Chronic renal failure medical history therapy. Download medical textbooks, lectures

Date: 08.03.2020

Chronic renal failure (CRF) is a clinical syndrome caused by irreversible, usually progressive, kidney damage due to various pathological conditions.

With CRF, permanent damage to the kidney tissue occurs: normal tissue is gradually replaced by scar tissue. CRF is irreversible and often progresses. Acute renal failure, on the other hand, is reversible, and the architectonics of the kidney is usually preserved in this case. The leading manifestations of renal failure are an increase in the concentration of creatinine and blood urea nitrogen due to a decrease in the glomerular filtration rate. Other functions of the kidney, such as the synthesis of renal hormones, are also generally impaired. Various degrees of renal failure are accompanied by a wide variety of symptoms and changes in laboratory parameters.

Several terms are used to describe chronic kidney damage. CRF is a general term to describe an irreversible drop in glomerular filtration rate over a long period of time, usually several years. means a chronic process, accompanied by a decrease in the functional capacity of the kidneys, although the degree of renal failure for this term is not fully defined. Under azotemia understand the increase in blood urea nitrogen and serum creatinine, without having in mind any obvious clinical manifestations of both chronic and acute renal failure. Uremia - this is the phase of renal failure in which symptoms and signs of renal dysfunction are detected. In many patients, the manifestations of uremia do not occur until the glomerular filtration rate falls below 10 ml / min (norm -120 ml / min). End stage renal disease means any form of chronic (i.e. irreversible) renal failure at a stage where permanent replacement treatment in the form of dialysis or kidney transplant is indicated.

CAUSES OF CHRONIC RENAL FAILURE

Many different kidney diseases can lead to CRF, just as many different heart diseases (eg, ischemia, valve damage, cardiomyopathy) can cause congestive heart failure. An idea of the causes of CRF can be obtained by analyzing data on the frequency of primary renal diagnoses in patients who are on dialysis.

MAIN CAUSES OF TERMINAL STAGE OF KIDNEY DISEASE IN THE USA

Causes of kidney disease Number of cases in%

Diabetes 34.2

Hypertension (nephrosclerosis) 29.2

Glomerulonephritis 14.2

Interstitial nephritis 3.4

Cystic kidney disease 3.4

Other or unknown 15.4

Diabetes is currently the most common cause of CRF leading to end-stage renal failure. About one third of people with insulin-dependent (i.e., ketosis-prone) diabetes (or type 1 diabetes) develop diabetic nephropathy, a generic term for diabetes-related kidney disease. Kidney disease develops in many patients with non-insulin dependent diabetes. Kidney disease is usually diagnosed in patients with diabetes for at least 10 years, and most of them also have diabetic complications, including diseases of the eyes (i.e., diabetic retinopathy) and peripheral sensory nerves (i.e., diabetic neuropathy). Histologically, in the kidneys, nodular or diffuse sclerosis of the glomeruli is detected. The first manifestation of kidney disease is the appearance of small amounts of albumin in the urine (microalbuminuria). In the future, albuminuria progresses and can reach the size of the nephrotic state (i.e.,> 3.5 g / day). Soon after the onset of proteinuria, azotemia develops, which progresses over 2-7 years to uremia and end-stage renal failure.

Hypertension - a recognized cause of end-stage renal failure, occurs in about 30% of patients. It causes kidney damage, manifested as a thickening of the renal arterioles; this phenomenon is called nephrosclerosis. The clinical syndrome includes slowly progressive renal failure, mild proteinuria, and a slight increase in urine sediment. But kidney disease itself can cause the development of hypertension or exacerbate preexisting hypertension. In patients with chronic renal failure and hypertension, it is often not clear which disease is primary. Although there is no definitive evidence, it still appears that treating hypertension can alleviate kidney damage.

Glomerulonephritis - the third most common and recognized cause of end-stage renal disease. A large number of primary and secondary forms of glomerulonephritis, such as membrane nephropathy, focal glomerulosclerosis, systemic lupus erythematosus, and Goodpasture's syndrome. ends in end-stage chronic renal failure.

The remaining pathological conditions leading to the development of end-stage renal failure include several relatively less frequent renal diseases. Polycystic kidney disease - it is a common disorder with an autosomal dominant inheritance. Although it accounts for only 3.4% of the causes of end-phase kidney disease, it is at the same time the most common recognized genetic disease. Chronic interstitial nephritis may result from prolonged exposure to analgesics, lead and other environmental toxins. In some patients with end-stage renal disease, the underlying cause remains unknown.

PATHOPHYSIOLOGY

Kidney damage can be caused by many diseases, which initially involve only one specific segment of the nephron and, along with it, blood vessels, glomeruli, tubules or interstitium. In the future, the process that affects any part of the nephron or the surrounding interstitium continues and reduces glomerular filtration, as well as the functions of this nephron. The normal architectonics of the kidney is lost, the tissue is replaced by collagen. When this happens, the size of the kidney usually shrinks.

The kidney usually loses its normal architectonics. Some nephrons become dysfunctional, while others continue to function at a higher than normal level to compensate for the loss of some of the nephrons. This sequence of events during the development of kidney failure is known as hypothesis of an intact nephron. It provides convenient approaches to understanding many aspects of CRF. Intact nephrons maintain fluid and solute homeostasis as long as a stable number of functional nephrons remain. After this point, the patient develops uremia and may die within weeks or months if dialysis or kidney transplantation is not performed. Intact nephrons adapt to the loss of damaged nephrons by increasing their size, increasing the glomerular filtration rate of each individual remaining nephron, and increasing the elimination of solutes in the blood. Such an increase in the filtration rate by an individual nephron (i.e., hyperfiltration) occurs due to the expansion of the afferent arterioles of the glomerulus, which leads to an increased plasma flow through this glomerulus. Filtration can be enhanced by increasing the tone of the efferent arterioles. The increase in plasma flow and filtration rate in the remaining nephrons is probably a short-term adaptive response designed to compensate for the loss of some of the nephrons. However, this increase in the preserved nephrons leads to an increase in the hydrostatic pressure in the glomeruli, which, if it acts for a long time, causes dysadaptation.

Chronic renal failure often progresses, even if the underlying cause has been eliminated. The rate of progression varies from person to person. In one, the development of end-stage renal failure occurs quickly, for example, in a year, while in the other, it is very slow, for example, in 10 years. The rate of progression of chronic renal failure can be monitored clinically by comparing in time the value inverse to the rate of increase in serum creatinine concentration. Considerable efforts have been made to clarify the causes of the progression of kidney disease and methods of stopping or slowing it down.

A common explanation of the nature of the progression of chronic renal failure is called the hypothesis hyperfiltration. According to her, an increase in plasma flow and hydrostatic pressure over time causes damage to intact nephrons. The remaining intact nephrons are damaged by prolonged action of increased capillary pressure and plasma flow. Hyperfiltration damage results in a characteristic change in glomerular structure known as focal glomerulosclerosis. This hypothesis probably explains why renal failure continues to progress even when the initial factors that caused the kidney disease (for example, some forms of glomerulonephritis) cease.

