What does the diagnosis of kidney nephrosclerosis mean? Nephrosclerosis (Shriveled kidney) Chronic pyelonephritis with outcome in nephrosclerosis

Kidney nephrosclerosis

Every urologist knows the causes of kidney nephrosclerosis, what it is, the outcome of the disease and the signs of this pathology. Nephrosclerosis (shrunken kidney) is a disease that occurs in a chronic form and is characterized by the growth of coarse scar tissue. Mostly adults are affected. If not properly treated, this condition can be fatal.

Types and causes of the disease

Kidney nephrosclerosis is primary (it occurs as an independent pathology against the background of damage to the renal vessels) and secondary (it is a complication of other diseases). The following forms of this pathology are distinguished:

• hypertonic;
• atherosclerotic;
• ischemic (develops as a result of blockage of the arteries that feed the kidneys);
• diabetic;
• hormonal (occurs during pregnancy and is a complication of toxicosis);
• benign (characterized by slow progression);
• malignant (characterized by the death of nephrons, capillaries and arterioles, which leads to atrophy of the organ).

The most commonly diagnosed diabetic and hypertensive nephrosclerosis. The reasons for the proliferation of connective tissue are:

1. Prolonged and persistent increase in blood pressure in the renal vessels (more than 139/89 mm Hg. Art.).
2. Frequent hypertensive crises.
3. Kidney infarction. This condition is characterized by tissue necrosis as a result of acute circulatory disorders.
4. Thrombosis of the renal arteries.
5. Thromboembolism (blockage of blood vessels by a detached blood clot).
6. Increased blood clotting.
7. antiphospholipid syndrome.
8. Blockage of arteries by plaque. This pathology often develops against the background of excessive consumption of fatty foods and simple carbohydrates, overeating, physical inactivity, smoking and dyslipidemia (changes in the blood lipid spectrum). With atherosclerosis, the lumen of the vessels decreases and the walls thicken. At the same time, elasticity decreases.
9. Congenital malformations of the kidneys.
10. Diabetes. It develops nephropathy. The reason is damage to the walls of blood vessels.
11. Toxicosis.
12. Chronic inflammatory diseases (pyelonephritis and glomerulonephritis).
13. The presence of kidney stones (nephrolithiasis).
14. Violation of the outflow of urine (hydronephrosis).
15. Stricture or compression of the ureter.
16. Tuberculosis.
17. Amyloidosis. With this pathology, an abnormal amyloid protein is formed, which is deposited in the tissues of the kidneys. In response, autoantibodies are produced that affect the nephrons and blood vessels.
18. Injuries.
19. Surgical interventions.
20. Exposure to ionizing radiation.
21. Systemic diseases (lupus erythematosus). With this pathology, circulating immune complexes are formed that attack their own tissues. There is damage to the renal tubules, an inflammatory reaction and tissue sclerosis.

Causes of kidney nephrosclerosis

Primary nephrosclerosis

Primary sclerosis of the kidney often occurs with a heart attack, atherosclerosis of the renal arteries, arterial hypertension and chronic plethora of the organ. Often this problem is faced by elderly people after 70 years. This is due to the natural aging process and the death of nephrons. In older people, there is thickening of the arteries, calcium deposition, and proliferation of connective tissue. The cortical layer of the kidneys becomes thinner, and the inner layer of the tubules atrophies. Symptoms of primary nephrosclerosis can be detected in a child.

Secondary nephrosclerosis

If hypertensive nephroangiosclerosis occurs primarily, then the secondary form is a complication of infectious and non-infectious pathology. It is necessary to consider what diabetic sclerosis is. Kidney damage is a late complication of type 1 and type 2 diabetes (occurs on average 15-20 years after the onset of the disease). Glomeruli are predominantly affected.

Forms of kidney nephrosclerosis

Symptoms and Diagnosis

If a person has atherosclerotic nephrosclerosis or another form of this pathology, then the following symptoms are possible:

1. Edema. They occur predominantly in the face, but may appear on the trunk. Edema is warm, mobile (going down) and paler than the surrounding skin.
2. Weakness.
3. Fast fatiguability.
4. Dyspepsia in the form of nausea and loss of appetite.
5. Skin itching.
6. Dryness and pallor of the skin.
7. Pain in the lumbar region.
8. Increase in blood pressure. It is manifested by headache, dizziness, impaired sensitivity and the presence of flies before the eyes.
9. Visual disturbances in the form of a veil before the eyes, loss of visual fields, decreased visual acuity and headache. With nephrosclerosis against the background of hypertension, swelling of the papilla or optic disc and retinal detachment often occur.
10. Bruising, bruising, bruising and bleeding. The reason is a decrease in the production of urokinase, which is responsible for blood clotting.
11. Signs of iron deficiency anemia in the form of weakness, dizziness, periodic fainting and shortness of breath.
12. Hematuria (an admixture of red blood cells in the urine).
13. Polyuria or oliguria. A decrease in urine volume is associated with the death of nephrons and a violation of blood filtration. With the death of more than 90% of kidney cells, anuria develops. With it, urine does not enter the bladder.
14. signs of azotemia. The reason is the accumulation of nitrogenous substances (creatinine and urea) in the blood. Thirst, palpitations, dyspepsia and drowsiness are observed. The extreme degree of this condition is uremia.
15. Pain behind the sternum.
16. Signs of cardiac asthma in the form of a feeling of lack of air, sweating, cyanosis of the skin, wheezing, shortness of breath and asthma attacks.
17. Intolerance to meat food.

In the early stages of the disease, there may be no complaints. The consequences (complications) of nephrosclerosis in children and adults are: chronic renal failure (the most common outcome of the disease), severe intoxication of the body and uremia. With the development of CRF (chronic renal failure) and the absence of proper treatment, the prognosis is unfavorable. Regular medication, blood purification and monitoring of laboratory parameters can prolong life.

Symptoms of kidney nephrosclerosis

Diagnosis requires:

1. Collection of anamnesis.
2. Palpation, percussion and auscultation.
3. Measurement of blood pressure.
4. General urine analysis. Detects proteinuria (protein admixture), erythrocyturia (blood admixture) and a decrease in its relative density.
5. General and biochemical blood tests. With this disease, hemoglobin, erythrocytes and platelets decrease. Leukocytosis is observed, creatinine, urea and uric acid increase. In the later stages, the concentration of trace elements increases.
6. ultrasound. Reveals a decrease in the size of the kidneys, salt deposits and atrophy of the cortical substance.
7. Test according to Zimnitsky.
8. excretory urography.
9. CT or MRI.
10. Angiography.
11. radioisotope scanning.
12. Dopplerography.
13. Renography (radiography).
14. Biopsy.

Treatment Methods

With renal sclerosis, treatment should be comprehensive. It includes:

1. Compliance with a salt-free diet. Patients should reduce protein intake, eat 5-6 times a day in small portions.
2. The use of medications (anticoagulants, antiplatelet agents, antihypertensive drugs, potassium and iron preparations, bisphosphonates, sorbents, Canephron or Cyston). With nephrosclerosis against the background of hypertension, ACE inhibitors (Perindopril, Kapoten, Enap), calcium channel blockers (Amlodipine, Verapamil) and beta-blockers (Egilok, Betalok, Concor) can be prescribed.
3. Micronutrient intake.
4. Purification of the blood by hemodialysis.

Treatment of kidney nephrosclerosis

In severe cases, a kidney transplant is required.

NEPHROSCLEROSIS (nephrosclerosis; Greek, nephros kidney + sclerosis) - replacement of the parenchyma of the kidney with connective tissue, leading to their compaction, wrinkling and dysfunction.

"Nephrosclerosis" is a clinical and anatomical concept. The process can develop due to various diseases of the kidneys and their vessels. In 1872, Gall and Sutton (W. W. Gull, H. G. Sutton) for the first time suggested that the cause of N. is damage to the vessels of the kidneys, and called it arteriolocapillary fibrosis. In 1914 Folhard and Far (F. Volhard, Th. Fahr) singled out arteriolosclerotic changes in the kidneys as an independent nozol, a form of diffuse bilateral kidney disease and associated them with hypertension; they also proposed to distinguish between simple sclerosis of the kidneys - in a benign form of hypertension and its combined form - in hypertension with a malignant course.

Etiology and pathogenesis

Replacing the renal parenchyma with connective tissue can be observed with advanced hypertension (see) and is most often associated with narrowing of the renal arteries - primary N. (angiogenic N.), primary wrinkled kidney. Due to insufficient blood supply, increasing hypoxia, dystrophic and atrophic changes in the kidney parenchyma occur, followed by proliferation of connective tissue. Depending on the nature of the process leading to the narrowing of the renal arteries, N. is distinguished hypertonic, or arteriolosclerotic, and atherosclerotic. In a pathogeny of primary N. also hron, a venous plethora matters, at Krom growth of connecting fabric in kidneys is connected with the increased synthesis of tropocollagen in the conditions of oxygen insufficiency. Carry postinfarction N. developing at scarring of multiple heart attacks of kidneys to primary N. (see).

