Abstract
The term “acute renal failure” (ARF) describes a curtailment of glomerular function and tubular reabsorptive and secretory processes. The kidneys loose their ability to concentrate the urine and to lower the urinary sodium concentration to values below approximately 40 mmol per 1. Glomerular filtration rate (GFR) is always considerably reduced, which leads to an accumulation of creatinine and urea in the blood. The impairment of cellular metabolism, either through oxygen deprivation or nephrotoxins, is the causal event in the generation of ARF. Each etiological factor leading to the phenomenon of ARF will initially affect different individual cellular functions; for example, ATP formation during anoxia, the formation of membrane characteristics by metal ions, or DNA synthesis by toxic peptides. Although their initial effects differ, the final changes in overall cellular function induced by anoxia or nephrotoxic substances are similar and reflect the inherent function of the tubular cells. In the kidney it is the diminished reabsorptive and secretory functions of the tubular cells which determine the excretory function of the kidney during ARF. Because of the different etiological factors different intrarenal pathophysiological reactions follow and dominate, such as intratubular cast formation, increased tubular permeability, reduced filtration area or filtration permeability of the glomerular capillaries, stimulation of the tubuloglomerular feedback system, and renal vasoconstriction. A specific combination of the various abnormalities becomes typical during ARF and the significance of the various pathogenetic factors may differ during its course over time.
Published Version
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