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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.

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PURPOSE: Though currently asymptomatic, a sickle cell trait can be responsible for renal abnormalities with macroscopic hematuria. METHODS: Ten patients were admitted to our department with gross hematuria in sickle trait. RESULTS: Six blacks men and four blacks women, aged from 17 to 53 years, had recurrent episodes of gross hematuria with clots in five patients with lumbar pain in four patients. Duration of gross hematuria varied from two weeks to two years. Imaging findings were normal. Urinary concentration ability was abnormally low in all patients but none had an impairement of the ability to dilute the urine or tubular dysfunction. Resolution of hematuria was obtained by abundant and alkaline hydratation in three patients. In six patients, aminocaproic acid was successfully employed, with a complete (3/6) or partial (3/6) efficiency. In one last patient, oral urea permitted a partial improvement. CONCLUSION: Combination of chemical and physical factors in renal medullary of sickle cell trait are responsible for gross hematuria and impaired capacity to concentrate the urine. A cautious care must still be given to make this association a diagnostic of exclusion. Clinical is usually benign. When resting and alkaline hydration are not sufficient to resolve hematuria, antifibrinolytic agents such as aprotinin, oral urea, urologic technical are sometimes necessary.

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Microscopic hematuria is an uncommon inaugural sign of kidney tumors in young asymptomatic patients. Renal clear-cell carcinoma was diagnosed in a 23-year-old female explored for microscopic hematuria. Radical nephrectomy removed a 7-cm tumor without local extension. The cytogenic study of the tumor disclosed X;1 translocation. The patient also had IgA deficiency. Von Hippel-Lindau disease or a cytogenetic abnormality in the tumor are to be searched for in young adults with renal clear-cell carcinoma.

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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.

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INTRODUCTION: IgD myeloma is a rare disease, comprising only 1-2% of all cases of myeloma. EXEGESIS: A 71-year-old woman was admitted with acute renal failure, hypercalcemia and IgD lambda multiple myeloma. Dialysis was necessary. Six monthly cures of chemotherapy of induction according to the protocol VAD (vincristine, doxorubicin and dexamethasone) allowed to achieve moderate chronic renal failure (serum creatinine = 120 mumol/L). Sixteen months later, the patient developed an abdominal mass due to an IgD plasmocytoma in spite of treatment with interferon alpha and dexamethasone. Chemotherapy with melphalan and dexamethasone allowed to the disappearance of plasmocytoma and remission. The death occurred 36 months after the diagnosis. CONCLUSION: This observation allows to display the particularities of IgD myeloma: remarkable preponderance of lambda-type light chains, small or no visible monoclonal spike on serum electrophoresis, frequent extraosseous spread of tumor, renal failure and presence of osteolytic lesions. Over the last years, management and prediction of the survival time of IgD myeloma patients have improved.

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The simultaneous occurrence of acute poststreptococcal glomerulonephritis and thrombotic microangiopathy is rare. A 47-year-old woman was admitted with acute renal failure, hematuria, edematous nephrotic syndrome and severe hypertension. This acute nephritic syndrome occurred two weeks after left leg erysipelas. The patient also had signs of intravascular hemolysis, low serum levels of C3 and C4 and elevated antistreptolysin-O titer. Kidney biopsy confirmed postinfectious glomerulonephritis with diffuse hypercellularity and humps, and simultaneous subendothelial hyalin deposits and fibrinoid arteriolar thrombi. The patient received four antihypertensive drugs, acetylsalicyclic acid and plasma infusions. Renal function improved, hypertension was controlled and serum levels of C3 and C4 complement components returned to normal within three months. This case illustrates the occurrence of thrombotic microangiopathy in association with acute poststreptococcal glomerulonephritis. This simultaneous appearance supports a role of neuraminidase in this disease.

