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
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.