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  • Title: Renal hemodynamics in renal transplant recipients. The role of reduced kidney mass and cyclosporine administration.
    Author: Pluvio C, DePascale E, Pluvio M, Carone M, Giordano M, Luzi L, Sabella F, Castellino P.
    Journal: Transplantation; 1996 Mar 15; 61(5):733-8. PubMed ID: 8607176.
    Abstract:
    It has been hypothesized that both the cyclosporine (CsA) treatment and the reduction of renal mass may affect the renal hemodynamic regulation in kidney transplant recipients. To address this question, we evaluated the renal hemodynamic response to hyperaminoacidemia (i.v. mixed amino acid infusion 3.3 mg/kg/minute for 150 minutes) in four study groups: (1) 16 renal transplant recipients (Tx), (2) 6 uninephrectomized (Nx) subjects, (3) 7 subjects treated with CsA for chronic uveitis (CsA), and (4) 9 normal controls (NC). In response to amino acid administration (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 recipients (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 recipients (243 +/- 27 vs. 235 +/- 25 ml/minute) but rose significantly in all other groups (257 +/- 17 vs. 344 +/- 33 in NX, 364 +/- 6l vs. 441 +/- 55 in CsA, 412 +/- 49 vs. 472 +/- 72 ml/min in NC subjects; P<0.05 vs. basal). Basal renal vascular resistances were significantly higher in Tx (0.29 +/- 0.04 mmHg/mlxmin; P<0.01 vs. all other groups) than in Nx (0.21 +/- 0.01 mmHg/mlxmin), CsA (0.23 +/- 0.04 mmHg/mlxmin) (both P<0.01 vs. NC subjects), and NC subjects (0.13 +/- 0.02 mmHg/mlxmin). Renal vascular resistance failed to decline in Tx (0.31 +/- 0.04 mmHg/mlxmin) during AA infusion but declined significantly in all other groups. In Tx, basal GFR was positively correlated to renal allograft volume (r=0.547, P<0.03); however, no relationship was found between the latter and basal 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 impaired. This is at variance to what is observed in normal controls and uninephrectomized 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 administration.
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