Twenty eight patients who had received haemodialysis for more than 10 years were reviewed to establish the incidence of joint problems. Only six patients had no joint symptoms, one had avascular necrosis, one had had recent septic arthritis, and four had hyperparathyroidism. The remaining 16 patients had no evidence of hyperparathyroidism yet had an arthropathy causing pain and stiffness in many joints, particularly the shoulders. Ten of these 16 patients had a recurrent carpal tunnel syndrome requiring repeated surgical decompressions, which resulted in only partial improvement. Of the eight patients who had received dialysis for more than 15 years, seven had this "dialysis arthropathy" and six had recurrent carpal tunnel syndrome.Dialysis arthropathy is a common and often severe and disabling complication of long term treatment with haemodialysis. The cause is not known, but amyloid was found in a synovial biopsy specimen from one patient.

The prevalence of heart failure is increasing.1 Patients usually present to their general practitioner but a definitive diagnosis of left ventricular systolic dysfunction can only be achieved by cardiac imaging. Measuring plasma concentrations of brain natriuretic peptide has been advocated as a screening test that might reduce demands on cardiological services. 2 We report the results of a community based study designed to investigate the effectiveness of measuring brain natriuretic peptide to diagnose left ventricular systolic dysfunction. The study was approved by the local research ethics committee. Participants, methods, and resultsGeneral practitioners were invited to refer patients with suspected heart failure to our clinic. The results of transthoracic echocardiography were reported by a single, experienced observer (IA). Ischaemia was diagnosed if Q waves, bundle branch block, T wave inversions, or left ventricular hypertrophy were present on an electrocardiogram. Evidence of heart failure on a chest radiograph was defined as the presence of pulmonary oedema or cardiomegaly. Concentrations of brain natriuretic peptide were measured by immunoradiometric assay (Shionoria assay, Shionogi, Osaka, Japan) of plasma stored at − 70°C. A concentration > 17.9 pg/ml was considered abnormal based on the results of a large study of left ventricular systolic dysfunction. 3 Altogether, 126 patients (68 men) with a mean age of 74.4 (SD 8.9) years were included in the study. Concentrations of the peptide were raised in the 40 patients with left ventricular systolic dysfunction (median concentration 79.4 pg/ml, interquartile range 35.9-151.0) compared with those with normal ventricular systolic function (26.7 pg/ml, 12.2-54.3; P < 0.001). A concentration > 17.9 pg/ml had a sensitivity of 88% and specificity of 34%. Choosing different cut points did not improve the predictive characteristics: at 10 pg/ml sensitivity was 92% but specificity was 18%, and at 76 pg/ml sensitivity was 66% and specificity 87%.The prior probability that a disease exists (its prevalence) and the extent to which a test result alters the chance of the disease existing determine whether further investigation is needed; this is the likelihood ratio of positive and negative tests. In the case of heart failure it is unlikely that a single positive test result will remove the need for further cardiac imaging before treatment is started. In contrast, a negative result may give a low posterior probability of disease so that further investigations are unnecessary.The prevalence (or prior probability) of left ventricular systolic dysfunction in this study was 32%; this is consistent with that reported in other studies. 4 The likelihood ratio for a patient without a history of myocardial infarction, with negative results on chest radiography and electrocardiography, and with concentrations of brain natriuretic peptide below the cut off, individually and in combination, are shown in the table. Measuring the concentration of brain natriuretic peptide ...

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A 41-year-old Asian woman presented with mild congestive cardiac failure, initially controlled with a small dose of diuretic. Subsequently there was a marked deterioration in her condition with severe cardiac failure resistant to treatment. At this time biochemistry revealed a hyperphosphataemic variety of osteomalacia. Her cardiac failure improved promptly on correcting the hypocalcemia. Although hypocalcaemia is a recognised cause of cardiac failure it has not been described in privational osteomalacia.

SummaryWe present the case of a 77-year-old woman who initially presented with pyrexia of unknown origin, anaemia and mild renal impairment. When her omeprazole was stopped she improved rapidly. When omeprazole was re-started she developed fever and acute renal failure, which again settled quickly on discontinuation of omeprazole. This case demonstrates how drugs can cause severe multisystem disorders that may appear to be infective or inflammatory.Keywords: omeprazole; acute renal failure; anaemia; pyrexia; adverse drug reaction A 77-year-old woman initially presented with a one-week history of malaise, nausea, rigors and sweats with weight loss of 2.5 kg. She had nonpleuritic left-sided lower back pain and nonproductive cough for two days. Oral cefuroxime (250 mg bid) had been started before admission without improvement. She had had malaria and possible pyelonephritis in Africa. She was taking omeprazole 20 mg daily, prescribed empirically for dyspepsia for two months. She had never smoked.On admission she was pyrexial at 38.5°C and tachypnoeic. No other abnormality was found on clinical examination. The initial full blood count was normal with haemoglobin 12.0 g/dl and white cell count 9.9 x 109/l (eosinophils 2.6%). Renal function was impaired with serum creatinine 202 jmol/l. Other biochemistry was normal. The erythrocyte sedimentation rate (ESR) was markedly raised at 96 mm/h. A midstream specimen of urine sent before commencing antibiotics was normal but a repeat specimen demonstrated sterile pyuria. Blood cultures were negative at seven days. A chest X-ray was normal.Investigations to identify the cause of the pyrexia, including further cultures of blood, urine and stool, specimens for acid-fast bacilli, serology for Legionella and other atypical infections, Mantoux-testing and autoantibody screen, were negative. Ultrasound examination of the abdomen and computed tomography of the chest and abdomen were normal on two occasions, one month apart, as was echocardiography. Lumbar spine X-rays and skeletal scintigraphy were normal. There was no improvement after seven days treatment with intravenous cefuroxime 750 mg eighthourly.