End stage chronic kidney disease treatment. Stages of acute and chronic renal failure and features of their course

Modern methods of treating chronic renal failure
Modern methods of treating chronic renal failure

CHRONIC RENAL FAILURE

Until recently, chronic renal failure (CRF) was defined as a clinical and biochemical syndrome that occurs with kidney damage of any etiology, caused by a gradually progressive loss of excretory and endocrine functions of the organ due to the irreversible loss of functioning nephrons.
In this case, unlike acute renal failure, the pathophysiological processes are irreversible, which lead to these disorders. Their development only partially depends on the etiology of the underlying renal disease, since the leading pathogenetic mechanisms of damage to functioning nephrons in this situation are intraglomerular hypertension, hyperfiltration in the glomerulus and the nephrotoxic effect of proteinuria (more precisely, disorders of renal protein transport).
The discovery of the unity of the mechanisms of pathogenesis of kidney tissue damage in chronic diseases of this organ was one of the important factors that led to the creation of a fundamentally new concept - chronic kidney disease (CKD).
Reasons for the emergence of the concept of CKD.
Currently, there is a dramatic increase in the number of patients with chronic renal pathology.
This is primarily determined by the increase in the incidence of diabetes mellitus, the aging of the population and, accordingly, the increase in the number of patients with kidney damage of a vascular nature.

The progressive increase in the number of such patients is regarded as a pandemic. The above factors have led to a catastrophic increase in the number of people who require renal replacement therapy (RRT) - various types of dialysis or kidney transplantation.
The long-standing approach to secondary prevention of end-stage renal disease (ESRD) has also contributed to the increase in the number of patients on RRT.

When a certain degree of decline in renal function was achieved, it was not considered necessary to resort to any special methods to slow the progression of the pathological process in the renal tissue.
In addition, over the past decades, the quality of RRT technologies has continuously improved, which has caused a sharp increase in life expectancy for patients receiving such treatments.

All this has led to an increased need for dialysis beds, organ transplants and rising costs.
Already in the sixties of the last century, it became clear that many mechanisms of progression of chronic kidney diseases are quite universal and largely operate regardless of etiology. Equally important was the identification of risk factors for the development and progression of a chronic pathological process in renal tissue.
Like the mechanisms of progression, they turned out to be basically the same in various chronic kidney diseases and quite similar to cardiovascular risk factors.

Clarification of the pathogenetic mechanisms of progression of chronic kidney diseases, identification of risk factors for their occurrence and development has made it possible to develop well-founded treatment regimens that can actually delay the onset of RRT or reduce the number of lethal complications.
Approaches to renoprotection for different kidney diseases turned out to be basically identical (angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor antagonists, non-dihydropyridine calcium channel blockers, low-protein diet).
All of the above required rethinking, primarily to develop effective measures to further improve medical and social care for patients with chronic kidney disease.
One of the prerequisites for this should be unity or at least similarity of criteria for identifying, describing, assessing the severity and rate of progression of renal pathology.
However, there was no such unity among nephrologists. For example, in the English-language literature one could find about one and a half dozen terms used to designate conditions associated with the appearance of chronic renal dysfunction.

It should be noted that in domestic nephrology the terminological problem was less acute. The phrase “chronic renal failure” (CRF) or, in appropriate cases, “end-stage renal failure”, “end-stage chronic renal failure”, etc. was usually used.
However, there was no common understanding of the criteria for chronic renal failure and assessment of its severity.

Obviously, the adoption of the concept of CKD should sharply limit the use of the term “chronic renal failure”.

In the NKF classification, the phrase “renal failure” remains only as a synonym for stage V. CKD.
At the same time, in the English-language nephrological literature, the name “end-stage renal disease” has become widespread.
The developers at NKF thought it would be appropriate to retain the use of this term since it is widely used in the United States and refers to patients who are receiving therapy various methods dialysis or transplantation, regardless of the level of kidney function.
Apparently, in domestic nephrological practice it is worth preserving the concept of “end-stage renal failure”. It is advisable to include patients both already receiving RRT and patients with stage V CKD who replacement treatment has not yet started or is not being carried out due to organizational problems.
Definition and classification of CKD.
A number of issues briefly mentioned above have been addressed by the National Kidney Foundation (NKF). The Foundation created a group of experts who, as a result of analyzing many publications on diagnostics and treatment, assessing the significance of a number of indicators in determining the rate of progression of kidney diseases, terminological concepts and agreements with administration representatives, proposed the concept of chronic kidney disease (CKD). ).

When developing the concept of CKD, the experts of the NKF working group pursued several goals: Definition of the concept of CKD and its stages, regardless of the cause (etiology) of renal failure (disease).
Selection of laboratory parameters (research methods) that adequately characterize the course of CKD.
Determination (study) of the relationship between the degree of renal dysfunction and complications of CKD.
Stratification of risk factors for the progression of CKD and the occurrence of cardiovascular diseases.

NKF experts proposed a definition of CKD, which is based on a number of criteria:
Kidney damage lasting > 3 months, which manifests itself as structural or functional impairment of the organ with or without a decrease in GFR.
These damages are manifested either by pathomorphological changes in the renal tissue, or by changes in the composition of the blood or urine, as well as changes when using methods of visualization of the structure of the kidneys GFR< 60 мл/мин/1,73 м2 в течение трех и более месяцев, при наличии или отсутствии других признаков повреждения почек.
In other words, chronic kidney disease can be defined as “the presence of kidney damage or decreased levels of kidney function for three months or more, regardless of diagnosis.”

NKF experts have identified five stages of CKD depending on the severity of the decrease in GFR

Let us again draw attention to a very important point.
In the classification, risk factors for the development and progression of CKD are highlighted in a separate line.
One of the most important among them is systemic arterial hypertension or proteinuria.
It should be borne in mind that, according to the conclusion of NKF experts, the presence of risk factors alone does not provide grounds for making a diagnosis of CKD, but requires a certain set of preventive measures).

The concept of CKD, which is not directly related to a nosological diagnosis, does not negate the nosological approach to the diagnosis of a specific kidney disease.
However, it is not a purely mechanical combination of chronic kidney damage of various natures.
As noted earlier, the development of this concept is based on the unity of the leading pathogenetic mechanisms of progression of the pathological process in renal tissue, the commonality of many risk factors for the development and progression of kidney diseases and the resulting similarity in methods of therapy, primary and secondary prevention.

In this sense, CKD is close to the concept of coronary heart disease (CHD).
The term CKD, as soon as it appeared, won citizenship rights not only in the United States, but also in many other countries.
The VI Congress of the Scientific Society of Nephrologists of Russia, held on November 14-17, 2005 in Moscow, clearly supported the need for widespread introduction of the concept of CKD into the practice of domestic healthcare.

General clinical manifestations of late stages of CKD.
Signs associated with the development of renal dysfunction and little dependent on the underlying pathological process in the kidneys usually begin to appear at the third stage of CKD and reach maximum severity by the fifth. At first, moderate polyuria, nocturia, decreased appetite, and a tendency to anemia are usually recorded.

A drop in GFR below 30% of the normal level leads to the appearance of symptoms of uremic intoxication, an increase in hyporegenerative anemia (due to a decrease in erythropoietin production), disturbances in phosphorus-calcium metabolism and the formation of symptoms of secondary hyperparathyroidism (due to a decrease in the intrarenal synthesis of the active metabolite of vitamin D-1, 25(OH)2D3; synonyms: 1,25-dihydroxy-cholecalciferol, calcitriol, D-hormone, etc.), metabolic acidosis (due to a decrease in renal excretion of hydrogen ions and suppression of bicarbonate ion reabsorption).

Compensation for metabolic acidosis is carried out by the lungs by increasing alveolar ventilation, which leads to the appearance of deep, noisy breathing. Secondary hyperparathyroidism, along with acidosis, leads to the development of osteodystrophy, which can manifest itself as pathological fractures. In addition, disturbances in calcium-phosphorus homeostasis often cause the appearance of extraosseous calcifications, including vascular calcification. Secondary hyperparathyroidism, skeletal damage, and soft tissue calcification are most severe in patients receiving RRT and represent a very serious clinical problem in these patients.
As CKD progresses, patients develop hemocoagulation disorders, which is accompanied by easy education they have subcutaneous hematomas and an increased risk of bleeding, including gastrointestinal bleeding.

Dry skin (“brights don’t sweat”) is typical; many patients experience painful itchy skin, leading to scratching.
The initial polyuria may be replaced by oliguria, leading to overhydration and edema internal organs, including pulmonary and cerebral edema.
IN late stages CKD can develop uremic polyserositis, in particular uremic pericarditis, which is a poor prognostic sign and requires immediate initiation of RRT.

Sometimes the so-called "terminal nephrotic syndrome".
General cerebral symptoms gradually increase: lethargy, drowsiness, apathy, and sometimes sleep rhythm disturbances.
Almost all patients are characterized by uremic dyslipoproteinemia, leading to acceleration of atherogenesis processes and increased cardiovascular risks.

Diagnostics. Provided early detection of the underlying renal pathological process (GN, secondary nephropathies, diabetic nephropathy, etc.) and follow-up of the patient, diagnosis usually does not cause difficulties. To monitor renal function in practical work, the level of plasma creatinine and GFR are monitored over time.
Some diagnostic difficulties may arise when managing patients in whom azotemia is detected for the first time. In these cases, the issue of distinguishing between acute and chronic renal failure may become relevant.

Now a little mathematics, which, unfortunately, cannot be done without in this section.
Speed ​​estimation problem glomerular filtration in practical medicine. Glomerular ultrafiltration is the initial and main mechanism of urine formation.
The way the kidneys perform all their diverse functions depends decisively on its condition.
It is not surprising that members of the NKF working group chose glomerular filtration rate (GFR) not only as the main criterion for distinguishing specific stages of CKD, but also as one of the most important basis for making a diagnosis of chronic kidney disease. The developers of the National Kidney Foundation have convincingly shown that the degree of decline in GFR is very closely associated with other clinical or metabolic changes that occur as chronic nephropathies progress.

