• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.37-41
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• 2018

Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function as well as their biogenesis and dynamics, especially in renal proximal tubule, to elicit ATP depletion. Mitochondrial fatty acid ${\beta}$-oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.39-40
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• 2003

Ochratoxin A (OA), a potent nephrotoxin in several species, is knownto be a renal carcinogen in animals and is implicated in the etiology of Balkan endemic nephropathy (BEN). The NTP (National Toxicology Program) classified Ochratoxin A as having clear evidence of carcinogenic activity, based on uncommon tubular adenomas and tubular cell carcinomas of the kidney and multiple fibroadenomas of the mammary gland, seen in the rat.(omitted)

• Journal of Yeungnam Medical Science
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• v.1 no.1
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• pp.13-23
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• 1984

Acute renal failure refers to a rapid reduction in renal function that usually occurs in an individual with no known previous renal disease. Development of a complication of acue renal failure in critically ill surgical patients is not unusual, and it causes high morbidity and mortality. Acute renal failure can be divided as Pre-renal (functional), Renal (organic), and Post-renal (obstructive) azotemia according to their etiologies. Early recognition and proper correction of pre-renal conditions are utter most important to prevent an organic damage of kidney. These measures include correction of dehydration, treatment of sepsis, and institution of shock therapy. Prolonged exposure to ischemia or nephrotoxin may lead a kidney to permanent parenchymal damage. A differential diagnosis between functional and organic acute renal failure may not be simple in many clinical settings. Renal functional parameters, such as $FENa^+$ or renal failure index, are may be of help in these situations for the differential diagnosis. Provocative test utilyzing mannitol, loop diuretics and renovascular dilators after restoration of renal circulation will give further benefits for diagnosis or for prevention of functional failure from leading to organic renal failure. Converting enzyme blocker, dopamine, calcium channel blocker, and propranolol are also reported to have some degree of renal protection from bioenergetic renal insults. Once diagnosis of acute tubular necrosis has been made, all measures should be utilized to maintain the patient until renal tubular regeneration occurs. Careful regulation of fluid, electrolyte, and acid-base balance is primary goal. Hyperkalemia over 6.5 mEq/l is a medical emergency and it should be corrected immediately. Various dosing schedules for medicines excreting through kidney have been suggested but none was proved safe and accurate. Therefore blood level of specific medicines better be checked before each dose, especially digoxin and Aminoglycosides. Indication for application of ultrafiltration hemofilter or dialysis may be made by individual base.