Abstract
The kidney, along with the liver, represents the most important excretory organ for drugs and their metabolites. Since the kidney has both a particularly high blood through-put, in fact some 25% of the coronary output, and because it is the major site for the elimination of many pharmaceutical preparations, this organ is particularly predisposed to drug-dependent damage. Drug-induced damage of the kidney is facilitated by a number of aspects of renal physiology including the metabolic activity of the kidney and the high concentration of drugs and their metabolites, produced by the counter current effect, in the relatively unvascularised renal medulla. In addition drugs may become particularly concentrated in tubular cells through the mediacy of active resorption and secretion processes. Furthermore, the vulnerability of the kidney to drug damage may be to some extent a product of the filtration process itself since the deposition of circulating immune complexes or the in situ immune complex formation in glomeruli may subsequently lead to a damaging of the glomerular structures. Drug-in- duced renal damage might also be expected in cases of renal insufficiency where the reduced elimination of a drug results in its accumulation in the kidney. Since the kidney plays a major role in water and electrolyte balance, acute or chronic alterations in the plasma ion levels or plasma volume may lead to both morphologically and clinically detectable kidney changes.
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Gärtner, HV. (1980). Drug-Associated Nephropathy. In: Grundmann, E. (eds) Drug-Induced Pathology. Current Topics in Pathology, vol 69. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67861-5_4
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DOI: https://doi.org/10.1007/978-3-642-67861-5_4
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-67863-9
Online ISBN: 978-3-642-67861-5
eBook Packages: Springer Book Archive