A concept concerning the role of evolution in human disease is presented on the basis of literature data and own clinical and experimental observations. According to our understanding, a seeming inadequacy of many chronic pathologic processes is based on the fact that such processes have emerged and became reinforced in the course of evolution primarily as the compensatory tools aimed to override the acute, but not chronic, pathological processes. Since in the course of natural selection, chronic diseases were not a factor of evolution, we believe that the inability to fix chronic disease by means of natural evolution could be fixed only by the technological evolution.

The review concerns nephroprotective (antihypertensive and antiproteinuric) effects of blockers of angiotensin II receptor and of ACE inhibitors in patients with chronic kidney disease. Complications of treatment with RAS antagonists including early and late onset acute renal failure and their association with aldosterone and renin escape are discussed.

Chronic kidney diseases are often and associated with bad prognosis in chronic heart failure patients. Decreasing of cardiac output, neurohumoral activation, inflammation and oxidative stress take part in pathophysiology of CKD in CHF. Blood pressure and glycemia control, angiotensin-II converting enzyme inhibitors and angiotensin II receptor blockers may improve outcomes in these patients. Nephroprotective and prognostic value of adenosine 1 and endotelin receptor blockers, antagonists of V2 vasopressin receptors, erythropoietin needs in further evaluation.

Aim: to characterize clinical features and pathology of chronic glomerulonephritis (CGN) in patients with genetic thrombophilia. Material and methods. Morphological data of 25 pts (12 F, 13 M, 34,0 ± 10,6 years) with HT diagnosed with CGN were analyzed. Average duration of nephropathy at biopsy time was 41,2 months. Criteria of patients’ selection for genetic analysis were: clinical manifestation of thromboses of various localization; syndrome of fetus loss, especially with early preeclampsia (earlier than 34 weeks of pregnancy), arterial hypertension which is inappropriate to the activity of renal disease; negative serological markers of APS. Polymorphisms of genes MTHFR С677Т; PTG G20210A; FV Leiden G1691A; FGB G455A; ITGB3 T176C L33P; PAI-1 4G/5G 675 were determined with PCR. For each biopsy glomerulosclerosis, arterio/arteriolosclerosis and the degree of interstitial fibrosis were analyzed semiquantitatively. Results. Mutation in one of the genes was detected in 24% patients, a multigenic form of thrombophilia – in 76% patients. All 25 patients had biopsy proven TMA, 3 of them had a combination of acute and chronic TMA features. ТМА was the only morphological sign of nephropathy in 3 (13%) pts. TMA was combined with various morphological variants of CGN in all other pts: mesangioproliferative CGN – in 39% pts including 2 with IgA – nephropathy, membranous CGN – in 8% and membranoproliferative CGN I type in 4%, 16% pts had FSGS, 5 (20%) – nephrosclerosis. Sclerotic alterations were more severe in combined carriage of the alleles 4G PAI-1 and T MTHFR. A correlation was found between the renal end point and number of mutant alleles (r = 0,6; p < 0,05), the presence of allele 4G (r = 0,46; p = 0,05) and interstitial sclerosis (r = 0,5; p = 0,05). Conclusion. Hereditary thrombophilia promotes induction of nephrosclerosis, leads to activation of intraglomerular blood clotting which contributes to the CGN progression. Patients with genetic thrombophilia may develop acute TMA without any other kinds of renal damage.

Overweight (body mass index, BMI = 25–29,9 kg/m2) and obesity (BMI >30 kg/m2) lead to the development of a metabolic syndrome (MS) and related complications. Patients with MS belong to the high-risk group for various forms of coronary heart diseases (CHD), diabetes mellitus and dysmetabolic nephropathy and in same cases develop chronic kidney failure. The direct influence of adipocytokines produced by adipose tissue may induce functional and structural lesions of the kidney. This research analyses the role of adiposity, and hormones produced by adipose tissue in development of kidney diseases in patients with MS. Methods. 70 patients have been examined (54,8% males, 45,2% females), age 52,8 ± 11,8 years with overweight (BMI 25–29,9 kg/m2) or obesity (BMI >30 kg/m2). Anthropometrics data, plasma leptin and adiponectin concentration, glomerular filtration rate (GFR) and the presence of albuminuria were analyzed. Results. Among the examined patients 77% obesity and 23%, overweight. Increased BMI was accompanied by a rise in leptin and increased degree of albuminuria and a decrease in GFR. The concentration of adiponectin declined with increase in BMI and rose with decrease GFR. A statistically significant positive correlation of leptin with the anthropometrics data and negative correlation with kidney functional parameters (GFR and albuminuria) have been found. The results allow us to consider adiposity as a risk factor for nephropathy in MS.