Growth in the kidneys of connective tissue can occur a second time, as a result of various diseases (secondary N., secondary wrinkled kidney). Secondary N. represents an outcome of the inflammatory and dystrophic processes arising in kidneys at hron, glomerulonephritis, pyelonephritis (pyelonephritic wrinkling of kidneys, pyelonephritically wrinkled kidneys), nephrolithiasis (calculous N.), tuberculosis (tuberculous N.), syphilis (syphilitic N.). ), rheumatism (rheumatic N.), systemic lupus erythematosus (lupus N.), amyloidosis (amyloid wrinkling of the kidneys, or amyloid-wrinkled kidneys), diabetes mellitus (diabetic N.).

Secondary N. can develop after such adverse effects as trauma (including after repeated operations on the kidneys), the effects of ionizing radiation, as well as in severe forms of nephropathy in pregnant women - preeclampsia and eclampsia. The spasm of arteries characteristic of nephropathy, inflammation of the renal glomeruli and tubular dystrophy after delivery in some cases are transformed into hron, glomerulonephritis, to-ry, slowly progressing, leads to wrinkling of the kidneys, the severity of changes and features of the course distinguishes two forms - benign and malignant. The benign form is characterized by arteriolosclerosis (Fig. 1), often in combination with atherosclerosis of the renal artery and its large branches, atrophic changes in groups of nephrons with secondary glomerular hyalinosis (Fig. 2), an increase in the connective tissue stroma, hyalinosis of the papillae of the pyramids. Macroscopically, the surface of the kidneys is fine-grained, and when combined with atherosclerosis, it is coarse-grained. As arteriolosclerotic changes increase, combining

Such sharp inf. diseases, such as hemorrhagic nephrosonephritis, leptospirosis, typhoid and typhus, scarlet fever, measles, and sepsis, are accompanied by changes in the parenchyma, interstitium and renal vessels of various mechanisms and severity - from focal glomerulonephritis without impaired renal function to tubular necrosis and acute renal insufficiency. After these inflammatory and necrotic changes N. develops varying degrees of severity, which usually does not progress.

Allocate also involutive N., to-ry is caused by age-related changes in the vessels of the kidneys, as well as atherosclerosis or hypertension, often observed in elderly and senile people.

pathological anatomy

Of the primary N., hypertensive, or arteriolo-sclerotic, nephrosclerosis is most common. Headlights (Th. Fahr), depending on the nature, prevalence, degree of plasmorrhagia (see) and hyalinosis (see), and the exclusion of new groups of nephrons, kidney failure develops (see).

The malignant form is characterized by fibrinoid necrosis of arterioles (arteriolonecrosis) and capillary loops of the glomeruli (Fig. 3, a), stromal edema, hemorrhage, protein degeneration of the tubular epithelium. Renal sclerosis develops very quickly in response to necrotic changes (Fig. 3, b). Similar changes can also occur in eclampsia (malignant post-eclamptic N.).

Macroscopically, the surface of the kidneys is motley, fine-grained (Fig. 4); the kidneys at the same time are not much different from the "big motley kidney" with glomerulonephritis (see). Arteriolonecrosis of the kidneys leads to renal failure.

According to Lelein (M. Lohlein), the benign form of arteriolosclerotic N. corresponds to the first stage of N. (initial N.), which occurs clinically without manifestations from the kidneys, and the malignant form corresponds to the second stage of N. (progressive N.), for which characterized by a rapid course with the development of renal failure.

However, this sequence of the process is not recognized by everyone.

According to H. N. Anichkov, K. G. Volkova, M. A. Zakharyevskaya, the morphology of arteriolosclerotic nephrosclerosis reflects the features of the course of hypertension.

Atherosclerotic N. arises at narrowing (caused by an atherosclerotic plaque) of a renal artery at the place of its discharge or division into branches of the first and second order.

More often this process is unilateral, rarely bilateral. In the kidney, wedge-shaped areas of parenchyma atrophy develop with stromal collapse and replacement of these areas with connective tissue or infarctions, followed by their organization and scarring (atherosclerotic wrinkled kidney, atherosclerotic nephrocyrrhosis). Macroscopically, in this case, the night becomes large-tuberous, it is often difficult to distinguish it from a kidney with iostinfarction N. The function of such a kidney (kidneys) suffers little, since most of its parenchyma remains intact. As a result of ischemia of the renal tissue, in some cases, with stenosing atherosclerosis of the renal arteries, symptomatic (renal) hypertension develops.

Secondary N., most often developing with hron, glomerulonephritis, is associated not only with glomerulonephritis as such (fibroplastic transformation of glomerular changes), but also with those changes in the vessels of the kidneys, which are constantly found in this disease, reflecting the state of renal allergy (proliferative endarteritis ), arterial hypertension (arteriolosclerosis, arteriolonecrosis), adaptation of the vascular system to turn off the "peripheral bed" of the kidneys (progressive elastofibrosis of the arteries with secondary lipoidosis). Thus, secondary N. always has the features of angiogenic.

Therefore, the morphological criteria for the differential diagnosis of primary (hypertonic) and secondary (nephritic) kidney contraction are usually unclear.

Involutive changes in the kidneys are detected starting from the age of 40-50 and by the age of 70 lead to a reduction in the mass of active nephrons by about 40%.

Age-related atrophy of the kidneys is accompanied by a gradual thinning of the cortical layer of both kidneys, atrophy of the tubular epithelium up to the death and replacement of the tubules with scar tissue. The glomeruli undergo hyalinosis, and their number gradually decreases. Increased vascular resistance with age leads to desolation of the glomerular capillaries, the formation of anastomoses between the afferent and efferent arteries, bypassing the glomeruli.

N. in old age is associated primarily with age-related changes in the vessels of the kidneys, so it approaches the primary mechanism of development.

Main clinical signs. A wedge, displays of primary N. arise usually in late stages of an idiopathic hypertensia both at high-quality, and its malignant course. One of the early signs of kidney damage may be polyuria (see) and nocturia (see), however, nocturia is not always the result of polyuria and may indicate a violation of the daily rhythm of the kidneys. Proteinuria (see), observed at N., usually small and changeable.

Quite often at N. the microhematuria is observed, in some cases there can be a macrohematuria (see. Hematuria ). A decrease in renal clearance (see) with a relative increase in the filtration fraction is manifested by a decrease in the concentration ability of the kidneys (hyposthenuria), which is detected using the Zimnitsky test. Accordingly, the specific gravity of urine and its osmolarity decrease. In the case of severe vascular damage to the kidneys, leading to a significant decrease in renal blood flow, their pressor effect on the level of blood pressure increases, the cut stabilizes at a high level and is difficult to correct with medication (see Arterial hypertension).

An increase in diastolic blood pressure is especially characteristic, a cut is always higher than 120-130 mm Hg. Art.

In this regard, there may be phenomena of overload and insufficiency of the left ventricular myocardium, coronary insufficiency, cerebral hemorrhages, edema of the optic nerve papilla, retinal detachment, and in some cases progressive renal failure.

Survey pictures reveal a decrease in the affected kidney (in whole or in part), the unevenness of its contours.

Prevention nephrosclerosis is the timely treatment of diseases leading to its development.

Radiation nephrosclerosis

Radiation nephrosclerosis refers to the long-term effects of ionizing radiation on the body (see) and is detected many months or years after exposure.

Morphologically, radiation N. is expressed by atrophy of the renal tubules, interstitial fibrosis, and sclerosis of the vessels of the kidneys. There is no single view on the development of radiation N.. The hypothesis of primary damage to the renal glomeruli is dominant, a cut, according to a number of researchers, can be caused by factors immunol, character. There is a point of view that radiation N. develops as a result of primary damage to vessels by ionizing radiation. It is possible that this process is based on damage to the genetic apparatus of the endothelium of the kidney vessels. It is also assumed that the cause of radiation N. is the primary damage to the renal tubules. Sometimes radiation N. is considered as a result of simultaneous damage to the parenchyma / kidneys and the vascular system. It is believed that radiation N. is based on interdependent vascular disorders and changes in the interstitial substance of the kidneys.

Basic information about radiation N. was obtained in experiments on animals, as well as as a result of observations of victims of the atomic bomb explosions in Hiroshima and Nagasaki and patients who were subjected to local radiation for tumors of the lumbar region. The severity of radiation N. depends on the type of ionizing radiation, its dose and the nature of the dose distribution in time and space (see Doses of ionizing radiation, Exposure time factor). After acute irradiation in absolutely lethal doses, radiation N. does not occur, because in the short period preceding the death of the organism, sclerotic processes in the kidneys do not have time to develop. Acute radiation sickness of mild to moderate severity in the long term may result in the development of radiation N. With total irradiation, the development of radiation N. in at least 50% of animals, according to most researchers, occurs when exposed to a dose close to 500 rad. There is information about the occurrence of radiation N. after total exposure to ionizing radiation in doses of 100-300 rad. Under conditions of local irradiation of the kidneys, N.'s development can be observed in the range of doses of ionizing radiation from 1000 to 2500 rad.

In radiol, practice, the kidneys are considered as critical organs (see) during radiation therapy for cancer metastases in paraortal lymph nodes, ribs or vertebrae from ThXI to LIV, as well as for tumors of the intestine, uterus, cardial esophagus and some other organs . The greatest care should be taken when carrying out neutron and proton therapy, since these types of ionizing radiation have a more pronounced effect on radiation H. Alpha radiation is also characterized by high efficiency in this regard. In experiments it is shown that at defeat by polonium which is removed which is generally carried out through kidneys, in the remote terms radiation N. is formed against the developing hron, radiation sickness.

