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Nephrol Dial Transplant. 2004 Mar;19(3):664-9.

Diabetic muscle infarction in end-stage renal disease.

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Department of Medicine, Division of Nephrology, Stanford University School of Medicine, Stanford, CA, USA.



Diabetic muscle infarction (DMI) is an unusual disorder of type 1 and type 2 diabetic patients with advanced microvascular damage including nephropathy. Few reports describe this complication among dialysis patients.


We studied four patients with terminal renal failure due to diabetic nephropathy who developed isolated skeletal muscle infarction at our institution between January 1998 and January 2003, and reviewed 15 additional cases of DMI reported among dialysis patients (Medline database search).


Analysis of available data for all 19 cases revealed the following features: mean age at symptom onset of 46.4 years; average duration of renal replacement 25.7 months (range 36 h to 72 months); male predominance (2.2:1); higher prevalence of type 2 vs type 1 diabetes (2.2:1); and more common use of haemodialysis than peritoneal dialysis (2.6:1). One patient developed symptoms after being immobilized during surgery and initiating dialysis. Thigh involvement was frequent (17/19). Fever, leucocytosis and elevated serum creatine kinase levels were noted inconsistently, but were seen commonly with early evaluation after symptom onset. Erythrocyte-sedimentation rate and C-reactive protein levels were high when checked. All 16 instances of magnetic resonance imaging (MRI) demonstrated increased T2-weighted signal from affected muscles. Seven patients were managed without muscle biopsy. Histological features included myofibre necrosis (8/12), inflammatory infiltrates (8/12) and microvasculopathy (6/12). Symptoms resolved with conservative therapy, but patients were at high risk for subsequent infarctions of other muscles (14/19).


DMI should be suspected in any diabetic dialysis patient who develops a painful, swollen muscle. A conservative MRI-based diagnostic approach may lead to satisfactory outcomes. The pathogenesis of the disorder is controversial, but the clinical sequence of one of our cases suggests precipitation by immobilization, direct pressure and/or haemoconcentration.

[Indexed for MEDLINE]

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