The study presents the results of a retrospective one-center 10-years follow up study for outcome of idiopathic steroid-resistant nephrotic syndrome in 65 children including 5 patients who had low birth weight (<2500 g) due to prematurity. Low birth weight group had the high relative risk (RR) of low renal function (eGFR >10 ml/min, RR = 2,53; p < 0,05) and low 5-year cumulative renal survival (0 vs 61%; р = 0,00084) compared to normal birth weight patients. Low birth weight that reflects adverse effects on development in utero is a risk factor for progression of idiopathic SRNS in children that is often accompanied by a decline of renal function.

The aim of the study was to determine relations between homocysteine level and indicators of endotelial dysfunctions in patients treated with program hemodialysis. During inspection of 89 program hemodialysis patients concentrations of homocysteine, stable metabolites of oxyde nitrogen and lipidogram indicators were determined. It was found that average homocysteine concentration in hemodialysis patients was higher than in control group (р < 0,001). Concentration of stable metabolites of oxyde nitrogen in surveyed groups was also lower than in practically healthy people; increase in atherogenic lipoproteins in program hemodialysis patients was also revealed. Correlation analysis revealed negative relations between homocysteine concentration and stable metabolites of oxyde nitrogen: nitrates (r = –0,21, р < 0,05), nitrites (r = –0,3, р < 0,01), total metabolites of oxyde nitrogen (r = –0,34, р < 0,05). A positive correlation between homocysteine concentration аnd the total cholesterol (r = 0,28, р < 0,04), low density cholesterol (r = 0,26, р < 0,04), triglycerides (r = 0,22, р = 0,05) were found. Also positive correlation between serum nitrites and the total concentration of stable metabolites of oxyde nitrogen (r = 0,8, р < 0,0001), nitrates (r = 0,4, р < 0,0001) was revealed. Multiple regression analysis revealed a negative relation of concentration of nitrites and homocysteine concentration (b –0,198, р = 0,008) and its direct relation with the total concentration stable metabolites of oxyde nitrogen in blood serum (b = 1,05, р < 0,00001). Conclusions: 1. In hemodialysis patients the levels of homocysteine, atherogenic indicators lipid's spectrum are higher than in practically healthy people. 2. Concentration of final metabolites of oxyde nitrogen in blood serum is in hemodialysis patients authentically lower than in the control group. 3. Statistically significant correlation between concentration of metabolites of oxyde nitrogen and homocysteine level is revealed. 4. Hyperhomocysteinemia can be regarded as an additional marker of endothelial dysfunction in hemodialysis patients.

The aim of the study was to evaluate the activity of human kidneys using water load test at various initial levels of decompression-induced intravascular gas formation (DIGF) arising in the course of a simulated descent to moderate depths. Forty-four male volunteers aged 20–25 years participated in this study. The subjects were divided into groups according to baseline values of IDGF in the first series of tests. During the second series of tests the subjects consumed water, 20 ml / kg body weight 5 minutes before the end of isopression (endurance/exposition) in a pressure chamber at the depth of 30 m (0,4 MPa). The parameters of the reaction of the excretory system to water load under the immersion differ from those in standard conditions. The kidney activity of persons who have high DIGF after immersion was characterized by reducing excretion of urine, sodium and chloride and increase in excretion of potassium. Differences in the kidney response to high pressure under conditions of decompression-induced intravascular gas formation of varying intensity can be associated with individual human resistance to these factors.

The main milestones in the development of peritoneal dialysis are reviewed. The history of the method from the first attempts of its clinical application to modern state is presented.