[The mechanisms of the development of arterial hypertension in patients with chronic kidney failure treated by hemodialysis]. / Nekotorye mekhanizmy razvitiia arterial'noi gipertenzii u bol'nykh s kronicheskoi pochechnoi nedostatochnost'iu, lechennykh gemodializom.

Hypertensive patients out of 50 with chronic renal failure degree IIIA on programmed hemodialysis were divided into those with uncontrolled (group 1) and controlled (group 2) arterial hypertension. Group 1 was found to have hyperactive renin-angiotensin aldosterone system and marked unbalance in the system of cyclic nucleotides. In group 2 the activity of renin and plasma aldosterone levels were not so high. In both groups the above hormonal abnormalities followed the pattern of progressive hyperkinetic syndrome running with an inadequate fall in peripheral vascular resistance responsible for arterial hypertension in these patients.

[The malignant hypertension syndrome: incontrovertible and questionable truths]. / Sindrom zlokachestvennoi arterial'noi gipertenzii: istiny besspornye i somnitel'nye.

A total of 42 patients with malignant arterial hypertension (MAH) were examined. Of these, 32 patients had essential hypertension (26 with normal renal function and 6 with renal failure treated by programmed hemodialysis) and 10 suffered from chronic glomerulonephritis. The patients were examined for central hemodynamics, hormonal background (plasma renin activity) (PRA), plasma aldosterone and cortisol concentration. 14 patients underwent closed puncture biopsy of the kidneys. All the patients manifested high PRA associated activation of gluco- and mineralocorticoid adrenal function along with the hyperkinetic syndrome. MAH was characterized by dramatic discrepancy between the stroke and cardiac indices and specific peripheral resistance. Nephrosclerosis whose extent varied, attaining maximum in patients with associated essential hypertension and renal failure and in autopsy material, in addition to severe lesions of the renal vessels appeared to be the common feature of all morphological alterations. Plasmic impregnation and fibrinoid necrosis of the arterioles were not detectable in all the patients, being of focal character. The same alterations were identified in the patients during exacerbation of glomerulonephritis and in the absence of MAH. The data obtained point to the nonuniformity of MAH. Four clinicomorphological variants of MAH are suggested.

[The role of atrial natriuretic peptide in the pathogenesis of arterial hypertension in chronic glomerulonephritis]. / O roli atria'lnogo natriiureticheskogo peptida v patogeneze arteria'lnoi gipertenzii pri khronicheskom glomerulonefrite.

Radioimmunoassay was used in 39 patients with chronic glomerulonephritis and secondary hypertension to measure atrial natriuretic peptide concentration in blood plasma. The latter concentration appeared unrelated to the patients' age, duration and gravity of hypertension, the degree of renal insufficiency, hyperhydration and activation of renin-angiotensin-aldosterone++ system. The conclusion is made on minor contribution of this short-acting peptide to pathogenesis of arterial hypertension in chronic glomerulonephritis.

[Criteria for the early diagnosis of chronic kidney failure]. / Kriterii rannei diagnostiki khronicheskoi pochechnoi nedostatochnosti.

Comprehensive study of blood and urinary levels of beta 2-microglobulin and cAMP in patients with chronic renal failure (CRF) demonstrated their significant alterations in the disease development. Therefore the levels of beta 2-microglobulin and cAMP could be of great aid in reaching the early diagnosis of CRF.

[Central hemodynamic indices of patients with chronic kidney failure treated by hemodialysis]. / Pokazateli tsentral'noi gemodinamiki u bol'nykh s khronicheskoi pochechnoi nedostatochnost'iu, lechennykh gemodializom.

Examination of the central hemodynamics in patients with chronic renal failure and of symptomatic arterial hypertension revealed two hemodynamic variants of hypertension, namely, that corrected by dialysis arterial hypertension is based on an increase of the cardiac output associated with decrease of the peripheral resistance in the course of treatment and that noncorrectable by dialysis hypertension characterized by a stably high resistance of the arteriolar bed associated with an increased minute blood volume. It was also established that working overloading by resistance and volume results in essential disorders of the intracardiac hemodynamics.