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Background. Diabetes mellitus is an important cause of end-stage renal failure (ESRF). Although classic diabetic nephropathy accounts for the majority of patients reaching ESRF, renovascular disease, which is frequent in such patients, plays an increasingly important role. Percutaneous transluminal renal angioplasty (PTRA) has been proven to be an efficacious measure for renal revascularization. Methods. Ninety-nine patients with diabetes mellitus and renal artery stenosis, corresponding to 16.6% of the entire population of diabetic patients, were treated by PTRA or with the Palmaz-Schatz stent in our clinic. Technical success was achieved by PTRA in 92/99 patients, in 10 patients a Palmaz Schatz stent was implanted. Results. Hypertension was cured in eight and improved in 44 patients. In 47 patients, there was no impact on blood pressure. An improvement in renal function was evident 1 month after PTRA in 8/27 patients. A further improvement occurred in another four patients after 6 months. The re-stenosis rate was 22% after 5 years. Serious complications occurred in seven patients (one patient required surgery and two patients had regular dialysis treatment). Conclusions. Renovascular disease is an important cause of ESRF in diabetic patients. PTRA is a valid tool to revascularize renal artery stenosis and improve blood pressure control and renal function both in diabetic and non-diabetic patients.

A multicentre, randomized, placebo-controlled study was performed in 39 adult patients with biopsy-proven IgA nephropathy with the aim of comparing the effects of the ACE inhibitor fosinopril and placebo on proteinuria. All patients had normal blood pressure and normal renal function. Proteinuria ranged from 1.0 to 2.5 g/24 h. After a 3-month run-in period, fosinopril and placebo were randomly administered in two 4-month sequences separated from cross-over treatment by a 1-month interval. The mean values of creatinine clearance did not change during either the placebo or the treatment sequences. The mean values of mean arterial pressure (MAP) were significantly lower during the fosinopril sequence (90.4 +/- 9.0 mmHg) than in basal conditions (92.8 +/- 9.1 mmHg) (P = 0.034). The mean basal values of proteinuria were 1.74 +/- 0.84 g/24 h. They were unchanged during the placebo sequence (1.79 +/- 1.20) and fell to 1.37 +/- 0.98 g/24 h after 4 months of fosinopril treatment. Using a multivariate statistical analysis, the treatment effect by time on proteinuria was significantly evident only in the fosinopril sequence (Wilks test, P = 0.033). Changes in protein excretion were not correlated with changes in MAP, baseline plasma renin activity, and urinary sodium excretion. This controlled study shows that fosinopril can significantly reduce proteinuria even in normotensive patients with IgA nephropathy. Obviously, the results of treatment with ACE inhibitors on long-term renal prognosis remain to be elucidated.

Hypertension is frequently present in glomerulonephritis without renal insufficiency but its pathogenesis is poorly understood. Eighty-five patients with glomerulonephritis and normal renal function, including 55 hypertensive patients, and 24 normal subjects were studied to obtain data on the mechanisms responsible for hypertension. Plasma renin activity (PRA), plasma noradrenaline, total exchangeable sodium, and urinary prostaglandin E (PGE) were determined. Moreover, the autonomic nervous system was explored with the following tests: tilt test, diving reflex, lying down, and deep-breathing tests. In 15 of the 30 normotensive patients with glomerulonephritis, PRA was measured after the administration of propranolol and then indomethacin. No significant differences were found in the mean values of PRA, plasma noradrenaline, total exchangeable sodium, urinary PGE, and autonomic nervous system behaviour between glomerulonephritis patients with and without hypertension or between hypertensive glomerulonephritis patients and control subjects. In many of the normotensive glomerulonephritis patients we found an elevated PRA that was normalised by propranolol but not by indomethacin. In summary, hypertension in glomerulonephritis is not associated with abnormalities in the sodium balance, with renin-angiotensin or with autonomic nervous system abnormalities. A renin hypersecretion seems to be present only in some normotensive patients with glomerulonephritis.