1. Untersuchungen zur Nierenfunktion nierengesunder Patienten unter Ciclosporin.
- Author
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Heering, P., Kutkuhn, B., Kreuzpaintner, G., Reinhard, T., Sundmacher, R., and Grabensee, B.
- Abstract
Long-term administration of ciclosporin has been complicated by side-effects, the predominant being nephrotoxicity. We performed renal function studies on 20 patients treated with ciclosporin (group 1) and on 12 patients serving as controls (group 2). Only patients with serum creatinine less than 1.3 mg/dl entered the study. The renal function studies consisted of: Inulin clearance, PAH clearance, sodium sulphate loading, sodium bicarbonate loading. Plasma renin activity (PRA), inactive renin (IR) and aldosterone (ALDO) were measured basally and after stimulation with 40 mg furosemide i.v. Serum creatinine was not significantly impaired under ciclosporin with 1.1±0.1 mg/dl vs 0.9±0.1 mg/dl in the control group (ns). Glomerular filtration rates as measured by creatinine and inulin clearance were significantly impaired in group 1 as compared to group 2. Inulin clearance was impaired by ciclosporin with 93.5±4.4 ml/min/1.73m as compared to 121±6.6 ml/min/1.73 m ( p<0.05) in patients of group 2. The PAH clearance in ciclosporin treated patients was impaired, with 379±22.1 ml/min/1.73 m in group 1 as compared to 605±39 ml/min/1.73 m ( p<0.001) in group 2. Mean arterial pressure and renovascular resistance were significantly increased in ciclosporin treated patients. We demonstrated, by means of sodium sulphate and bicarbonate loading, incomplete distal tubular acidosis in 3 patients from group 1 but in none of group 2. There was no difference in basal plasma renin activity (PRA), but during volume contraction induced by furosemide there was only blunted response by PRA in patients receiving ciclosporin with 2.7±0.3 ng/ml/h as compared to 7.7±0.5 ng/ml/h in controls. Inactive renin was significantly increased during administration of ciclosporin and did not respond to volume contraction. Ciclosporin induced a significant impairment of renal perfusion and glomerular filtration and an increased mean arterial pressure and renovascular resistance. The decreased PRA may be due to an impaired conversion of inactive to active renin. It is possible, using appropriate methods, to prove that ciclosporin induced nephrotoxicity is also located to the distal tubular segment. [ABSTRACT FROM AUTHOR]
- Published
- 1991
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