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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Antigens, Tumor-Associated, Carbohydrate, Cells, Cultured, Estradiol, Gonadal Steroid Hormones, Humans, Kidney Glomerulus, Kidney Tubules, Progesterone, Shiga Toxin 1, Testosterone, Toxicity Tests.
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Do sex steroids affect shigatoxin cytotoxicity on human renal tubular or glomerular cells? Context: The greater susceptibility of children to renal injury in post-diarrheal hemolytic-uremic syndrome (HUS) may be related, at least in part, to heightened renal cell sensitivity to the cytotoxic effect of Shiga toxin (Stx), the putative mediator of kidney damage in HUS. We hypothesized that sexual maturation, which coincides with a falling incidence of HUS, may induce a relatively Stx-resistant state in the renal cells. Cultured human glomerular endothelial (HGEN), human glomerular visceral epithelial (HGEC) and human proximal tubule (HPT) cells were exposed to Stx-1 after pre-incubation with progesterone, beta-estradiol or testosterone followed by determination of cytotoxicity. Under basal conditions, Stx-1 potently and dose-dependently killed HPT and HGEC, but had relatively little effect on HGEN. Pre-incubation for 1, 2 or 7 days with physiologic or pharmacologic concentrations of progesterone, beta-estradiol or testosterone had no effect on Stx-1 cytotoxicity dose-response on any cell type. In addition, no steroid altered Gb3 expression (Stx receptor) by any cell type at any time point.
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These data do not support the notion that hormonal changes associated with puberty induce an Stx-resistant state within kidney cells. Final Decision: no