Hyperfiltration damage can be reduced by lowering the hydrostatic pressure in the glomerulus. Several methods have been used to slow down the filtration rate in attempts to slow or stop the progression of CRF. In patients with hypertension, this progression, apparently, can be slowed down. treatment of hypertension. Most drugs selectively dilate afferent arterioles, causing increased blood flow in the glomerular capillaries. At the same time, there is a decrease in capillary pressure in the glomerulus as a result of a drop in pressure in the systemic circulation. These two processes partially counterbalance each other, but the net effect of antihypertensive treatment is to slow down the progression of chronic renal failure. Angiotensin-converting enzyme inhibitors are a specific class of antihypertensive drugs that block the conversion of angiotensin I to angiotensin II in the kidneys. Angiotensin II has a vasoconstrictor effect that is relatively more specific for efferent arterioles. By blocking its formation, angiotensin-converting enzyme inhibitors dilate efferent arterioles to a greater extent than afferent. This selective expansion of arterioles leads to a decrease in pressure in the capillaries of the glomerulus and to weakening of hemodynamic damage to the walls of the capillaries. In experimental animals, angiotensin-converting enzyme inhibitors slow or prevent the progression of renal failure. Recent studies have confirmed the effectiveness of angiotensin-converting enzyme inhibitors in slowing the rate of renal failure in humans. Protein restriction in food can also prevent the development of hyperfiltration damage by reducing blood flow and pressure in the glomerular capillaries in intact nephrons. Despite numerous studies, the degree of protein restriction required and the specific role of this type of exposure are not well defined.

Other hypotheses have been proposed for the cause of the progression of renal failure. For example, changes in blood coagulation, lipid deposits, and the uptake of macromolecules by mesangium can lead to progressive damage to intact nephrons.

CLINICAL CONSEQUENCES OF CHRONIC RENAL FAILURE

Almost every organ and every function of the body can be impaired due to kidney failure. Usually the earliest symptoms of uremia are fatigue, disturbed sleep, decreased appetite, nausea and vomiting. The manifestations of uremia occur as a result of the accumulation of toxins (mostly unidentified), as well as due to a violation of the secretion and function of hormones. The following are the manifestations of uremia, although not all of them are necessarily observed in every patient.

NEUROLOGICAL CONSEQUENCES

The accumulation of uremic toxins has a negative effect on the central nervous system. The threshold of convulsive reaction is reduced, which initially manifests itself in the form of tremor, but with possible progression to severe convulsions. Cognitive function may also be affected. Initially, small changes in the electroencephalogram are recorded, and later in patients, depression of consciousness may develop. Prolonged CRF also affects the peripheral nervous system; peripheral sensory neuropathy is observed.

HEMATOLOGICAL CONSEQUENCES

These patients are characterized by anemia as a result of reduced production of erythropoietin by the kidney. Anemia is normochromic and normocytic and can be largely corrected by the administration of exogenous erythropoietin. The platelet count is normal, but their function is impaired due to the action of uremic toxins. As a result, patients have hemorrhagic diathesis. The number of leukocytes is normal, but some studies indicate a violation of their immune and phagocytic functions, which is why patients have an increased risk of developing infections.

CARDIOVASCULAR EFFECTS

Most people with chronic renal failure have hypertension. In some cases, hypertension precedes the onset of kidney damage and may cause or worsen kidney failure. In others, hypertension is clearly secondary to the underlying kidney disease. Sometimes it is impossible to determine which came first. Hypertension is caused by a retention of sodium and fluid in the body (i.e., an increase in the volume of extracellular fluid) and the release of vasoconstrictor substances such as renin into the blood. Treatment consists of regulating extracellular fluid volume with diuretics, dialysis, and vasodilation. Patients with CRF also have dyslipidemia and, possibly, a predisposition to atherosclerosis. Due to the multiplicity of cardiovascular risk factors, patients with CRF are more likely to develop cardiovascular diseases such as myocardial infarction and stroke.

With CRF, the ability to secrete salt load may be impaired, which leads to an increase in the volume of extracellular fluid and the formation of edema. Congestive heart failure and pulmonary edema may develop, especially in patients with heart disease.

With severe renal failure, pericarditis sometimes develops, which, apparently, is an inflammatory and hemorrhagic reaction to uremic toxins accumulating in the pericardial cavity. With the development of this serious complication, the patient develops chest pain, shortness of breath and the sound of pericardial rubbing. Tamponade may occur with hypotension and circulatory collapse. Dialysis treatment, which removes harmful toxins, often cures the problem, although additional treatment is sometimes required.

After a long existence in conditions of poor absorption of calcium and hypocalcemia, hyperthyroidism and metabolic acidosis (in the bones, the buffering of the H ion occurs due to the release of calcium), there is a tendency to bone degeneration in patients with renal failure; this process is called renal osteodystrophy. In children with CRF, bone development may slow down. In adult patients, bone pain occurs and the frequency of fractures increases.

The most common form of bone damage is fibrous osteodystrophy, caused by an excess of parathyroid hormone. The rate of removal of minerals exceeds the rate of their deposition, which leads to the growth of the osteoid, a bone matrix consisting of soft tissue. Another manifestation of bone disease in patients with chronic renal failure is osteomalacia. It is characterized by a low level of bone mineral metabolism and its demineralization. The main cause of osteomalacia in patients with renal failure is aluminum intoxication. This intoxication is, unfortunately, an iatrogenic problem that occurs in patients who take aluminum antacids for a long time, usually to bind dietary phosphate. Classically, osteomalacia is a disorder of vitamin D deficiency.However, although patients with renal failure are deficient in the active metabolite of vitamin D, calcitriol, most do not develop osteomalacia until the body has accumulated sufficient amounts of aluminum. Every effort is being made to minimize the effect of aluminum in patients with chronic renal failure, but this is still a problem.

Calcification of soft tissues often occurs in patients with CRF as a result of severe, poorly regulated hyperphosphatemia. Calcium phosphate precipitates and is deposited in soft tissues such as skin, heart, joints, tendons, muscles, and blood vessels, and elsewhere. Serious disorders have been observed including pruritus, cardiac arrhythmias, arthritis, muscle weakness, and peripheral tissue ischemia. These problems can occur earlier than bone pathology in renal failure, but often occur against its background.

GASTROINTESTINAL EFFECTS

Nausea and vomiting are early symptoms of uremia and can cause anorexia and weight loss. Severe renal failure is accompanied by inflammation and hemorrhage of the mucous membranes. In patients with uremia, the risk of gastrointestinal bleeding is increased due to the formation of arterio-venous anastomoses in the intestine in combination with a defect in platelet function.

METABOLIC AND ENDOCRINE EFFECTS

Patients with CRF have a number of metabolic disorders, regardless of the diseases that cause renal failure. These include glucose intolerance and insulin resistance, hyperlipidemia, and decreased testosterone and estrogen levels. In women with chronic renal failure, fertility is sharply reduced.

