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Acute Renal Failure and Toxic Nephropathy

  • Chapter
Contemporary Nephrology

Abstract

Acute renal failure is a common clinical syndrome. This syndrome can be caused by prerenal functional hemodynamic processes, intrarenal structural injury, or postrenal obstructive disorders. Prerenal acute renal failure, or prerenal azotemia, results from a persistent, significant decline in renal blood flow (RBF), which leads to a decline in the rate of glomerular filtration (GFR) and rising levels of blood urea nitrogen (BUN) and plasma creatinine. Usually this decline in renal perfusion is a component of a generalized process of poor tissue perfusion, but selective declines in RBF, and hence GFR, may develop disproportionately to blood flow to other tissues. A variety of drugs, most notably agents that inhibit prostaglandin synthesis, have been demonstrated to produce nephrotoxic side effects by an ability to promote selective declines in RBF and GFR.1 With regard to intrarenal structural processes, several factors make the kidney especially susceptible to toxic injury. The high rates of delivery of compounds to the kidney, concentration of drugs in tubule lumens and interstitium, and transcellular transport of toxins by the kidney make the renal tubular cells especially vulnerable to toxic injury.2. The high metabolic demands for the normal transport activities of renal tubular cells and the virtual absolute requirement for oxidative metabolism as an energy source by proximal tubular cells make the renal tubular cells also keenly susceptible to ischemic injury.3 Both toxic and ischemic insults have the ability to cause substantial renal structural damage to procedure acute renal excretory failure.

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© 1987 Plenum Publishing Corporation

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Humes, H.D., Nguyen, V.D. (1987). Acute Renal Failure and Toxic Nephropathy. In: Klahr, S., Massry, S.G. (eds) Contemporary Nephrology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1859-0_9

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  • DOI: https://doi.org/10.1007/978-1-4613-1859-0_9

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