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We investigated the serum and urine chemokine levels of patients with schistosomal mansoni glomerulonephritis. This cross-sectional study was conducted in the Southeast of Brazil. Overall, 160 subjects were enrolled and divided into five groups: 1) hepatosplenic schistosomiasis with renal disease (N = 12); 2) hepatosplenic schistosomiasis without renal disease (N = 68); 3) hepatointestinal schistosomiasis (N = 27); 4) glomerulopathy caused by other diseases (N = 22); and 5) healthy controls (N = 31). The patients with microalbuminuria > 30 mg in 24 hours were considered to have renal disease. The sera and urine chemokines CCL2, CCL3, CCL5, CCL11, and CXCL8 were measured using an enzyme-linked immunosorbent assay test. A similar profile was observed between the patients with schistosomal glomerulopathy and the patients with glomerulopathy caused by other diseases, with the exception of serum CCL2 ≤ 634.3 pg/mL. In cases with sera CCL2 > 634.3 pg/mL, the diagnosis of schistosomal glomerulopathy should be considered.

INTRODUCTION: The current prevalence of glomerulonephritis in patients with hepatosplenic schistosomiasis mansoni in Brazil was evaluated. METHODS: Sixty three patients (mean age 45.5±11 years) attending the outpatient infectious disease clinic of a University Hospital in Belo Horizonte, Brazil, from 2007 to 2009, were consecutively examined and enrolled in the present investigation. Diagnosis of hepatosplenic schistosomiasis was based on epidemiological, clinical and parasitological data and imaging techniques. Eight patients, who presented >30mg/day albuminuria, were submitted to percutaneous ultrasound guided renal biopsy. Kidney tissue fragments were examined under light, direct immunofluorescence and electron microscopy. RESULTS: All patients showed mesangial enlargement. In five, mesangial hypercellularity was observed and four presented duplication of the glomerular basement membrane. Areas of glomerular sclerosis were diagnosed in four. Deposits of immunoglobulin M and C3 were present in six samples; deposits of IgG in four, IgA in three and C1q in two samples. In all patients, immunoglobulin A was reported in the lumen of renal tubules. Deposits of kappa and lambda were observed in six samples. Electron microscopy revealed dense deposits in the glomerular tissue of three patients. Arterial hypertension, small esophageal varices, slight increases in serum creatinine and decreases in serum albumin were associated with glomerular disease. CONCLUSIONS: Renal disease associated with hepatosplenic schistosomiasis was verified in 12.7% of patients and type I membranoproliferative glomerulonephritis was observed in 50% of them. Schistosomal glomerulopathy still is an important problem in patients with hepatosplenic schistosomiasis in Brazil. INTRODUÇÃO: Avaliou-se a frequência de glomerulonefrite em pacientes com esquistossomose hepatosplênica no Brasil. MÉTODOS: Selecionou-se para o estudo, 63 pacientes (idade média de 45,5±11 anos) avaliados consecutivamente no ambulatório de doenças infecciosas de um hospital universitário de Belo Horizonte, Brasil, no período de 2007 a 2009. O diagnóstico da esquistossomose foi baseado em dados epidemiológicos, clínicos, parasitológicos e de imagem. Os oito pacientes que apresentaram albuminúria acima de 30mg em 24 horas submeteram-se a biópsia renal percutânea dirigida por ultrassonografia. As amostras de tecido renal foram analisadas à microscopia óptica, eletrônica e de fluorescência direta. RESULTADOS: Havia expansão do mesângio em todos. Em cinco, houve proliferação de células mesangiais e em quatro observou-se duplicação da membrana basal glomerular. Áreas de esclerose glomerular foram diagnosticadas em quatro. Depósitos de imunglobulinas M e C3 foram patentes em seis amostras; IgG em quatro, IgA em três e C1q em duas. Em todos os pacientes relatou-se fluorescência para IgA dentro dos túbulos renais. Depósitos de kappa e lambda foram vistos em seis amostras. A microscopia eletrônica demonstrou depósitos eletrondensos em tecido glomerular. A presença de hipertensão arterial, varizes do esôfago de pequeno calibre, pequenos aumentos de creatinina e diminuição de albumina sérica associaram-se à ocorrência de dano renal. CONCLUSÕES: A frequência de lesão renal foi de 12,7%, no presente estudo, e a glomerulonefrite membranoproliferativa do tipo I foi encontrada em 50%. A lesão renal associada à esquistossomose permanece um problema importante no Brasil.

platelet clotting caused pseudohyperkalemia and pseudohyperphosphatemia. A 42-year-old male patient with hepatosplenic schistosomiasis was admitted to hospital in January 2007, with bleeding esophageal varices and was operated on for portal hypertension (splenectomy + portal variceal disconnection + suturing of varices). He was discharged from hospital 15 days after surgery in good clinical condition. One year later he came to our hospital reporting recurrent episodes of dizziness, syncope and right hemiparesis and, in his hometown, he was treated for epilepsy with anticonvulsants, without improvement. After admission he was found to have nephrotic syndrome (12g of protein in the urine/day). The mean platelet count was 2.7 million measured in 3 different occasions. The serum level of potassium was 7.0mmol/L (normal range: 3.5-5.1mmol/L) and the serum level of phosphorus was 8.9mg/dl (normal range: 2.5-4.9mg/dl). There were no clinical signs or symptoms of electrolyte imbalances, nor electrocardiograph alterations. No clinical response was obtained with the routine treatment for hyperkalemia (exchange resin and intravenous glucose + insulin). Hemodialysis sessions were mistakenly used to correct the electrolyte imbalance. After pseudohyperkalemia was suspected, potassium and phosphorus were measured in plasma (with heparin), and both were found to be within the normal range. Post-splenectomy thrombocytosis is an important cause of pseudohyperkalemia, and this is, in fact, an incorrect laboratory result because it appears in patients with thrombocytosis, only when the electrolytes are measured in blood collected in tubes without anticoagulants