TREATMENT OF CHRONIC RENAL FAILURE

SPECIFIC DISEASE TREATMENT

To stop the progression of kidney disease, which causes tissue scarring and irreversible kidney failure, specific treatment is necessary. It is also possible in some inflammatory diseases, such as systemic lupus erythematosus, vasculitis, and a number of forms of glomerulonephritis. There is evidence that intensive care for diabetes and hypertension reduces the chance of kidney damage.

TREATMENT OF HYPERTENSION

The regulation of blood pressure is a mandatory component in the treatment of all patients with hypertension and renal failure. A decrease in systemic pressure in the glomeruli causes a corresponding decrease in capillary pressure and the magnitude of hyperfiltration. Any medication or activity that lowers blood pressure appears to be helpful. At the same time, angiotensin-converting enzyme inhibitors make a special contribution to reducing damage to the glomeruli by selectively reducing the resistance of the efferent arterioles of the glomeruli and dilating the capillaries.

A low-protein diet helps to reduce pressure in the capillaries of the glomeruli and slow the progression of renal failure. Limiting protein intake in food to 40-60 g per day is often recommended for patients with chronic renal failure, if they do not have protein deficiency. With severe renal failure, it is necessary to limit the intake of potassium and sodium salts due to the current trend towards the development of hyperkalemia and an increase in the volume of extracellular fluid. Restriction of water intake is necessary in patients predisposed to the development of hyponatremia. A diet low in phosphate should be eaten to avoid hyperphosphatemia.

Diuretics in the treatment of edema

Patients with chronic renal failure often experience edema due to the limited ability of the kidneys to excrete salt. In nephrotic syndrome, edema can develop due to a low concentration of albumin in the blood serum; oncotic pressure, which determines the amount of fluid retained in the intravascular space, largely depends on albumin. Peripheral edema causes increased stress on the heart and often contributes to the development of systemic hypertension. Pulmonary edema leads to shortness of breath and respiratory failure. Edema should be treated with dietary salt restriction and diuretics. The actual level of salt intake for a non-hospitalized patient is 2 g per day (88 mmol / day). Patients with a serum creatinine concentration above about 20 mg / L do not respond to thiazide diuretics and should receive loop diuretics such as furosemide, bumetanide, or ethacrynic acid.

PREVENTION AND TREATMENT OF RENAL OSTEODYSTROPHY

A number of measures are used to prevent and treat disorders of mineral metabolism in bones in chronic renal failure. Patients should be on a low phosphorus diet to correct hyperphosphatemia. Phosphate absorption is reduced by products containing phosphate binders. For this purpose, calcium salts are preferred. They not only bind food phosphates, but also provide the necessary calcium supplement. In the past, aluminum gels were traditionally used, but in some patients, after many years of taking these gels, aluminum intoxication developed. To increase the absorption of calcium and direct suppression of the secretion of parathyroid hormone, the active form of vitamin D - 1,25 (OH) 2D, or calcitriol is prescribed. The goal of preventive treatment is to correct hyperphosphatemia and hypocalcemia, but without the occurrence of aluminum toxicity. If this goal is achieved, it seems that the normal state of the bones is maintained. If their pathology is pronounced, additional measures may be required, including parathyroidectomy.

CONTROL OF MEDICINE APPLICATION

The body of patients with chronic renal failure will accumulate those drugs that should be excreted by the kidneys. Therefore, it is important to reduce their dose or lengthen the interval between administration. The same drugs that are removed by the liver usually do not require dose adjustment in patients with CRF.

TREATMENT OF TERMINAL STAGE KIDNEY DISEASE

SUBSTITUTION THERAPY

The measures described above should be carried out as needed in patients with chronic renal failure. In many patients, symptoms of CRF may be absent until the glomerular filtration rate falls below 10 ml / min. At a lower glomerular filtration rate, clinical manifestations of renal failure such as hyperkalemia, me Tabolic acidosis, increased extracellular fluid, and symptoms of uremia (i.e., vomiting, pruritus, sleep disturbances, pericarditis, tremors, and seizures). At this terminal stage, replacement therapy for impaired kidney functions becomes absolutely necessary, otherwise the patient will die from complications. Such therapy includes dialysis or kidney transplant. There are two forms of dialysis: hemodialysis and peritoneal dialysis.

Hemodialysis is carried out with a special apparatus through which the patient's blood is passed at a rate of more than 250 ml / min. The dialyzer is a semi-permeable membrane through which fluid and uremic toxins pass. Dialysis fluid is located on the other side of this membrane, which facilitates the exchange diffusion of solutes. After passing through the dialyzer, the purified blood is returned to the patient. Typically, hemodialysis is performed for 4 hours up to three times a week.

PERITONEAL DIALYSIS

In peritoneal dialysis, the exchange of fluids and solutes occurs through the semipermeable lining of the peritoneal cavity (Fig. 8-7). A sterile catheter is inserted into the peritoneal cavity through the subcutaneous canal on the anterior abdominal wall. Sterile dialysis fluid is pumped into the peritoneal cavity and left to equilibrate with the patient's extracellular fluid. When equilibrium is reached, the dialysate containing metabolic end products is removed. This procedure can be carried out at the patient's home and thereby save him from frequent visits to the center for routine therapeutic dialysis. There are several options for dialysis; the most common is continuous ambulatory dialysis, involving four sessions evenly distributed throughout the day. In one session, the patient is injected with approximately two liters of dialysate.

Kidney transplantation has become the accepted treatment for end-stage renal disease and, for many patients, represents the most physiological and well-tolerated form of replacement therapy. Organs for transplantation are obtained from living relatives or, more often, from strangers, as well as from the corpses of people who have died of sudden death, provided that the organ is removed before the cessation of life support measures. The donor organ is transplanted to a patient with end-stage renal failure into the iliac fossa with vascular anastomoses with the iliac vessels. Careful identification of the type and pre-existing antibodies is necessary to prevent immunological rejection of the transplanted organ. In addition, the patient should receive prophylactic immunosuppressants to reduce the risk of acute rejection. For this, substances such as corticosteroids, cyclosporine and azathioprine are used. To prevent acute rejection, preparations of polyclonal and monoclonal antibodies against lymphocytes are also used. In addition to rejection, kidney transplant patients have an increased risk of developing infections and malignant neoplasms. However, the survival rate for a year after a cadaveric kidney transplant reaches 80%.

