To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40 ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm. These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.

No abstract

Thirty-one renal transplant recipients, submitted to treatment with cyclosporin in association with other immunosuppressive agents, were also treated for 9 months with two hydroxymethylglutaryl coenzyme A reductase inhibitors, simvastatin (10 mg/day) or pravastatin (20 mg/day), for concomitant hypercholesterolemia and hypertriglyceridemia. Both drugs significantly decreased total cholesterol and triglyceride serum levels, but they did not modify whole-blood trough concentrations of polyclonal and monoclonal cyclosporin or polyclonal/monoclonal cyclosporin ratio. No alterations of the clinical and laboratory parameters investigated were found. The results of this study show the efficacy and safety of hydroxymethylglutaryl coenzyme A reductase inhibitors in the treatment of hyperlipidemia in kidney transplant patients.

Forty kidney-transplanted patients with hypertriglyceridemia, under treatment with cyclosporine alone or associated with other immunosuppressive drugs, were treated with gemfibrozil. This drug, for a long-term treatment (ranging from 4 to 6 months), was able to decrease hypertriglyceridemia and did not modify either polyclonal (P) and monoclonal (M) cyclosporine blood levels or P/M ratio. These data seem to exclude an effect of gemfibrozil on cyclosporine blood concentrations. Therefore, the use of gemfibrozil in kidney-transplanted patients does not require modifications of cyclosporine dose.

Severe perirenal hemorrhage is a major, although rare, postbiopsy complication. We report a case of a 48-year-old man with a postbiopsy massive bleeding from a ramification of the renal artery supplying the lower pole of the left kidney. Treatment consisted of complete obliteration of the bleeding vessel by helding a percutaneous catether in wedge position during a renal arteriographyc study. Our case shows that percutaneous arterial obliteration is a successful procedure in treating postbiopsy renal hemorrhage, representing an effective alternative to surgical therapy.