TY - JOUR
T1 - Renal and metabolic effects of L-arginine infusion in kidney transplant recipients
AU - Zhang, X. Z.
AU - Ghio, L.
AU - Ardissino, G.
AU - Tirelli, A. S.
AU - Daccò, V.
AU - Testa, S.
AU - Claris-Appiani, A.
PY - 1999
Y1 - 1999
N2 - Aim and methods: In order to investigate the role of kidney damage on renal response to L-arginine (L-Arg) infusion in transplant patients receiving cyclosporine A (CsA) treatment, we assessed systemic and glomerular hemodynamic variables, the fraction excretion of urinary sodium, albumin, cyclic GMP (as an index of nitric oxide (NO) production from L-Arg) and urea excretion (as an index of ureagenesis), and glucoregulatory hormone levels in five normal volunteers and 21 renal allograft recipients (aged 10-20 years) treated with CsA, 10 with normal renal function and II with chronic renal insufficiency. Results: In the normal subjects, L-Arg infusion (290 mg/min/1.73 m2 for 1 h) significantly reduced mean arterial pressure (MAP) (76 ± to 70 ± 5 mmHg) and renal vascular resistance (RVR), and increased GFR (103 ± 9 to 122 ± 7 min/1.73 m2), RPF urinary cyclic GMP excretion (0.40 ± 0.1 to 0.60 ± 0.1 nmol/100 ml glomerular filtrate (GF)), and sodium and albumin excretion. Neither the patients with chronic graft dysfunction nor those with a normal graft responded to L-Arg infusion: RVR remained high, and MAP. GFR, RPF, fractional excretion of sodium and urinary excretion of albumin and cyclic GMP were unchanged in both groups of patients. Glucagon, insulin and urinary urea excretion rose significantly in controls and both patient groups. Conclusion: The hemodynamic effects of L-Arg infusion were inhibited in the patients, regardless of their degree of renal function, possibly because L-Arg-NO production was blunted.
AB - Aim and methods: In order to investigate the role of kidney damage on renal response to L-arginine (L-Arg) infusion in transplant patients receiving cyclosporine A (CsA) treatment, we assessed systemic and glomerular hemodynamic variables, the fraction excretion of urinary sodium, albumin, cyclic GMP (as an index of nitric oxide (NO) production from L-Arg) and urea excretion (as an index of ureagenesis), and glucoregulatory hormone levels in five normal volunteers and 21 renal allograft recipients (aged 10-20 years) treated with CsA, 10 with normal renal function and II with chronic renal insufficiency. Results: In the normal subjects, L-Arg infusion (290 mg/min/1.73 m2 for 1 h) significantly reduced mean arterial pressure (MAP) (76 ± to 70 ± 5 mmHg) and renal vascular resistance (RVR), and increased GFR (103 ± 9 to 122 ± 7 min/1.73 m2), RPF urinary cyclic GMP excretion (0.40 ± 0.1 to 0.60 ± 0.1 nmol/100 ml glomerular filtrate (GF)), and sodium and albumin excretion. Neither the patients with chronic graft dysfunction nor those with a normal graft responded to L-Arg infusion: RVR remained high, and MAP. GFR, RPF, fractional excretion of sodium and urinary excretion of albumin and cyclic GMP were unchanged in both groups of patients. Glucagon, insulin and urinary urea excretion rose significantly in controls and both patient groups. Conclusion: The hemodynamic effects of L-Arg infusion were inhibited in the patients, regardless of their degree of renal function, possibly because L-Arg-NO production was blunted.
KW - Cyclosporine A
KW - Glucagon
KW - L-arginine
KW - Nitric oxide
KW - Renal allograft recipients
KW - Renal hemodynamics
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M3 - Article
C2 - 10442494
AN - SCOPUS:0032792677
SN - 0301-0430
VL - 52
SP - 37
EP - 43
JO - Clinical Nephrology
JF - Clinical Nephrology
IS - 1
ER -