Clinically, radiation N. in mild cases is manifested by proteinuria, slight hypertension; kidney function is not impaired. In severe cases, hypertension develops, which is not amenable to drug treatment, renal failure.

Treatment is symptomatic (salt restriction, antihypertensives).

Bibliography: Vepkhvadze R. Ya. Radiation complications of the kidneys, Tbilisi, 1967; Zakharyevskaya M. A. Pathological anatomy of vascular nephrosclerosis, M., 1952; Kalugina G. V. Differential diagnosis of vascular nephrosclerosis, L., 1975, bibliogr.; Kushakovsky M. S. Hypertension, M., 1977; Lang G. F. Hypertension, L., 1950; Metabolism in radiation sickness, ed. I. I. Ivanova, p. 198, Moscow, 1956; Fundamentals of Nephrology, ed. E. M. Tareeva, vol. 1, p. 372 and others, M., 1972; Postnov Yu. V., Perov Yu. L. and Tribunov Yu. P. Sclerosis of the medulla of the kidney in hypertension, Arkh. patol., t. 36, No. 7, p. 75, 1974; Kidneys, ed. F. K. Mostofi and D. E. Smith, trans. from English, p. 294, M., 1972; Chebotarev D. F. Geriatrics in the clinic of internal diseases, Kyiv, 1977; Fahr Th. Nephrosklerose, Handb. spez. path. Anat. u. Histol., hrsg. v. V. F. Henke u. O. Lubarsch, Bd 6, T. 1, S. 368, B., 1925, T. 2, S. 909, V., 1931; HeptinstallR. H. Pathology of the kidney, Boston, 1974; Yolhard F.a. Fahr Th. Die Brightsche Nierenkrankheit (Klinik, Pathologie und Atlas), B., 1914; Z o 1 1 i n-g e r H. U. Niere und ableitende Harnwege, in: Spez. path. Anat., hrsg. v. W. Doerr u. E. Uehlinger, Bd 3, B. u. a., 1966.

E. M. Tareev; P. Ya. Vepkhvadze (med. glad.), B. B. Serov (stalemate. An.).

usually develops as a result nephrosclerosis- loss of functional kidney tissue and its replacement with functionally inactive connective tissue.

Sclerotic changes in the renal glomeruli (glomerulosclerosis) and tubulointerstitium (tubulointerstitial fibrosis) are combined in different ways in kidney diseases of various nature.

The advanced development of tubulointerstitial fibrosis with relatively intact glomeruli (the phenomenon of "atubular nephrons" in the morphological study of the kidney) is typical for interstitial kidney diseases, as well as for vascular nephropathies, in which tubulointerstitium ischemia is observed.

In "glomerular" kidney diseases (glomerulonephritis, diabetic nephropathy), glomerulosclerosis is combined with secondary changes in the renal tubulointerstitium, and the severity of tubulointerstitial fibrosis, and not glomerulosclerosis, most highly correlates with the rate of decline in kidney function.

Mechanisms of progression of chronic renal failure

Nephrosclerosis is a complex, potentially reversible pathological process in which, under the influence of various external damaging factors or functional overload of the kidneys, the dynamic balance between the production and destruction of the extracellular matrix is ​​disturbed. As a result, there is an accumulation of proteins in the renal tissue - both typical for the interstitium (collagen types I, III, V, VII, XV, fibronectin), and those that are normally components of the basement membrane (collagen type IV, laminin), as well as proteoglycans and polysaccharides.

The cellular composition of the kidney tissue undergoes significant changes: the death of own kidney cells occurs (necrosis in acute toxic effects and ischemia; apoptosis or "programmed death" in chronic injuries), active migration to the site of damage of phagocytes and fibroblasts is noted.

The phenotype and functional properties of renal cells change: they begin to actively synthesize adhesion factors that regulate the migration of cells of the immune system into damaged tissue, proliferate, acquire the properties of immunocompetent cells themselves, producing pro-inflammatory cytokines; like fibroblasts, they begin to synthesize components of the extracellular matrix (the so-called transdifferentiation). The complex processes of intercellular interactions that underlie nephrosclerosis at its various stages and their molecular mediators are the subject of close study, since the modern development of molecular medicine makes it possible to synthesize agents that suppress their synthesis or inhibit their effects, which can have a nephroprotective effect.

The causes and mechanisms that cause kidney damage and activate the processes of intercellular interactions that lead to the development of nephrosclerosis are diverse.

Adverse Influence arterial hypertension on renal prognosis has been shown in numerous studies. Essential hypertension is one of the most common causes of ESRD according to many registries; an unfavorable prognostic value of secondary renal hypertension was established in relation to the rate of decline in kidney function in diabetic nephropathy, chronic glomerulonephritis, lupus nephritis. At the same time, adequate control of elevated blood pressure can significantly slow down the onset of ESRD.

The damaging effect of systemic arterial hypertension on the kidneys is realized through violations of renal hemodynamics. Expansion of preglomerular renal vessels (from renal arteries to afferent arterioles) under the action of vasodilators (prostaglandins, kinins, endothelial relaxing factor - NO) leads to glomerular hyperperfusion, causing damage due to shear stress of endothelial cells, and contributes to the transmission of systemic arterial hypertension on the glomeruli with an increase in hydrostatic pressure in them (glomerular hypertension).

hyperperfusion glomeruli is accompanied by an increase in their volume, which causes mechanical damage to the mesangium due to its overstretching. There is a proliferation of mesangial cells and increased production of collagen fibers by them, leading to glomerulosclerosis. Another, even more powerful mechanism for increasing glomerular pressure is the narrowing of the efferent arteriole under the action of angiotensin II. When this mechanism is activated, glomerular hypertension can develop even against the background of normal systemic blood pressure.

Violation of self-regulation of renal blood flow develops in response to local ischemia of the renal tissue, observed in patients diabetes , may occur with immune damage to the kidneys. It is important to emphasize that under conditions of impaired regulation of renal blood flow, the level of blood pressure that does not go beyond the general population norm (130/80 - 139/89 mm Hg) can have negative consequences, causing hemodynamic damage to the kidneys.

Ischemia - type of renal hemodynamic disorders, opposite hyperperfusion, also causes damage to the kidney tissue and the development nephrosclerosis. The most sensitive to ischemic damage is the epithelium of the renal tubules, which performs energy-intensive transport and synthetic functions and is supplied with blood worse than the glomeruli. In acute severe ischemia, necrosis of the epithelium of the renal tubules develops with the development of acute renal failure. Chronic ischemia is associated with atrophy and apoptosis of the tubular epithelium, the development of tubulointerstitial fibrosis. The ischemic tubular epithelium loses its ability to self-heal and becomes more sensitive to the effects of toxins.

Renal ischemia can be total in nature (hemodynamically significant bilateral stenosis of the renal arteries in ischemic kidney disease, congestive heart failure). At the same time, there is a decrease in function, which at an early stage is not associated with glomerulosclerosis, but with a drop in pressure in the renal glomeruli and is reversible if the normal blood supply to the kidneys is restored. Approximately 10% of the minute volume of blood entering the glomeruli is used to ensure the vital activity of cells and 90% to ensure the function. Therefore, even with severe ischemia, the glomeruli remain relatively intact for a long time, while the tubulointerstitium undergoes severe atrophy and fibrosis (the “atubular nephrons” phenomenon). Obliteration of the capillary bed, which is closely associated with the development of tubulointerstitial fibrosis, seems to be, on the one hand, a reflection of tubulointerstitial ischemia, which leads to a slowdown in blood flow, and, on the other hand, contributes to its aggravation.

Local ischemia of the renal tissue is much more common than total ischemia and can be caused by a variety of causes (hypertensive nephroangiosclerosis, unilateral atherosclerotic stenosis of the renal artery or stenosis of individual segmental arteries, cholesterol embolism, vasculitis, thrombotic microangiopathy, immune inflammation with edema and microthrombosis, volumetric formations, destructive processes in kidneys). As a result of compensatory vasodilation of the preglomerular vessels and narrowing of the efferent arterioles, hyperperfusion and glomerular hypertension are noted in non-ischemic nephrons. Thus, in local ischemia, changes in renal blood flow are of a mosaic nature: ischemic areas of the renal tissue alternate with tissue in a state of hyperperfusion; both violations lead to the development of nephrosclerosis.

The triggering factor that causes a disorder in the self-regulation of renal blood flow in CKD, regardless of the nature of the kidney disease, is the very critical decrease in the number of functioning nephrons due to their irreversible loss - absolute oligonephronia (with severe nephrosclerosis, after nephrectomy, etc.) or temporary shutdown (for example, with acute glomerulonephritis). There is also a relative oligonephronia - a discrepancy between the number of active nephrons and the increased needs of the body (obesity, pregnancy).

The restructuring of renal blood flow associated with efferent arteriole stenosis and glomerular hypertension occurs under the influence of the reninangiotensin system (RAS). In the kidneys, there is a local synthesis of not only renin, but all the components of the RAS - from angiotensinogen to aniotensin II. In the lumen of the proximal renal tubules and in the cytoplasm of tubulocytes, angiotensinogen is found, the molecules of which cannot penetrate from the systemic circulation through the basement membrane of the glomerular capillaries due to their large size. The level of the main effector component of the RAS, angiotensin II, in the lumen of the proximal renal tubules is approximately 100 times higher than in the blood. This suggests the presence of local renal RAS, which plays a key role in the progression of CKD and is the main point of application of nephroprotective therapy.

