Diabetic muscle infarction is a rare microangiopathic complication occurring in patients with advanced diabetes mellitus. Diabetic patients with chronic kidney disease stage Vd are prone to develop this complication. The presenting symptom is a localized painful swelling of the affected limb. Symptoms usually resolve spontaneously during the following weeks, but frequent relapse can occur and in some cases swelling may lead to compartment syndrome. Biochemical blood analyses show an elevated C-reactive protein, but creatine kinase is often normal. Diagnosis can be made on clinical presentation and imaging, with magnetic resonance imaging as the gold standard. Histology is often not contributive. Treatment consists of rest, analgesics, rigorous glycemic control and low-dose aspirin. Severe cases of compartment syndrome require fasciotomy. In the current paper, we present two diabetic patients with cystic fibrosis, who are treated with automated peritoneal dialysis and suffered from episodic lower limb infarction. We subsequently review 48 episodes of diabetic muscle infarction previously reported in the literature in patients with end-stage renal disease. 1. Introduction Diabetic muscle infarction (DMInf) is a rare microangiopathic complication in patients with advanced diabetes mellitus (DM). Patients having terminal diabetic nephropathy are prone to develop DMInf and nearly one-fourth of DMInf, patients receive renal replacement treatment [1]. Consequently, nephrologists are likely to be increasingly confronted with this disease entity. 2. Case Reports Case 1. A 27-year-old woman with cystic fibrosis started insulin treatment at the age of 11. When she was 16 years old, she received bilateral lung transplantation (SSLTx). Her immune-suppressive therapy consisted of tacrolimus and steroids. At the age of 24, she developed chronic kidney disease stage V (CKD-Vd) for which peritoneal dialysis (PD) was started. Two years later, she presented with acute pain in the right calf. Biochemical evaluation showed an elevated creatine kinase (CK 218？U/L) and C-reactive protein (CRP 97？mg/L). HbA1c was 5.8%. Ultrasound and computed tomography (CT) showed diffuse muscular and subcutaneous edema of the affected calf. Muscular biopsy demonstrated muscular atrophy, macrophages, and myophagia. The symptoms resolved within four weeks. There was a new onset of pain in the left calf 18 months later. CK was normal, but CRP levels were elevated (215？mg/L). HbA1c was 7.2%. The clinical and biochemic characteristics are shown in Table 1. Magnetic resonance imaging (MRI) showed
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