Angela Volpi

Acute Renal Failure Due to Hypersensitivity Interstitial Nephritis Induced by Warfarin Sodium

Dr. A. Volpi, Unità Operativa di Nefrologia e Dialisi, Ospedale di Vimercate, Via Cereda, 2, I-20059 Vimercate (Italy) Sir, Adverse reaction to a growing number of drugs is being recognized as a cause of acute renal failure [1]. The clinician should suspect the possibility of acute drug-induced tubulointerstitial nephritis in all cases of acute renal failure of unknown etiology. Acute drug-induced hypersensitivity reaction is a common form of tubulointerstitial nephritis with sudden deterioration of renal function and oliguria. Renal function usually returns toward baseline after withdrawal of the drug. Systemic signs and symptoms such as fever, skin rash, arthralgias, myalgias, eosinophilia and seldom lym-phoadenopathy suggest a hypersensitivity mechanism; certain observations suggest that immunologically mediated tissue damage is the consequence of cell-mediated injury [2]. We have observed a 65-year-old female who developed fever, arthralgias, gross hematuria, sterile pyuria and oliguric acute renal failure (serum creatinine rose from 1.2 to 6.8 mg/dl). She was treated for 25 days with diltiazem, nitroglycerine discs and warfarin sodium (20 mg/day) because of myocardial infarction. Renal biopsy showed a typical picture of acute tubulointerstitial nephritis, with several interstitial eosino-phils, mononuclear cells, patchy focal tubular necrosis and intratubular casts of eosinophil cells (fig. 1). The glomeruli showed mild mesangial hypercellularity with IgA and C3 mesangial deposits at immunofluorescence. Late assay of serum IgE was normal. Withdrawal of warfarin sodium and treatment with corticosteroids (1 mg/kg/day) returned renal function to the normal level in 45 days (serum creatinine 1 mg/dl). Acute renal failure due to acute drug-induced tubulointerstitial nephritis is seen more frequently in older patients and, usually, the mean latent period of treatment is 15 days (from 2 to 44 days) [2]. In the absence of other apparent causes we think that warfarin sodium hypersensitivity has likely been the

Acute Glomerulonephritis in Human Brucellosis

Acute Glomerulonephritis in Human Brucellosis C. Cecilia Doregatti A. Angela Volpi L.T. Laura Torri Tarelli M. Mario Brognoli F. Ferdinando Giordano M. Mietta Meroni G. Giancarlo Orlandini A. Adalberto Sessa Servizio di Nefrologia e Dialisi, Ospedale di Leno, Leno, Italia;Servizio di Nefrologia e Dialisi, Ospedale di Vimercate, Vimercate, Italia; Istituto di Anatomia Umana Normale, Università degli Studi, Milano, Milano, Italia

Two Brothers With Idiopathic Membranous Nephropathy and Familial Sensorineural Deafness

Genetic factors could play an important role in the pathogenesis of idiopathic membranous nephropathy, and a few cases of familial membranous nephropathy have been described: an increased incidence of some HLA antigens as DR3 and others has been reported. We present two brothers with idiopathic membranous nephropathy and sensorineural deafness. HLA typing was performed in the two patients and in the members of the family, and it showed the absence of linkage of an HLA antigen with the renal disease in the family.