Activation of type 1 angiotensin receptors causes a powerful vasoconstriction, an increase in systemic and glomerular pressure, a decrease in tubulointerstitium perfusion, but these are far from being limited to the renal effects of RAS. The decrease in hydrostatic pressure in the interstitium and the direct action of angiotensin II on tubulocytes lead to an increase in sodium reabsorption. Angiotensin II increases the permeability of the basement membrane of the glomerular capillaries for proteins, activates the production of inflammatory cytokines, cell proliferation and the synthesis of profibrogenic factors, stimulates the production of plasminogen activator inhibitor type 1 (PAI-1), which suppresses the destruction of the extracellular matrix. Activation of the RAS accelerates the development of nephrosclerosis also by increasing the production of aldosterone, which stimulates fibrogenesis both in the heart, the vascular wall, and in the kidneys.

Proteinuria not only reflects the severity of glomerular damage, but also has a pronounced toxic effect on the tubulointerstitium. Large epidemiological and clinical studies have shown that the presence of severe proteinuria is an unfavorable prognostic sign, and its decrease under the influence of therapy is accompanied by inhibition of the progression of CKD.

Normally, tubulocytes reuptake by pinocytosis of proteins that have passed through the glomerular filter into the primary urine, and their destruction with the participation of lysosomal enzymes to amino acids, which then enter the systemic circulation and are used for biosynthesis. With massive proteinuria, a functional overload of tubulocytes occurs, manifested by the accumulation of vacuoles in their cytoplasm containing undigested proteins. This is accompanied by the production of chemokines that activate the migration of immune cells with the formation of an inflammatory infiltrate in the tubulointerstitium, and also leads to apoptosis of tubulocytes. When the glomeruli are damaged, fragments of the basement membrane of the glomerular capillaries with immunogenicity, immune complexes, complement, inflammatory cytokines, lipids and other substances penetrate into the primary urine, leading to the spread of inflammation to the renal tubules and interstitium, damage to tubulocytes and activation of tubulointerstitial fibrosis.

Proteinuria and arterial hypertension potentiate the adverse effect of each other on the kidneys. The most rapid progression of CKD is observed with a combination of severe proteinuria and elevated blood pressure, and strict control of arterial hypertension is most effective in relation to renal prognosis in proteinuric forms of kidney damage. Of interest is the evidence that severe proteinuria, not accompanied by an increase in blood pressure, causes significant damage to the tubular epithelium, however, these changes can be reversible for a long time and do not lead to tubulointerstitial fibrosis.

Progression nephrosclerosis is associated with metabolic disorders that are very common in the population and can cause kidney disease (diabetic nephropathy, urate nephropathy) or, not being the main etiological factor, potentiate the action of other causes and mechanisms of nephrosclerosis. At the same time, kidney damage (active nephritis, nephrotic syndrome, renal failure) leads to severe disorders of various types of metabolism - purine, lipid, phosphorus-calcium. The adverse effects of metabolic disorders in relation to the kidneys are realized both through the direct toxic effect of metabolites on the renal structures, and indirectly through disorders of renal hemodynamics. Metabolic disorders not only cause and accelerate the development of nephrosclerosis, but also lead to cardiovascular complications, worsening the overall prognosis.

In recent years, it has been established that anemia is not only one of the manifestations of CKD and is closely associated with the development of left ventricular myocardial hypertrophy, vascular wall remodeling and an increased risk of cardiovascular complications, but is also accompanied by accelerated progression of renal failure (apparently due to hypoxia of the kidney tissue and aggravation of violations of renal hemodynamics); treatment with erythropoietin preparations, according to some studies, leads to a slowdown in the rate of decline in function.

Thus, CKD is associated with a whole range of complications, each of which contributes to the further progression of nephrosclerosis, even in the case of complete remission of the primary kidney disease. Knowledge of the risk factors and mechanisms of CKD progression forms the basis of a nephroprotective strategy and makes it possible to determine the main directions of treatment.

Kidney nephrosclerosis is a secondary chronic disease usually associated with high blood pressure. Nephrosclerosis leads to the death of the kidney tissue and organ dysfunction.

It is no secret that the functionality of an organ is determined by the structure and functions of its tissues. However, with certain types of disease, a situation often arises when the functional tissue is replaced by an ordinary connective tissue. The latter plays the role of a neutral filler, but, alas, does not take on the function of the replaced fabric. It is clear that in this case the activity of the body is irrevocably disrupted.

These diseases include kidney nephrosclerosis.

Kidney nephrosclerosis - what is it

This definition refers to the replacement of the parenchyma with connective tissue. To understand the essence of this disease, you need to turn to the structure of the organ.

The kidneys are a paired parenchymal organ in the form of beans, located behind the parietal sheet of the peritoneum. The organ is protected by a connective tissue fibrous membrane and includes the parenchyma and systems for the accumulation and excretion of urine. The parenchyma, in turn, consists of an outer cortical layer and an inner medulla.

The cortical substance of the parenchyma consists of nephrons - functional units of the organ that perform the task of forming urine. The tubules of these structures form a kind of loop, as it were, connecting the cortical and medulla. In the medulla there are excretory tubules, through which the accumulated urine enters the renal cups - an element of the excretion system.

The task of the parenchyma is the formation of urine. The process is carried out in 2 stages:

• formation of primary fluid - as a result of filtration, several liters of primary urine are formed. Its volume is much larger than the amount of urine that is usually excreted by the body: 150–180 liters per day, while the volume of urine does not exceed 2 liters. Primary urine is reabsorbed;
• with reabsorption, excess water, as well as salts and trace elements necessary for the body, are returned back to the blood. Secondary urine is characterized by a high content of urea, uric acid and other things. It travels to the renal pelvis and then is excreted through the ureter into the bladder.

Thus, not only the blood is purified from frankly toxic substances, but the water-salt balance is also maintained, as well as the required concentration of osmotic substances in the blood.

With nephrosclerosis, nephrons die, and their place in the parenchyma is occupied by connective tissue, which is unable to perform this function. At the same time, the organ decreases in size, thickens and loses functionality, which leads to kidney failure. It is no longer possible to restore kidney function in this case.

According to the International Classification of ICD-10 diseases, the disease code is I12.9.

Healthy kidney and kidney with nephrosclerosis

Classification and reasons

Nephrosclerosis is not an independent disease. The impetus for its appearance is hypertension, atherosclerosis and any other vascular or kidney diseases that lead to impaired blood supply to the organ. The classification of the types of the disease is associated with a variety of causes that provoke nephrosclerosis.

There are primary and secondary nephrosclerosis.

The primary is caused precisely by disturbances in the work of the vessels - narrowing of the working section of the artery, which leads to ischemia of the organ, the development of heart attacks, the appearance of scars, and so on. Age-related changes can also be the reason, if they lead to a decrease in the cross section of the bloodstream and venous blood stagnation.

There are several types of primary nephrosclerosis:

• Atherosclerotic - the cause of vasoconstriction in this case is the deposition of atherosclerotic plaques of a fatty nature. Plaques significantly reduce the elasticity of the vessel, thicken the walls, which ultimately leads to a decrease in the lumen, and, in turn, to kidney ischemia. Most often, plaques are deposited at the entrance of the renal artery or at the branching sites.

The surface of the kidney becomes coarsely knotted, irregularly shaped scars are visible on it. However, it is atherosclerotic nephrosclerosis that can be considered the most harmless, since in this case most of the parenchyma remains functional. However, the disease can be accompanied by hypertension.

• Hypertensive nephrosclerosis got its name due to the cause - spasms of blood vessels caused by hypertension. The result is the same: narrowing of the arteries and ischemia. At the same time, the connective tissue gradually replaces the parenchyma: the surface of the organ seems fine-grained. There are 2 subspecies of the disease:
  • arteriosclerotic - or benign. Connective tissue grows in the inner walls of the arteries, causing a decrease in the lumen and loss of elasticity of the vessel;
  • arteriolonecrotic - malignant. This is necrosis of arterioles and glomeruli, accompanied by hemorrhage in the urinary tubules, impaired protein metabolism, and so on.
• Involutive - associated with age-related changes. For example, after 45–50 years, calcium begins to deposit on the walls of the arteries, which causes a thickening of the walls and, accordingly, a decrease in the lumen. In addition, with age, thinning of the layer of the cortical substance and atrophy of the cells of the urinary tubules are possible, which leads to a decrease in the functionality of the organ.

There are other possible options. The cause, for example, may be chronic venous plethora. It is fraught with stagnation of venous blood, which provokes the synthesis of collagen, the main protein of connective tissue, in the walls of blood vessels.

Secondary nephrosclerosis is caused by dystrophic or inflammatory processes occurring directly in the kidney.