It is clear that the introduction of the concept of CKD requires the availability of a reliable, simple and inexpensive method of measuring GFR in clinical practice.

To date, a very large number of methods and their modifications have been developed that make it possible to estimate GFR with varying degrees of accuracy. However, their use in widespread clinical practice is limited by complexity and high cost.
Therefore, they are usually used for specific research purposes.

Throughout the world in practical medicine, the main estimates of GFR until recently remained the serum creatinine concentration (Cgr) or endogenous creatinine clearance (Ccreatinine clearance).
Both of these methods have a number of significant disadvantages. Serum creatinine concentration as an index of GFR.

Creatinine is a low molecular weight product of nitrogen metabolism.
It is mainly excreted by the kidneys by glomerular filtration, although some is secreted in the proximal tubules. In streets with unimpaired filtration capacity, the proportion of creatinine secreted by the tubules is small. However, the contribution of tubular secretion to the distortion of estimates of glomerular filtration rate may increase sharply with a decrease in renal function.

The process of creatinine formation in healthy people occurs at an almost constant rate.
This determines the relative stability of Cgr.
Despite the relative stability of creatinine production, there are a significant number of reasons, including those not directly related to the functional state of the kidneys, that can affect the level of Cgr. The main determinant of serum creatinine levels.
apparently, is the volume of muscle mass, since the production of this metabolite is proportional to this volume.
An important factor influencing serum creatinine levels is age.
GFR in adults declines progressively after age 40.
Decreased creatinine generation caused by age naturally increases GFR levels. Sgr in women is usually slightly lower than in men. The main significance in the appearance of these differences, apparently, is also associated with lower muscle mass in females.
Thus, clinical assessment of GFR based on serum creatinine levels cannot be carried out without taking into account anthropometric, gender and age characteristics patient.

Under conditions of pathology, including kidney pathology, all factors that determine the level of serum creatinine can be modified to one degree or another.
The available information does not make it possible to come to a final conclusion about whether creatinine formation is increased, unchanged, or decreased in patients with chronic kidney disease.

However, when GFR decreases to 25-50 ml/min, patients usually spontaneously reduce protein intake (nausea, vomiting, anorexia).
Serum creatinine levels can be affected by various medications.
Some of them (amnoglycosides, cyclosporine A, platinum preparations, X-ray contrast agents, etc.) are nephrotoxic drugs, when prescribed, an increase in Cg reflects a real decrease in GFR.
Others are capable of undergoing the Jaffe reaction.
Finally, some drugs selectively block proximal tubular creatinine secretion without any significant effect on GFR.
Cimetidine, trimethoprim and, possibly, to some extent phenacetamide, salicylates and vitamin D3 derivatives have this property.

The determined value of creatinine concentration in blood serum depends quite significantly on the analytical methods used to measure this indicator. Until now, the level of creatinine in biological fluids is most often assessed using the Jaffe reaction.
The main disadvantage of this reaction is its low specificity.
This reaction can involve, for example, ketones and keto acids, ascorbic and uric acids, some proteins, bilirubin, etc. (“non-creatinine chromogens”). The same applies to some cephalosporins, diuretics, if they are prescribed in high doses, phenacetamide, acetohexamide and methyldopa (when administered parenterally). With normal serum creatinine values, the contribution of non-creatinine chromogens to its total concentration can range from 5 to 20%.

As kidney function declines, serum creatinine concentrations naturally rise.
But this increase is not accompanied by a proportional increase in the level of non-creatinine chromogens.
Therefore, their relative contribution to the concentration of total chromogen (creatinine) in the serum decreases and usually in this situation does not exceed 5%. In any case, it is clear that creatinine levels measured using the Jaffe reaction will underestimate the true GFR values.
Rapid changes in the latter parameter also lead to disruptions in the clarity of the inverse relationship between the concentration of serum creatinine and GFR.
In relation to them, the increase or decrease in Cgr may be delayed by several days.
Therefore, special care must be taken when using Cgr as a measure of renal function during the development and resolution of acute renal failure.
Use of creatinine clearance as a quantitative measure of GFR. The use of SSG compared to Sgr provides one significant advantage.
It allows you to obtain an estimate of the glomerular filtration rate, expressed as a numerical value with a dimension corresponding to the nature of the process (usually ml/min).

However, this method of assessing GFR does not resolve many issues.
Obviously, the accuracy of the measurement of CVg largely depends on the correctness of urine collection.
Unfortunately, in practice, the conditions for determining the volume of diuresis are often violated, which can lead to either overestimation or underestimation of Cg values.
There are also categories of patients in whom quantitative urine collection is almost impossible.
Finally, when assessing the value of GFR, the amount of tubular secretion of creatinine is of great importance.
As noted above, in healthy people the proportion of this compound secreted by the tubules is relatively small. However, under conditions of kidney pathology, the secretory activity of proximal tubular epithelial cells in relation to creatinine can sharply increase.

However, in a number of individuals, including those with a significant decrease in GFR, creatinine secretion may even have negative values. This suggests that they actually have tubular reabsorption of this metabolite.
Unfortunately, it is impossible to predict the contribution of tubular secretion/reabsorption of creatinine to the error in determining GFR based on CFR in a particular patient without measuring GFR using reference methods. “Calculation” methods for determining GFR.

The very fact of the presence of an inverse, although not direct, relationship between Cgr and GFR suggests the possibility of obtaining an estimate of the glomerular filtration rate in quantitative terms based only on the concentration of serum creatinine.

Many equations have been developed to predict GFR values ​​based on Cgr.
However, in real practice In “adult” nephrology, the Cockcroft-Gault and MDRD formulas are most widely used.

Based on the results of the multicenter study MDRD (Modified of Diet in Renal Disease), a series of empirical formulas were developed that make it possible to predict GFR values ​​based on a number of simple indicators. The best agreement between the calculated GFR values ​​and the true values ​​of this parameter, measured by the clearance of 125I-iothalamate, was shown by the seventh version of the equations:

However, it should be borne in mind that there are situations where “calculated” methods for determining GFR are unacceptable.

In such cases, at least a standard creatinine clearance measurement should be used.
Situations in which it is necessary to use clearance methods for determining GFR: Very old age. Non-standard body sizes (patients with limb amputations). Severe emaciation and obesity. Diseases of skeletal muscles. Paraplegia and quadriplegia. Vegetarian diet. Rapid decline in kidney function.
Before prescribing nephrotoxic drugs.
When deciding whether to start renal replacement therapy.
It must also be remembered that the Cockcroft-Gault and MDRD formulas are not applicable in children.

Cases of acute deterioration of renal function in patients with pre-existing chronic kidney pathology, the so-called “acute on chronic renal failure”, or, in the terminology of foreign authors, “acute on chronic renal failure” deserve special attention.
From a practical point of view, it is important to emphasize that timely elimination or prevention of factors leading to acute impairment of kidney function in patients with CKD can slow the rate of progression of deterioration of organ function.

The causes of acute renal dysfunction in patients with CKD may be: dehydration (limited fluid intake, uncontrolled use of diuretics); CH; uncontrolled hypertension; the use of ACE inhibitors in patients with bilateral renal artery stenosis; obstruction and/or urinary tract infection; systemic infections (sepsis, bacterial endocarditis, etc.); nephrotoxic drugs: NSAIDs, antibiotics (aminoglycosides, rifampicin, etc.), thiazides, radiocontrast agents.
It should also be mentioned that patients with CKD are especially sensitive to any potentially nephrotoxic factors, and therefore the problems of iatrogenicity and self-medication (herbs, sauna, etc.) in these cases should be given Special attention.

Another important indicator of the rate of progression of CKD is proteinuria.
In an outpatient setting, to assess it, it is recommended to calculate the protein/creatinine ratio in the morning urine, which is almost equivalent to measuring daily protein excretion.
An increase in daily proteinuria always means an acceleration in the rate of progression of CKD.

Treatment. Dietary recommendations.
The basic principles of the diet for CKD come down to the following recommendations:
1. Moderate limitation of NaCl consumption depending on the level of blood pressure, diuresis and fluid retention in the body.
2. The maximum possible fluid intake depending on diuresis, under the control of body weight.
3. Limiting protein intake (low-protein diet).
4. Limit foods rich in phosphorus and/or potassium.
5. Maintaining the energy value of the diet at the level of 35 kcal/kg body weight/day.
Taking into account the fact that as tubulointerstitial sclerosis develops, the ability of the kidneys to reabsorb Na may decrease, in some cases the salt regime must be expanded to 8 or even 10 g of salt per day. This is especially true for patients with the so-called “salt-losing kidney.”
In any situation, it is necessary to take into account the concomitant use of diuretics and their dose.
In a number of patients taking loop diuretics in large doses (over 80-100 mg/day of furosemide), restrictions on the consumption of table salt with food are not required.
The most adequate method of monitoring NaCl intake is daily urinary Na excretion.
A healthy person excretes at least 600 milliosmoles (mosm) of osmotically active substances (OAS) per day.
Intact kidneys are capable of significantly concentrating urine, and the total concentration of OAS (osmolality) in urine can be more than four times higher than the osmolality of blood plasma (1200 or more and 285-295 mOsm/kg H2O, respectively).
The kidneys cannot eliminate OAS (mainly urea and salts) without excreting water.
Therefore, a healthy individual is theoretically capable of excreting 600 mol in 0.5 liters of urine.

With the progression of CKD, the concentrating ability of the kidneys steadily decreases, the osmolality of urine approaches the osmolality of blood plasma and amounts to 300-400 mOsm/kg H20 (isosthenuria).

Since in the advanced stages of CKD the total excretion of OAV does not change, it is easy to calculate that to excrete the same 600 my OAV, the volume of diuresis should be 1.5-2 l/day.
This makes it clear that polyuria and nocturia appear; ultimately, limiting fluid intake in such patients accelerates the progression of CKD.

