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- W1825583669 abstract "This chapter provides significant information on mitochondrial diseases of the kidney. Many chronic renal progressive diseases result from nephron degeneration. Focal segmental glomerosclerosis could represent the final common pathway for this degenerative disorder. The initial changes are believed to occur in glomerular epithelial cells. The A3243G point mutation in the tRNALeu is considered to be the most common mtDNA defect. The A3243G mutation is shown to cause type II diabetes with deafness, cardiomyopathy, or progressive external ophthalmoplegia. Oncocytomas are benign tumors predominantly occurring in the kidney. Histologically, they reveal epithelial cells with granular eosinophilic cytoplasm. These cells have an increased number of mitochondria and the mitochondria are dysmorphic. While patients with Fanconi’s syndrome show many electrolyte abnormalities such as hypophosphatemia, hypokalemia, and hypomagnesemia, there are a large number of patients with electrolyte abnormalities and mitochondrial mutations who lack aminoaciduria, acidosis, and glucosuria. There is no effective treatment for diseases of the mitochondria. Treatment is primarily symptomatic. In addition, patients should avoid respiratory chain toxic medications. Patients with complex III deficiency may benefit from vitamin K-3 or coenzyme Q10. Patients with complex I deficiency may be treated with riboflavin. Vitamin C has been prescribed to prevent reactive oxidative species (ROS) damage. Dichloroacetate, an activator of pyruvate dehydrogenase complex, accelerates the oxidation of glucose, lactate, and pyruvate to acetylcoenzyme A. This product has been used at 25-200 mg/kg and improvement has been observed in patients with lactic acidosis." @default.
- W1825583669 created "2016-06-24" @default.
- W1825583669 creator A5003040736 @default.
- W1825583669 date "2009-01-01" @default.
- W1825583669 modified "2023-09-23" @default.
- W1825583669 title "Mitochondrial Diseases of the Kidney" @default.
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