The causes can be a variety of diseases:

• Diabetic - elevated blood sugar provokes deposits on the walls of blood vessels, especially small ones. At the same time, the wall swells, thickens, but its permeability increases. As a result, protein enters the blood. To compensate for this damage, substances that increase clotting are released into the blood. At the same time, the blood flow in the capillary vessels slows down, which leads to damage not only to the kidneys, but also to other organs.
• Nephropathic - during pregnancy, hormonal changes often lead to failures in different systems. One of them is capillary spasm, which causes an increase in blood pressure and impaired blood supply to the kidneys. Against this background, edema is formed, the pressure is kept at a high level, which all together leads to the death of nephrons and their replacement with connective tissue.
• In chronic glomerulonephritis, circulating immune complexes are not destroyed and eventually reach the kidneys. CECs damage the lining of blood vessels in the glomeruli. To compensate, substances are synthesized that increase thrombosis, which leads to vasoconstriction.
• In pyelonephritis, bacteria enter the renal glomeruli and tubules and form bacterial thrombi in them. Leukocytes accumulate around the latter. During recovery, scars remain in such areas, with a protracted course of the disease, abscesses form. Both of these formations lead to the death of nephrons.
• Urolithiasis - when urine stagnates, bacteria multiply in it, and when the fluid is thrown back, the latter enter the urinary tubules and damage the inner walls.
• Tuberculosis - a tubercle bacillus can settle on the walls of the renal glomeruli, which provokes inflammation. At the same time, the vessels narrow, and even recovery is fraught with scarring.
• Lupus erythematosus is a systemic disease in which synthesized immune complexes "attack" their own organs. Once in the kidneys, CECs destroy the tissues of the renal glomeruli.
• The situation is similar with amyloidosis - a violation of protein metabolism. The CEC, designed to fight an abnormal protein - amyloid, damages the kidney tissue.
• Trauma or even surgery on the kidney can cause a piece of kidney tissue to enter the artery and block it. In this case, blood circulation is severely disturbed, which leads to the rapid death of nephrons.

Possible causes of kidney nephrosclerosis

Stages and degrees

The cells of the kidney tissue die gradually, and therefore the disease develops in stages. Symptoms of the disease appear months and years after the onset of the disease.

There are 2 stages of development:

• The first period is the formation of a factor that leads to impaired blood supply to the kidneys. Symptoms are characteristic of the disease that provokes this factor.
• The second period is the actual death of nephrons and their replacement with connective tissue. The process causes kidney failure, which is also divided into 4 types depending on the severity of the disease:
  • in the first stage, fatigue after exercise, some general weakness and decreased performance may be observed. Polyuria, an increase in the volume of urine excreted at night, may appear. The patient is often thirsty and has dry mouth. Protein can be detected in the urine - not always, the content of sodium, calcium and phosphorus changes in the blood;
  • at the second stage, the level of urea in the blood rises, its volume decreases. Blood pressure is kept at a high level and is poorly amenable to antihypertensive treatment. There are headaches, nausea, vomiting against the background of lack of appetite and weakness. With successful treatment of the underlying ailment, the symptoms usually disappear;
  • for the third stage, the characters are severe weakness, lack of appetite, and a tendency to viral diseases. The volume of urine decreases against the background of constant strong thirst. The skin acquires a characteristic yellowish tint due to the bile pigment - according to the norm, it should be excreted in the urine;
  • at the fourth stage, urine is completely absent or is excreted in a critically small amount. Poisoning develops - uremia, there is a violation of blood clotting. Blood pressure is very high, pulmonary edema develops. All changes at this stage are irreversible.

In addition, according to the rate of development of the disease, 2 forms of nephrosclerosis are distinguished.

• Benign - characterized by gradual development. In this case, the walls first thicken in small vessels, then in large ones. Fat is deposited in the altered tissue, an excess of elastic tissue appears in large vessels, which contributes to blockage of the bloodstream. All together leads to impaired blood supply and the gradual death of nephrons.

The likelihood of developing the disease increases with age, since age-related changes already aggravate the condition of the vessels.

• The malignant form is characterized by the rapid development of the same process. As a rule, without timely hemodialysis, the prognosis is extremely unfavorable. The disease is more common in people of the Negroid race. In general, malignant nephrosclerosis is not very common and rarely occurs in people with persistently elevated blood pressure.

Signs and symptoms

Symptoms of the first stage do not differ in expressiveness, moreover, since they are associated with the main ailment, they can be inconsistent.

The first signs include symptoms that are characteristic of almost any disease associated with increased blood pressure or cardiac ischemia:

• general weakness and lethargy;
• nonspecific headaches;
• increase in blood pressure - unstable and unstable;
• poor appetite and weight loss;
• change in daily urine output.

The symptomatology of the disease is also determined by the form of nephrosclerosis - primary and secondary. The most informative is the last sign - a change in the volume of urine. It is directly related to the number of dead nephrons, which indicates the stage of the disease.

The primary symptoms include the following.

• Polyuria - fluid from the primary urine does not return to the blood, but is absorbed by the urinary tubules. As a result, the volume of daily urine is higher than the volume of liquid drunk - more than 2 liters.
• - the volume of urine excreted at night is usually less than during the day. However, when the disease occurs at night, the vessels relax, and the volume of nighttime urine exceeds the daytime one. This symptom usually appears first.
• Cylindriuria is an indirect sign, inconsistent. In the general analysis of urine, cylinders are found - casts of blood proteins.
• Proteinuria - observed in both primary and secondary nephrosclerosis. Due to a violation in the walls of blood vessels, protein from the blood enters the primary urine, but does not return to the blood and is excreted in the urine. Protein is found in OAM.
• Iron deficiency anemia - due to problems with the synthesis of erythropoietin, red blood cells are not produced in the proper amount. This is the main cause of weakness and dizziness.
• High blood pressure is a common symptom, the severity depends on the stage. With poor blood supply in the kidneys, renin begins to be produced, which maintains blood pressure at a high level, significantly worsening the patient's condition. In this case, headaches, numbness of the limbs, vomiting, nausea appear. There are hypertensive crises - up to 250/130 and 300/140. The effect of conventional drugs that reduce blood pressure is very weak.
• Tendency to bleeding - due to a decrease in the production of urokinase, blood clotting decreases. Bleedings from the nose, from the gums become possible, hematomas appear on the skin from the weakest mechanical impact.
• Headaches are caused by an increase in blood pressure. At the same time, all the vessels narrow and there is an imbalance between the blood entering the brain and its outflow - stagnation. It causes headaches. Most often, it is concentrated in the occipital region, but with a steady increase in blood pressure, it turns into pressing and not localized.
• The tendency to viral diseases is associated not so much with the state of the vessels, but with the medications taken during treatment. Drugs in this group reduce immunity.

Secondary signs develop with significant damage to the kidney tissue and obvious organ dysfunction:

• Oliguria - observed in violation of blood filtration. The volume of daily urine is significantly reduced - up to 500–800 ml. This is a sign of the death of 70-75% of nephrons.
• Anuria is the absence of urine. Accompanied by lethargy, nausea, vomiting and other signs of poisoning. Anuria appears when about 90% of nephrons die. In the absence of urgent treatment, the patient dies.
• - erythrocytes penetrate into the primary urine, but are not absorbed in the urinary tubules and are excreted along with the secondary urine. The latter at the same time acquires a characteristic red color, the analysis shows the presence of erythrocytes in it.
• Edema - the same renin contributes to the retention of water and sodium ions. The fluid enters the surrounding tissues, and is not excreted. Edema, as a rule, appears first on the face and legs, and then "hidden edema" is formed. The patient's weight increases to 0.5-1 kg per day. Protein is found in the urine.
• Azotemia - the products of protein metabolism - urea are not excreted. Manifested as drowsiness, nausea, palpitations, intense thirst. The skin acquires a yellowish color, a characteristic ammonia smell is heard from the mouth. Azotemia appears when 65-70% of nephrons are damaged.
• Uremia - products of protein metabolism and other toxic substances are not excreted from the body. Self-poisoning develops. To the symptoms listed above, atrophy of muscle tissue, impaired sensitivity are added, urea crystals are deposited on the skin - “uremic frost”. Uremia indicates the death of 90% of the cells.
• Visual impairment - two characteristic lesions are distinguished: retinal detachment and edema of the papilla of the optic nerve. In the first case, the accumulation of fluid under the retina leads to detachment, which is accompanied by sparks, a veil before the eyes, and the appearance of dark spots. In the second case, fluid stagnates near the optic nerve in the cavity of the orbit. Edema leads to squeezing of the nerve fibers and damage to it. It is accompanied by the appearance of a veil, headaches and rapidly progressive blindness.
• - vasospasm ultimately leads to disruption of the blood supply to the heart. With physical exertion or an emotional outburst, there is a strong sharp pain in the region of the heart or behind the sternum.
• Cardiac asthma - in later stages, cardiac ischemia and edema lead to left ventricular failure. As a result, blood begins to stagnate in the pulmonary vessels, which causes swelling of the lung tissue. The first asthma attacks appear during physical exertion, then night attacks begin. The cough is usually almost dry or with little mucus. In this case, cold sweat appears, the skin turns blue, and the heartbeat rises significantly. In the lungs, when listening, moist rales are fixed.

Diagnostics

The nonspecificity of signs in primary nephrosclerosis and even in secondary nephrosclerosis at the first stage makes it difficult to diagnose. However, laboratory studies help to quickly clarify the picture.

A biochemical blood test for violations in the work of the kidney will reveal the following factors:

• increased urea and creatinine;
• decreased protein levels;
• an increase in the content of potassium - at 3-4 stages of the disease, since potassium is not excreted in the urine;
• increased sodium content - this sign may be absent if the patient is on a diet;
• an increase in the level of magnesium in the blood is also characteristic of the last stages.

A general urine test is no less eloquent:

• there is an increase in the amount of protein;
• the appearance of red blood cells;
• the relative density of urine decreases.

