Glomerular and tubular function in renal transplant patients treated with and without ciclosporin A

Citation
Jm. Hansen et al., Glomerular and tubular function in renal transplant patients treated with and without ciclosporin A, NEPHRON, 80(4), 1998, pp. 450-457
Citations number
27
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
NEPHRON
ISSN journal
00282766 → ACNP
Volume
80
Issue
4
Year of publication
1998
Pages
450 - 457
Database
ISI
SICI code
0028-2766(199812)80:4<450:GATFIR>2.0.ZU;2-1
Abstract
The present study evaluated whether chronically administered low-dose (<5 m g/kg) ciclosporin A (CsA) affects renal haemodynamics and tubular function in renal transplant recipients (RTx) when studied at nadir CsA blood levels . The renal clearance of lithium was used as an index of proximal tubular o utflow of sodium and water. Effective renal plasma flow, glomerular filtrat ion rate, and renal clearance of lithium were studied in 67 stable non-diab etic RTx and 44 healthy controls. Forty-eight of the RTx were treated with CsA, prednisone, and azathioprine. Nineteen were treated exclusively with p rednisone and azathioprine. In RTx with a good graft function (serum-creati nine <125 mu mol/l), no specific CsA-induced renal haemodynamic and tubular dysfunctions were evident. In CsA-treated RTx with a slightly reduced rena l function (serum creatinine 125-180 mu mol/l) a decrease in fractional pro ximal tubular reabsorption was found. The renal clearances of urate and mag nesium were comparable between RTx treated with or without CsA, and a signi ficant correlation between glomerular filtration rate and renal clearance o f urate was found. CsA-treated RTx had a significantly higher blood pressur e, independent of glomerular filtration rate and segmental tubular function . In conclusion, at nadir CsA blood levels, no specific CsA-induced tubular dysfunction evaluated by the renal lithium clearance method could be demon strated in RTx receiving chronically low-dose CsA. The hyperuricaemia commo nly seen in RTx seems to be mainly caused by the reduced glomerular filtrat ion rate.