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Am J Physiol Renal Physiol 284: F718-F726, 2003. First published December 17, 2002; doi:10.1152/ajprenal.00009.2002
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Vol. 284, Issue 4, F718-F726, April 2003

Male gender increases sensitivity to renal injury in response to cholesterol loading

Diana M. Attia1, Roel Goldschmeding2, Mahmoud A. Attia3, Peter Boer1, Hein A. Koomans1, and Jaap A. Joles1

1 Departments of Nephrology and Hypertension and 2 Pathology, University Medical Center, 3508 GA Utrecht, The Netherlands; and 3 Department of Pathology, Centre International de Toxicologie, 27005 Evreux Cedex, France

Males are at greater risk for renal injury than females. This may relate to nitric oxide (NO) availability, because female rats have higher renal endothelial NO synthase (NOS) levels. Previously, our laboratory found susceptibility to proteinuria induced by NOS inhibition in male compared with female rats. Dyslipidemia and hypercholesterolemia dose dependently decreased renal NOS activity and caused renal injury in female rats. We hypothesized that exposure of male rats to hypercholesterolemia would lead to more renal injury in male than in female rats due to an a priori lower renal NO system. Female and male rats were fed no, low-dose, or high-dose cholesterol for 24 wk. Cholesterol feeding dose dependently increased proteinuria in both female and male rats, but male rats developed more proteinuria at similar plasma cholesterol (P < 0.001). Control males had lower renal NOS activity than control females (4.44 ± 0.18 vs. 7.46 ± 0.37 pmol · min-1 · mg protein-1; P < 0.05), and cholesterol feeding decreased renal NOS activity in males and in females (P < 0.05). Cholesterol-fed males developed significantly more vascular, glomerular, and tubulointerstitial monocyte/macrophage influx and injury than females. Thus under baseline conditions, male rats have lower renal NOS activity than female rats. This may explain why male rats are more sensitive to renal injury by factors that decrease NO availability, such as hypercholesterolemia.

hypercholesterolemia; proteinuria; renal nitric oxide synthase activity


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