Lactic Acidosis Coma in Continuous Ambulatory Peritoneal Dialysis

Dr. A. Tommasi, Servizio di Nefrologia e Dialisi, Ospedale di Vimercate, Via Cereda 2, 20059 Vimercate (Italy) Dear Sir, We have recently observed a case of lactic acidosis coma in a patient on continuous ambulatory peritoneal dialysis (CAPD). The patient, a 69-year-old female, weighing 78.5 kg and 162 cm tall, had been on CAPD treatment for 2 months because of analgesic nephropathy, proved by anamnestic investigation and by kidney biopsy. She developed severe lactic acidosis with abrupt onset and without warning, during an episode of peritonitis and circulatory failure. The maintenance therapy consisted of digoxine, nifedipine and aluminum hydroxide. Laboratory data were: arterial blood pH 7.19, Pa02 64.1 mm Hg, PaC02 32.6 mm Hg, plasma bicarbonate 11.5 mEq/1, plasma lactate concentration 120 mg/l00 ml (normal values 5–22 mg/l00 ml), sodium 136 mEq/1, potassium 6.49 mEq/1, chloride 95 mEq/1, BUN 77 mg/l00 ml, creatinine 8.35 mg/l00 ml, glucose 91 mg/l00 ml, hema-tocrit 24.7%, hemoglobin 7.6 g/l00 ml. We treated lactic acidosis with sodium bicarbonate infusion (600 mEq in 48 h) and acetate hemodialysis (4 h twice a day for the 1st day and once a day for the following 2 days). The patient recovered after 2 days of treatment. Laboratory data were: arterial blood pH 7.41, Pa02 59.7 mm Hg, PaC02 37.9 mm Hg, plasma bicarbonate 24.7 mEq/l, plasma lactate 17 mg/l00 ml; and after 4 days of treatment: arterial blood pH 7.43, Pa02 68.8 mm Hg, PaC02 46 mm Hg, plasma bicarbonate 30 mEq/l, plasma lactate 13 mg/l00 ml. An increased plasma lactate concentration has been reported to occur during intermittent peritoneal dialysis (IPD) [1], but lactic acidosis has never been reported during CAPD. It is possible that more concomitant mechanisms have determined the severe lactic acidosis in our patient: (a) hepatic failure because of hepatitis following long-term exposure to paracetamol [2,3]; that may justify the lack of a metabolic way of lactate to piruvate; (b) circulatory failure, which may induce a shift from aerobic metabolism to anaerobic glycolysis and thereby produce lactic acidosis [4]; (c) fasting in the presence of obesity, which may induce accumulation of lactic acid in significant amounts [4].

Thrombolysis in Myocardial Infarction and Double Aortocoronary Bypass in a Patient on Continuous Ambulatory Peritoneal Dialysis

Dr. A. Volpi, Servizio di Nefrologia e Dialisi, Ospedale di Vimercate Via C. Battisti 23, I-20059 Vimercate (Italy) Sir, Cardiovascular diseases appear to be the leading cause of death in patients receiving long-term dialysis, and accelerated atherosclerosis is mainly responsible for vascular lesions in uremic patients [1,2]. Moreover hypertension, coronary artery disease, myocardial failure, cardiac calcifications, arrhythmias, and pericarditis are more common in these patients compared to the general population [3]. We have observed a 53-year-old woman admitted in October 1983 because of microhematuria and proteinuria with clinical and renal histological features of Henoch-Schönlein syndrome: her serum creatinine was 1.4 mg/dl. In November 1984 she was readmitted for rapid deterioration of renal function (serum creatinine, 6 mg/dl) and she was treated with pulses of steroid and plasma exchange: serum creatinine returned to 3.17 mg/dl. She developed diabetes and hypertension during steroid treatment. Eighteen months later (March 1985) she was begun on continuous ambulatory peritoneal dialysis for end-stage renal failure. She had experienced angina pec-toris during the previous 6 months and therefore she was treated with calcium channel blockers and nitrates. In April 1986 she presented with prolonged anginal pain and hypotension: ECG tracings showed signs of an acute ischemic lesion of the inferior cardiac wall. Laboratory examinations showed: lactate dehydrogenase 1,031 IU, and creatine kinase 1,366 IU with high levels of MB isoenzyme. She was treated with urokinase by intravenous infusion (a ‘pulse’ of 600,000 U followed by 1,500,000 U in 60 min) with partial regression of the ischemic lesion; afterwards the patient was treated with heparin and nitrates.

