The incidence of urinary tract infections (UTI) in 299 renal graft transplantations (281 patients) was analyzed. UTI episodes were demonstrated in 185 grafts (62%), most frequently in the first month after transplantation. The infectious episodes were mostly recurrent. Persistent infection, detected in 11% of grafts, was associated with urologic complications in almost all cases. No significant correlation between the primary renal disease and the UTI rate was found, and there was no significant correlation between UTI and sex. In grafts with recurrent infectious episodes, vesicoureteral reflux was more common. No significant difference was observed in the residual bladder volume, irrespective of whether infection was present or not. The urine was infected by a number of hospital strains, particularly Klebsiella, Enterobacter and indole-positive Proteus strains. An overwhelming majority of UTI episodes (96%) were asymptomatic. Antibody-coated bacteria in urinary sediment were present in only 19% of infectious episodes. Clinically severe courses were observed in infections associated with urologic complications (especially urinary fistulae); these were difficult to treat and were often a source of sepsis and a risk factor in graft loss.

Very little is known about bile composition in the end stage of chronic renal sufficiency. Patients with this condition are either assigned to a dialysis-transplantation programme, or are treated temporarily with a low-protein diet. Our study was designed to determine bile composition both in a group of ten patients treated with a low-protein diet over a long period of time, and in 11 patients on regular haemodialysis. The patients on haemodialysis were found to have increased bile cholesterol and an increased saturation index in the bile, i.e. changes implying increased risk of cholecystolithiasis. These changes were further enhanced by the effect of a low-protein diet with subsequent increases in cholesterol values and the bile saturation index, as well as a decrease in primary and an increase in secondary bile acids in the bile, i.e. a change in the spectrum of bile acid characteristic for cholecystolithiasis.

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