However, it should also be taken into account that with CKD stages III-V. The ability to excrete osmotically free water is gradually impaired, especially if the patient takes diuretics.
Therefore, fluid overload is fraught with the development of symptomatic hyponatremia.

Guided by the above principles, it is permissible to allow patients a free water regime, taking into account self-monitoring of daily diuresis, adjusted for extrarenal fluid losses (300-500 ml/day). Regular monitoring of body weight, blood pressure, clinical signs of overhydration, determination of daily Na excretion in urine and periodic testing of Na levels in the blood (hyponatremia!) are also necessary.

For many decades, in practical nephrology there has been a recommendation to limit the intake of proteins with food, which is based on a number of theoretical premises.
However, only recently has it been proven that a low protein diet (LPD) reduces the rate of progression of CKD.

Adaptive mechanisms of MBD in patients with CKD include: improvement of intraglomerular hemodynamics; limiting hypertrophy of the kidneys and glomeruli; positive effect on dyslipoproteinemia, effect on renal metabolism, limitation of O2 consumption by renal tissue; reduction in oxidant production; effects on T cell function; suppression of AN and transforming growth factor b, limiting the development of acidosis.
MBD is usually prescribed to patients starting from stage III. CKD.
At II st. A diet with a protein content of 0.8 g/kg body weight/day is advisable.

The standard MBD involves limiting protein intake to 0.6 g/kg/day.
In order to enrich the diet with essential amino acids, a low-protein diet can be prescribed with supplements.
Low protein diet options:
- standard MBD - protein 0.6 g/kg/day (again, regular food);
- MBD, supplemented with a mixture of essential amino acids and their keto analogues (preparation “Ketosteril”, Fresenius Kabi, Germany); food protein 0.4 g/kg/day + 0.2 g/kg/day ketosteril;
- MBD supplemented with soy proteins, protein 0.4 g/kg/day + 0.2 g/kg/day soy isolate, for example “Supro-760” (USA).

As mentioned above, when using MBD it is very important to maintain normal energy value diet due to carbohydrates and fats at a level of 35 kcal/kg/day, since otherwise the body’s own proteins will be used as energy material.
In practical work, the issue of monitoring patient compliance with the MBD is essential.

The amount of protein consumed per day can be determined based on the concentration of urea in the urine and knowing the amount of daily diuresis using the modified Maroni formula:
PB = 6.25 x EMM + (0.031 x BMI) + *SP x 1.25
where PB is protein consumption, g/day,
EMM - urea excretion in urine, g/day,
BMI - ideal body weight (height, cm - 100),
*SP - daily proteinuria, g/day (this term is entered into the equation if SP exceeds 5.0 g/day).
In this case, the daily excretion of urea can be calculated based on the volume of daily urine and the concentration of urea in the urine, which in the practice of Russian clinical laboratory diagnostics is usually determined in mmol/l:
EMM = Uur x D/2.14
where Uur is the concentration of urea in daily urine, mmol/l;
D - daily diuresis, l.

Renoprotection.
In modern nephrology, the principle of renoprotection has clearly been formed, which consists in carrying out a set of therapeutic measures in patients with kidney disease, aimed at slowing the rate of progression of CKD.

The complex of treatment measures is carried out in three stages, depending on the degree of renal dysfunction:
Stage I - nitrogen excretion function of the kidneys is preserved (CKD stages I-II), a decrease in functional reserve may be noted (no increase in GFR by 20-30% in response to a protein load).
Stage II - kidney function is moderately reduced (CKD stage III).
Stage III - kidney function is significantly reduced (CKD stage IV - beginning of stage V CKD).

Stage 1:
1. Adequate therapy for the underlying renal disease in accordance with the principles of evidence-based medicine (evaluation indicator - reduction of daily proteinuria below 2 g/day).
2. In diabetes, intensive control of glycemia and the level of glycosylated hemoglobin (evaluation indicator - control of microalbuminuria).
3. Adequate control of blood pressure and proteinuria using ACE inhibitors, ATj receptor antagonists to AII, or a combination thereof.
4. Timely and adequate treatment complications: heart failure, infections, urinary tract obstruction.
5. Exclusion of iatrogenic causes: medications, Rg-contrast studies, nephrotoxins.
6. Normalization of body weight with a mass index >27 kg/m2.
Successful pathogenetic therapy of the underlying renal disease is of paramount importance in preventing the formation of glomerulo- and tubulointerstitial sclerosis, and, consequently, in slowing the rate of progression of CKD.
In this case, we are talking not only about the treatment of newly diagnosed pathology, but also about the elimination of exacerbations.
The activity of the main inflammatory process (or its relapses) involves the activation of humoral and tissue immune reactions, naturally leading to the development of sclerosis.
In other words, the more pronounced the activity of the inflammatory process and the more often its exacerbations are noted, the faster sclerosis forms.
This statement is in full agreement with the traditional logic of the clinician and has been repeatedly confirmed by clinical studies.
In glomerular diseases, hypertension is usually formed long before the decline in renal function and contributes to their progression.
In parenchymal diseases, the tone of preglomerular arterioles is reduced and the system of their autonomous autoregulation is disrupted.
As a result, systemic hypertension leads to an increase in intraglomerular pressure and contributes to damage to the capillary bed.

When choosing antihypertensive drugs, it is necessary to proceed from the main three pathogenetic mechanisms of parenchymal renal hypertension; Na retention in the body with a tendency to hypervolemia; increased RAS activity; increased sympathetic activity nervous system due to increased afferent impulses from the affected kidney.

For any renal pathology, including diabetic nephropathy, if the creatinine level is normal and the GFR is more than 90 ml/min, it is necessary to achieve a blood pressure level of 130/85 mm Hg. Art.
If daily proteinuria exceeds 1 g/day, it is recommended to maintain blood pressure at 125/75 mm Hg. Art.
Considering modern data that nocturnal hypertension is the most unfavorable from the point of view of kidney damage, it is advisable to prescribe antihypertensive drugs taking into account these data daily monitoring blood pressure and, if necessary, reschedule their administration to the evening hours.

The main groups of antihypertensive drugs used for nephrogenic hypertension:
1. Diuretics (for GFR< 70мл/мин - преимущественно петлевые диуретики). 2. Ингибиторы АПФ и антагонисты АТ1 рецепторов к АII.
3. Non-dihydropyridine calcium channel blockers (diltiazem, verapamil).
4. Dihydropyridine CCBs are exclusively long-acting.
5. b-blockers.
Medicines are listed in descending order of recommended frequency of use.
Any antihypertensive therapy for parenchymal renal disease should begin with the normalization of Na metabolism in the body.
In kidney diseases, there is a tendency to Na retention, which is higher, the higher the proteinuria.
At least in experimental studies, the direct damaging effect of sodium contained in the diet on the glomeruli, regardless of blood pressure levels, has been proven.
In addition, sodium ions increase the sensitivity of smooth muscles to the action of AII.

The average dietary salt intake for a healthy person is approximately 15 g/day, so the first recommendation for patients with kidney disease is to limit salt intake to 3-5 g/day (an exception may be tubulointerstitial kidney damage - see above).
In an outpatient setting, a measure to monitor patient compliance with prescribed recommendations is to monitor urinary sodium excretion per day.
In cases where there is hypervolemia or the patient is not able to follow a hyposodium diet, diuretics are the first-line drugs.
If renal function is preserved (GFR > 90 ml/min), thiazides can be used; if GFR decreases< 70мл/мин назначаются петлевые диуретики (допустима комбинация петлевых диуретиков с тиазидами).
Potassium-sparing diuretics are absolutely contraindicated.

During treatment with diuretics, careful dose monitoring is necessary to prevent the development of hypovolemia. Otherwise, kidney function may acutely deteriorate - “ACF on chronic renal failure.”

Drug renoprotection.
Currently, many prospective placebo-controlled studies have proven the renoprotective effect of ACE inhibitors and AT1 receptor antagonists, which is associated with both hemodynamic and non-hemodynamic mechanisms of action of AN.

Strategy for using ACE inhibitors and/or AT1 antagonists for the purpose of nephroprotection:
- ACE inhibitors should be prescribed to all patients early stages development of any nephropathies with SPB > 0.5-1 g/day, regardless of blood pressure level.
ACE inhibitors have renoprotective properties even at low plasma renin levels;
- the clinical predictor of the effectiveness of the renoprotective effect of drugs is partial (SPB< 2,5 г/сут) или полная (СПБ < 0,5 г/сут) ремиссия протеинурии через несколько недель или месяцев после начала приема медикаментов.
When treating with ACE inhibitors, a dose-dependence phenomenon is observed: the higher the dose, the more pronounced the antiproteinuric effect;
- ACE inhibitors and AT1 receptor antagonists have a renoprotective effect regardless of the systemic hypotensive effect.
However, if the blood pressure level does not reach the optimal level during their use, it is necessary to add antihypertensive drugs of other pharmacological groups. If you are overweight (body mass index > 27 kg/m2), it is necessary to achieve weight loss, which enhances the antiproteinuric effect of the drugs;
- if the antiproteinuric effect of any drug from one of the groups (ACE inhibitors or AT1 antagonists) is insufficient, a combination of them can be used.

The third-line drugs are non-dihydropyridine CCBs (diltiazem, verapamil). Their antiproteinuric and renoprotective effects have been proven in diabetic and non-diabetic nephropathies.
However, they can only be considered as an addition to basic therapy with ACE inhibitors or AT1 antagonists.

Less effective, from the point of view of nephroprotection, is the use of dihydropyridine CCBs.
This is associated with the ability of these drugs to dilate the glomerular afferent arterioles.
Therefore, even with a satisfactory systemic hypotensive effect, conditions are created that promote intraglomerular hypertension and, consequently, the progression of CKD.
In addition, short-acting dihydropyridine CCBs activate the sympathetic nervous system, which in itself has a damaging effect on the kidney.
The negative effect of non-extended dosage forms of nifedipine on the course of diabetic nephropathy has been proven.
Therefore, the use of this drug in DN is contraindicated.
On the other hand, in recent years, data have emerged indicating the effectiveness of the renoprotective properties of a combination of ACE inhibitors and long-acting dihydropyridine CCBs.