Plasma Exchange in Acute Renal Failure Due to Postpartum Hemolytic-Uremic Syndrome

Dr. A. Sessa, Servizio di Nefrologia e Dialisi, Ospedale di Vimercate, Via C. Battisti 23, I-20059 Vimercate (Italy) Dear Sir, In females with early or late postpartum hemolytic-uremic syndrome (HUS), the features of the illness are acute renal failure and microangiopathic hemolytic anemia in association with thrombocytopenia and increased serum bilirubin levels [1]. Severe irreversible renal failure is the rule; nevertheless, cases have been reported with a favorable outcome [2]. The pathogenesis of the HUS is still unknown: circulating substances (en-dotoxins, vasoactive amines, etc.) are likely to produce the primary injury to the endothelial cells of the glomeru-lar capillaries [3]. Moreover, some patients appear to have a lack of a prostaglandin plasma inhibitor [4], and intravascular coagulation also might be induced by im-munoglobulin factors [5]. Therefore, plasma exchange treatment with fresh plasma infusion has been suggested [6]. We have observed a 32-year-oîd female affected with early postpartum HUS. The kidney biopsy showed glom-erular thrombotic microangiopathy. The patient received plasma exchange treatment for 3 consecutive days and then every 3rd day the following week with an exchange of one plasma volume at each procedure, using fresh plasma as 50% of the substitution fluids. Regression of the HUS and partial recovery of renal function were observed. The patient was discharged on the 16th hospital day with normal blood pressure, renal function, and hematologic picture. For 3 years she has been well (fig. 1). The early treatment with plasma exchange and fresh plasma infusion possibly conditioned a favorable course of the disease. ππ Plasmapheresis Bilirubin, mg/l00 ml Pla†ele† 500 · coun†/mm3 ¿λ∩ 300 200–100 Serum crea†inine, mg/l00 ml Urine 1,500

Recurrent Hemolytic Uremic Syndrome: Case Report

Dr. M. Meroni, Servizio di Nefrologia e Dialisi, Ospedale di Vimercate, via C. Battisti 23, I-20059 Vimercate (Italy) Dear Sir, Hemolytic-uremic syndrome (HUS) is a disease of infants and children, but this condition may be found in adults too. Females are more commonly affected, and they usually show a history of oral contraception or recent delivery [1]. At present, however, a clear distinction between HUS and thrombotic thrombocytopenic pur-pura is quite difficult. Recurrent attacks of HUS in adults have been seldom recordered, and the factors responsible for the recurrences were not always known [2]. We have observed a 52-year-old female with acute renal failure in course of classic manifestations of HUS: weakness, petechiae, and ecchymoses in the skin, hema-temesis, melena, and hematuria with mild proteinuria. Hemoglobin was 8.8 g/dl, reticulocytes 21%o, white blood cells, 12,000/mm3, platelets 105,000/mm3, plasma fibri-nogen 140 mg/dl, fibrin split products 80 μg/ml, blood urea nitrogen 131 mg/dl, and serum creatinine 6.22 mg/dl. The renal biopsy specimen has been studied by light, immunoñuorescent, and electron microscopy and showed pathognomonic lesions of HUS (fig. 1). The patient was treated with prednisolone pulses, hemodialysis, plasmapheresis and she left the hospital after 42 days. Serum creatinine was 1.36 mg/dl. In coincidence with abrupt withdrawal of prednisolone, she developed a relapse of HUS with slight renal involvement (serum creatinine 1.79 mg/dl, blood urea nitrogen 32 mg/dl), but with severe involvement of skin, intestinal tract, myocardium, and brain. She died after 25 days in spite of prednisolone, plasmapheretic, and vitamin E treatment. At autopsy the pathologic findings were small microthrombi in brain, myocardium, kidney, thyroid, peritoneum, omentum, jejunum, and ileum. Fig. 1. Electron micrograph from a biopsy specimen showing thickening of the capillary wall, effacement of foot processes, wrinkling of the basement membrane (asterisks), widening of the suben-dothelial space, which contains rarefied and granular material of variable electron density