A general blood test reports a decrease in the level of hemoglobin, erythrocytes and platelets. At the same time, the proportion of leukocytes increases, which indicates poisoning.

A laboratory study allows you to localize the lesion, as it clearly indicates a violation in the work of the kidneys.

For a more accurate assessment of the state of the organ, instrumental research methods are used.

• Ultrasound of the kidneys - with a disease, the size of the cortical layer and its functionality decrease. In the parenchyma, specific salt deposits are noted.
• - Obtaining an x-ray of the kidney and urinary tract. With nephrosclerosis, the size and contours of the organ change. Also, urography allows you to assess the deposition of salts.
• Angiography - gives the most complete picture of the condition of the vessels in the kidneys. With nephrosclerosis, there is a narrowing and brokenness of the branches of the artery - the effect of a "burnt tree".
• Vascular Doppler - carried out to assess blood flow in the kidneys: in case of illness, blood circulation is slowed down.
• Radiography is the most informative method in the early stages of the disease. Allows you to assess the condition of the glomeruli and urinary tubules.
• (CT) - a comprehensive study, as a result of which information is obtained about the structure, structure, size of the kidney and the state of the vessels.
• A biopsy is the removal of tissue for analysis. A biopsy is the only type of analysis that allows you to accurately determine what form of the disease - benign or malignant, in question.

Treatment

Treatment is primarily focused on treating the underlying disease. Attempts to restore kidney function without eliminating the main acting factor are doomed to failure.

To restore the organ, a complex treatment is carried out, designed for a long time. Usually, therapy is prescribed in courses with short intervals between treatments.

Depending on the stage, degree of damage to the organ, medications are prescribed.

• Anticoagulants - heparin, and antiplatelet agents - trental. The drugs prevent the formation of blood clots.
• Drugs from the group that reduce blood pressure are used with great caution in the last stages of the disease, since a sharp drop in blood pressure is fatal for the patient.
• ACE inhibitors - berlipril, diroton, block the synthesis of angiotensin, due to which the vessels in the kidneys expand.
• Calcium antagonists - falipamil, dilate arteries, including those in the kidneys.
• Diuretic drugs - indapamide, remove excess fluid and sodium ions.
• Locators of b-adrenergic receptors - propranolol, reduce the production of renin, thereby reducing blood pressure.
• Alpha-blockers - prazosin, increase the rate of blood passing through the glomerular arteries.
• To adjust the water-salt balance, special potassium preparations, panangin, can be prescribed.
• To improve the general condition, multivitamin preparations are administered.

For other disorders associated with kidney dysfunction, special medications are also additionally prescribed. So, with osteoporosis, often observed in involutive nephrosclerosis, treatment includes calcium preparations. Iron or erythropoietin preparations are prescribed to treat anemia.

Treatment is necessarily accompanied by a diet that limits the intake of salt and animal proteins.

In the first stages, it is possible to treat the patient with folk remedies:

• For example, birch sap helps to eliminate toxins, as well as alcohol infusion of aspen buds, which is taken in the amount of 30 drops before meals.
• Lingonberry infusion - 1 tablespoon per 200 ml of boiled water, helps to reduce pressure.
• Licorice infusion - 2 teaspoons per 200 ml of hot water, also helps to remove toxins.
• An infusion of strawberry, birch, nettle and flax leaves - 10 g, 20 g, 20 g and 50 g, respectively, allows you to get rid of edema.

Folk remedies can only act as supporters. It is very useful to use herbal infusions between courses of drug therapy.

At stages 3–4 of nephrosclerosis, drug therapy is ineffective in most cases.

It is almost impossible to restore kidney function with such a large damage - 70-75% of nephrons:

• Hemodialysis - the patient's blood is passed through an artificial kidney machine. Thus, it is cleared of toxic substances, protein metabolism products, and so on. The frequency of the procedure depends on the severity of the disease. In fact, this is not a cure, but a support.
• A kidney transplant is a method that allows you to return to your normal lifestyle. However, such an operation is quite risky, even in cases where the donor organ was provided by a close relative. The probability of rejection and the development of urological complications is very high. Surgical intervention of this kind is resorted to only as a last resort.

Forecast

Nephrosclerosis is a chronic disease. At stages 1-2, it is quite possible to maintain kidney function, but at the same time, all the necessary restrictions must be observed: a minimum of table salt, mainly vegetable protein, control over the level of calcium, potassium and phosphorus in the blood and replenishment of these elements if they are not enough in the daily diet. In this case, the drug course has to be taken again with an exacerbation of the disease.

The periods of remission are the longer, the more successfully the underlying disease is treated.

At stages 3-4, the course of therapy is carried out more often, restrictions on diet and life are more stringent. It is impossible to restore the dead kidney tissue, so here the treatment is reduced to maintaining the functionality of the remaining nephrons, which may not be enough.

The course of benign nephrosclerosis is determined by the state of the heart. In the absence of cardiac pathologies, the outcome of the disease is always favorable. But against the background of heart failure, treatment is difficult.

The prognosis for malignant nephrosclerosis is unfavorable. Usually, if it is not possible to transplant a kidney, the patient can live no more than a year.

Nephrosclerosis is a secondary disease that is directly related to the state of the vessels and the magnitude of blood pressure. There are no special preventive measures to prevent it, but the most common recommendations - diet, physical activity, lack of overstrain, sufficient rest, may well prevent its occurrence.

Nephrosclerosis- chronic kidney disease, in which the functional cells of the kidneys (nephrons) gradually die, and connective tissue grows in their place (it is not responsible for the functioning of the organ).

As a result, the kidneys thicken, shrivel, decrease in size and cease to perform their functions - chronic renal failure (international name - chronic kidney disease) develops.

Nephrosclerosis is not an independent disease. A large number of severe ailments lead to its formation: diabetes mellitus, arterial hypertension and others.

Statistics

In Europe, according to statistics, CRF occurs in 600 cases per 1,000,000 inhabitants.

The number of patients with nephrosclerosis who are on hemodialysis (artificial kidney) with CRF is from 10 to 20%. Moreover, mortality among patients with chronic renal failure reaches 22% per year.

Story

Then, in 1914, Volgard and Fahr proved that arteriosclerotic changes (deposition of "harmful" fats) occur in the vessels of the kidneys, linking them to high blood pressure. They also singled out nephrosclerosis as a separate disease, proposing to divide it into a simple and malignant form.

A doctor by education and a writer by vocation, Mikhail Bulgakov, passed away from nephrosclerosis. His pen belongs to famous works that have not lost their relevance even today: “The Master and Margarita”, “Notes of a Young Doctor” and others.

In a letter sent to his friend a few months before his death, Bulgakov wrote: “Dying is painful, tedious and vulgar. As you know, there is one decent type of death - from a firearm, but I, unfortunately, do not have this.

Anatomy and function of the kidneys

The kidney contains renal tissue (parenchyma) and the pelvicalyceal system.

kidney tissue consists of cortical substance (contains nephrons - the smallest units of the kidney) and medulla (contains urinary tubules). Urine is produced in the kidney tissue.

pelvicalyceal system consists of cups and pelvis, in which urine accumulates and then is excreted.

Outside, each kidney is covered with a capsule.

The structure of the nephron

The renal artery, having reached the renal tissue, decreases in diameter and branches, forming an introductory atreriole (a small-caliber artery).

Entering the capsule, the introducing arteriole branches into the smallest vessels - a glomerulus is formed, which has about 50 loops. When leaving the nephron capsule, the vascular loops unite and form the efferent arteriole.

The walls of the vessels of the glomerulus have a complex structure, due to which "windows" are formed.

The structure of the capsule

It consists of outer and inner sheets, and between them there is a cavity into which the liquid part of the blood from the glomerulus with substances dissolved in it penetrates.

From the capsule of the glomerulus, the urinary tubules of the nephron begin, which flow into the collecting urinary tubules. Then they unite with each other and open into the renal cups of the pelvicalyceal system.

The mechanism of blood filtration and urine formation

Moreover, the “windows” let in both useful substances (for example, amino acids) and harmful substances (toxins, drugs). However, with such filtration, blood elements (erythrocytes, leukocytes), blood proteins and large molecules are retained. This is how primary urine is formed (150-180 liters per day).

Further, the primary urine enters the urinary tubules, in which useful substances (vitamins, fats, glucose) and water are reabsorbed, while harmful substances, on the contrary, accumulate. So primary urine turns into secondary urine (about 1.5-2.0 liters per day).

Then the secondary urine enters the collecting ducts, then into the pyelocaliceal system of the kidney, then into the ureter and bladder. During the act of urination, secondary urine is excreted from the body.

Kidney Functions

• Removal from the body excess fluid, toxins, metabolic end products of certain substances (urea, creatinine, bilirubin), allergens, medicines and others.
• Hormone production:
  • Renin, which is involved in the regulation of vascular tone and blood pressure (the conversion of angiotensin I to angiotensin II), the content of sodium and potassium salts in the body, as well as the reverse absorption of water in the urinary tubules,
  • Erythropoietin, which stimulates the formation of erythrocytes (red blood cells) in the bone marrow.
• Maintaining blood acidity(normal blood pH - from 7.37-7.44).
• Synthesis of a substance (urokinase), which regulates blood clotting.
• Converting vitamin D to its active form improves the absorption of calcium and phosphorus in the small intestine.

