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+A 37-year-old Caucasian man was referred to our department from an external hospital because of severe abdominal pain of unclear aetiology.
+The patient suffered from Friedreich's ataxia.1 2 His most recent transthoracic echocardiography, performed on the day of admission, showed a dilated cardiomyopathy, impaired left ventricular function with an ejection fraction of 30% and a pulmonary artery pressure of 55 mm Hg; all findings were unchanged from previous examinations.
+At that time, he lived alone in a residential home and was mobile using a wheelchair.
+On arrival at our emergency department, the patient was somnolent and disoriented.
+His axillary body temperature was 35.7 °C and his arterial blood pressure 125/89 mm Hg, with a pulse rate of 84 rhythmic beats/min.
+He complained of an increasing, diffuse abdominal pain during the whole day, combined with absence of appetite and vomiting on a single occasion.
+His daily medication was perindopril 2.5 mg, torasemide 7.5 mg and esomeprazole 40 mg.
+On physical examination, we found a tender abdomen with painful epigastric palpation.
+Normal bowel sounds were auscultated in the upper right and lower left quadrants.
+The renal bed was free of pain on palpation.
+On cardiac auscultation, a 2/6 systolic murmur was audible.
+Lung auscultation showed normal respiration.
+Laboratory findings were slightly elevated C reactive protein (CRP) of 16 mg/l (normal: <5 mg/l), elevated troponin-T-hs of 0.070 µg/l (normal: <0.014 µg/l) and highly elevated pro-B-type natriuretic peptide of 7382 pg/ml (normal: <63 pg/ml).
+Kidney function parameters were in the upper normal range, with creatinine of 100 µmol/l and a calculated glomerular filtration rate of 73 ml/min.
+Blood count revealed leucocytosis of 15.6×109/litre.
+Regarding thyroid function, thyroid-stimulating hormone, f-T3 and f-T4 were in the reference range.
+Urine analysis showed no pathology.
+In abdominal sonography, all organs were normal, especially the kidneys.
+No free fluid was detected (figure 1).
+As the severe pain persisted all night, despite analgesia with paracetamol 1 g, metamizole 1 g and pethidine 75 µg, a contrast-enhanced abdominal CT was performed revealing infarction of the right kidney, which appeared as a hypodense area although kidney arteries and veins were assessed as open (figures 2 and ​3).
+Cardiac dysfunction is the most frequent cause of death in patients affected by Friedreich's ataxia, most commonly from congestive heart failure or arrhythmia.
+Renal artery embolism is not a rare event in these patients.
+However, other non-abdominal viscous causes of severe diffuse abdominal pain such as porphyria, familial Mediterranean fever, diabetic ketoacidosis, tocopherol deficiency also had to be excluded.
+The negative cardiolipin test excluded tabetic crises.
+No evidence for pre-existing porphyria was encountered for example, quantitative determination of δ-aminolevulinic acid, porphobilinogen and porphyrin in 24-h urine was negative.
+Further genetic diagnosis regarding, for example, clotting disorder, was also not conclusive.
+Hypovitaminosis was not present.
+The patient had no endocrinopathies, for example, no diabetes and no evidence for hypothyreosis or hyperthyreosis.
+The patient was hospitalised without delay at the department of nephrology.
+Immediate anticoagulation with heparin was initiated and later replaced by lifelong oral anticoagulation with phenprocoumon.
+During 11 days of hospitalisation, no complications occurred.
+Kidney function parameters remained normal.
+Transoesophageal echocardiography on the fifth day showed no cardiac thrombus and no patent foramen ovale.
+Deep vein thrombosis was excluded with duplex sonography.
+Anticardiolipin antibody testing and genetic testing regarding clotting disorders were both negative.
+Urine tests revealed no evidence of porphyria.
+During hospitalisation the patient remained stable regarding cardiological function, while diuretics were adjusted according to the fluid balance.
+The patient had already been treated with levofloxacin for pneumonic infection prior to hospitalisation.
+The antibiotic treatment was continued because of increasing inflammatory parameters in the further course of disease.
+A CRP increase of up to 200 mg/l was interpreted as an inflammatory response to renal infarction.
+By discharge, laboratory parameters were significantly decreased.