Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype.

BACKGROUND: Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG). CASE REPORT: A 35-year-old male was admitted for hypertension and an eight-month history of lower-limb edema, foamy urine, and increased abdominal girth. He had a recent diagnosis of hepatosplenic SM, treated with praziquantel, without clinical improvement. Laboratory tests revealed serum creatinine 1.89mg/dL, blood urea nitrogen (BUN) 24mg/dL, albumin 1.9g/dL, cholesterol 531mg/dL, low-density lipoprotein 426mg/dL, platelets 115000/mm3, normal C3/C4, antinuclear antibody (ANA), rheumatoid factor (RF), and antineutrophil cytoplasmic antibodies (ANCA), negative serologies for hepatitis C virus (HCV) and human immunodeficiency virus (HIV), HBsAg negative and AntiHBc IgG positive, no hematuria or leukocyturia, 24 hour proteinuria 6.56g and negative serum and urinary immunofixation. Kidney biopsy established the diagnosis of CG. A treatment with prednisone was started without therapeutic response, progressing to end-stage kidney disease 19 months later. Molecular genetics investigation revealed an HRG. CONCLUSIONS: This is the first report of CG associated with SM in the setting of an HRG. This case highlights the two-hit model as a mechanism for CG pathogenesis, where the high-risk APOL1 genotype exerts a susceptibility role and SM infection serves as a trigger to CG.

Effect of Mineral and Bone Metabolism on Restless Legs Syndrome in Hemodialysis Patients.

STUDY OBJECTIVES: Restless legs syndrome (RLS) is a highly prevalent sleep disease among patients on hemodialysis. The physiopathology is still unclear, and may be multifactorial. Because of the association between iron metabolism and chronic kidney disease-mineral and bone disorders (CKD-MBD), we hypothesized that both factors would be associated with RLS. METHODS: We have evaluated hemodialysis patients, in a face-to-face interview for the diagnosis and severity of RLS, as measured by the International Restless Legs Syndrome Study Group. Clinical, demographic, and biochemical characteristics were measured. RESULTS: Out of 101 adult patients included, RLS was found in 29 (28.7%). Adjusted multinomial regression analysis revealed that age older than 35 years, transferrin saturation less than 47%, serum ferritin level less than 700 ng/mL, hemoglobin level less than 9.8 g/dL, serum phosphate level higher than 5.2 mg/dL, FGF-23 higher than 2,000 RU/mL, and C-reactive protein less than 1.24 mg/dL were independently associated with RLS. RLS was classified as mild, moderate, severe, and very severe in 3.4%, 41.7%, 44.8%, and 10.1% of patients, respectively. Scores of severity correlated significantly with erythropoietin dose/kg/w (p = 0.046), phosphate (p = 0.003), and inversely with serum albumin (p = 0.003) and calcium (p = 0.008). Phosphate and 25(OH)-vitamin D correlated with transferrin saturation. Patients with severe/very severe symptoms were mostly women, presented with lower serum iron, ionic calcium, and serum albumin levels and higher levels of serum phosphate, and higher percentage of 25(OH)-vitamin D deficiency and levels of FGF-23 higher than 2,000 RU/mL than did those with mild/moderate symptoms. CONCLUSIONS: CKD-MBD factors besides iron metabolism are associated with RLS in patients on hemodialysis, providing new insights into the understanding of RLS in this population.

Coronary Artery Calcification Seen Through Chest Radiography.

Patients with end-stage renal disease (ESRD) on dialysis have poor overall survival, and cardiovascular (CV) is the main cause of mortality among these patients. Coronary calcification is an independent predictor of mortality and CV events in dialysis patients and can be accessed by using a computerized tomography scanning. The high cost of this procedure, however, precludes routine implementation of this method for the purposes of risk stratification. Aortic arch calcification has been associated with CV mortality in the general population. Also, vascular calcification beyond the thoracic aorta has been shown to be associated with mortality in ESRD patients. We presented here a case of a young patient with ESRD in which the coronary calcification could be cleared seen through simple chest radiography. This is a 35-year-old man with a history of ESRD secondary to pyelonephritis, who was receiving conventional hemodialysis thrice a week for the last 5 years. He was submitted to chest radiography as part of routine annual cardiac screening. His blood pressure was within the target limits, although much higher in lower limbs, generating a high ankle brachial index of 1.3. He also had secondary hyperparathyroidism. His physical examination was unremarkable, except for the presence of non-functioning arteriovenous fistulas in both arms and a central venous catheter. The last routine blood test showed calcium 9.0 mg/dL, phosphate 5.7 mg/dL, potassium 4.7 mEq/L, creatinine 7.4 mg/dL, alkaline phosphatase 175 U/L, and parathyroid hormone 1,745 pg/mL. Surprisingly, the chest radiography revealed a calcified aortic valve and a calcified coronary artery. This patient had sudden cardiac death few months after this radiography had been taken. We present here a case of coronary calcification that can be seen through simple chest radiography. Such images are not usually seen, although the risk of vascular calcification is high in this population, and is closely related to CV risk. Chest radiographs, nearly universally available provide a method for assessing coronary artery calcification. Such a finding is intriguing and should alert nephrologists and cardiologists for the high risk of CV death in these patients.

Acute kidney injury after massive attack of Africanised bees.

Acute kidney injury (AKI) is a well-documented complication of massive attack by Africanised bees and can be observed 48-72 h after the accident. We report a case of Africanised bees attack followed by severe and lethal AKI. A 56-year-old man was admitted to emergency department after a massive attack of Africanised bees (>1000 bee stings). He was unconscious, presenting with hypotension and tachycardia. Mechanical ventilation, volume expansion and care for anaphylaxis were instituted. The patient was transferred to the intensive care unit (ICU) and after 48 h he developed rhabdomyolysis, oliguria, increased creatinine levels, hyperkalaemia and refractory acidosis. A diagnosis of AKI secondary to rhabdomyolysis and shock was made. The patient was treated with a prolonged course of haemodialysis. However, he progressed to refractory shock and died 5 days after admission.