Causes and classification of nephrosclerosis

Causes of primary nephrosclerosis (primary wrinkled kidney)

A prolonged increase in blood pressure (BP) causes spasm and narrowing of the vessels of the kidneys, they lose their elasticity, they increase pressure and resistance to blood flow.

Hypertensive nephrosclerosis occurs in two variants:

• Benign nephrosclerosis(arteriolosclerotic nephrosclerosis) - when connective tissue grows in the walls of the arteries of the kidneys, which leads to a decrease in their elasticity. The disease develops over 10 years or more. Often this form is combined with atherosclerosis (vascular disease).
• Malignant nephrosclerosis(arteriolonecrotic nephrosclerosis, Fara nephrosclerosis) develops within a short time (several years) in severe arterial hypertension (AH). With this disease, the arterioles and capillaries of the glomeruli die. Hemorrhages also occur in the wall of the urinary tubules, leading to atrophy of the cells of their inner layer (they decrease in size and lose their viability).

There is a partial or complete blockage of the lumen of the renal artery by a detached blood clot (thrombosis) or an embolism (for example, an accumulation of microbes in pyelonephritis). As a result, the lumen of the arteries narrows. Therefore, the flow of blood to the kidney, or its individual zones, decreases - heart attacks develop (areas of living tissue die).

With single and small heart attacks, the work of the kidney is compensated. Whereas with repeated and extensive heart attacks, a greater number of nephrons die, leading to the development of nephrosclerosis.

Atherosclerosis

Fat-like substances - "harmful" fats (atherosclerotic plaques) are deposited on the inner wall of the arteries of the whole organism. Therefore, the lumen of the arteries narrows, and their walls thicken and become less elastic. As a result, the cells of organs and tissues are not sufficiently supplied with blood, dying over time. The smaller the caliber of the arteries, the faster the changes occur in them.

The most "favorite" areas of atherosclerotic plaques in the kidneys are the places of entry into the kidney of the renal artery, or its division into smaller branches.

Age changes

Starting from the age of 40-50, the walls of the arteries thicken, and their gaps also narrow. The reason is the deposition of calcium on the inner lining of the artery wall, the accumulation of smooth muscle fibers and connective tissue.

Age-related changes in the kidneys lead to thinning of the cortex and atrophy of the cells of the inner layer of the urinary tubules (they lose function and viability).

By the age of 70, the number of nephrons in the kidneys decreases by about 40%.

Chronic venous plethora of the kidneys

It leads to a violation of the outflow of venous blood from the kidneys, creating conditions for excessive growth of collagen (a protein that is the basis of connective tissue) in the wall of the kidney vessels. Therefore, their elasticity decreases.

Changes develop over a long time (10 years or more) with nephroptosis (prolapse of the kidneys), narrowing of the renal vein and chronic venous thrombosis.

Causes of secondary nephrosclerosis (secondary wrinkled kidney)

Against the background of an increased level of sugar in the blood, complex compounds are formed that are deposited on the inner wall of blood vessels (primarily small ones), damaging them. As a result, the vascular wall swells and thickens, and its permeability increases. Therefore, protein enters the urine (diabetic nephropathy develops).

Also, when the cells of the inner wall of blood vessels are damaged, blood clotting factors are released into the blood. Therefore, the formation of blood clots in the lumen of the vessels of the kidneys increases.

Changes lead to a slowdown in blood flow in the capillaries (small vessels) and a decrease in the supply of oxygen to cells in almost all organs and tissues. That is, not only the kidneys are affected, but also other organs (eyes, heart).

Nephropathy of pregnancy (late toxicosis)

Against the background of hormonal changes in the body during pregnancy, the work of the brain changes, which gives “wrong commands” to all capillaries, leading to their spasm.

Therefore, resistance to blood flow in the vessels increases, and blood pressure rises. As a result, the blood supply to the kidneys deteriorates, and the nephrons die.

The permeability of the capillary wall of the glomerulus also increases, so salts are retained in the body, and protein is lost in the urine. Such changes contribute to the formation of edema (the release of liquid honor into the surrounding tissues) and maintain high blood pressure.

In response to an infection (tonsillitis, pharyngitis), antibodies are formed in the body (immune system proteins that fight "foreigners"), which, interacting with an antigen (a protein or a toxin of a bacterium), form circulating immune complexes (CICs) - a protective reaction of the body. Normally, CECs are destroyed by the liver and phagocytes (cells of the immune system). However, in the presence of disturbances in the functioning of the immune system, this does not happen.

With the blood flow, CECs enter the kidneys and damage the inner lining of the glomerular vessels. At the same time, substances are released into the blood that enhance the formation of blood clots in the lumen of the vessels of the glomerulus, and hyaline (a protein substance of a dense consistency) is deposited in their wall. As a result, the elasticity decreases and the permeability of the vessel wall of the glomerulus increases, which leads to impaired blood flow.

Chronic pyelonephritis

Microbes with blood flow or reverse reflux of urine from the bladder enter the renal glomeruli and the lumen of the urinary tubules, settling in them. White blood cells accumulate around bacterial thrombi. During recovery, scars form in their place, if recovery does not occur, abscesses. When the disease proceeds for a long time, the number of scars increases, leading to the death of a large number of nephrons.

Urolithiasis, narrowing or compression of the ureter

In the pyelocaliceal system and ureters, the outflow of urine is disturbed. Therefore, it stagnates, creating conditions for the reproduction of bacteria in it (normally, urine is sterile, but during inflammatory processes it contains bacteria). Then the microbes enter with the reverse reflux of urine into the urinary tubules and vessels of the glomerulus, damaging their inner wall.

Tuberculosis of the kidney

With the blood flow from the focus (for example, easily), tubercle bacilli enter the kidneys, settling on the inner wall of the vessels of the glomerulus. White blood cells gather around the accumulation of bacteria, forming foci of inflammation. As a result, blood flow slows down, and the vessels narrow, disrupting the flow of blood to the glomeruli.

Systemic lupus erythematosus

In this disease, the immune system “does not recognize” its own tissues, mistaking them for their “foreign” ones. Therefore, it tries to destroy the normal cells of the body, damaging them. As a result, circulating immune complexes (CICs) are formed in the blood, which consist of an antibody (a protein of the immune system designed to fight “foreigners”) and an antigen (particles from the surface of normal body cells).

CECs with the blood flow reach the renal tissue and damage the inner wall of the vessels of the glomeruli. Therefore, inflammation develops, which leads to the death of nephrons.

Renal amyloidosis

There is a violation of protein metabolism: an abnormal protein is formed - amyloid, which becomes a "stranger" (antigen) for the body. Therefore, the immune system fights it by producing antibodies. The antibody and antigen, interacting, form CECs, which reach the kidneys with the blood flow and damage the inner wall of the glomerular vessels. As a result, the nephrons die. Simultaneously with kidney damage, the lungs, heart and other organs are involved in the process.

Kidney injury or surgery

Particles of renal tissue can clog the lumen of the arteries and arterioles of the kidney. Therefore, the blood supply to a separate section of the kidney is sharply disrupted, leading to the death of nephrons.

ionizing radiation

Causes the development of the disease years or months after exposure to the body. Moreover, changes occur in all vessels of organs and tissues. The degree of their severity depends on the dose and type of ionizing radiation.

What's happening? The walls of the vessels of the kidneys gradually thicken, and their lumen also narrows, therefore, the blood flow in the nephrons decreases.

Symptoms

Signs of nephrosclerosis

Periods of nephrosclerosis

Second period characterized by the gradual death of nephrons and the replacement of the parenchyma of the kidneys with connective tissue - chronic renal failure (CRF) develops. Depending on the volume of the dead renal tissue, CRF goes through several stages in its formation.

Stages of chronic renal failure

First stage

Patients quickly get tired during physical exertion or in the evening. They have reduced ability to work, there is a slight dryness in the oral cavity, thirst, polyuria, nocturia. But in general, the health of the patients is good. In the biochemical analysis of blood, the content of sodium, phosphorus and calcium sometimes changes. Protein may be found in the TAM, and the relative gravity of the urine may decrease.

Second stage

Symptoms of azotemia appear: appetite decreases, there is lethargy, itching, nausea and vomiting. Vision is disturbed, headaches occur, the heartbeat quickens, the heart rhythm is disturbed. Blood pressure rises to high numbers and is difficult to lower. The volume of daily urine decreases. In a biochemical blood test, the level of urea and creatinine increases.

At this stage, when the course of the underlying disease improves, the analyzes and the volume of daily urine normalize, and the well-being of patients improves.

Third stage

The work of the kidneys deteriorates sharply, the volume of daily urine decreases. Patients are weakened, get tired quickly, eat poorly, constantly want to drink. They are prone to frequent and severe bacterial or viral infections (SARS, stomatitis, pustular skin infections). The skin is dry, acquires a yellowish tint - due to the accumulation of derivatives of bile pigments in the body (normally excreted in the urine, turning it yellow). Increased levels of creatinine and urea in the blood.

Fourth stage

Urine is absent, or its daily volume is sharply reduced, so the symptoms of self-poisoning (uremia) increase. Sleep is disturbed, memory is reduced, pulmonary edema develops, there are blood clotting disorders, blood pressure is kept at high numbers, and so on. There is a persistent increase in creatinine, uric acid and urea in the blood, and the total protein is lowered.

All changes that have arisen in the fourth stage are irreversible.