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We describe the case of a 51-year-old woman who developed a hemolytic uremic syndrome nine weeks after the end of chemotherapy with mitomycin C for cancer of the anus. Episodes of hemolytic uremic syndrome recurred within a period of up to six months. They were treated with plasma infusion and exchange, antiplatelet agents and rigorous control of blood pressure. The patient was followed for eight years. Her blood pressure has been normal without the use of antihypertensive agents and the renal function has remained stable with serum creatinine at 110 mumol/1. The tumor has remained in remission. This case suggests that recovery from the acute phase of hemolytic uremic syndrome leads to good long-term prognosis.

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Renal failure secondary to acute tubular necrosis is a common complication of severe Plasmodium falciparum malaria. The purpose of this report is to describe two cases of severe malaria featuring acute renal failure observed in young patients who had failed to comply with chemoprophylaxis. Occurrence of renal failure was delayed four to seven days in relation to the beginning of the malaria attack. Hemodialysis was required in one case. Both patients were successfully treated by quinine perfusion. The main pathophysiology mechanisms underlying acute tubular necrosis are obstruction of capillaries and post-capillary venules by infected red blood cells and activation of monocytes that release cytokines such as tumor necrosis factor. Other nonspecific mechanisms may come into play including hypovolemia, release of catecholamines and subsequent activation of the rennin-angiotensin system, complement activation, and rhabdomyolysis. Acute tubular necrosis is the main renal complication of Plasmodium falciparum malaria but latent forms of acute glomerulonephritis have also been documented. Prognosis is usually favorable depending mainly on early diagnosis and prompt treatment.

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Renal involvement in parasitic infections are polymorphic. Plasmodium malariae often leads to membranoproliferative glomerulonephritis whereas acute tubular necrosis or post-infectious acute glomerulonephritis are observed with Plasmodium falciparum. Urogenital taxis of Schistosoma haematobium is responsible for frequency of chronic tubular and interstitial nephritis. Without specific treatment, the renal function progressively deteriorates and urological complications appear. Schistosoma mansoni mainly leads to mesangial and membranoproliferative glomerulonephritis. Membranoproliferative and membranous glomerulonephritis are reported with loasis. Onchocerca volvulus also leads to membranoproliferative glomerulonephritis and lipoid nephrosis. Renal involvement with Wuchereria bancrofti is rare. With leishmaniosis, it is often mild but more serious observations are described: acute glomerulonephritis, nephrotic syndrome or acute interstitial nephritis. Renal hydatic cysts are diagnosed in two or three per cent of cases. Surgery is the only treatment. Immunosuppressive or antimalarial treatments seem to be ineffective in the outcome of chronic glomerulonephritis.

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PURPOSE: Clinical renal outbreaks occurring in the course of sarcoidosis are polymorphous. METHODS: Nine patients presenting with sarcoidosis were followed up for 18 years. RESULTS: Five patients presented with chronic interstitial nephritis. Renal failure accompanying granuloma was also present in three of them. Corticotherapy allowed rapid improvement in renal function in three patients. In two other cases, late treatment prevented recovery and led to end-stage renal failure in one case. In another case, persistent hypercalciuria was responsible for bilateral nephrolithiasis further treated via extracorporeal lithotrity. One case of mesangial glomerulonephritis and two morbid associations (retroperitoneal fibrosis and Henoch-Schönlein purpura) were observed. CONCLUSION: Interstitial nephritis is still a severe clinical renal outbreak. Corticotherapy must be prescribed early to avoid renal failure. Calcium metabolism disorders are frequent and often combined with interstitial nephritis. Hypercalcemia can often and rapidly be improved via corticotherapy, while monitoring of hypercalciuria proves to be more difficult. Membranous glomerulonephritis is still the most frequently reported glomerular lesion.

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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.

