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DEFINITION OF HYPOURICEMIA: Hypouricemia (serum uric acid less than 120 micro mol/l) is a biological abnormality often discovered accidentally and with a low prevalence depending on its permanent or transitory nature ranging from 0.15 to 3.38%. NEW PHYSIOLOGICAL CONCEPTS OF ITS PATHOGENESIS: Recently, our knowledge of the physiopathological mechanisms of hypouricemia has been emphasized by the identification of three systems of renal and extra-renal uric acid transport: a Cl/urate (URAT1) transporter, a multispecific organic anion transporter (OAT) and a urate transporter/channel. ETIOLOGY AND COMPLICATIONS OF HYPOURICEMIA: Through questioning, drugs and toxics (allopurinol.) are generally rapidly recognized as responsible for half of the hypouricemia encountered. It can be concomitant to a known disease: severe liver disease, neoplasia, diabetes, AIDS, syndrome of inappropriate antidiuretic hormone secretion. Hypouricemia can also be isolated and justifies the measurement of uric acid clearance, the normality or reduction of which orients towards a deficiency in xanthine-oxydase, the increase in which suggests an abnormality in uric acid transport in the proximal tubule (Fanconi syndrome, primary hereditary anomaly of tubular uric acid transport). Hypouricemia does not appear to expose the patient to any danger, but the onset of nephrolithiasis or acute renal failure secondary to the combination of severe hypouricemia and oxidant stress is always possible.

Introduction: This study reports the largest series of acute renal failure following collective poisoning by Cortinarius orellanus since 1957., Patients: Twelve men, in whom altered renal function appeared following ingestion of mushroom soup (Cortinarius orellanus) when they were 20 to 23 year-old, were followed up for 13 years., Results: After a period of latency of between 2 to 5 days, the patients complained of asthenia, intense thirst and digestive and neurological disorders. On admission, 4 were anuretic and two exhibited polyuria. Leukocyturia was detected in all patients but without proteinuria. Renal biopsy was performed on day 14 in seven patients. It revealed severe tubulo-interstitial lesions with polymorphous cell infiltration, oedema, loose fibrosis and epithelial necrosis. Eight patients required haemodialysis. Nine patients received corticosteroids for less than 6 months. Over a follow-up period of 13 years, seven patients recovered normal renal function, four underwent transplantation and one was still under haemodialysis and died, victim of a car accident., Conclusion: The incidence of acute renal failure varies from 30 to 46%. It depends on individual sensitivity, pre-existing nephropathy and the cumulated dose of toxin ingested. Early and severe interstitial fibrosis, marked interstitial oedema and tubular epithelial necrosis are the most characteristics renal lesions. Renal failure regresses progressively over several months in 60% of cases. In the other patients, terminal renal failure appears immediately or after several years. The evolution is not influenced by corticosteroid therapy.

Background: Diagnosis of familial benign hypercalcemia can be challenged by the association with a urinary lithiasis, which, in the presence of hypercalcemia, will most frequently lead to affirm primary hyperparathyroidism., Case Reports: We report the case of a 23 year-old patient who presented with a left ureteral stone composed of calcium oxalate. His serum total calcium value was 2.92 mmol/l. Serum PTH value was inappropriately in the normal range (32 ng/l, normal values 10 to 58 ng/l). Hypercalcemia persisted despite a subtotal parathyroidectomy and new investigation biochemical revealed familial benign hypercalcemia., Conclusion: This diagnosis is usually made fortuitously, since most patients have few, if any, symptoms. A past familial history of hypercalcemia and several biochemical features (such as a reduced fractional excretion of calcium, mild hypermagnesemia, and a normal serum inorganic phosphorus level) are helpful dues to the diagnosis of familial benign hypercalcemia. In some cases, however, searching for an inactivating mutation of the extracellular calcium-sensing receptor gene is necessary to distinguish this autosomal dominant disease from primary hyperparathyroidism.

Background: In the very large majority of cases, nephrotic syndrome with minimal glomerular lesions is an idiopathic condition. Drugs can favor the glomerulopathy. The effect of non-steroidal antiinflammatory drugs is well known, but other drugs, particularly tiopronin may be incriminated., Case Report: A 73-year-old patient developed severe nephrotic syndrome with minimal glomerular lesions 6 weeks after tiopronin therapy was initiated. Complete and spontaneous remission of the nephrotic syndrome was achieved 5 weeks after drug withdrawal. No recurrent lipoidic nephrosis has been observed at 3 years follow-up., Conclusion: Tiopronin-induced nephrotic syndrome with minimal glomerular lesions is usually severe and develops rapidly. Remission occurs rapidly after drug withdrawal. Weekly urine checks with dip-strips should be proposed in patients treated with tiopronin.