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Fig. 1 Putative mechanisms leading from medullary cell hypoxia to renal failure. Physiological homeostatic signals that improve medullary oxygenation (by increased blood flow and decreased transport) and often contribute to reduced renal function are shown on the left. Some pathophysiological consequences of more advanced medullary hypoxia, such as tubular damage and reduced insulin-like growth factor 1 (IGF-1), are shown on the right. The potential adverse effects of some nephrotoxicants and volume depletion are shown. Non-steroidal anti-inflammatory drugs (NSAIDs) disable the beneficial prostanoid-mediated medullary vasodilatatory response to local hypoxia. Volume depletion enhances the tubuloglomerular feedback reflex decrease in glomerular filtration. In myeloma kidneys, Bence-Jones proteins (BJP) coprecipitate with the Tamm-Horsfall protein released by damage to medullary thick ascending limbs, increasing the likelihood of tubular obstruction and renal failure from other insults (such as NSAIDs, volume depletion, or radiographic contrast agent). Renal failure results from tubular obstruction (by casts), backleak of glomerular filtrate from the lumen to blood (through damaged epithelium), impaired intrarenal microcirculation such as activation of tubuloglomerular feedback (by increased distal delivery of solute to the macula densa), and failure of the local production of growth factors.

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