Rapidly Progressive Nephropathy in a Young Patient with Mitochondrial Gene Mutation.
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A 26-year-old man was diagnosed with NIDDM in 1991. Since his mother had diabetes and deaf as well, we tested him for mitochondrial DNA and detected the 3243bp mutation. In 1994, he developed the nephrotic syndrome (BUN 16.4 mg/d/, Cr 0.8 mg/d<I>l</I>, Ccr 39.6 m<I>l</I>/min.) without retinopathy, and a renal biopsy was performed. Light microscopy showed mild mesangial expansion that seemed to represent diabetic nephropathy, but in addition to segmental sclerosis, immunofluorescent staining showed granular deposition of IgM and Ciq, and Electron microscopy revealed dense deposits. Asa result, the renal lesion was concluded to be accompanied by focal segmental sclerosis. On March in 1996, the patient was admitted with dyspnea, cough, and edema. His renal function had rapidly deteriorated to end-stage. We examined the renal biopsy specimen again, and found that the kidney was in the histological endstage. Hemodialysis was instituted in July, five years after thediagnosis of diabetes. The rapid deterioration in renal functionseemed to be attributable to the mitochondrial gene mutation in addition to the poor glycemic control (HbAic 8.3%-16.7%) and insufficient restriction of protein intake.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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