METHOD FOR TRACKING THE PROGRESSION OF CHRONIC KIDNEY DISEASE

From the moment that significant impairments have occurred in the kidney, it can be expected that after a certain time there will be a progressive deterioration in kidney function. It can occur due to a current disease, such as diabetes, or due to the damaging effects of glomerular hypertension in intact nephrons. As renal failure progresses, the glomerular filtration rate tends to decrease linearly over time. This empirical observation can be used to infer changes in kidney status and to predict the timing of end-stage renal disease (ie, when dialysis becomes necessary). In clinical practice, regular measurements of glomerular filtration rate and even creatinine clearance are difficult and imprecise. Instead of these indicators, the reciprocal of the plasma creatinine concentration can be used to assess the rate of disease progression. Recall that creatinine clearance creates the possibility of a fairly accurate estimate of the glomerular filtration rate:

Glomerular filtration rate = creatinine clearance = (Ucr x V): Pcr,

where Ucr is the urine creatinine concentration, V is the urinary flow rate and Pcr is the plasma creatinine. Creatinine is a metabolic product of skeletal muscle. If lean body mass is constant, the rate of creatinine production and excretion per unit time (ie, UcrV) will be relatively constant. Then this equation can be written as follows:

Glomerular filtration rate = creatinine clearance = (Ucr х V): Per = = constant / Рсг

1 / Pcr, from which it follows that the reciprocal of the plasma creatinine concentration (1 / Pcr) can be used to trace changes in the glomerular filtration rate.

Changes in the slope of the 1 / Pcr ratio with time can be used as an indicator of the rate of dynamics of the progression of renal failure. A steeper slope indicates faster than expected progression. Possibly due to a concomitant lesion such as pyelonephritis or renal vein thrombosis. Shallower slope - slower than expected progression; this is the goal of antihypertensive and dietary treatment. In most patients, indications for starting dialysis appear by the time plasma creatinine reaches 10 mg% (100 mg / l), in other words, the reciprocal value reaches 0. 1. For a patient with a known rate of progression, extrapolation of this ratio 1 / Pcr in time is necessary for a rough estimate of the approximate time before the start of the dialysis procedure. The assumption of a linear nature of the decrease in 1 / Pcr over a certain time is disputed, but this method of calculation is useful if the existing limitations are taken into account.

Medicine abstracts

Chronic renal failure

QUESTIONNAIRE FOR BASIC KNOWLEDGE

1. Give a definition of CRF.

2. Options for the course of chronic renal failure.

3. Etiology of chronic renal failure.

4. To characterize the pathogenesis of chronic renal failure.

5. List and describe the clinical symptoms of chronic renal failure.

6. Justify the examination program for chronic renal failure.

9. What is the prognosis for a patient with the development of chronic renal failure?

10. List the indications for hemodialysis.

DIAGNOSTICS OF CHRONIC RENAL FAILURE

Purpose of the topic... to study the issues of diagnostics of chronic renal failure.

Objectives of the topic:

1. To teach how to identify the main symptoms and syndromes in chronic renal failure.

2. To teach how to diagnose CRF with kidney disease

3. To teach how to use the possibilities of diagnosing chronic renal failure (complaints, medical history, objective data, laboratory and instrumental studies).

4. To study the principles of modern treatment of chronic renal failure:

a) drug treatment of syndromes;

b) indications for the initiation of dialysis treatment for chronic renal failure.

Chronic renal failure - a symptom complex caused by a sharp decrease in the number and function of nephrons, which leads to impaired excretory and endocrine function of the kidneys, homeostasis, disorder of all types of metabolism, acid-base balance, the activity of all organs and systems.

The prevalence of chronic renal failure (the number of new patients with chronic renal failure who require hemodialysis treatment per 1 million population per year) varies within a very wide range: from 18-19 to 67-84. Data on the prevalence of chronic renal failure are the basis for planning specialized care - the number of hemodialysis beds and the volume of transplantation.

The incidence of chronic renal failure (the number of patients per 1 million population) is approximately 150-200, reflecting to a certain extent the level of provision with extrarenal cleansing methods.

The most common causes of CRF are:

1. Diseases occurring with a predominant lesion of the glomeruli of the kidneys - CGN, subacute glomerulonephritis.

2. Diseases occurring with a predominant lesion of the renal tubules and interstitium, chronic pyelonephritis, interval nephritis.

3. Diffuse connective tissue diseases, SLE, systemic scleroderma, periarteritis nodosa, hemorrhagic vasculitis.

4. Metabolic diseases, diabetes mellitus, amyloidosis, gout,

hypercalcemia.

5. Congenital kidney disease: polycystic kidney disease, kidney hypoplasia (Fanconi syndrome, Alport syndrome, etc.).

6. Primary vascular lesions, malignant hypertension, renal artery stenosis. hypertonic disease.

7. Obstructive nephropathy - urolithiasis, hydronephrosis, tumors of the genitourinary system.

CGN and chronic pyelonephritis remain the most common kidney diseases leading to the development of chronic renal failure. They cause end-stage renal failure in more than 80% of patients. Among other nosological forms, amyloidosis, diabetes mellitus and polycystic disease most often lead to the development of uremia. In the United States, one in four patients admitted to programmed hemodialysis treatment has diabetes mellitus as a cause of chronic renal failure.

A special group is represented by urological diseases, accompanied by obstruction of the urinary tract, in which surgical treatment makes it possible to hope for a partial restoration of renal function even with a prolonged existence of an obstruction to the outflow of urine.

Speaking of renal failure, we must bear in mind the disturbances in water-salt metabolism, CBS, delay in nitrogenous toxins, disturbance of endocrine and enzymatic function.

Azotemia - an excess in the blood concentration of urea, amino nitrogen, creatinine, uric acid, methylguanidine, phosphates, etc. An increase in the level of amino nitrogen may be associated with increased protein catabolism due to its excessive intake, or its sharp restriction during starvation.

Urea is the end product of protein metabolism, formed in the liver from the nitrogen of deaminated amino acids. In conditions of renal failure, not only the difficulty of its excretion is noted, but also, for still unknown reasons, an increase in its production by the liver.

Creatinine is formed in the muscles of the body from its precursor creatinine. The content of creatinine in the blood is quite stable, an increase in creatinemia in parallel with an increase in the level of urea in the blood occurs, as a rule, with a decrease in glomerular filtration to 20-30% of the normal level. The overproduction of parathyroid hormone as a possible major toxin of uremia has attracted even more attention. This is confirmed by the effectiveness of at least partial parathyroidectomy. There are more and more facts indicating the toxicity of substances of unknown nature, the relative molecular weight of which is 100-2000, as a result of which they are called "average molecules". They are the ones that accumulate in the blood serum of patients with chronic renal failure. However, it is becoming more and more obvious that the syndrome of azotemia (uremia) is not caused by one or several toxins, but depends on the rearrangement of cells in all tissues and changes in the transmembrane potential. This occurs as a result of violations, both of the function of the kidneys and of the systems that regulate their activity.

Anemia. Its causes are blood loss, shortening of the life span of erythrocytes due to a deficiency of protein and iron in the body, toxic effects of nitrogen metabolism products, hemolysis (deficiency of glucose-6-phosphate dehydrogenase, excess guanidine), decreased erythropoietin. The growth of medium molecules also inhibits erythropoiesis.

