A 44-year old woman of Greenlandic origin was referred to Queen Ingrid's Hospital. She was previously healthy apart from excessive alcohol consumption and pulmonary tuberculosis diagnosed two years earlier for which she had received full antimycobacterial treatment. The patient initially complained of a painful traumatic skin lesion of the right lower extremity with a diameter of approximately 2 cm. A few days later, her temperature rose to 39.5 C and bullous erysipelas of the area of initial trauma was noted. Laboratory tests revealed a markedly elevated sedimentation rate of 111 mm/L hour [2-21], an elevated C reactive protein of 144 mg/L [<10], leukocytosis 18x109/L [4.4-11] with neutrophilia and x10>9/L [150-450]. Intravenous dicloxacillin and phenoxymethylpenicillin were administered. Culture from the lesion of the right lower extremity was positive for group A beta-hemolytic streptococci (GABHS). In spite of relevant antibiotic treatment, the clinical condition rapidly deteriorated with involvement of the deeper layers of the skin and subcutaneous tissue, spreading across the fascial planes of the subcutis (Figure 1). Necrotizing fasciitis (NF) was diagnosed. Based on positive skin cultures, this condition was considered to be due to GABHS. The patient had no other predisposing factors to NF, specifically no diabetes mellitus, no intravenous abuse and no daily intake of non-steroidal anti-inflammatory drugs (NSAID). Radiological examination of the right lower extremity and foot showed no signs of osseous involvement. Extensive surgical revision of the NF-lesion was performed and meropenem, ciprofloxacin and clindamycin were administered. Approximately three weeks after the initial presentation, impairment of renal function with azotemia and severe nephrotic syndrome with periorbital and peripheral edema were noted. Laboratory tests showed an elevated creatinine of 386 umol/L [44-115], BUN: 23.6 mmol/L [2.5-6.7], normochromic, normocytic anemia with hemoglobin: 4.9 mmol/L [7.5-9.0], as well as macroscopic hematuria, renal-creatinine clearance: 30 mL/min and U-protein: 5.8 g/24 h [<0.15]. Anti nuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA), IgA, IgG, IgM and protein electrophoresis were all normal. Blood pressure was increased to 165/100. The hypertension was efficiently treated by ACE-inhibitors and beta blockers. The patient was transferred to Rigshospitalet, Copenhagen where a renal biopsy was performed. The biopsy demonstrated endocapillary glomerulonephritis with proliferation of endothelial cells and infiltration of polymorphonuclear cells. Using immunofluorescence techniques, granular deposits of IgG and C3 were identified as typically seen in acute post-streptococcal glomerulonephritis (APSGN) (Figure 2). During the same period, the patient complained of chest pain. Electrocardiogram (ECG) showed sinus rhythm with no signs of ischemia and no elevation of cardiac troponin I was found. Echocardiography showed moderate reduced left ventricular ejection fraction (LVEF): 35% [50-65%] and moderate mitral regurgitation (grade II). Pulmonary pressure was significantly increased > 60 mm Hg [18-25]. Brain natriuretic peptide (BNP) was significantly increased >8000 pg/mL [<100]. There were complaints of arthralgia of the left elbow. There were no other signs of acute rheumatic fever (ARF) and no signs of pharyngitis in the whole period. Chest X ray and HR-CT of the thorax showed changes in both lungs consistent with old tuberculosis. Two weeks after the first analysis, renal function had improved and U-protein had decreased to 2.6 g/24 h, creatinine 139 umol/L, BUN 9.5 mmol/L. Ultrasound of the kidneys was normal. Echocardiography still showed moderate reduced left ventricular ejection fraction (LVEF): 35% with mild mitral regurgitation (grade I). Continued follow-up of renal and cardiac function is planned.