Angiotensin converting enzyme inhibition and chronic cyclosporine-induced renal dysfunction in type 1 diabetes
Aim. This study was designed to evaluate whether the angiotensin converting enzyme inhibitor enalapril could prevent cyclosporine-induced renal dysfunction in diabetic patients treated with CsA in monotherapy. Design. Twenty-four recent onset insulin-dependent diabetic patients without prior renal i...
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Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 1996-04, Vol.11 (4), p.673-678 |
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Sprache: | eng |
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Zusammenfassung: | Aim. This study was designed to evaluate whether the angiotensin converting enzyme inhibitor enalapril could prevent cyclosporine-induced renal dysfunction in diabetic patients treated with CsA in monotherapy. Design. Twenty-four recent onset insulin-dependent diabetic patients without prior renal involvement were randomized to receive a 3 month course of either cyclosporine (CsA) alone (7.5 mg/kg. b.i.d. in olive oil) or CsA$enalapril (20 mg p.o. oad.). End points. were mean arterial pressure, plasma creatinine, GFR, renal plasma flow, renal vascular resistance, sodium and lithium clearances measured before and after 3 months of treatment. Results. Baseline values were identical in both groups except for mean arterial pressure which was slightly higher in the subjects subsequently receiving CsA$enalapril. Three month treatment with CsA increased significantly mean arterial pressure and renal vascular resistance by 9 and 24% respectively, while decreasing significantly glomerular filtration rate and renal plasma flow by 17 and 14% respectively. Enalapril was able to prevent the decline in GFR and the increase in blood pressure induced by CsA. This effect was demonstrated despite a similar increase in renal vascular resistance suggesting a dissociation between changes in glomerular filtration rate and renal vascular resistance during angiotensin converting-enzyme inhibition. Conclusion. Chronic angiotensin converting-enzyme inhibition could afford some degree of protection against CsA-induced renal dysfunction. Whether these results can be extrapolated to transplant recipients in whom CsA is usually associated to treatment by glucocorticosteroids, deserves further evaluation. |
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ISSN: | 0931-0509 1460-2385 |
DOI: | 10.1093/oxfordjournals.ndt.a027358 |