Osteodystrophy due to impaired metabolism of calciferol. In the kidneys, an active metabolite of 1,25-dehydroxycalciferol is formed, which affects the transport of calcium by regulating the synthesis of specific proteins that bind it. With chronic renal failure, the transfer of calciferol and exchange-active firms is blocked. The water-electrolyte balance remains close to physiological for a long time, up to the terminal phase. Under conditions of impaired ion transport and tubular tubular defects, sodium loss increases, which, if it is insufficiently replenished, leads to hyponatremia syndrome. Hyperkalemia is regarded as the second most important sign of chronic renal failure. This is associated not only with the increasing catabolism characteristic of renal failure, but also with an increase in acidosis, and most importantly, with a change in the distribution of potassium outside and inside the cells.

The change in CBS occurs in connection with a violation of the function "carbonic acid-bicarbonate". With various options for impaired renal function, depending on the nature of the process, one or another type of impairment of CBS may be observed. With glomerular - the possibility of acid valences entering the urine is limited, with tubular - the predominant inclusion of ammonio acidogenesis occurs.

Arterial hypertension. In its appearance, the role of inhibition of the production of vasodilators (kinins) is undoubted. The imbalance of vasoconstrictors and vasodilators in chronic renal failure is caused by the kidney's loss of the ability to control sodium levels and circulating blood volume in the body. In the terminal phase of chronic renal failure, a persistent hypertensive reaction can be adaptive, maintaining filtration pressure. In these cases, a sudden drop in blood pressure can be fatal.

Hemorrhagic manifestations are associated with a violation of thrombus formation, coagulation, with the state of the vascular bed. DIC may appear. For CRF, it is not so much a decrease in the number of platelets that is characteristic as platelet dysfunction (a decrease in the functional activity of the 3rd platelet factor), generalized damage to the vascular eidothelium in the coagulation and fibrinolysis links.

Immunodeficiency state - decreased immune reactivity, predisposition to infectious diseases, afebrile course of the infectious process. Lymphopenia is noted, depending on the deficiency of both T- and B-lymphocytes.

Clinical manifestations

Asthenic syndrome: weakness, fatigue, drowsiness, loss of hearing, taste.

Dystrophic syndrome: dry and excruciating itching of the skin, traces of scratching on the skin, weight loss, real cachexia, muscle atrophy is possible.

Gastrointestinal syndrome: dryness, bitterness and an unpleasant metallic taste in the mouth, lack of appetite, heaviness and pain in the epigastric region after eating, often diarrhea, an increase in gastric acidity is possible (due to a decrease in the destruction of gastrin in the kidneys), in the later stages there may be gastrointestinal bleeding, stomatitis, parotitis, enterocolitis, pancreatitis, liver dysfunction.

Cardiovascular syndrome: shortness of breath, pain in the heart, arterial hypertension, hypertrophy of the left ventricular myocardium, in severe cases - attacks of cardiac asthma, pulmonary edema; with advanced CRF - dry or exudative pericarditis, pulmonary edema.

Anemic hemorrhagic syndrome: pallor of the skin, nasal, intestinal, gastric bleeding, skin hemorrhages, anemia.

Osteoarticular syndrome: pain in bones, joints, spine (due to osteoporosis and hyperuricemia).

Damage to the nervous system: uremic encephalopathy (headache, memory loss, psychosis with obsessive fears, hallucinations, convulsive seizures), polyneuropathy (paresthesia, itching, burning sensation and weakness in the arms and legs, decreased reflexes).

Urinary syndrome: isohypostenuria, proteinuria, cylindruria, microhematuria.

The manifestations of chronic renal failure depend on: 1) the stage of chronic renal failure; 2) the severity of disorders of various components of homeostasis.

In the initial stage of chronic renal failure, patients may not present any complaints; the clinical picture is due to the manifestation of the disease, as a result of which chronic renal failure developed. With the progression of chronic renal failure, first of all, symptoms of a neurological syndrome appear: weakness, drowsiness, fatigue, apathy. Gastroenterological syndrome is expressed by nausea, vomiting, loss of appetite up to aversion to food, diarrhea (less often constipation). Sometimes the sick can only be fed in the morning. Usually, dyspeptic complaints are associated with the development of uremic gastritis, however, uremic intoxication is probably of greater importance, since after hemodialysis the complaints quickly disappear. With an increase in renal failure, gastroenterological syndrome progresses, signs of encephalopathy appear (lethargy, irritability, insomnia), as well as symptoms of peripheral neuropathy (sensory and motor disorder).

Itching, epistaxis and gastrointestinal bleeding, subcutaneous hemorrhages are explained by the delayed "uremic toxins". With a prolonged delay in the body of uric acid, pain in the joints may appear - a manifestation of "uremic" gout. Arterial hypertension leads to decreased vision due to the development of severe retinopathy.

In the history of some patients, any kidney disease is detected, so these complaints are not a surprise to the doctor. The rapidity of the onset of CRF symptoms from the moment of detection of kidney disease is different: sometimes many years pass; with malignant (subacute) glomerulonephritis, chronic renal failure develops several months after the onset of the disease.

An objective study in the initial period of chronic renal failure reveals a decrease in body weight, dry skin (including in the armpits), a pale yellowish color of the skin due to the development of anemia and delayed urochromes. An ammoniacal odor appears from the mouth. Skin with traces of scratching, peeling, subcutaneous hemorrhages are often found.

When examining the circulatory system, hypertension, expansion of the borders of the heart to the left, an accent of the II tone in the second intercostal space to the right of the sternum are revealed. However, some patients with CRF may have normal blood pressure. In the terminal stage, uremic pericarditis develops, manifested by pericardial rubbing noise, shortness of breath. Serous-articular syndrome can also be expressed in the development of pleurisy (usually dry) and the appearance of "uremic" gout (tophus, joint deformity). Tongue dry, coated with a brownish bloom. Palpation of the abdomen reveals diffuse pain in the epigastrium and along the colon.

In patients with chronic renal failure, there is a tendency to infections: pneumonia is often noted, which sharply worsen the functional state of the kidneys. An increase in neurological symptoms is also manifested by convulsive twitching, polyneuropathy, the development of a coma with large, noisy breathing (Kussmaul), which is caused by progressive acidosis. Hypothermia is often noted, with infections (pneumonia), the body temperature sometimes does not rise.

As a result of developing osteoporosis, pathological fractures can be observed.

In a laboratory study, first of all, it is necessary to assess the functional state of the kidneys and the degree of retention of nitrogenous toxins.

When carrying out the Zimnitsky test, there is a monotonous excretion of urine of low relative density (iso, hypostenuria). In the sediment, the content of formed elements decreases, the level of proteinuria is reduced.

The degree of creatinine retention and glomerular filtration measured by endogenous creatinine versus creatinuria are reliable measures of renal function. A decrease in filtration to 40 ml / min indicates severe chronic renal failure, to 15-10-5 ml / min - to the development of terminal uremia. The level of creatininemia increases as the patient's condition worsens.

With advanced chronic renal failure in the blood, the content of uric acid rises - hyperuricemia appears. In peripheral blood, hypochromic anemia is determined, combined with toxic leukocytosis (6.0-8.0x10 9 / l) and neutrophilia. Thrombocytopenia is noted with a decrease in platelet aggregation, which is one of the causes of bleeding.

