Pathophysiology of acute kidney injury

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Edited by Neil Turner, Norbert Lameire, David J. Goldsmith, Christopher G. Winearls, Jonathan Himmelfarb, and Giuseppe Remuzzi. Pathophysiology of acute ...

Pathophysiology of acute kidney injury

Oxford Textbook of Clinical Nephrology (4 ed.) Edited by Neil Turner, Norbert Lameire, David J. Goldsmith, Christopher G. Winearls, Jonathan Himmelfarb, and Giuseppe Remuzzi Publisher: Oxford University Press Print ISBN-13: 9780199592548 DOI: 10.1093/med/9780199592548.001.0001

Print Publication Date: Oct 2015 Published online: Oct 2015

Pathophysiology of acute kidney injury Chapter: Pathophysiology of acute kidney injury Author(s): Michael S. Goligorsky, Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff DOI: 10.1093/med/9780199592548.003.0221

Introduction Acute kidney injury (AKI), in the past variously referred to as ‘acute haematogenic interstitial nephritis’ (Kimmelstiel, 1938), ‘lower nephron nephrosis’ (Lucke, 1946), ‘haemoglobinuric nephrosis’ (Mallory 1947), ‘acute tubular necrosis’ (Bull et al. 1950), ‘glomerulo-tubulo-nephrosis with pigmented casts’ (Zollinger, 1952), and ‘tubulointerstitial nephritis’ (Brun, 1954) is a syndrome of graded severity of acute renal functional impairment which, depending on the nature of the insult —nephrotoxic, endotoxic, or ischaemic—may or may not be accompanied by the commensurate morphologic changes (Brun and Munck, 1966). The diversity of nomenclature is a reflection on the panoply of morphologic presentations in cases secondary to nephrotoxins, like ethylene glycol, mercury compounds, or others, which are accompanied by a conspicuous tubular necrosis, and in cases of haemorrhage, sepsis, mismatched transfusions, and others, which offer morphologic presentations far less dramatic than clinical presentation with oliguria.

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