1. Renal Effects of Metabolic Acidosis in the Normal Rat
- Author
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A. J. Howie, J. Walls, P. N. Furness, K. P. G. Harris, Alan Bevington, and D. Throssell
- Subjects
medicine.medical_specialty ,Kidney Glomerulus ,Renal function ,Kidney ,Mucoproteins ,Internal medicine ,Uromodulin ,medicine ,Animals ,Rats, Wistar ,Acidosis ,Proteinuria ,urogenital system ,business.industry ,Body Weight ,Metabolic disorder ,Kidney metabolism ,Metabolic acidosis ,Hypertrophy ,Organ Size ,medicine.disease ,Immunohistochemistry ,Rats ,Kidney Tubules ,medicine.anatomical_structure ,Endocrinology ,Tubular proteinuria ,Immunoglobulin G ,Female ,Hydrochloric Acid ,Blood Gas Analysis ,medicine.symptom ,business - Abstract
Metabolic acidosis causes renal growth and proteinuria, and may contribute to the progression of CRF. This study assessed the effects of HCI-induced acidosis on the structure and function of normal kidneys. Acidosis was induced in 12 rats by dietary HCl. After 2 weeks, acidotic animals had higher kidney/body weight ratios (0.47 +/- 0.10 vs. 0.35 +/- 0.10 g%, p < 0.001) and higher kidney protein content (123 +/- 3 vs. 111 +/- 4 mg/kidney, p < 0.05) than controls, but tubular nuclear densities were lower, suggesting tubular hypertrophy. Acidotic animals developed tubular proteinuria (16.4 +/- 2.6 mg/day after 2 weeks of acidosis vs. 2.9 +/- 0.3 mg/day at baseline; p < 0.001), and the pattern of immunohistochemical staining for Tamm-Horsfall protein suggested tubular injury. These data suggest that a tubulotoxic effect of metabolic acidosis may contribute to the progression of CRF.
- Published
- 1996
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