Ramón Rodrigo1, Gonzalo Rivera, Rodrigo Castillo, Cristián Guichard. 1. Renal Pathophysiology Laboratory, Molecular and Clinical Pharmacology Program, ICBM, Facultad de Medicina, Universidad de Chile, Casilla 70058, Santiago 7, Chile. rrodrigo@med.uchile.cl
Abstract
BACKGROUND: Ethanol consumption is known to cause structural and functional renal damage in rat kidney. Acutely, ethanol impairs acid-base regulation, but a chronic effect on urine acidification has not been well elucidated. The aim of the present study was to assess urinary acidification in rats subjected to chronic ethanol consumption and renal function stressors, such as unilateral nephrectomy and/or metabolic acidosis. MATERIAL/ METHODS: Ethanol-fed rats received aqueous ethanol 20% (v/v) as the sole drinking fluid for ten weeks. Then unilateral nephrectomy was performed and, five days later, metabolic acidosis was induced by administration of NH(4) Cl (1.5 mmol/kg body weight) twice a day for two days. The urinary acidification rate was assessed seven days after unilateral nephrectomy by determining urine pH, ammonium and titratable acid. RESULTS: Chronic ethanol consumption, with or without unilateral nephrectomy, did not change urine pH, titratable acid, or ammonium excretion. Although NH(4)Cl-induced metabolic acidosis resulted in a significant increase of the acidification rate, the changes were not significantly different between ethanol- fed and control groups. Renal (Na + K)-ATPase was enhanced by chronic ethanol consumption, as well as by unilateral nephrectomy, but not by NH(4)Cl-induced metabolic acidosis. CONCLUSIONS: Chronic ethanol consumption does not impair the urinary acidification function of the rat, even under stressful conditions, such as acid loading and/or unilateral nephrectomy. Although these data cannot be extrapolated to human settings, there is possible application when considering drinkers as potential kidney donors.
BACKGROUND:Ethanol consumption is known to cause structural and functional renal damage in rat kidney. Acutely, ethanol impairs acid-base regulation, but a chronic effect on urine acidification has not been well elucidated. The aim of the present study was to assess urinary acidification in rats subjected to chronic ethanol consumption and renal function stressors, such as unilateral nephrectomy and/or metabolic acidosis. MATERIAL/ METHODS:Ethanol-fed rats received aqueous ethanol 20% (v/v) as the sole drinking fluid for ten weeks. Then unilateral nephrectomy was performed and, five days later, metabolic acidosis was induced by administration of NH(4) Cl (1.5 mmol/kg body weight) twice a day for two days. The urinary acidification rate was assessed seven days after unilateral nephrectomy by determining urine pH, ammonium and titratable acid. RESULTS: Chronic ethanol consumption, with or without unilateral nephrectomy, did not change urine pH, titratable acid, or ammonium excretion. Although NH(4)Cl-induced metabolic acidosis resulted in a significant increase of the acidification rate, the changes were not significantly different between ethanol- fed and control groups. Renal (Na + K)-ATPase was enhanced by chronic ethanol consumption, as well as by unilateral nephrectomy, but not by NH(4)Cl-induced metabolic acidosis. CONCLUSIONS: Chronic ethanol consumption does not impair the urinary acidification function of the rat, even under stressful conditions, such as acid loading and/or unilateral nephrectomy. Although these data cannot be extrapolated to human settings, there is possible application when considering drinkers as potential kidney donors.