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Renal Failure

Terms in this set (102)

The pathogenesis of ARF is not clear. One hypothesis is that the damaged tubules cannot conserve sodium normally, which activates the renin-angiotensin-aldosterone system. The effect is to redistribute the renal vascular supply by increasing the tone of both the afferent and efferent arterioles. The resulting ischemia may cause an increase in vasopressin, cellular swelling, inhibition of prostaglandin synthesis, and further stimulation of the renin-angiotensin system. The reduced blood flow decreases glomerular pressure, GFR, and tubular flow; thus oliguria occurs.
Another theory is that cellular and protein debris in the tubule obstructs the lumen, which raises the intratubular pressure. The increasing oncotic pressure opposes filtration pressure until glomerular filtration stops. A biochemical theory claims that decreased renal blood flow leads to decreased oxygen delivery to the proximal tubules; this causes a reduction in cellular adenosine triphosphate, which increases cytosolic and mitochondrial calcium concentrations. The result of this process is cell death and tubular necrosis. Vasomotor nephropathy, which causes spasms of peritubular capillaries, may result in tubular damage. Other possible pathogenic mechanisms include leakage of filtered urine through damaged tubules back into the peritubular capillaries and chemical or morphologic changes in the basement membrane of the glomerular capillary, which decrease nephron filtration. The reversibility of this mechanism depends on the level of destruction of the basement membrane.