Nephrotoxicity of acyclovir and ganciclovir in rats: Evaluation of glomerular hemodynamics
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1997-03-01
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Santos, Maria de Fatima Fernandes dos [UNIFESP]
Santos, Oscar Fernando Pavão dos [UNIFESP]
Boim, Mirian Aparecida [UNIFESP]
Razvickas, Clara Versolato [UNIFESP]
Moura, Luís Antonio Ribeiro de [UNIFESP]
Ajzen, Horacio [UNIFESP]
Schor, Nestor [UNIFESP]
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Whole-kidney function and glomerular hemodynamics were evaluated after acute (50 mg/kg, iv, in bolus) and short-term-chronic (50 mg mg/kg, ip, 5 days) acyclovir (ACV) and short-term chronic ganciclovir (Gan; 30 mg/kg, ip, 5 days) treatment in euvolemic Munich-Wistar rats. The evaluation of whole-kidney function of the ACV groups showed a significant reduction in total GFR (0.96 +/- 0.10 to 0.28 +/- 0.02 mL/min in the acute group, P < 0.05, and 1.04 +/- 0.09 to 0.33 +/- 0.04 mL/min in the chronic group, P < 0.05) with a marked increase in total renal vascular resistance (TRVR) (33 +/- 5 to 122 +/- 26 mm Hg . min/mL in the acute group and 28 +/- 3 to 74 +/- 18 mm Hg . min/mL in the chronic group, P < 0.05) and a reduction in RPF (2.29 +/- 0.25 to 0.81 +/- 0.15 mL/min in the acute group and 2.57 +/- 0.36 to 1.30 +/- 0.40 mL/min in the chronic group, P < 0.05). Conversely, urinary flow (V') was unchanged (3.6 +/- 0.4 to 3.6 +/- 0.2 mu L/min in the acute group) or elevated (3.7 +/- 0.6 to 6.6 +/- 1.4 mu l/min in the chronic group, P < 0.05). The evaluation of glomerular hemodynamics after ACV treatment showed a reduction in single-nephron GFR (SNGFR) (46.4 +/- 5.3 to 26.2 +/- 3.4 nL/min in the acute group and 38.7 +/- 5.7 to 21.1 +/- 5.7 nL/min in the chronic group, P < 0.05), a significant elevation in total arteriolar resistance (R(T)) (2.90 +/- 0.44 to 4.94 +/- 0.77 X 10(10) dyn . s . cm(-5) in the acute group and 3.72 +/- 0.45 to 9.00 +/- 2.40 X 10(10) dyn . s . cm(-5) in the chronic group, P < 0.05) and a severe reduction in glomerular plasma flow rate (Q(A)) (152.6 +/- 29.5 to 103.8 +/- 27.8 nL/min in the acute group and 149.1 +/- 29.8 to 68.5 +/- 10.0 nL/min in the chronic group, P < 0.05). However, the glomerular ultrafiltration coefficient, K-f, was changed only in the chronic group (0.1002 +/- 0.0165 to 0.0499 +/- 0.0090 nL/(s . mm . Hg), P < 0.05). After Can treatment, no changes were observed in GFR (1.04 +/- 0.09 to 0.96 +/- 0.08 mL/min, with the maintenance of RPF (2.57 +/- 0.36 to 2.66 +/- 0.34 mL/min) and a nonsignificant reduction in TRVR (28 +/- 3 to 20 +/- 3 mm Hg . min/mL. The short-term Can treatment also showed a different pattern in glomerular hemodynamics by inducing an elevation in SNGFR (38.7 +/- 5.7 to 50.3 +/- 2.8 nL/min, P < 0.05) with no changes in Q(A) (150 +/- 30 to 135 +/- 22 nL/min) and a mild vasodilation, R(T) (3.7 +/- 0.5 to 2.7 +/- 0.3 X 10(10) dyn . s . cm(-5), P < 0.05) associated with an increment in K-f (0.1002 +/- 0.0165 to 0.2400 +/- 0.0700 nL/(s . mm Hg), P < 0.05). Thus, ACV induced acute renal failure by reducing GFR and SNGFR by an increase in TRVR and R(T) with a reduction in RPF and Q(A). Also, after short-term treatment with ACV, a reduction in K-f led to a reduction of SNGFR. On the other hand, can treatment did not induce acute renal failure by the adopted techniques.
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Journal Of The American Society Of Nephrology. Baltimore: Williams & Wilkins, v. 8, n. 3, p. 361-367, 1997.