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Aim: To evaluate effects of corticosteroids, cytostatics, ACE inhibitors, Ang-II receptor blockers, HMG-CoA-reductase inhibitors on the levels of blood cholesterol in patients with progressive glomerulonephritis (PGN)., Material and Methods: The influence of medications which are used for treatment of chronic glomerulonephritis on the serum levels of total cholesterol (TCh) was investigated in 53 patients with chronic glomerulonephritis and persistent nephrotic syndrome (NS). All the patients with NS or nephrotic range proteinuria were divided into five groups depending on the type of therapy: corticosteroids, cytotoxic agents, ACE inhibitors, Ang-II receptor blocker, HMG-CoA-reductase inhibitors., Results: No negative change of serum TCh was revealed after the courses of treatment with corticosteroids and cytotoxic agents. Moreover, treatment with ACE inhibitors and Ang-II receptor blockers was accompanied with a significant reduction of the TCh level., Conclusion: ACE inhibitors and Ang-II receptor blockers affect some mechanisms of glomerulonephritis progression including hypercholesterolemia.

The activity of gamma-glutamyl transferase (GGT), alkaline phosphatase (AP), lactate dehydrogenase (LDG), N-acetyl-beta-D-glucosaminidase (NAG) was assessed in 53 patients with psoriasis (PS), 24 PS patients with affected kidneys, 50 patients with type 1 diabetes mellitus(DM). Enhanced activity of the enzymes occurred not only in nephropathy patients but also in those without proteinuria. AP and NAG were more active in PS, while LDG and NAG in DM. Both in PS and DM, NAG activity rose 3-4-fold compared to control. A direct correlation was found between enzymuria and uremia, glycemia (in hyperglycemia only) and cholesterolemia. An inverse relationship existed between enzymuria and uricosuria. The above changes in enzymic activity are attributed to impairment of tubules of the kidney induced by PS and DM. Diagnostic significance of enzymuria as a marker of early tubular involvement is confirmed by investigations of renal biopsies.

In view of weak implication of immunoinflammatory mechanisms in pathogenesis of noninflammatory nephropathy one may expect the disease course improvement and more slow progression of renal dysfunction. The mechanism of this action can be realized through hypolipidemic effect. In recent research there are data on a direct lovastatin action on the mechanism underlying nephritis progression by means of inhibiting proliferation of mesangial cells.

An extracellular matrix (collagens I, III, IV) was studied in the glomeruli of patients demonstrating glomerular low density lipoproteins (LDL) and free of them. These two patients' groups were not found significantly different by age, nephropathy duration, blood pressure, serum concentrations of creatinine, triglycerides, HDL cholesterol. The LDL deposit group differed by longer duration of the nephrotic syndrome, higher 24-h proteinuria, lower serum albumin levels, higher total cholesterol in the serum and the proportion VLDL and LDL cholesterol to HDL cholesterol. They had noninflammatory nephropathies more frequently, collagen IV accumulated in the glomerulus more actively, there appeared interstitial collagens I and III. The discussion concerns the role of hypercholesterolemia with the above proportion of cholesterols, its duration, a type of cells dictating mesangial proliferation, in the development of LDL-deposit-induced glomerulosclerosis.

Boyden camera tests, chemiluminescence of urinary supernatant, passive hemagglutination tests were used in measuring chemotactic properties of the urine, intensity of free-radical processes, fibronectin urine concentrations, respectively, in 31 glomerulonephritis (GN) patients. The above parameters were closely related to nephritis activity. These were much lower in patients with nephritis remission, than in subjects with nephrotic syndrome or exacerbation of latent nephritis. Chemotactic activity and intensity of free-radical processes were unrelated to protein urea which, however, correlated with fibronectin concentrations (r = 0.35, p < 0.05). The authors discuss the role of the mediators' values in evaluation of local renal inflammation and feasibility of their use as criteria of nephritis activity and prognosis.

To determine the mechanisms underlying diabetic nephropathy (DN) onset, a clinical and morphological study was initiated of 14 diabetics with insulin-dependent disease free of clinical renal manifestations. The patients were examined for intraglomerular hypertension, blood lipid spectrum and renal tissue morphology. In high intraglomerular hypertension, i. e. in renal functional reserve depletion, there is dyslipidemia with a characteristic significant rise in the levels of very low density lipoprotein cholesterol and low density lipoprotein cholesterol, in the value of atherogenic index. Morphologically, renal tissue of the hypertensive and dyslipidemic patients experienced hyperperfusion and massive lipid infiltration in glomerular cells. In contrast, renal tissue underwent only minimal nonspecific changes when intraglomerular hemodynamics and lipidemia were normal. The findings suggest that associated effects of intraglomerular hypertension and dyslipidemia may promote DN onset.

A study was made of urine lipids and their fractions in chronic glomerulonephritis (CGN) and renal amyloidosis with nephrotic syndrome (NS). 91 patients suffering from NS were examined. 2 subgroups were distinguished among these patients: with CGN of the nephrotic type and with the nephrotic stage of renal amyloidosis. The reference groups were made up of patients with latent CGN and healthy subjects. Measurements were made in the blood and urine of total lipids (TL) and their fractions--phospholipids (LP), free cholesterol (FC), mono- and diglycerides, triglycerides (TG), and cholesterol esters (CE). The presence of the NS was attended by a rise in the blood of TL concentration, relative content of FC, TG and by a decline of RL and CE, with the decrease of the relative content being more manifest in amyloidosis. Nephrotic lipiduria was largely characterized by an increase of the concentration of TL and of the relative content of PL, with the changes of the latter parameter being mostly characteristic of CGN patients. Thus, NS was associated with a high excretion of lipids with urine which is likely to reflect their elevated filtration under nephrotic hyperlipidemia. Still, in nephropathies whose pathogenesis is determined by an important role of inflammatory and membrane-destructive processes, of definite role is also the local (renal) formation of PL.

The main classes of serum lipids (fatty acids, phospholipids, triglycerides, cholesterol) were studied and compared in 36 patients aged 20 to 41 years with the renal hypertensive syndrome of different etiology, in 25 patients aged 30 to 51 years with essential hypertension, and in 20 practically healthy subjects aged 20 to 42 years. The mechanism of changes in the content of serum lipids in different diseases associated with the hypertensive renal syndrome and in patients with essential hypertension allows an assumption that these changes are linked to a large degree with arterial hypertension.

A study was made of the content of blood lipids in patients with associated chronic nephritis and arterial hypertension (AH). It has been established that the reduction of arterial pressure as a result of hypotensive therapy (administration of central action drugs, vasodilators of direct action, calcium antagonists, blockers of the angiotensin-transforming enzyme) was followed by a decrease in the blood of the concentration of fatty acids, glycerin, triglycerides, low density lipoproteins, total cholesterol, free cholesterol, phospholipids, characteristics of lipid peroxidation and by the rise of cholesterol concentration in high density lipoproteins. The data obtained are of clinical importance in view of the possibility of correcting dyslipidemia in patients with associated chronic nephritis and arterial hypertension during hypotensive treatment.