Violation of the release of hydrogen ions causes the appearance of metabolic acidosis.

In the terminal stage of chronic renal failure, the appearance of hyperkalemia is noted. The data of instrumental research methods characterize in more detail the state of organs in chronic renal failure. On the ECG syndrome of left ventricular hypertrophy (a consequence of hypertension), with the appearance of hyperkalemia, the ECG may change: the ST segment increases and the amplitude of the positive T wave increases.

When examining the fundus, severe retinopathy is noted. X-ray examination of the chest reveals peculiar changes in the lungs: the so-called uremic lung (bilateral focal darkening from the gate of the lung, caused by left ventricular failure or increased extravasation from the pulmonary capillaries). Bone X-ray reveals their demineralization. Gastric secretion is reduced, and gastroscopic examination reveals changes in the mucous membrane (atrophy and its rearrangement prevail).

Flow. To a large extent, the course of chronic renal failure is determined by the underlying disease. With CGN, renal failure progresses more rapidly than with other diseases.

Gradual progression of chronic renal failure is observed in persons of mature age with a calm course of the disease, rare exacerbations and relatively stable hypertension.

CRF progresses rapidly in persons under 30 years of age, in whom an exacerbation of the underlying kidney disease contributes to the growth of hypertension: edema often appears at the same time.

Examination program

1. OA of blood

2. OA of urine.

3. Daily urine output and the amount of fluid you drink.

4. Analysis of urine but Zimnitsky, Nechiiorsnko.

5. LHC: total protein, protein fractions, urea, krsatinin, bilirubin, trassaminase, aldolases, potassium, calcium, sodium, chlorides, acid-base balance.

6. Radioisotope renography and nocturnal scanning.

7. Ultrasound scanning of the night.

8. Research of the fundus.

9. Electrocardiography.

Early diagnosis of CRF is often difficult. On the one hand, there is often a long-term asymptomatic course of chronic renal failure, especially characteristic of chronic pyelonephritis, latent nephritis, polycystic disease. On the other hand, in connection with the polymorphism of lesions of internal organs with advanced CRF, its nonspecific "masks" may come to the fore: anemic, hypertensive, asthenic, gouty, osteopathic.

The presence of persistent normochromic anemia in a patient in combination with polyuria and arterial hypertension should be alarming in relation to chronic renal failure. However, early diagnosis of CRF is based primarily on laboratory and biochemical methods.

Determination of the maximum relative density (osmolarity) of urine, the value of glomerular filtration (CF) and the level of creatinine (Cr) in the blood serum is informative and reliable. A decrease in the maximum relative density of urine below 1018 in Zimnitsky's sample along with a decrease in CF in Reberg's sample to less than 60 ml / min indicates the initial stage of chronic renal failure. Azotemia (Kp> 0.12 mmol / l) joins at a later stage - with a decrease in CF to 40 - 30 ml / min.

In favor of chronic renal failure in terms of its differentiation from acute renal failure, data from a long "renal history", impaired calcium-phosphorus metabolism, and a decrease in the size of the kidneys speak.

Ryabov S.I. 1982

Stage phase name creatinine filtration form

Patient ___________________________ 72 years

Referring institution diagnosis: MKB, xr. pyelonephritis of the only left kidney.

Diagnosis on admission: chronic pyelonephritis latent course of "chronic renal failure III-IV"

Passport data

FULL NAME.: _________________________________

Age: 72

Place of residence: ___________________________

Place of work: disabled person of group II

Date of admission to the hospital: 16.06.08 10-00

Time of supervision: 27.06.08

Gr. blood: III, Rh “+“

Clinical diagnosis: chr. pyelonephritis of the only left kidney latent course of "chronic renal failure III-IV"

Complaints

At the time of examination, complaints of weakness, dizziness, minor recurrent pain in the left lumbar region.

morbi

Considers himself ill since 1989, when the right kidney was removed for m to b. After that, 18 years later, chronic pyelonephritis of the only left kidney was diagnosed. He is annually treated in a hospital, takes ketoterrol. Suffering from hypertension for a long time. Directed to a course of steroid treatment. She was hospitalized in the urology department in a planned manner.

At the time of admission, she complained of weakness, dry mouth, nausea, dry skin, constipation, poor appetite, periodic pain in the left lumbar region. Was diagnosed with chronic pyelonephritis of the only left kidney latent course, chronic renal failure 3-4.

vitae

Born on January 09, 1936. Was the third child in the family. She grew and developed normally, she did not lag behind her peers in mental and physical development. Received an incomplete secondary education. In 1952 she entered the technical school. Then she worked as a radio operator all her life. Hereditary history is not burdened. In 1985, the uterus with appendages was removed, 1989 - nephrectomy of the right kidney. Injury - fracture of the left hand in 2007.

Epidemic history: tuberculosis, Botkin's disease, venereal diseases. Of the past diseases, she notes colds of the upper respiratory tract. Denies bad habits. Allergic history: data on food and drug allergies were not identified. No blood transfusions were performed.

praesens communis

General inspection: The general state of moderate severity, clear consciousness, the patient's position is active, the patient's physique is proportional, the constitution is normosthenic, the gait is heavy, the posture is straight, height 165 cm, weight 83 kg, body temperature is normal (36.6 o C).

Examination of individual body parts:

Skin

· The color is pale, without depigmentation;

· The elasticity of the skin is reduced;

Thinning of the skin or seals are not detected, keratoderma is absent;

· The moisture of the skin is moderate;

· No rashes detected.

Fingernails

· Round shape;

· No brittleness or cross striation.

Subcutaneous tissue

· Development of the subcutaneous fat layer is excessive (the thickness of the fold in the subclavian region is 3.5 cm);

· Place of the greatest deposition of fat on the abdomen;

· No edema.

The lymph nodes

· Palpable single submandibular lymph nodes on the right and left, the size of millet grain, round, elastic consistency, painless, mobile, not adhered to the skin and surrounding tissue; no ulceration or fistula;

The occipital, cervical, supraclavicular and subclavian, ulnar, bicipital, axillary, popliteal, inguinal lymph nodes are not palpable.

Subcutaneous veins

· Subtle. Thrombi and thrombophlebitis were not revealed.

Head

· Oval shape. Head circumference 57 cm;

· The position of the head is straight;

Shaking and rocking (Musset symptom) is negative.

Neck

· Curvature - not curved;

· Palpation of the thyroid gland - not enlarged, uniform plastic consistency, painless.