Today, b-blockers occupy the last place as renoprotective drugs.
However, in connection with recent experimental studies that have proven the role of activation of the sympathetic nervous system in the progression of chronic nephropathy, the view on the validity of their use in nephrogenic hypertension should be reconsidered.

Stage II(patient with any renal pathology and GFR 59-25 ml/min).
The treatment plan at this stage includes:
1. Dietary measures.
2. Use of loop diuretics to control hypertension and hypervolemia.
3. Antihypertensive therapy, taking into account possible side effects of ACE inhibitors. If the blood plasma creatinine level is 0.45-0.5 mmol/l, do not use ACE inhibitors in high doses.
4. Correction of phosphorus-calcium metabolism disorders.
5. Early correction of anemia using erythropoietin.
6. Correction of dyslipoproteinemia.
7. Correction of metabolic acidosis. When GFR decreases below 60 ml/min (CKD stage III), all drug therapy is carried out against the background of a low-protein diet.
In order to avoid the occurrence of hypo- or hypervolemia, a more strict regimen regarding sodium and fluid intake is necessary.
Only loop diuretics are used as diuretics. Sometimes their combination with thiazides is acceptable, but the use of thiazide diuretics alone is not recommended.
It is necessary to take into account the possibility of side effects from the use of ACE inhibitors with a GFR of 59-30 ml/min, namely: deterioration of renal excretory function, which is explained by a decrease in intraglomerular pressure; hyperkalemia, anemia.
At a plasma creatinine level of 0.45-0.5 mmol/l, ACE inhibitors are not first-line drugs and are used with caution.
A combination of long-acting dihydropyridine CCBs and loop diuretics is more preferable.
When GFR is below 60 ml/min, treatment for disorders of phosphorus-calcium metabolism, anemia, dyslipoproteinemia, and acidosis begins. A low-protein diet with limited dairy products helps reduce the total amount of inorganic calcium entering the body. In addition, in CKD, the adaptive capacity of the intestine to increase calcium absorption is impaired (due to 1,25(OH)2D3 deficiency).
All these factors predispose patients to the development of hypocalcemia.
If a patient with CKD has hypocalcemia with a normal level of total blood plasma protein, it is recommended to use 1 g of pure kalysh per day exclusively in the form of calcium carbonate to correct the blood calcium level.
This type of therapy requires monitoring calcium levels in the blood and urine. Hyperphosphatemia in patients with chronic renal failure contributes to the occurrence of calcifications of soft tissues, blood vessels (aorta, aortic valve) and internal organs. It is usually recorded when GFR decreases below 30 ml/min.

A low-protein diet usually involves restricting the intake of dairy products, and therefore the intake of inorganic phosphorus into the patient’s body is reduced.
However, it should be taken into account that prolonged and significant restriction of protein intake can lead to negative protein catabolism and exhaustion.
In these cases, it is recommended to add complete proteins to the diet with the simultaneous administration of drugs that interfere with the absorption of phosphates in the intestine.

The most well-known and widely used in practice at present are calcium carbonate and calcium acetate, which form insoluble phosphate salts in the intestine.
The advantage of these drugs is the additional enrichment of the body with calcium, which is especially important for concomitant hypocalcemia. Calcium acetate is distinguished by greater phosphate-binding capacity and less release of calcium ions.

Calcium preparations (acetate and carbonate) should be taken with food, doses are selected individually and on average range from 2 to 6 g/day.
Currently, aluminum hydroxides are not used as phosphate binders due to the potential toxicity of the latter in patients with CKD.

Several years ago, phosphate binding agents that did not contain aluminum or calcium ions appeared abroad - the drug Renagel (sevelamer hydrochloride 400-500 mg).
The drug has high phosphate-binding activity; no side effects are observed with its use, but it is not registered in the Russian Federation.

In patients with CKD due to impaired endocrine renal function, there is a deficiency of the active form of vitamin D.
The substrate for the active form of vitamin D3 is 25(OH)D3 - 25-hydroxycholecalciferol, which is formed in the liver.
Kidney disease itself usually does not affect 25(OH)D3 levels, but in cases of high proteinuria, cholecalciferol levels may be reduced due to loss from vitamin D-carrying proteins.
Reasons such as insufficient insolation and protein-energy deficiency should not be ignored.
If the level of 25(OH)D3 in the blood plasma of patients with chronic renal failure is below 50 nmol/l, then patients require cholecalciferol replacement therapy.
In cases where high concentrations of parathyroid hormone (more than 200 pg/ml) are observed with normal concentrations of cholecalciferol, the use of drugs 1,25(OH)2D3 (calcitriol) or 1a(OH)D3 (alpha-calicidiol) is necessary.
The last group of drugs is metabolized in the liver to 1.25(OH)203. Low doses are usually used - 0.125-0.25 mcg based on 1,25-dihydroxycholecalciferol. This treatment regimen prevents a rise in the level of parathyroid hormone in the blood, but the extent to which it can prevent the development of hyperplasia of the parathyroid glands has not yet been clarified.

Correction of anemia
Anemia is one of the most characteristic signs of CKD.
It usually forms when GFR decreases to 30 ml/min.
The leading pathogenetic factor of anemia in this situation is an absolute or, more often, relative deficiency of erythropoietin.
However, if anemia develops in the early stages of CKD, factors such as iron deficiency (low plasma ferritin levels), blood loss in the gastrointestinal tract due to the development of erosive uremic gastroenteropathy (the most common cause), protein-energy deficiency (as a consequence) should be taken into account in its genesis inadequate low-protein diet or due to dietary self-restraints of the patient in the presence of severe dyspeptic disorders), lack folic acid(rare cause), manifestations of the underlying pathology (SLE, myeloma, etc.).

Secondary causes of anemia in CKD must be excluded whenever low hemoglobin values ​​(7-8 g/dL) are recorded in patients with GFR above 40 ml/min. In all cases, basic therapy with iron supplements (oral or intravenous) is recommended.
Currently, a common point of view has emerged among nephrologists regarding the early initiation of erythropoietin therapy for anemia.
Firstly, in experimental and some clinical studies Evidence has been obtained that correction of anemia in CKD using erythropoietin slows the rate of progression of PN.
Secondly, early use of erythropoietin inhibits the progression of LVH, which is an independent risk factor for sudden death in chronic renal failure (especially subsequently in patients on RRT).

Treatment of anemia begins with a dose of erythropoietin 1000 units subcutaneously once a week; It is first recommended to restore iron reserves in the body (see).
The effect should be expected within 6-8 weeks from the start of treatment.
Hemoglobin levels should be maintained between 10-11 g/dL. Failure to respond to treatment usually indicates iron deficiency or intercurrent infection.
Even with a slight improvement in red blood counts, patients, as a rule, significantly improve their overall health: appetite, physical and mental performance increase.
During this period, some caution should be exercised in the management of patients, since patients independently expand their diet and are less serious about maintaining the water and electrolyte regime (overhydration, hyperkalemia).

Among the side effects of treatment with erythropoietin, a possible increase in blood pressure should be noted, which requires increased antihypertensive therapy.
Currently, when using small doses of erythropoietin subcutaneously, hypertension rarely acquires a malignant course.

Correction of dyslipoproteinemia
Uremic dyslipoproteinemia (DLP) begins to form when GFR decreases below 50 ml/min.
Its main cause is a violation of the processes of VLDL catabolism. As a result, the concentration of VLDL and intermediate-density lipoproteins in the blood increases, and the concentration of the antiatherogenic fraction of lipoproteins - high-density lipoproteins (HDL) - decreases.
In practical work, to diagnose uremic DLP, it is enough to determine the levels of cholesterol, triglycerides, and a-cholesterol in the blood. Characteristics disorders of lipid metabolism in CKD will be: normal or moderate hypercholesterolemia, hypertriglyceridemia and hypo-a-cholesterolemia.

Currently, there is an increasingly clear trend towards lipid-lowering therapy in patients with CKD.
This is explained by two reasons.
Firstly, lipid metabolism disorders in chronic renal failure are potentially atherogenic. And if we take into account that in CKD there are also other risk factors for the accelerated development of atherosclerosis (hypertension, impaired carbohydrate tolerance, LVH, endothelial dysfunction), the high mortality rate of patients with PN from cardiovascular diseases (including patients on hemodialysis) becomes understandable.
Secondly, DLP accelerates the rate of progression of renal failure in any renal pathology. Given the character lipid disorders(hypertriglyceridemia, hypo-a-cholesterolemia), theoretically, fibrates (gemfibrozil) should be the drugs of choice.
However, their use in PN is fraught with the development of serious side effects in the form of rhabdomyolysis, since the drugs are excreted by the kidneys. Therefore, it is recommended to take small doses (no more than 20 mt/day) of 3-hydroxy-3-methylglutaryl reductase inhibitors - coenzyme A - statins, which are metabolized exclusively in the liver.
Moreover, statins also have a moderate hypotriglyceridemic effect.
The question of how lipid-lowering therapy can prevent the accelerated formation (development) of atherosclerosis in chronic renal failure remains open to this day.

Correction of metabolic acidosis
In CKD, the renal excretion of hydrogen ions, which are formed in the body as a result of the metabolism of proteins and partly phospholipids, is impaired, and the excretion of bicarbonate ions is increased.
A low-protein diet helps maintain ABS, so pronounced symptoms of metabolic acidosis occur in the later stages of CKD or in cases of non-compliance with the diet.
Typically, patients tolerate metabolic acidosis well until bicarbonate levels fall below 15-17 mmol/L.
In these cases, it is recommended to restore the bicarbonate capacity of the blood by administering sodium bicarbonate orally (1-3 g/day), and in case of severe acidosis, administering a 4% sodium bicarbonate solution intravenously.

