Skip to main content

Archived Comments for: Advances in understanding ischemic acute kidney injury

Back to article

  1. Hypoxic and histotoxic renal injury

    Heikki Savolainen, Dept. of Occup.Safety & Hlth., Tampere, Finland

    28 February 2011

    Dear Editor,

    The excellent review of Munshi et al. (1) covers the salient features of the ischemic kidney injury. Perhaps, it could be added, though, that inhibitors of the mitochondrial cytochrome oxidase cause comparable acute renal failure. They include e.g. formic acid (2) which causes tubular cell necrosis and calcium deposits. At lower exposure levels, significant calciuria can be found in exposed persons (3).

    It may be added that in severe infections a circulatory shock due to excessive NO is associated with renal hypoperfusion. In addition to the hypoxia the NO competes also with oxygen for the binding in the terminal cytochrome oxidase thus adding a histotoxic element to the hypoxia.

    1 Munshi R, Hsu C, Himmelfarb J. Advances in understanding ischemic acute kidney injury. BMC Medicine 2011; 9: 11.

    2 Liesivuori, J, Kosma, V-M, Naukkarinen A, Savolainen H. Kinetics and toxic effects of repeated intravenous dosage of formic acid in rabbits. Br J Exp Path 1987; 68: 853-61.

    3 Liesivuori J, Laitinen J, Savolainen H. Kinetics and renal effects of formic acid in occupationally exposed farmers. Arch Toxicol 1992; 66: 522-4.

    Competing interests