RENAL HEMODYNAMICS IN RENAL-TRANSPLANT RECIPIENTS - THE ROLE OF REDUCED KIDNEY MASS AND CYCLOSPORINE ADMINISTRATION

Citation
C. Pluvio et al., RENAL HEMODYNAMICS IN RENAL-TRANSPLANT RECIPIENTS - THE ROLE OF REDUCED KIDNEY MASS AND CYCLOSPORINE ADMINISTRATION, Transplantation, 61(5), 1996, pp. 733-738
Citations number
29
Categorie Soggetti
Immunology,Surgery,Transplantation
Journal title
ISSN journal
00411337
Volume
61
Issue
5
Year of publication
1996
Pages
733 - 738
Database
ISI
SICI code
0041-1337(1996)61:5<733:RHIRR->2.0.ZU;2-X
Abstract
It has been hypothesized that both the cyclosporine (CsA) treatment an d the reduction of renal mass may affect the renal hemodynamic regulat ion in kidney transplant recipients, To address this question, we eval uated the renal hemodynamic response to hyperaminoacidemia (i.v, mixed amino acid infusion 3.3 mg/kg/minute for 150 minutes) in four study g roups: (1) 16 renal transplant recipients (Tx), (2) 6 uninephrectomize d (Nx) subjects, (3) 7 subjects treated with CsA for chronic uveitis ( CsA), and (4) 9 normal controls (NC), In response to amino acid admini stration (AA), glomerular filtration rate (GFR) rose significantly in NC subjects (80+/-6 vs. 91+/-6 ml/minute; P<0.01) and Nx patients (57/-3 vs, 68+/-7 ml/minute; P<0.01) and failed to increase in Tx recipie nts (39+/-3 vs. 37+/-3 ml/minute) and CsA-treated patients (58+/-3 vs, 53+/-4 ml/minute). Renal plasma flow (RPF) did not change in Tx recip ients (243+/-27 vs, 235+/-25 ml/minute) but rose significantly in all other groups (257+/-17 vs, 344+/-33 in NX, 364+/-61 vs. 441+/-55 in Cs A, 412+/-49 vs, 472+/-72 ml/min in NC subjects; P<0.05 vs. basal). Bas al renal vascular resistances were significantly higher in Tx (0.29+/- 0.04 mmHg/ml . min; P<0.01 vs. all other groups) than in Nx (0.21+/-0. 01 mmHg/ml . min), CsA(0.23+/-0.04 mmHg/ml . min) (both P<0,01 vs, NC subjects), and NC subjects (0.13+/-0.02 mmHg/ml . min). Renal vascular resistance failed to decline in Tx (0.31+/-0.04 mmHg/ml . min) during AA infusion but declined significantly in all other groups. In Tx, ba sal GFR was positively correlated to renal allograft volume (r=0.547, P<0.03); however, no relationship was found between the latter and bas al RPF or the AA induced changes in GFR, In summary, the present study demonstrates that in kidney transplant recipients and in CsA-treated subjects, the renal functional reserve to hyperaminoacidemia is impair ed, This is at variance to what is observed in normal controls and uni nephrectomized subjects. In renal transplant recipients, basal but not amino acid stimulated GFR correlates with renal allograft volume, We conclude that basal GFR is related to renal volume in Tx and that the response to hyperaminoacidemia seems to be affected by chronic CsA adm inistration.