Patients subjectively tolerate mild degrees of acidosis easily, so it is optimal to manage patients at the level of base deficiency (BE - 6-8).
With long-term oral administration of sodium bicarbonate, strict control over sodium metabolism in the body is necessary (hypertension, hypervolemia, and increased daily sodium excretion in urine are possible).
With acidosis, the mineral composition is disrupted bone tissue(bone buffer), renal synthesis of 1,25(OH)2D3 is suppressed.
These factors may be important in the origin of renal osteodystrophy.

Stage III carrying out a complex of therapeutic measures in patients with CKD marks the immediate preparation of the patient for the start of renal replacement therapy.
NKF standards prescribe starting RRT when GFR is less than 15 ml/min, and in patients with diabetes it is advisable to start such treatment at higher levels of GFR, although the question of its optimal value in this situation is still a matter of debate.

Preparing patients to start RRT includes:
1. Psychological monitoring, training, information for relatives of patients, solving employment issues.
2. Formation of vascular access (during hemodialysis treatment) - an arteriovenous fistula with a GFR of 20 ml/min, and in patients with diabetes and/or with a poorly developed venous network - with a GFR of about 25 ml/min.
3. Vaccination against hepatitis B.

Naturally, the initiation of hemodialysis or peritoneal dialysis therapy is always a drama for patients and their family members.
In this regard, psychological preparation is of great importance for subsequent treatment results.
Clarification is needed regarding the principles of the upcoming treatment, its effectiveness in comparison with treatment methods in other areas of medicine (for example, in oncology), the possibility of a kidney transplant in the future, and so on.

From the standpoint of psychological training, group therapy and patient schools are rational.
The issue of employment of patients is significant, since many patients are able and willing to continue working.
Early creation of vascular access is preferable, since the formation of an arteriovenous fistula with satisfactory blood flow requires from 3 to 6 months.

According to modern requirements, vaccination against hepatitis B should be carried out before starting hemodialysis treatment.
Vaccines against the hepatitis B virus are usually administered three times, intramuscularly, with an interval of one month after the first administration, then six months after the start of vaccination (0-1-month schedule).
A faster immune response is achieved by administering the vaccine according to the 0-1-2 month schedule. The dose of HBsAg for an adult is 10-20 mcg per injection.
Post-vaccination AT persist for 5-7 years, but their concentration gradually decreases.
When the AT titer to the surface antigen of the hepatitis B virus decreases to a level of less than 10 IU/l, revaccination is necessary.

Kidney transplant
The most promising treatment method.
Kidney transplantation is a dramatic treatment.
In the long term, the patient is a healthy person if everything goes smoothly, if the kidney is transplanted according to all the rules.
In 1952, in Boston, at the transplant center, J. Murray and E. Thomas successfully transplanted a kidney from a twin, and 2 years later - from a corpse.
This success made the surgeons laureates Nobel Prize.
The same prize was awarded to A. Carrel for his work on transplantation.
The introduction of modern immunosuppressants into transplantation practice has ensured an exponential increase in the number of kidney transplants.
Today, kidney transplantation is the most common and most successful developing species internal organ transplants.
If in the 50s. While we were talking about saving patients with GN, kidneys are currently being successfully transplanted into patients with diabetic nephropathy, amyloidosis, etc.
To date, more than 500,000 kidney transplants have been performed worldwide.

Graft survival has reached unprecedented levels.
According to the United Network for Organ Allocation (UNOS) kidney registry, the 1-year and 5-year survival rates of cadaveric kidney transplants are 89.4% and 64.7%, respectively.
Similar figures for transplants from living donors are 94.5% and 78.4%.
The survival rate of patients at the same time with cadaveric transplants was 95% and 82% in 2000.
It is slightly higher in patients with kidneys transplanted from living donors - 98% and 91%.

The steady development of immunosuppression techniques has led to a significant increase in the half-life of transplants (almost 2 times).
This period is 14 and 22 years for cadaveric and living donor kidneys, respectively.
According to the Freiburg University Hospital, which summarized the results of 1086 kidney transplantations, 20 years after the operation, the survival rate of recipients was 84%, the graft functioned in 55% of those operated on.
The survival rate of grafts decreases noticeably, mainly in the first 4-6 years after surgery and especially significantly during the first year. After 6 years, the number of graft losses is negligible, so over the next 15 years the number of transplanted kidneys that maintain function remains almost unchanged.

The spread of this promising method of treating patients with end-stage CKD is hampered primarily by the shortage of donor kidneys.
A big problem in transplantation is the issue of providing donor organs.
Finding a donor is very difficult, since there are diseases that can prevent the donation of a kidney (tumors, infections, changes in the functional state of the kidneys).
It is mandatory to select a recipient based on blood type and histocompatibility antigens.
This achieves improved long-term functioning of the transplanted kidney.
This circumstance led to a significant increase in the waiting time for surgery.
Despite the high cost of immunosuppressive therapy in the postoperative period, kidney transplantation is more cost-effective than other methods of RRT.

In developed country settings, successful surgery can result in savings of approximately $100,000 over 5 years compared to a patient receiving dialysis treatment.
Despite the enormous successes of this treatment method, many issues still require further solutions.

A complex problem is the indications and contraindications for kidney transplantation.
When establishing indications for surgery, it is assumed that the course of chronic renal failure has many individual characteristics: the level of creatininemia, the rate of its increase, the effectiveness of other treatment methods, as well as complications of chronic renal failure.

A generally accepted indication for kidney transplantation is the condition of patients when the developing complications of chronic renal failure are still reversible.
Contraindications to kidney transplantation are: age over 75 years, severe pathology of the heart, blood vessels, lungs, liver, malignant neoplasms, active infection, active vasculitis or glomerulonephritis, severe degrees of obesity, primary oxalosis, uncorrectable pathology of the lower urinary tract with obstruction of urine outflow, drug or alcohol addiction, severe psychosocial problems.

Without dwelling on the purely technical details of the operation, we will say right away that the postoperative period occupies a special place in the problem of kidney transplantation, since at this time the future fate of the patient is determined.

The most important are immunosuppressive therapy, as well as the prevention and treatment of complications.
In terms of immunosuppressive therapy, the leading place belongs to “triple therapy” - GCS, cyclosporine-A (tacrolimus), mycophenolate mofetil (sirolimus).
To monitor the adequacy of immunosuppression when using cyclosporine-A and to monitor complications of treatment, the concentration of this drug in the blood should be monitored.
Starting from the 2nd month after transplantation, it is necessary to maintain the level of CSA in the blood within 100-200 μg/l.

In recent years in clinical practice The antibiotic rapamycin was included, which prevents the rejection of transplanted organs, including kidneys. Of interest is the fact that rapamycin reduces the likelihood of secondary narrowing of blood vessels after balloon angioplasty. Moreover, this medicine prevents the metastasis of certain cancerous tumors and suppresses their growth.

The results of new animal experiments at the American Mayo Clinic suggest that rapamycin increases the effectiveness of radiation treatment of malignant brain tumors.
These materials were presented by Dr. Sarkario and his colleagues in November 2002 to participants in an oncology symposium in Frankfurt.
In the early postoperative period, in addition to rejection crises, patients are threatened with infection, as well as necrosis and fistula of the bladder wall, bleeding, and the development of a steroid gastric ulcer.

In the late postoperative period there remains a danger infectious complications, development of graft artery stenosis, relapse of the underlying disease in the graft (GN).
One of current problems modern transplantology is to preserve the viability of the transplanted organ.
The chances of restoring graft function are sharply reduced if the period of renal ischemia exceeds 1 hour.
Preservation of a cadaveric kidney is achieved by non-perfusion preservation in a hypothermic solution resembling intracellular fluid.

Chronic renal failure never occurs “by itself” - this pathology is a complication of many kidney diseases. But if we talk about the symptoms of chronic renal failure, they will be absolutely the same, regardless of what caused the development of the pathology.

Causes of development of chronic renal failure

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It is believed that the disease in question most often occurs against the background of inflammatory and/or infectious kidney pathologies. But there are also diseases of other organs and systems that can also lead to chronic renal failure.

Doctors have identified a list of pathologies that contribute to the development of the disease in question:

• sustainable high blood pressure – ;
• amyloidosis;

It is not at all necessary that when diagnosing the above diseases, the patient will experience chronic renal failure - this pathology is a complication and for its development several factors must come together.

Renal failure in the latent stage - symptoms

The clinical picture of renal failure in the latent stage will depend on what disease led to the development of the pathology. Symptoms can be very different - swelling that occurs during the day and is independent of the amount of fluid consumed, increased blood pressure without visible reasons, pain syndrome concentrated in the lumbar region. Doctors often note that the first symptoms of chronic renal failure in the latent stage are completely ignored - this happens with progressive glomerulonephritis and/or polycystic kidney disease.

In the latent stage of the disease in question, the patient will complain of increased fatigue and decreased appetite, up to complete refusal of food. These complaints are absolutely not specific, therefore, the doctor will be able to make a correct diagnosis and associate such changes in the patient’s well-being with problems with kidney function only after a thorough examination of the patient.

Both the patient and the attending physician should be alerted during the night hours, which occur even with a minimal amount of fluid consumed in the evening. This condition may indicate that the kidneys are unable to concentrate urine.

In kidney diseases, some of the glomeruli die, and the remaining ones cannot cope with the function of this organ - the liquid is absolutely not absorbed in the tubules, the density of urine decreases so much that in some cases the indicators approach those of the blood plasma. To clarify this point, doctors prescribe the patient according to Zimnitsky - if a density of 1018 is not present in any portion of urine, then we can talk about the progression of renal failure. A urine density of 1010 is considered critical - this means that fluid reabsorption has completely stopped, and the disturbances in kidney function have gone too far.

