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We performed a retrospective study on 26 patients with moderate renal failure (mean GFR = 51 +/- 21 ml min-1 1.73 m-2), hypertension and atherosclerosis. Apart from three patients who had completely normal renal Doppler ultrasonography, all patients underwent renal angiography. Three groups of kidneys with different atherosclerotic renal artery involvement were identified: Group 1, 24 kidneys with no renal artery stenosis (RAS); Group 2, 18 kidneys with mild (> 25% and < 50% diameter) RAS; and Group 3, 10 kidneys with moderate (> 50% diameter) RAS. We used a two-day protocol with frusemide plus enalapril 99Tcm-MAG3 scintigraphy. The mean parenchymal transit time (MPTT), time to the maximum activity (time to peak) of the renal curve (Tmax), residual activity and split renal uptake were evaluated. The measured parameters did not differ before and after enalapril in Group 1 or in Group 2. In Group 3, MPTT and residual activity differed significantly (P < 0.025) before and after enalapril. The Tmax before and after enalapril, MPTT before and after enalapril and residual activity after enalapril differed significantly (P < 0.05) between Groups 1 and 3 and between Groups 2 and 3. Threshold values were obtained to maximize diagnostic accuracy. The Tmax, MPTT and residual activity after enalapril gave satisfactory results, and MPTT performed best with a 75% positive predictive value and a 98% negative predictive value for the diagnosis of renal artery stenosis. We conclude that MPTT, measured after enalapril administration, is a useful parameter to detect renal artery stenosis in patients with hypertension, atherosclerosis and moderate renal insufficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) may induce a variety of acute and chronic renal lesions. Acute interstitial nephritis can follow the use of nearly all NSAIDs, but the number of reported cases is low. Most of these patients are elderly and develop a nephrotic syndrome with acute renal failure while taking NSAID for months. Renal biopsy shows acute tubulo-interstitial lesions with minimal changes in the glomeruli. The renal signs usually improve after discontinuing the drug, with or without steroid therapy, but chronic renal insufficiency or even end-stage renal disease (ESRD) are possible hazards. There is evidence that interstitial nephritis results mainly from a delayed hypersensitivity response to NSAID, and nephrotic syndrome results from changes in glomerular permeability mediated by prostaglandins and other hormones. Nephrotic syndrome without interstitial nephritis may occur, as well as immune-complex glomerulopathy, in a small subset of patients receiving NSAIDs. Patients taking NSAID for months or years may develop papillary necrosis, chronic interstitial nephritis, or even ESRD. Case-control studies suggest that patients at risk are older men who suffer from chronic heart disease and renal hypoperfusion. Impaired medullary circulation and direct toxicity due to a drug metabolite seem to play a critical role in inducing interstitial fibrosis, which can be facilitated by a sustained production of some growth factors and cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the potential benefit of drug-induced renal haemodynamic changes in patients with chronic renal failure, we have evaluated the effects of the beta-blocking agent tertatolol on blood pressure, glomerular filtration rate, and renal plasma flow. Inulin and PAH clearances were performed before and after 3 months treatment and oral tertatolol, 5 mg daily in eight hypertensive patients with moderate chronic renal failure. After 3 months of treatment, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) increased significantly by 10% and 13% respectively, whereas renal vascular resistance decreased by 16% and the filtration fraction was unchanged. These results indicate that tertatolol possesses novel renal haemodynamic properties in hypertensive patients with chronic renal failure. However, the long-term benefit of such a therapy is yet to be confirmed.

A girl aged 17 developed a nephrotic syndrome with renal insufficiency after narcotic abuse. Renal biopsy showed a diffuse glomerulonephritis with crescents and dense deposits within the glomerular basement membrane; glomerular C3 deposits were present without immunoglobulin. The serum complement profile was typical of activation via the alternative pathway, and tests for C3 nephritic factor were strongly positive. Terminal renal failure occurred within 6 months and required chronic hemodialysis. It is likely that the narcotics used or their contaminants were responsible for the renal damage, presumably by activating the complement system via the alternative pathway.