Face

· Facial expression is calm;

· The palpebral fissure is moderately widened;

• The eyelids are pale, not edematous; trembling, xanthelasma, barley, dermatomyosin glasses are absent;

· Eyeball: no retraction and protrusion;

· The conjunctiva is pale pink, moist, without subconjunctival hemorrhage;

· Sclera pale with bluish tinge;

· The shape of the pupils is round, the reaction to light is friendly;

· Symptoms: Greffe, Shtelvag, Moebius negative;

· Snub nose; there are no ulceration of the tips of the nose, the wings of the nose do not participate in the act of breathing;

· Lips: the corners of the mouth are symmetrical, there are no clefts in the lips, the mouth is slightly open, the color of the lips is cyanotic; rashes, no cracks, lips are moist;

· Oral cavity: no smell from the mouth; the presence of aft, pigmentation, Belsky-Filatov-Koplik spots, hemorrhages, telangiectasis on the oral mucosa are absent, the color of the mucous membrane of the hard palate is pale pink;

· Gums: hyperemic, loose, bleeding when touched, no border;

Inserted teeth, an abundance of hard dental deposits on the lower incisors from the oral surface

K - crown; L - cast tooth; P - filling; О - absent

· Tongue: the patient sticks out the tongue freely, there is no tremor of the tongue, the color of the tongue is pale pink, with misprints of the teeth, partially overlaid with white, no cracks or ulcers;

· Tonsils of the correct shape, do not protrude from the arches, pale pink in color; plaque, purulent plugs, no ulcers.

Examination of the musculoskeletal system:

Inspection

· There are no swelling, deformity and defiguration of the joints;

· The color of the skin over the joints is not changed;

· Muscles are developed according to age; no atrophy, muscle hypertrophy;

· No joint deformities and no bone curvature.

Superficial palpation

· Skin temperature above the joint surface is not changed;

· The volume of active and passive movements in all planes is preserved;

· No joint murmurs.

Deep palpation

· The presence of effusion in the joint cavity and compaction of the synovial membrane in the bimanual is not revealed;

· The presence of "articular mice" was not identified;

· Two-finger bimanual palpation is painless;

· Symptom of fluctuation is negative; symptom of the anterior and posterior "drawer", Kushelevsky's symptom are negative;

· Muscle tone without pathological changes.

Percussion

· When beating the bones, there is no soreness.

Respiratory examination:

Chest examination

The shape of the chest is not changed, without curvature, symmetrical, the excursion of both sides of the chest during breathing is uniform, the type of breathing is mixed, the respiratory rate is 18, the breathing rhythm is correct, there is no difficulty in nasal breathing;

Excursion of the chest 5 cm

Palpation of the chest

· The chest is resistant, painless on palpation;

· There is no sensation of pleural friction on palpation.

Comparative lung percussion

· With comparative percussion of the lungs, a clear percussion sound in 9 paired points.

Topographic percussion

Lower bounds

Mobility of the lower pulmonary margin

Lung auscultation

Right and left vesicular breathing,

Side respiratory noises: dry, moist, fine bubbling rales are not heard, crepitus and pleural friction noise are not so.

· Bronchophonia is carried out in the same way in all paired points.

Study of the circulatory system

Examination of the area of the heart and blood vessels

· There is no defiguration in the region of the heart; the apical and cardiac impulse is not visually determined; systolic retraction in

the area of the apical impulse is not defined; there is no pulsation in the second and fourth intercostal spaces on the left;

· Pulsations in the extracardiac region: "dance of carotids" pulsation of the cervical veins in the jugular fossa, epigastric pulsation was not detected; Quincke's pulse is negative;

Palpation of the region of the heart

· The apical impulse is palpable in the fifth intercostal space along the midclavicular line, diffuse, resistant, high; systolic and diastolic tremors (a symptom of "cat's purr") is absent; pulse 84 / min., synchronous on both hands, pulse even, regular.

Percussion

The boundaries of the relative and absolute dullness of the heart

· The length and diameter of the heart according to Kurlov are 13 and 11 cm, respectively.

· Percussion of the vascular bundle in II m / p 5 cm;

· Heart of mitral configuration;

Auscultation of the heart and blood vessels

· Muffled heart sounds, weakening of I tone at the apex of the heart; accent of the II tone over the aorta; minor tachycardia;

Bifurcation, splitting, the appearance of additional noises (gallop rhythm, quail rhythm) is not heard;

Intracardiac murmurs

Decreasing systolic murmur at the apex

Extra-cardiac murmurs

· Noise of pericardial friction and pleuropericardial is not heard; vascular murmurs are not heard

BP on the right hand 140/90; BP on the left hand 140/90; BP on the right thigh 140/90; BP on the left thigh 145/95

Abdominal examinations:

Examination of the abdomen

· The abdomen is rounded, symmetrical, participates in the act of breathing; peristaltic and antiperistaltic movements are not visually determined; subcutaneous venous anastomoses on the anterior abdominal wall are not developed; abdominal circumference 96 cm.

Palpation of the abdomen

· On superficial palpation, the abdomen is painless; there is no tension in the abdominal wall. Hernial openings in the umbilical ring and along the white line of the abdomen were not found. Shchetkin-Blumberg's symptom is negative; no tumor formations were found;

With deep palpation, the sigmoid colon in the left iliac region is in the form of a smooth dense cylinder, 2 cm in diameter, 4-5 cm long, painless, non-rumbling, mobile. Blind, ascending colon, appendix are not palpable. The lower border of the stomach is not determined by the "splash noise" method. By auscultofriction and auscultopercussion, the border of the stomach is determined 3.5 cm above the navel to the right and left of the midline;

Transverse colon, stomach and pancreas are not palpable. On palpation of the liver, the edge is rounded, the hepatic surface is smooth, soft, elastic consistency; the gallbladder is not palpable. Courvoisier's symptom, Frenicus phenomenon, Obraztsov-Murphy's symptom are negative. The spleen is not palpable.

Abdominal percussion

· With percussion, a tympanic percussion sound is detected. Mendel's symptom is negative; no free fluid was found in the abdominal cavity.

· Borders of the liver according to Kurlov 9 * 8 * 7 cm; symptom Ortner, Vasilenko, Zakharyin negative;

The dimensions of the spleen according to Kurlov are 5 * 7 cm.

Auscultation of the abdomen

· Above the abdominal cavity, intestinal motility is heard. There is no peritoneal rubbing noise. Systolic murmur above the aorta, above the renal arteries is not heard.

Examination of the urinary organs

Inspection

· Redness, swelling, swelling in the lumbar region is not observed, there are no protrusions above the pubis. There is a scar in the right lumbar region.

Palpation

· In the horizontal and vertical position, the kidneys are not palpable. On palpation in the suprapubic region, there were no foci of compaction; palpation is painless.

Percussion

· Symptom of Pasternatsky is negative;

· Percussion the bladder is not defined.

Status localis

The lumbar region is symmetrical, without visible depressions or deformations. Palpation of the area of the left kidney is painless, the left kidney is not palpable. Palpation of the right kidney area is painless, on the right there is a postoperative scar. The tapping symptom is negative on both sides. There is no pain along the ureters. The external genital organs are formed according to the female type, corresponding to age.

Bladder: no protrusions above the pubic region, painless on palpation.