The latent stage of development of chronic renal failure acquires more and more pronounced symptoms over time - for example, the patient begins to complain of increased thirst, but there is no high blood pressure (unless it was the cause of the development of the complication in question), a blood test does not show a decrease in the level of hemoglobin and electrolytes shifts. If a doctor examines a patient at this stage of development of the disease in question, a reduced amount of vitamin D and parathyroid hormone will be detected, although there will be no signs of progression of osteoporosis.

Note:at the latent stage of development of chronic renal failure is characterized by the reversibility of symptoms - with timely diagnosis and professional medical care can prevent progression.

Azotemic stage of renal failure - signs

If the latent stage of development of the disease in question was diagnosed in a timely manner, but treatment does not produce any results, then the progression of the pathology will occur at a rapid pace - the irreversible stage of chronic renal failure begins. In this case, the patient will complain about very specific symptoms:

1. Blood pressure rises, constant headaches occur and this is associated with a decrease in the synthesis of renin and renal prostaglandins in the kidneys.
2. Muscle mass becomes smaller, the patient loses weight sharply, intestinal upset appears, appetite decreases, and he is often worried - these symptoms are due to the fact that the intestines partially take over the function of removing toxins.
3. Erythropoietin in the kidneys begins to be produced in too small quantities, which leads to the development of persistent anemia.
4. There are complaints of numbness of the upper and lower extremities (feet and hands), corners of the mouth, pronounced muscle weakness– the cause of this condition is a lack of active calcium in the body and a decrease in calcium levels. For the same reason, the patient may experience disturbances in the psycho-emotional background - agitation or.

As chronic renal failure progresses, a more severe stage 4 of the disease occurs. It will have the following symptoms:

Manifestations of end-stage renal failure

At this stage of development of the disease in question, the patient receives only replacement treatment - he regularly undergoes hemodialysis and/or peritoneal dialysis.

The main signs of chronic renal failure in the terminal stage will be the following manifestations:

Note:The life of patients with chronic renal failure at stage 4 of development is not even calculated in days - in hours! Therefore, it is highly advisable to seek professional medical care much earlier, when the first symptoms of the disease in question appear.

Specific symptoms of chronic renal failure develop in later stages of pathology, when irreversible processes in the kidneys occur. And in order to identify the development of the disease in question at stages 1-2, you need to regularly take blood and urine tests - this is especially true for those patients who are at risk.

Tsygankova Yana Aleksandrovna, medical observer, therapist of the highest qualification category

To identify kidney problems and choose treatment tactics for chronic renal failure, the doctor will conduct a whole range of diagnostic tests. Among all examination methods, one of the most important is the determination of the level of nitrogen compounds in the blood. By the amount of nitrogen-containing waste that must be excreted from the body through the urinary tract, one can reliably determine the degree of renal dysfunction. Determining the stages of chronic renal failure by creatinine concentration is very indicative and highly informative, therefore it is widely used in the complex diagnosis of renal failure.

Variants of nitrogenous slags

The urinary function of the kidneys ensures constant removal from the human body. harmful substances and toxic compounds that are formed in the process of life. If this does not happen, then gradual poisoning occurs with disruption of the functioning of all organs and systems. Some unnecessary substances are very difficult to identify, while others are quite simple. One of the main diagnostic criteria for identifying chronic renal failure are nitrogen-containing wastes, which include:

• residual nitrogen;
• urea;
• uric acid;
• creatinine

Of these biochemical compounds, the last one is most indicative for the diagnosis of chronic renal failure: based on the concentration of creatinine, one can confidently determine the stage of the disease. The levels of other nitrogenous wastes are ineffective and do not affect the determination of the stage of chronic renal failure. However, urea and residual nitrogen concentrations can help diagnose renal failure.

Azotemia

When treating chronic renal failure, the doctor will dynamically determine the level of azotemia, a significant increase in which occurs when the condition worsens or in the absence of effect from treatment measures. Blood creatinine concentration is the most specific finding, but it is advisable to consider urea and uric acid levels. Sometimes determining the cause of the disease depends on this.

If blood urea levels are high and creatinine values ​​are normal, the doctor will look for conditions that are not associated with renal pathology:

• excessive consumption of protein foods;
• severe malnutrition and hunger;
• severe loss of fluid from the body;
• excess metabolic processes.

If all nitrogen-containing compounds increase simultaneously, then we can confidently speak of chronic renal failure.

Classifications of chronic renal failure

Quite a few types of classification of chronic renal failure have been proposed, in which different indicators are taken into account. Among laboratory classifications, doctors widely and actively use the following 2 options:

1. According to the degree of reduction in glomerular filtration.

• Initial. The reduction in the cleansing capacity of the kidneys reaches almost 50% of normal values.
• Conservative. Renal cleansing deteriorates significantly and is only 20-50% of what is required.
• Terminal. The filtration capacity of the kidney parenchyma drops to less than 20%, reaching extremely low levels in the worst case.

1. Based on the concentration of blood creatinine (at a norm of 0.13 mmol/l).

• latent or reversible stage (nitrogen compound level ranges from 0.14 to 0.71);
• azotemic or stable (creatinine level from 0.72 to 1.24);
• uremic or progressive stage (if the value exceeds 1.25 mmol/l).

In each classification, all stages are divided into phases, which are used to select the most effective methods of therapy. Both for diagnosis and for monitoring the treatment of chronic renal failure, it is best to use biochemical studies to identify the characteristics of nitrogen metabolism.

Treatment of chronic renal failure based on creatinine levels

One of the most important areas of treatment for chronic renal failure is the correction of azotemia: it is necessary to improve the filtration capacity of the renal parenchyma so that wastes and harmful substances are removed from the body. In addition, reducing the level of nitrogen compounds in the blood can be achieved using the following treatment methods:

1. Diet therapy.

At minimum concentrations creatinine in the latent stage of chronic renal failure, it is necessary to use a diet with a moderate protein content. It is advisable to consume vegetable protein, giving preference to soy and avoiding meat and fish. It is necessary to maintain normal calorie content of food to maintain energy expenditure.

In the azotemic and uremic stages of chronic renal failure, a significant reduction in protein foods and dietary restrictions on phosphorus and potassium are shown. To maintain the level of vital amino acids, the doctor will prescribe special medications. Be sure to exclude the following products:

• mushrooms;
• legumes and nuts;
• White bread;
• milk;
• chocolate and cocoa.

1. Detoxification.

Purification of the blood from nitrogenous compounds is achieved through intravenous administration of solutions that help bind and remove harmful substances that accumulate in the vascular bed. Typically, sorbent solutions and preparations of calcium salts (carbonate) are used. However, if therapy for chronic renal failure does not bring the desired effect (which will be evident from the level of azotemia), then replacement methods of treatment must be used.

1. Hemodialysis.

An important criterion for starting blood purification by dialysis is the concentration of nitrogen compounds. Against the background of concomitant severe diseases (diabetes mellitus, arterial hypertension), hemodialysis can be started at stage 2, when the creatinine level exceeds 0.71 mmol/l. However, the typical indication for dialysis is stage 3 with severe azotemia.

After each blood purification session, diagnostic studies are required to determine indicators such as:

• general clinical urine and blood tests;
• assessment of the level of azotemia by creatinine and urea 1 hour after the end of the hemodialysis session;
• determination of minerals (calcium, sodium, phosphorus) in the blood after hardware purification.

1. Treatment of concomitant diseases.

Improving the general condition of the body with the correction of pathological changes will help restore the processes of removing nitrogenous compounds. Sometimes it is the harmful substances that accumulate in the blood during chronic renal failure that contribute to the following problems:

• anemia;
• erosive gastritis;
• diseases of joints and bones;
• accumulation of phosphate compounds with an increased risk of urolithiasis.

All variants of pathologies detected in chronic renal failure require a course of therapy taking into account the capabilities of the kidneys. Do not use drugs that have even minimal nephrotoxic effects. Treatment should be carried out in a hospital setting under the constant supervision of a physician with regular monitoring of laboratory parameters. An important factor in therapy will be the correction of sugar and blood pressure in people with diabetes, obesity and hypertension.

Among all the classifications used for the diagnosis and treatment of chronic renal failure, one of the optimal, quite simple and informative ones is determining the stage of the disease by the level of azotemia. In a biochemical blood test, the concentration of creatinine and urea are most indicative for assessing the urinary function of the kidneys and for monitoring during course treatment of chronic renal failure. Assessing azotemia is almost always used for any replacement therapy provided in a hemodialysis unit. The best option for predicting future complications is dynamic monitoring of the concentration of nitrogen-containing compounds in the blood. That is why the doctor at all stages of examination and treatment of renal failure will use laboratory tests with the mandatory determination of creatinine concentration.

Kidney failure– this is a violation of the excretory (excretory) function of the kidneys with the accumulation of nitrogenous wastes in the blood, which are normally removed from the body in the urine. Can be acute or chronic.

(CRF) is a syndrome of irreversible renal dysfunction that occurs for 3 months or more. Occurs as a result of the progressive death of nephrons as a consequence of chronic kidney disease. It is characterized by impaired excretory function of the kidneys, the formation of uremia associated with the accumulation in the body and the toxic effect of nitrogen metabolism products (urea, creatinine, uric acid).

Causes of chronic renal failure

1. Chronic glomerulonephritis (damage to the glomerular apparatus of the kidneys).
2. Secondary kidney damage caused by:
- diabetes mellitus type 1 and 2;
- arterial hypertension;
- systemic diseases of connective tissue;
- viral hepatitis"B" and/or "C";
- systemic vasculitis;
- gout;
- malaria.
3. Chronic pyelonephritis.
4. Urolithiasis, urinary tract obstruction.
5. Anomalies in the development of the urinary system.
6. Polycystic kidney disease.
7. Effect of toxic substances and drugs.

Symptoms of chronic renal failure

Initial chronic renal failure is asymptomatic and can only be detected by laboratory testing. Only when 80-90% of nephrons are lost do signs of chronic renal failure appear. Early clinical signs may include weakness and fatigue. Nocturia appears (frequent urination at night), polyuria (excretion of 2-4 liters of urine per day), with possible dehydration. As renal failure progresses, almost all organs and systems are involved in the process. Weakness increases, nausea, vomiting, skin itching, and muscle twitching appear.