Diagnosis of nephrosclerosis

Laboratory research

Blood chemistry

Indicators indicating impaired renal function:

• The level of urea rises(2.5-8.3 mmol/l), creatinine(for women - 50-100 µmol / l, for men - 60-115 µmol / l) and uric acid(210 - 420 µmol/l).
• Total protein goes down(65-85 g/l).
• Potassium(3.5-5.5 mmol / l) in the initial stages remains normal or decreases, since it is excreted along with the fluid that the body loses in large volumes. At the final stage, the level of potassium rises, as it is not excreted in the urine, accumulating in the body.
• In the last stages, the level of magnesium increases(0.8-1.2 mmol/l) and phosphorus(0.81-1.45 mmol/l). Whereas the calcium content (2.15-2.65 mmol / l) decreases.
• Sodium rises(123-140 mmol/l). However, it may also decrease if the patient sharply limits the intake of table salt.

General urine analysis

• Increased protein content(absent or present up to 0.033 g/l)
• Red blood cells appear(0-2-3 erythrocytes in the field of view of the microscope) and cylinders (normally absent).
• Relative density of urine decreases (1.010 - 1.022 g/l)

General blood analysis

Decreased hemoglobin level(for men - 130-160 g / l, for women - 120-150 g / l), erythrocytes (3.5 * 10 12

/ l - 5.0 * 10 12 / l). While the level of leukocytes (4-9x10 9) due to self-poisoning, on the contrary, increases.

Decreased platelet count(180 - 320 * 10 9 / l). This increases the time of blood clotting (the beginning of clotting - from 30 seconds to 2 minutes, the end of clotting - from 3 to 5 minutes) and the duration of bleeding (2-3 minutes).

Instrumental research methods

Ultrasound examination (ultrasound)

With nephrosclerosis there is atrophy (reduction in size and cessation of function) of the cortical layer of the kidney in relation to the medulla. There is sometimes no separation (differentiation) between the two layers. Also visible are deposits of calcium salts in the kidney parenchyma (nephrocalcinosis), which indicate the death of the kidney tissue.

Excretory urography of the kidneys

The method is based on the fact that the kidneys are able to secrete some radiopaque iodine-containing substances introduced into the body intravenously. As a result, on radiographic images taken at regular intervals, images of the kidneys and urinary tract are obtained.

With nephrosclerosis the volume of the kidney and the size of the cortical substance is reduced. Often, deposits of calcium salts (nephrocalcinosis) are determined.

Angiography of the vessels of the kidneys

A contrast agent is administered intravenously. Then a series of images is taken, in which the doctor then evaluates the degree of narrowing of the kidney vessels, the presence of an obstruction to blood flow, and so on.

With nephrosclerosis there is deformation and narrowing of small arterial vessels, an uneven outer contour of the kidneys and thinning of the cortical substance. In addition, a symptom of a "burnt tree" is visible - when the branches of the renal artery are narrowed and broken, and there is also no fine drawing of the arteries.

Kidney scintigraphy

A special radioisotope substance is injected intravenously, which is excreted by the kidneys, emitting radiation. Such radiation is captured by special equipment, then the image is transmitted to a computer.

With nephrosclerosis radioisotope is distributed unevenly. Sometimes only separate sections of the renal tissue are preserved, and sometimes either the kidney is not visible at all.

Doppler of kidney vessels

Special equipment emits and directs ultrasonic waves, which, having reached the organ, are reflected and captured by special equipment. The information is then transferred to a computer where the data is processed.

With nephrosclerosis the method reveals a slowdown in blood flow in the renal vessels and nephrons.

Radionuclide renography

It is considered the most sensitive method in the early stages of kidney disease. Since it allows you to evaluate the function of each kidney, the state of blood flow in the glomeruli, as well as the excretion of urine by the tubules.

A radiopharmaceutical is given intravenously, which is filtered by the glomerulus and excreted from the body. The drug emits radiation, which is recorded by special equipment.

With nephrosclerosis a special drug accumulates and is excreted by the kidneys more slowly.

CT scan

For the diagnosis of nephrosclerosis, CT and angiography are combined (administration of a contrast agent intravenously before the study). That allows you to assess the structure, structure and position of the kidney, as well as the condition and functioning of the vessels of the kidneys.

With nephrosclerosis small arterial vessels are narrowed and deformed, the cortical layer is thinned, the kidney itself can be reduced in size. There are changes in the vessels: they are narrowed and broken.

Kidney biopsy

With the help of a special needle inserted through the skin into the kidney, the doctor receives a small section of the kidney tissue. Then he sends it for research.

Treatment of nephrosclerosis

Regarding the treatment of nephrosclerosis, drugs are prescribed comprehensively and for a long time (for years and months), courses of treatment are often repeated, but with short breaks between them.

Treatment of nephrosclerosis: hemodialysis and kidney transplant

With hemodialysis The patient's blood is passed through a special membrane in an artificial kidney machine. Due to this, the body is cleansed of toxins and end products of metabolism, the balance of water and salts is normalized.
The frequency of the procedure depends on the degree of impaired renal function and the device model used.

A patient on hemodialysis is prescribed drugs to lower pressure, vitamins, potassium and other drugs.

kidney transplant - a radical method that allows patients to lead an active lifestyle. A donor organ is taken either from a corpse (subject to all conditions) or from a living donor (for example, a brother or sister, with their consent).

After transplantation, patients take special drugs that suppress the activity of the immune system so that it does not reject the donor organ.

Is hospitalization necessary for nephrosclerosis?

However, when the condition worsens, there is a need inpatient treatment:

• Increased loss of fluid (polyuria) and salts
• Violated acid-base balance in the body (acidification of the blood) - when the pH is lower than 7.2
• Self-poisoning by metabolic products
• High urea and creatinine numbers
• Increased bleeding
• Severe anemia (hemoglobin below 40-50 g/l)

Lost fluid is replenished with intravenous fluids solutions of glucose, isotonic sodium solution and others.

Loss of salt solutions for intravenous administration or oral preparations containing sodium and potassium are used.

To lower creatinine and urea levels glucose solution is administered in the form of a drink or intravenously in combination with insulin.

Acid-base balance restored with intravenous sodium bicarbonate solution.

For the treatment of anemia erythrocyte mass (blood component containing red blood cells - erythrocytes) is transfused.

With self-poisoning solutions (glucose, reopoliglyukin and others) and hemodez are administered intravenously.

On a note

A patient on hemodialysis must carry a card (memo) with him indicating the diagnosis and the frequency of procedures, phone numbers and the address of the dialysis center. Since in emergency cases (poisoning, accident, loss of consciousness on the street), doctors must know which patient they are dealing with in order to create conditions for timely hemodialysis.

Nutrition for nephrosclerosis (diet)

Nephrosclerosis: diet and drinking regimen

The principles of nutrition include the creation of conditions to reduce the load on the nephrons, but taking into account the stage of nephrosclerosis.

Protein restriction

Justified, since 30 grams of urea is formed from 100 grams of protein. Also, a protein-restricted diet encourages the body to reuse urea for protein synthesis.

In the absence of kidney protein deficiency is practically unlimited.

However if CKD has developed, it should be limited. In the early stages of the disease, protein is limited to 50-60 grams per day, in the later stages - up to 30-40. Moreover, 2/3 of the protein should be highly valuable: poultry meat, lean beef, egg white, fish, dairy products. Whereas only 1/3 of the protein should come from potatoes, bread, cereals and other protein-rich foods. However, dairy products and fish should not be abused, since they contain phosphorus.

Salt restriction

Reasonable, since sodium attracts water, increasing swelling. However Depending on the stage of CKD and symptoms, the approach is different:

• In the absence of edema and normal blood pressure figures salt is not limited.
• In the early stages of CKD salt is limited to 10-15 grams per day , at later- up to 3-7.

Maintaining levels of potassium, calcium and phosphorus close to normal

Traditionally, dairy products are rich in calcium. However, with nephrosclerosis, they should be limited, since they contain phosphorus. Whereas its level in the body is already increased with nephrosclerosis. Therefore, it is necessary to consume more other products in which contains calcium: legumes (peas, beans), green vegetables, whole grain flour.

Foods containing potassium are used if it is not enough in the body (in the initial stages). Whereas if potassium is in excess (late stages), foods with its content are limited. Potassium a lot in raisins, dried apricots, bananas, chocolate, baked potatoes.

Ensuring an adequate intake of calories and vitamins

Because if there are not enough calories, the body uses its own resources - its own proteins - to work. Whereas, breaking up, proteins increase the level of urea.

Therefore, the patient should receive food rich in carbohydrates, fats and vitamins: rice, potatoes, sweets, fresh vegetables and fruits, butter and vegetable oil, honey.

However, the patient should make his diet taking into account the underlying disease. For example, if you have diabetes, you should limit your intake of carbohydrates.

Drinking regime

In the early stages when there is no edema and blood pressure does not rise to high numbers, water restriction is not required. Moreover, with a sufficient water regime (2-2.5 liters per day), blood passes through the kidneys faster, creating conditions for better removal of toxins from the body.

At later stages(presence of edema and high blood pressure figures), the patient is recommended to take 500 ml of liquid more than he allocated for the previous day.

Consequences of nephrosclerosis

However, with an unfavorable course of the underlying disease, the work of the kidneys worsens, so a large number of nephrons die. As a result, chronic renal failure develops over time, and the patient after a few years often needs a hemodialysis procedure or a kidney transplant.