2. Gender: Male

3. Age: 22 years old

4. Place of work: GUPO food quality control center

5. Position: driver

7. Time and date of admission: 10.11.05 at 12.35 - 13.30

8. Date of supervision: 28.11.05 - 3.12.05

The patient complains of weakness, edema localized on the face, legs, abdomen, which appear in the morning and increase during the day, shortness of breath with little physical exertion, with impaired inspiration (inspiratory character), constant headaches in the occipital region of a pressing character, frequent urination in night time (nocturia), decreased urine output (oliguria), itching and dry skin.

III. History of this disease (Anamnesis morbi)

In childhood, there were frequent colds, bronchitis, at the age of 5-6 (he does not remember exactly) proteinuria was found, at the age of 14, when passing the commission, arterial hypertension was revealed.

Considers himself ill since 2001 after having bathed, subsequently appeared cough, headaches, general weakness, edema localized mainly on the face in the morning, shortness of breath. After the completed treatment in the mountains. Hospital No. 6, the patient began to be registered with a nephrologist, his condition worsened, there was an increase in the abdomen in volume. Ultrasound revealed VAR (congenital malformation): hypoplasia of both kidneys. In 2002, due to the deterioration of the patient's condition, he turned to the mountains. Hospital No. 5.

With a worsening of the general condition, an increase in edema, an increase in headache, he applied to the Burdenko Regional Clinical Hospital in 2005. Was diagnosed with chronic renal failure III-IV degree.

He was released from military service due to congenital malformation - hypoplasia of both kidneys.

Household history: The patient considers his living conditions to be good.

Bad habits:

He has been smoking for about 5 years, a pack a day, drinks alcohol often and in large quantities.

Past illnesses:

In childhood, there were frequent colds, bronchitis, proteinuria was found at the age of 5-6, at the age of 14 arterial hypertension was revealed at the time of the passed commission. The patient has urethritis, chlamydia, Raynaud's disease. Tuberculosis, jaundice, HIV infection denies.

There is no intolerance to drugs and food.

Not hereditarily burdened, all relatives are healthy.

Consciousness: clear, normally oriented in space.

Body type: constitutional type - normosthenic, height - 173 cm. Body weight - 83 kg. posture - stooped, gait - slow.

The ratio of body weight and height according to Broca's index is 1.137, which indicates the I degree of obesity, which may be associated with edema.

Body temperature: normal (ranges from 36.8 ° C to 37.2 ° C; from 8 to 10 days of illness, there is a short fever with a rise in temperature above 38 ° C).

Facial expression: calm.

There are no rashes, vascular changes, hemorrhages, scars, trophic changes, visible tumors.

Nails of the usual color and shape.

Moderately developed, edema on the legs and an increase in the volume of the abdomen are visible. Soreness on palpation of adipose tissue, no crepitus.

Zev: Pale pink, tonsils intact.

The shape of the bones is normal, the presence of deformities, pain on palpation, tapping, no symptom of "drumsticks".

There is no deformity or edema in the larynx area, the voice is clear.

Rib cage:

The shape of the chest is normosthenic, the supraclavicular and subclavian fossae are slightly smoothed, the width of the intercostal spaces is moderate, the epigastric angle is straight, the scapula and clavicle fit tightly to the posterior surface of the chest. The ratio of the anteroposterior to lateral dimensions is approximately 2: 3, the chest is symmetrical. There is no pronounced curvature of the spine.

Palpation

Topographic lung percussion:

Medicine abstracts

Chronic renal failure (CRF) is a clinical syndrome caused by irreversible, usually progressive, kidney damage due to various pathological conditions.

CAUSES OF CHRONIC RENAL FAILURE

MAIN CAUSES OF TERMINAL STAGE OF KIDNEY DISEASE IN THE USA

Causes of kidney disease Number of cases in%

Diabetes 34.2

Hypertension (nephrosclerosis) 29.2

Glomerulonephritis 14.2

Interstitial nephritis 3.4

Cystic kidney disease 3.4

Other or unknown 15.4

PATHOPHYSIOLOGY

CLINICAL CONSEQUENCES OF CHRONIC RENAL FAILURE

NEUROLOGICAL CONSEQUENCES

HEMATOLOGICAL CONSEQUENCES

CARDIOVASCULAR EFFECTS

GASTROINTESTINAL EFFECTS

METABOLIC AND ENDOCRINE EFFECTS

TREATMENT OF CHRONIC RENAL FAILURE

SPECIFIC DISEASE TREATMENT

TREATMENT OF HYPERTENSION

Diuretics in the treatment of edema

PREVENTION AND TREATMENT OF RENAL OSTEODYSTROPHY

CONTROL OF MEDICINE APPLICATION

TREATMENT OF TERMINAL STAGE KIDNEY DISEASE

SUBSTITUTION THERAPY

PERITONEAL DIALYSIS

METHOD FOR TRACKING THE PROGRESSION OF CHRONIC KIDNEY DISEASE

Glomerular filtration rate = creatinine clearance = (Ucr x V): Pcr,

Glomerular filtration rate = creatinine clearance = (Ucr х V): Per = = constant / Рсг

1 / Pcr, from which it follows that the reciprocal of the plasma creatinine concentration (1 / Pcr) can be used to trace changes in the glomerular filtration rate.

PENZA MEDICAL INSTITUTE AT PNZA STATE UNIVERSITY

6. Place of residence: Penza, - ————————

IV. ANAMNESIS VITAE

Brief biographical information:

The patient was born on 05.05. 1983 in an ordinary family. Grew and developed in accordance with age and gender. Received secondary education.

Family and sex history: not married, no children.

Labor history:

Immediately after school, he began working as a driver at the State Unitary Enterprise Center for Food Quality Control. Works on a rolling schedule. In connection with work activities, one has to be on long unforeseen business trips, experience a sharp change in temperature, psycho-emotional stress, the presence of harmful fumes, dust.

Nutrition: The patient considers nutrition to be complete.

Allergic history:

V. HERITAGE

Vi. PRESENT STATE (STATUS PRAESENS)

General inspection.

The general condition of the patient: the condition of the patient is of moderate severity.

Position: active.

The skin is dry, pale yellow, mucous membranes are pale pink. Skin turgor is not changed.

Subcutaneous fat:

Lymph nodes: not palpable.

The degree of muscle development is satisfactory, the tone is preserved, the muscle strength is not changed, pain and seals on palpation were not detected.

There is no normal configuration, swelling, pain on palpation, and no hyperemia. Local skin temperature is normal. The movements in the joints are not changed, not painful.

Respiratory system

The shape of the nose is not changed, breathing through the nose is free, there is no discharge from the nose and no nosebleeds.

The type of breathing is mixed, breathing movements are symmetrical, there is no lag of one half of the chest, there is no participation of additional muscles in breathing. Heart rate 24 per minute. Breathing is shallow, rhythmic.

There were no painful areas on palpation, the chest was elastic, the voice tremor was carried out equally on both sides, not changed.

Percussion

The percussion sound is pulmonary, no change is observed.

The height of the tops of the lungs.