Patients complain of dryness and bitterness in the mouth, lack of appetite, pain and heaviness in the epigastric region, and loose stools. I am concerned about shortness of breath, pain in the heart area, and increased blood pressure. Blood clotting is impaired, resulting in nasal and gastrointestinal bleeding, skin hemorrhages.

In the later stages, attacks of cardiac asthma and pulmonary edema occur, disturbances of consciousness, up to a coma. Patients are prone to infections ( colds, pneumonia), which in turn accelerate the development of renal failure.

The cause of renal failure may be progressive liver damage, this combination is called Hepatorenal syndrome). In this case, renal failure develops in the absence of clinical, laboratory or anatomical signs of any other causes of renal dysfunction. Such renal failure is usually accompanied by oliguria, the presence of normal urine sediment and low urinary sodium concentration (less than 10 mmol/L). The disease develops with advanced liver cirrhosis, complicated by jaundice, ascites and hepatic encephalopathy. Sometimes this syndrome can be a complication of fulminant hepatitis. As liver function improves in this syndrome, kidney condition often improves.

They are important in the progression of chronic renal failure: food intoxication, surgical interventions, injuries, pregnancy.

Diagnosis of chronic renal failure

Laboratory research.

1. A general blood test shows anemia (decrease in hemoglobin and red blood cells), signs of inflammation (acceleration of ESR - erythrocyte sedimentation rate, moderate increase in the number of leukocytes), a tendency to bleeding (decreased platelet count).
2. Biochemical blood tests - an increase in the level of nitrogen metabolism products (urea, creatinine, residual nitrogen in the blood), a violation electrolyte metabolism(increased levels of potassium, phosphorus and decreased calcium), decreased total protein in the blood, hypocoagulation (decreased blood clotting), increased blood cholesterol and total lipids.
3. Urinalysis - proteinuria (the appearance of protein in the urine), hematuria (the appearance of more than 3 red blood cells in the urine in the field of view during urine microscopy), cylindruria (indicates the degree of kidney damage).
4. The Reberg-Toreev test is performed to assess the excretory function of the kidneys. Using this test, the glomerular filtration rate (GFR) is calculated. This indicator is the main one for determining the degree of renal failure and the stage of the disease, since it is this indicator that reflects functional state kidney

At the moment, to determine GFR, not only the Reberg-Toreev test is used, but also special calculation methods that take into account age, body weight, gender, and blood creatinine level.

It should be noted that at present, instead of the term chronic kidney disease, which is considered outdated and characterizes only the fact of irreversible impairment of kidney function, the term CKD (chronic kidney disease) is used with a mandatory indication of the stage. It should be especially emphasized that establishing the presence and stage of CKD in no case replaces making the main diagnosis.

Stages of the disease:

CKD (chronic kidney disease) I: kidney damage with normal or increased GFR (glomerular filtration rate) (90 ml/min/1.73 m2). There is no chronic renal failure;
CKD II: kidney damage with a moderate decrease in GFR (60-89 ml/min/1.73 m2). Initial stage of chronic renal failure.
CKD III: kidney damage with a moderate degree of reduction in GFR (30-59 ml/min/1.73 m2). compensated chronic renal failure;
CKD IV: kidney damage with a significant decrease in GFR (15-29 ml/min/1.73 m2). CRF decompensated (not compensated);
CKD V: kidney damage with end-stage renal failure (< 15 мл/мин/1,73 м2).

Instrumental research.

1. Ultrasound examination urinary system with pulse Doppler (determination of renal blood flow). Conducted to diagnose chronic kidney diseases, and allows you to assess the severity of kidney damage.
2. Needle biopsy of the kidneys. Examination of kidney tissue allows you to make an accurate diagnosis, determine the course of the disease, and assess the extent of kidney damage. Based on this information, a conclusion is made about the prognosis of the course of the disease and the selection of a treatment method.
3. X-ray (survey, contrast) examination of the kidneys is carried out at the diagnostic stage and only for patients with I – II degrees of renal failure.

Consultations:

1. Nephrologist (to make a diagnosis and choose treatment tactics). All patients with renal failure are examined.
2. Oculist (monitors the condition of the fundus).
3. Neurologist (if damage to the nervous system is suspected).

Treatment of chronic renal failure

Each stage of kidney failure requires specific actions to be taken.

1. At stage I, the underlying disease is treated. Stopping the exacerbation of the inflammatory process in the kidneys reduces the severity of renal failure.
2. At stage II, along with treatment of the underlying disease, the rate of progression of renal failure is assessed and drugs are used to reduce its rate. These include lespenefril and hofitol - these are drugs plant origin, the dose and frequency of administration are prescribed by the attending physician.
3. Stage III is diagnosed and treated possible complications, drugs are used to slow the rate of progression of renal failure. They correct arterial hypertension, anemia, calcium-phosphate disorders, treat infectious and cardiovascular complications.
4. At stage IV, the patient is prepared for renal replacement therapy
5. and at stage V, renal replacement therapy is performed.

Renal replacement therapy includes hemodialysis and peritoneal dialysis.

is an extrahepatic method of blood purification, during which toxic substances are removed from the body and disturbances in water and electrolyte balances are normalized. This is done by filtering the blood plasma through the semi-permeable membrane of the artificial kidney apparatus. Treatment with maintenance hemodialysis is carried out at least 3 times a week, with a duration of one session of at least 4 hours.

Peritoneal dialysis. The human abdominal cavity is lined by the peritoneum, which acts as a membrane through which water and substances dissolved in it enter. A special catheter is surgically installed into the abdominal cavity, through which the dialysate solution enters the abdominal cavity. An exchange occurs between the solution and the patient’s blood, resulting in the removal of harmful substances and excess water. The solution sits there for several hours and then is drained. This procedure does not require special installations and can be performed independently by the patient at home or while traveling. Once a month he is examined at the dialysis center for control. Dialysis is used as treatment while waiting for a kidney transplant.

All patients with stage V chronic kidney disease are considered candidates for kidney transplantation.

Nutrition for chronic renal failure

Diet for kidney failure plays a very important role. It is determined by the stage, chronic disease, phase (exacerbation, remission). The attending physician (nephrologist, general practitioner, family doctor) together with the patient compiles a food diary indicating the quantitative and qualitative composition of food.

A low-protein diet with limited consumption of animal proteins, phosphorus, and sodium helps slow the progression of renal failure and reduces the possibility of complications. Protein consumption should be strictly dosed.

At stage I, the amount of protein consumed should be 0.9 -1.0 g per kg of body weight per day, potassium up to 3.5 g per day, phosphorus - up to 1.0 g per day. In stage II, the amount of protein is reduced to 0.7 g per kg of body weight per day, potassium to 2.7 g per day, phosphorus to 0.7 g per day. At stages III, IV and V, the amount of protein is reduced to 0.6 g per kg of body weight per day, potassium to 1.6 g per day, phosphorus to 0.4 g per day. Preference is given to proteins of plant origin, which contain less phosphorus. Soy proteins are recommended.

The main components of the patient's diet are fats and carbohydrates. Fats – preferably of plant origin, in sufficient quantities to ensure the calorie content of food. The source of carbohydrates can be products of plant origin (except legumes, mushrooms, nuts). If the level of potassium in the blood increases, exclude: dried fruits (dried apricots, raisins), potatoes (fried and baked), chocolate, coffee, bananas, grapes, rice. To reduce phosphorus intake, limit animal proteins, legumes, mushrooms, white bread, milk, and rice.

Complications of kidney failure

The most common complications of renal failure are infectious diseases (up to the development of sepsis) and cardiovascular failure.

Prevention of kidney failure

Preventive measures include timely detection, treatment and monitoring of diseases leading to the development of renal failure. Most often, renal failure occurs with diabetes mellitus (type 1 and 2), glomerulonephritis and arterial hypertension. All patients with renal failure are observed by a nephrologist. Examinations are carried out: blood pressure control, fundus examination, body weight control, electrocardiogram, ultrasound of organs abdominal cavity, blood and urine tests, receive recommendations on lifestyle, rational employment, and nutrition.

Consultation with a doctor for kidney failure

Question: How is a kidney biopsy performed?
Answer: The procedure is performed in a specialized medical institution (usually in the nephrology department) by a nephrologist. Under local anesthesia, under the control of an ultrasound probe, a tiny column of kidney tissue is taken with a thin disposable needle. In this case, the doctor performing the biopsy sees the kidney and all the movements of the needle on the screen. Contraindications to performing a puncture biopsy of the kidneys are:
1. single kidney;
2. hemorrhagic diathesis;
3. polycystic kidney disease;
4. purulent inflammation kidneys and perinephric tissue (purulent pyelonephritis, paranephritis);
5. kidney tumors;
6. kidney tuberculosis;
7. refusal of the patient to conduct the study.

Question: Are there age or other restrictions for kidney transplantation?
Answer: Age cannot be an obstacle to surgery. Has the meaning psychological readiness transplant candidate. It is determined by the patient's ability to comply with medical recommendations after kidney transplantation, since non-compliance with immunosuppressive medications is the most common cause of kidney transplant loss. Absolute contraindications for transplantation are: sepsis, AIDS, uncontrolled malignant neoplasms.

General practitioner Vostrenkova I.N.

Chronic renal failure or chronic kidney disease code according to ICD 10 - N 18 is a most complex kidney pathology. With this disease, the kidneys cease to perform their main functions. The incidence of kidney failure among the population of different ages is increasing every year. The role of the kidneys in the human body is very important, as they participate in very important processes that regulate and maintain the normal functioning of the body. The kidneys not only remove excess fluid, but also normalize the acid-base balance in the body and maintain blood pressure, and also remove metabolic products. There are several stages of chronic renal failure based on creatinine.