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We analyzed 33 patients with AILD T-NHL in a retrospective multicentric study. The median age was 62 yr (35-84 yr) (19 patients over 60 yr). Advanced disease (n = 31) and B-symptoms were consistently found (n = 29) and 20 patients had bone marrow involvement. The main laboratory abnormalities were: anemia (n = 13), hypereosinophilia (n = 13), lymphopenia (n = 14), hypergammaglobulinemia (n = 17), elevated lactate dehydrogenase (LDH) level (n = 24). First-line therapy was chemotherapy (ChT) alone (n = 25) or ChT after steroids (n = 8). Most patients received a CHOP-like regimen for a median number of 6 cycles and 3 patients received interferon alpha (IFN alpha) as consolidation after chemotherapy. With a median follow-up of 46 mo, 60% achieved a complete response but the outcome was poor with a relapse rate at 56%, a median survival referring to the total population was of 36 mo (2-108+ mo) and an overall survival at 5 yr of 36%. Two patients received high-dose chemotherapy (with total body irradiation) and autologous progenitor-cell transplantation for chemosensitive relapse and were free of disease at, respectively, 76 and 24 mo+. In conclusion AILD T-NHL still has a poor prognosis compared to other NHL. The role of intensive therapy and IFN alpha still remains to be evaluated.

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Although rare, renal involvement during hypereosinophilic syndromes can lead to life-threatening situations. Since eosinophilic renal lesions can occur in a wide range of primary or secondary diseases, diagnosis can pose difficult clinical dilemmas. In some settings, renal lesions may be a predictable complication as in essential hypereosinophilic syndrome or angiolymphoid hyperplasia with eosinophilia. In other cases, renal lesions may be a highly unusual event secondary to cholesterol embolization, drug-induced reactions, immunoallergic responses, eosinophilic helminthic infection, or maintenance hemodialysis. The mechanisms of renal involvement are complex. In hypereosinophilic syndromes, renal involvement has been attributed to the deleterious effects of eosinophil granules and possibly to micro-emboli from the heart in patients presenting fibroplastic endocarditis or eosinophilic myocarditis. Most secondary forms are usually due to an immuno-allergic process leading to deposit of immune complexes in glomeruli. The effects of polynuclear eosinophils could also be due to release of cytokines and other mediators such as leukotriens. Cholesterol embolization involves a different mechanism in which hypereosinophilia is often moderate and accessory to arteriolar lesions. Eosinophiluria may be observed in any setting but the prognostic value of this finding as well as the mechanism underlying remain unclear.

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A healthy 19-year-old recruit in a French artillery regiment drank 250 mL of a mixture of beer and wine that had rinsed in a hot 155-mm gun-barrel. Fifteen minutes later, he complained of nausea followed by seizures. He was comatose for 24 h, presenting signs of encephalopathy. A moderate renal failure was noted initially and worsened to an extensive tubular necrosis with anuria on the day after the incident. The first toxicological investigations only showed a 0.31 g/L blood ethanol. Then inductively-coupled plasma (ICP) emission-spectrometry revealed very high concentrations of tungsten in the "beverage" as well as in gastric content, blood and urine (1540 mg/L, 8 mg/L, 5 mg/L, and 101 mg/L, respectively). The nature of the metal was confirmed by ICP coupled to mass spectrometry. A simple and reliable ICP quantitative assay of tungsten in biological fluids, hair and nails was then developed. It showed high blood levels (> 0.005 mg/L) until day 13 in spite of six hemodialyses, and in urine until D33. Tungsten was also incorporated in hair and nails. To the best of our knowledge, such an intoxication has never been reported before though this drinking seems to be traditional in the French Artillery. It has probably been favored by the unusually high volume of beverage absorbed and by the new alloy of the gun, containing tungsten. The clinical evolution was satisfactory over weeks and the patient was declared totally cured after five months.

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A patient with a filarial infection due to Loa loa, received single oral dose of ivermectin A few hours after, he has presented a severe renal impairment. Native of the Cameroons, he was also treated for malaria. A renal biopsy has been done, because of chronic proteinuria. It has showed microfilariae in glomeruli, thickening of the basement membrane and a segmental and focal mesangial hyalinosis. By immunofluorescence microscopy there were granular deposits of IgM and C3 along this membrane. Electron microscopy has showed subepithelial electron- dense deposits. This suggests that the renal disease is immunologically induced. During the therapy, adverse reactions seemed to be related with massive liberation of filarial antigens. This is well known with diethylcarbamazine but also now, sometimes with ivermectin.

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