It has recently been suggested that selective parathyoidectomy modifies drug-induced acute renal failure. In the present study, we tested whether parathyroid hormone (PTH) could play a role in the pathogenesis of cisplatin (CP) nephrotoxicity. Parathyroidectomized rats (PTX) with normal blood calcium, were injected with two different doses of CP (group Ia: 10 mg/kg and group Ib: 6 mg/kg) and their renal functions were evaluated after 72 hours (group 1a) and 120 h (group 1b), respectively. All animals exhibited a milder course of acute renal failure when compared to sham-PTX CP treated rats, with lower serum creatinines (S(Cr)) (group Ia: 1.99 ± 0.14 vs 2.91 ± 0.56 mg/dl, p<0.05) (group Ib: 1.45 ± 0.08 vs 1.80 ± 0.09 mg/dl, p<0.05) and blood urea (BUN) (group Ia: 76 ± 5 vs 115 ± 19 mg/dl, p<0.05) (group Ib: 70 ± 9 vs 88 ± 10 mg/dl, p<0.05). Furthermore, the i.p. administration of PTH (50 I.U. twice daily for 9 days) to normal rats treated with CP (6 mg/kg) aggravated the CP-induced ARF as compared to vehicle injected animals (S(Cr) 2.23 ± 0.16 vs 1.63 ± 0.19 mg/dl, p<0.05 and BUN 153 ± 22 vs 97 ± 20 mg/dl, p<0.05). Treatment with the calcium channel blocker verapamil (4 mg/kg) nine days before and three days after CP (4 mg/kg) administration, had no significant effect on cisplatin nephrotoxicity. These data indicate that selective parathyroidectomy ameliorates experimental cisplatin-induced acute renal failure, while PTH aggravates CP nephrotoxicity through a mechanism that is not mediated by the voltage-dependent calcium channels.

Parathyroidectomy has a beneficial effect on experimental cisplatin nephrotoxicity

CAPASSO, Giovambattista;
1990

Abstract

It has recently been suggested that selective parathyoidectomy modifies drug-induced acute renal failure. In the present study, we tested whether parathyroid hormone (PTH) could play a role in the pathogenesis of cisplatin (CP) nephrotoxicity. Parathyroidectomized rats (PTX) with normal blood calcium, were injected with two different doses of CP (group Ia: 10 mg/kg and group Ib: 6 mg/kg) and their renal functions were evaluated after 72 hours (group 1a) and 120 h (group 1b), respectively. All animals exhibited a milder course of acute renal failure when compared to sham-PTX CP treated rats, with lower serum creatinines (S(Cr)) (group Ia: 1.99 ± 0.14 vs 2.91 ± 0.56 mg/dl, p<0.05) (group Ib: 1.45 ± 0.08 vs 1.80 ± 0.09 mg/dl, p<0.05) and blood urea (BUN) (group Ia: 76 ± 5 vs 115 ± 19 mg/dl, p<0.05) (group Ib: 70 ± 9 vs 88 ± 10 mg/dl, p<0.05). Furthermore, the i.p. administration of PTH (50 I.U. twice daily for 9 days) to normal rats treated with CP (6 mg/kg) aggravated the CP-induced ARF as compared to vehicle injected animals (S(Cr) 2.23 ± 0.16 vs 1.63 ± 0.19 mg/dl, p<0.05 and BUN 153 ± 22 vs 97 ± 20 mg/dl, p<0.05). Treatment with the calcium channel blocker verapamil (4 mg/kg) nine days before and three days after CP (4 mg/kg) administration, had no significant effect on cisplatin nephrotoxicity. These data indicate that selective parathyroidectomy ameliorates experimental cisplatin-induced acute renal failure, while PTH aggravates CP nephrotoxicity through a mechanism that is not mediated by the voltage-dependent calcium channels.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/229271
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