The diagnosis of chronic renal failure can only be made over time. If the manifestations of chronic kidney disease last for several months. Chronic renal failure is most likely to occur in a patient with a large number of kidney pathologies. Often the causes of chronic renal failure are diseases of the genitourinary system. Kidney performance gradually decreases, as there are fewer working nephrons. As the disease progresses, the functioning of the kidneys is disrupted and this leads to the fact that all processes stop. This is the essence of all problems and the disease develops according to this pattern.

The patient exhibits severe anemia due to chronic insufficiency. The course of the disease always occurs differently, the rate of destruction depends on many external and internal factors, as well as from the underlying disease that provokes chronic renal failure. The rate of development of the pathology is strongest with the underlying disease in diabetic nephropathy, nephritis, and also in the presence systemic lupus. A slow course of the disease occurs with polycystic disease and pyelonephritis.

Acute renal failure occurs due to injury or in the postoperative period, as well as from toxic drug treatment. It is extremely rare that both pregnancy and the postpartum period can cause changes in the condition of the kidneys. Acute renal failure and chronic renal failure develop differently, however, the course of the disease of all types of renal failure can lead to complete failure of all kidney functions.

To exclude chronic renal failure, it is necessary to carry out preventive measures. Preventive measures for chronic renal failure include timely seeking medical help for symptoms of renal pathology. To prevent all provoking factors means to avoid possible occurrence chronic renal failure. It is necessary to take measures to treat diseases such as pyelonephritis, kidney stones, glomerulonephritis.

Main classification

Regarding the stages of creatinine, there are several developed classifications, however, the vast majority of experts rely on the division of N.A. Lopatkina and I.N. Kuchinsky. This classification of chronic renal failure describes 4 stages:

1. Latent stage of chronic renal failure. This stage does not affect the patient’s condition and, as a rule, there are no complaints about well-being. Changes can only be detected by laboratory analysis. In this case, the glomerular filtration rate drops to 60-50 ml/min.
2. Clinical stage of chronic renal failure. At this stage, the patient experiences severe discomfort, as the volume of urine output increases significantly. Some functions of the kidneys change. Club filtration is reduced to 49-30 ml/min.
3. Decompensation stage of chronic renal failure. Club filtration is reduced to a minimum value and is approximately 29-15 ml/min. In the urine, a creatinine volume of up to 0.2-0.5 mlmol/l is observed.
4. End-stage chronic renal failure. This is the very last stage of the disease, in which there is no hope of restoring kidney function. During a blood test, the electrolyte composition changes, urea, uric acid and creatinine increase greatly. Such changes cause uremic intoxication, in which acid secretion is impossible.

The last stage is very destructive not only for the kidneys, but also for the health of the entire body. Disastrous problems develop of cardio-vascular system, blood flow deteriorates significantly, cardiac muscle dystrophy and pericarditis develop. And also in most cases, patients experience pulmonary edema. The immune system and hormonal levels are disrupted.

And also according to the increase in the value of creatinine in the blood, the stages of chronic renal failure are according to Ryabov:

1. Up to 440 µmol/l.
2. From 440 to 880 µmol/l.
3. Up to 1320 µmol/l.
4. From 1320 µmol/l.

International classifications may differ slightly from those generally accepted in our country. Each classification of ESRD divides stages into phases. When diagnosing chronic renal failure, it is necessary to clearly determine the stage of the lesion, since the correctness and success of treatment depends on the correct diagnosis. Thus, it becomes possible to control the development of the disease and prevent one form of chronic renal failure from passing into another.

Proper treatment

Treatment of chronic renal failure is recommended to begin with changing azotemia so that the removal of harmful substances occurs in a normal manner. Thus, the level of nitrogenous compounds will be reduced. IN medical practice There are several methods for treating chronic renal failure, depending on the level of creatinine in the blood.

Treatment methods for chronic renal failure at the latent stage of the disease consist of changing dietary habits, that is, therapeutic nutrition. The food you eat should contain protein in moderate doses. It is recommended to consume animal protein minimally, but vegetable protein is most preferable. As a result, the diet is replaced from meat or fish to legumes. It is strictly forbidden to limit yourself in food or overeat; however, you must calculate the required amount of calories consumed and adhere to the obtained value.

In more advanced stages, protein intake must be significantly reduced, and foods rich in phosphorus and potassium must also be removed from the diet. If there is a shortage of useful amino acids, they are replenished additionally with the use of drugs. Beans, nuts, white bread, milk, chocolate, cocoa and mushrooms are completely removed from the diet.

When treating chronic kidney failure, a detoxification method is mandatory. Harmful and toxic substances accumulating in the blood must be removed from the body. For this purpose, the patient is given special solutions intravenously. Most often, a carbonate solution or sorbents are used, but if these methods are ineffective, replacement therapy is used. During the treatment phase, it is recommended to measure the level of azotemia.

Treatment with folk remedies involves the use medicinal herbs. Signs can be removed with folk remedies such as decoctions of lemon balm, lingonberry, dandelion, etc. Treatment with folk remedies must be carried out under the guidance of a specialist and does not replace medications prescribed by the attending physician.

What is hemodialysis

Hemodialysis for chronic renal failure is used to detoxify the body. Hemodialysis is carried out using a special device, popularly called an artificial kidney. When the kidneys do not perform their main functions of removing toxic substances, an artificial kidney performs this function. The blood is cleansed of nitrogenous compounds.

The essence of the device is that the blood is purified under pressure with a dialysate solution, thus removing all toxic substances from the body. The device consists of several parts: a blood supply, a dialyser, and a dialysate supply.

In some situations, hemodialysis is recommended for grade 3 or 2, but treatment of end-stage chronic renal disease still requires a kidney transplant. After the procedure, the patient must have urine and blood tested, and the level of creatinine and urea and the amount of minerals must be measured.

Despite the fact that the hemodialysis procedure leads to significant improvements, it should not be performed in patients with the following diseases:

1. Active pulmonary tuberculosis, lung diseases.
2. Diseases that cause bleeding.
3. Unstable mental state.
4. Malignant neoplasms.
5. Circulatory disease.
6. Pathologies of the nervous system.
7. Elderly age.
8. Post-infarction condition and heart failure.
9. Chronic hepatitis cirrhosis of the liver.

As well as patients leading antisocial image lives who do not see the need for treatment, as a rule, do not undergo hemodialysis. Accordingly, people suffering from alcohol addiction or drug use do not resort to such a procedure. The course of treatment is developed by the attending physician, and in each specific case it is individual.

Treatment of concomitant diseases

If the general condition of the body worsens, it is necessary to treat all concomitant diseases. In chronic renal failure, problems arise due to an excess of harmful substances in the blood. Typically, signs of the following diseases occur:

1. Anemia.
2. Erosive gastritis.
3. Diseases of joints and bones.
4. Urolithiasis disease.
5. Renal osteodystrophy.

Therapy for concomitant diseases is mandatory, however, when carrying out it, it is necessary to remember the weak condition of the kidneys, and that not all treatment methods are suitable. If there is a risk of even a slight toxic effect on the kidneys, the drugs are replaced. In this case, only inpatient treatment is assumed, since constant monitoring of the patient’s condition and regular laboratory testing of all important indicators life activity.

If the patient has diabetes, therapeutic measures will be aimed at reducing sugar levels, and in case of obesity or hypertension, at controlling blood pressure. Since the main classifications of renal failure are based on the values ​​of creatinine and urea, constant measurement and monitoring of these indicators is necessary, because on their basis it is possible to draw conclusions about changes in the state of the urinary function of the kidneys and the stage of development of renal failure.

During hemodialysis, azotemia indicators must be monitored. If you keep all indicators under control, it is possible to predict how much the pathology will progress in the future and at what speed. During treatment, it is necessary to conduct laboratory tests and monitor creatinine levels. Negative symptoms and treatment are interrelated.

Chronic renal failure for children

IN childhood chronic renal failure occurs due to the following reasons: toxic effect of certain drugs, impairment of certain renal functions, progressive nephropathy, violation of the integrity of cell membranes, renal dysembryogenesis. As a rule, chronic renal failure in children occurs against the background of diseases such as severe uropathy, hereditary or sclerosing nephritis, renal tissue dysembryogenesis, and tubulopathy. The real cause is damage to the kidney, given that there is only one.

The cause of chronic renal failure may be acquired or congenital diseases. congenital - these are primarily pyelonephritis, glomerulopathy, vasculitis, polycystic kidney disease, nephrocalcinosis, as well as some systemic diseases.

In case of chronic renal failure, the symptoms in a child are pronounced. Children feel very lethargic, get tired quickly, the skin is pale, and it is also noticeable that there is a slight lag in growth and development. Chronic renal failure is often accompanied by anemia and its symptoms. Unfortunately, between the ages of 7 and 13 years, ESRD can cause fatal outcome The child has.

Arises this danger due to the fact that at this age the child’s body begins to grow and develop rapidly, however, the kidneys with pathology do not develop, which means it will be almost impossible to remove toxic substances from the blood. If in the first stages of the disease the child does not complain, then in the last stage life is supported only through the use of an artificial kidney apparatus.

Prognosis in children

For each case of illness, the prognosis for recovery is made based on the specific situation. How long people live with this disease depends on many factors. As a rule, kidney transplantation is performed in childhood, but this operation may not lead to the desired result, and the transplanted kidney may also stop functioning and require hemodialysis.

Modern treatment methods and medications allow a child to live for about 30 years with normal life activities, however, the mortality rate is very high and the disease can develop rapidly with sufficient treatment. According to statistics, a child who has been on dialysis since adolescence lives about 20 years.

To prevent the occurrence of chronic renal failure in a child, it is necessary to take preventive measures at an early stage. It is important for parents to monitor diseases of the urinary system, promptly and fully treat renal pathologies, and also assess the possibility of progression of renal diseases.

If a child has obstructive uropathy, it is necessary to resort to surgical correction measures. The slightest complaints of a child cannot be ignored and if symptoms of chronic renal failure occur, it is necessary to urgently consult a specialist; an individually selected treatment will allow achieving good results.