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.

Hemodialysis (HD) is associated with increasing thrombotic trend. Vascular access thrombosis (VAT) increases morbidity in HD patients. The aim of this study was to evaluate ADAMTS13 and VWF plasma levels from patients undergoing HD as putative biomarkers of the hypercoagulability state, as well the association between these markers and VAT occurrence. This study included 195 patients on HD for more than 6 months. HD patients were allocated into two groups according to the occurrence or not of previous episode of VAT; HD with VAT (N = 46) and HD without VAT (N = 149). ADAMTS13 and VWF were performed by ELISA. There was no significant difference between HD patients with and without VAT for ADAMTS13 and VWF levels. However, VWF levels were higher (P < 0.001) and ADAMTS13 were lower (P < 0.001) in HD patients, comparing to the control group composed by healthy subjects without kidney disease, age and sex-matched (N = 80). Taken together our data suggest a potential role of the kidneys function compromised on ADAMTS13 synthesis or metabolism, regardless other known sources of ADAMTS13. The imbalance between ADAMTS13 and VWF levels does not explain the development of VAT in HD patients by itself, although it should contribute for the hypercoagulability state. Therefore, additional studies to identify other risk factors are warranted and essential for better management of HD patients.

Pseudohyperkalemia has been described in patients with thrombocytosis caused by a variety of diseases 1 5 . To our knowledge, this is the first report of a patient with hepatosplenic schistosomiasis who developed extreme thrombocythemia after splenectomy 2 3 and in whom in vitro 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 5 . Potassium release from platelets is a universal phenomenon during coagulation, and the more platelets present, the more potassium will be released. In cases of extreme thrombocythemia, it becomes clinically significant to cause a spurious serum hyperkalemia. In normal subjects, the median serum potassium concentration is 0.2 mmol/L higher than the plasma potassium concentration. A diagnosis of pseudohyperkalemia can be confirmed when the difference is more than 0.4mmol/L in the presence of an elevated potassium level 5 . In our patient, the occurrence of glomerulonephritis 2 was a confounding factor in the diagnosis of real or pseudohyperkalemia and pseudohyperphosphatemia 4 . This patient was submitted to hemodialysis based on a mistaken diagnosis of hyperkalemia and hyperphosphatemia which brings a definite threat to life. Both clinicians and surgeons need to be aware of this phenomenon in order to avoid unwanted and potentially detrimental treatment including hemodialysis. Also, to our knowledge, this is the first description of pseudohyperphosphathemia 4 in patients with thrombocytosis. This ca...

Abstract. 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.