Steroid-induced hypertension in patients with nephrotic syndrome.

In 35 initially normotensive patients with chronic glomerulonephritis and lupus nephritis (including 27 patients with nephrotic syndrome; NS), blood pressure (BP), urinary sodium excretion, plasma renin activity (PRA), plasma aldosterone level (PA), urinary aldosterone excretion (Au and blood volume were measured before and during prednisolone treatment. In 7 patients (all with NS) steroid-induced hypertension has developed. The patients prone to develop hypertension were hypervolemic nephrotics with initial depression of PRA, PA, Au, and severe sodium retention. In these patients prednisolone did not produce diuresis of natriuresis nor did it decrease proteinuria. In normo- and hypovolemic patients prednisolone produced significant diuresis and natriuresis and failed to induce hypertension. Thus, two types of response to prednisolone could be observed in patients with NS.

Effects of heparin-induced aldosterone deficiency on renal function in patients with chronic glomerulonephritis.

The effects of heparin-induced aldosterone deficiency on renal sodium and potassium transport and renal function were studied in 65 patients with chronic glomerulonephritis and initial hyperaldosteronism. Heparin-induced aldosterone deficiency resulted in increased diuresis, in natriuresis due to decreased sodium reabsorption in the distal nephron, in a fall in serum sodium and an increase in serum potassium concentration. A transient reduction in potassium excretion occurred during the 2-4 days of heparin treatment. In patients with chronic glomerulonephritis and a compromised renin-angiotensin-aldosterone system, heparin may cause drug-induced selective hypoaldosteronism. The suppressive effect of heparin on aldosterone production was partially compensated for by increasing plasma renin activity. Heparin-induced aldosterone deficiency did not change glomerular filtration rate in patients without renal failure. In those with chronic sclerosing glomerulonephritis and a glomerular filtration rate less than 35 ml/min, heparin caused a further decrease in renal function.

Lupus nephritis in males and females.

The course of lupus nephritis in 51 males was compared to that of 337 females. Nephrotic syndrome occurred with equal frequency in males and females, hypertension was more frequent in males, rapidly progressive lupus nephritis was much more frequent in males. The overall 10-year survival rate from the onset of systemic lupus erythematosus was 41 per cent in males and 60 per cent in females. The 10-year 'renal survival' - from the clinical evidence of renal disease to 'renal death' - was 40 per cent in males and 57 per cent in females. Thus the prognosis of lupus nephritis in males was worse than in females. In 10 males and 65 females acetylation rate of sulfadimezine was studied. The predominance of slow acetylators was especially marked in males and in patients with more severe disease.

Effect of levamisole on cell sensitivity in rats with experimental Heymann's nephritis.

The development of cell-sensitization to renal antigen in rats with experimental Heymann's glomerulonephritis and the effect of levamisole on cell sensitivity have been studied. Morphologic changes in GN rats appeared after 14 days and were most pronounced on days 21-28, with focal proliferation of glomerular cells, an increase of mesangium, a focal increase of the basal membrane material. After day 49 the changes improved slightly and were still the same on day 147 when a location of IgG to the glomerular basal membrane was detected. In every GN rat, cell-sensitivity to renal antigen was revealed from day 21 of the experiment till its end. Levamisole treatment decreased renal morphologic changes and abolished cell-sensitivity to renal antigen. The possible mechanisms of preventing the development of cell-sensitization in rats treated with levamisole are discussed.

Effects of indomethacin on the renal function and renin-aldosterone system in chronic glomerulonephritis.

The effects of indomethacin on plasma renin activity (PRA), plasma and urine aldosterone levels and on renal function were studied in 37 patients with chronic glomerulonephritis (GN). Indomethacin produced a significant decrease in PRA, in plasma and urinary aldosterone levels and an increase in serum potassium levels. In 4 patients indomethacin induced the clinical syndrome of hyporeninemic hypoaldosteronism with hyperkalemia, which developed during the first weeks of treatment, persisted during treatment and disappeared without any additional drugs when indomethacin was stopped. In 14 patients with chronic GN, indomethacin caused a decrease in glomerular filtration rate (GRF). Their pretreatment PRA was significantly higher than that of patients with unchanged or increased GFR and most of them had prominent sclerotic changes on biopsy. Indomethacin considerably depressed diuresis and urinary sodium excretion. The antidiuretic and antinatriuretic effects of indomethacin were more pronounced in patients with the nephrotic syndrome. The results suggest that indomethacin exerts an effect on the renin-aldosterone axis, may be a cause of drug-induced hyporeninemic hypoaldosteronism and may cause a decrease in GFR in patients with high PRA.

Antiviral immunity in chronic glomerulonephritis.

Antiviral activity was evaluated in sera from 65 patients with chronic glomerulonephritis (GN), 58 patients with SLE and 59 healthy controls. Antibodies to influenza A2 and B, and parainfluenza I-II-III viruses occurred much more frequently in GN than in healthy controls. Geometric mean antibody titers to measles, influenza A2 and B, and parainfluenza I-II-III were found to be elevated. The frequency of antiviral antibodies and their level in GN patients were similar to those in SLE patients. Detection of increased antiviral activity in sera of patients with chronic GN extends the range of diseases where persistent latent viral infection may be relevant.

The effects of azathioprine and prednisolone on T- and B-lymphocytes in patients with lupus nephritis and chronic glomerulonephritis.

The effects of long-term treatment with azathioprine and prednisolone on T- and B-lymphocytes were studied in 52 patients with lupus nephritis (LN) and chronic glomerulonephritis (GN). The effect of azathioprine on lymphocyte populations was dose dependent; high doses decreased the number of T- and particularly, B-cells, while smaller doses produced a selective depletion of B-cells. The changes in T- and B-cells during prednisolone treatment were variable with alternating increases and decreases in their numbers. The patients with increased B-lymphocyte levels showed the best response to immunosuppressive therapy.