Kidney Function Changes after Acute Exposure to Lead

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HILDA VARGAS ROBLES1, CARLOS CASTILLO HENKEL1, FRANCISCO POSADAS DEL RIO2, .... ACKNOWLEDGMENTS: We thank Elizabeth Hernan-.
Proc. West. Pharmacol. Soc. 45: 97-98 (2002)

Kidney Function Changes after Acute Exposure to Lead HILDA VARGAS ROBLES1, CARLOS CASTILLO HENKEL1, FRANCISCO POSADAS DEL RIO2, ROCIO BAUTISTA PÉREZ3 & BRUNO ESCALANTE ACOSTA3* 1

Escuela Superior de Medicina IPN, México D.F.; Departments of 2Pharmacology and 3Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del IPN, Avenida Instituto Politécnico Nacional 2508, México D.F., CP 07300, México *e-mail: [email protected]

Kidney is a target organ for lead (Pb) toxicity. The toxic effects of Pb on the kidney appear to be primarily localized in the proximal tubule and are manifested as excessive urinary excretion of amino acids, glucose and phosphate [1], natriuresis, kaliuresis [2] and intranuclear bodies inclusion [3]. These changes may be related to one or more factors, including increased plasma levels or decreased ion reabsorption by alteration in tubular transport mechanisms, as well as structural lesions in the nephron [4]. The aim of the present study was to correlate the effects of acute lead exposure to those of renal function, by evaluating urinary excretion and renal enzymatic activity. Therefore, in the present study we investigate kidneyspecific enzymes localized on the extracellular surface of the proximal tubule brush borders, such as γ-glutamyl transpeptidase (GGT) [5], alanine aminopeptidase (AAP) [6] and dipeptidyl aminopeptidase IV (DAP-IV) [7].

RESULTS: The results obtained show that the Pb exposed group decreased urinary sodium in 24-h urine, after the exposure. Urinary sodium decreased 49% as compared to control group (from 131 ± 9 mmol/L to 68 ± 13 mmol/L; p