Although patients who received Polymyxin B plus vancomycin had more favorable clinical profile and higher previous GFR, they presented a higher AKI incidence than those patients who received Polymyxin B alone. Cumulative Polymyxin B dose > 10 million IU was independently associated to AKI.

Leptospirosis showed significant changes over time in this region. The main changes point to a decrease in disease severity and complications, such as acute kidney injury. Mortality has decreased, being close to 11%.

BackgroundVisceral leishmaniasis (VL) is an important and potentially fatal neglected tropical disease. The aim of this study was to investigate hyponatremia and risk factors for death among VL patients.MethodsThis is a cross-sectional study with VL patients admitted to a tertiary hospital in Northeast Brazil, from 2002 to 2009. Patients were divided into two groups: non-survivors and survivors. Hyponatremia was defined as serum sodium < 135 mEq/L. A logistic regression model was done to investigate risk factors for death.ResultsA total of 285 VL patients were included, with mean age 37 ± 15 years, and 74% were males. Thirty-four patients died (11.9%). Non-survivors had a significantly higher prevalence of dyspnea (38.2 vs. 16.7%, p = 0.003), pulmonary crackles (11.8 vs. 4.0%, p = 0.049), dehydration (23.5 vs. 10.8%, p = 0.033), oliguria (8.8 vs. 0.8%, p = 0.001) and jaundice (47.1 vs. 14.3%, p < 0.001). They also presented higher prevalence of hyponatremia (41.9 vs. 24.1%, p = 0.035), thrombocytopenia (91.2 vs. 65.3%, p = 0.002) and severe hypoalbuminemia (78.3 vs. 35.3%, p < 0.001). In multivariate analysis, moderate/severe hyponatremia (OR = 2.278, 95% CI = 1.046–4.962), thrombocytopenia (OR = 5.482, 95% CI = 1.629–18.443), jaundice (OR = 5.133, 95% CI = 1.793–14.696) and severe hypoalbuminemia (OR = 6.479, 95% CI = 2.124–19.766) were predictors of death.ConclusionHigher prevalence of dehydration, oliguria, pulmonary symptoms and liver involvement was found in non-survivors VL patients. Hypoalbuminemia and hyponatremia were frequent and significantly associated with mortality.

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SUMMARY INTRODUCTION: Paroxysmal Nocturnal Haemoglobinuria (PNH) is an acquired genetic disorder characterized by complement-mediated haemolysis, thrombosis and variable cytopenias. Renal involvement may occur and causes significant morbidity to these patients. OBJECTIVE: To review the literature about pathophysiology and provide recommendations on diagnosis and management of renal involvement in PNH. METHODS: Online research in the Medline database with compilation of the most relevant 26 studies found. RESULTS: PNH may present with acute kidney injury caused by massive haemolysis, which is usually very severe. In the chronic setting, PNH may develop insidious decline in renal function caused by tubular deposits of hemosiderin, renal micro-infarcts and interstitial fibrosis. Although hematopoietic stem cell transplantation remains the only curative treatment for PNH, the drug Eculizumab, a humanized anti-C5 monoclonal antibody is capable of improving renal function, among other outcomes, by inhibiting C5 cleavage with the subsequent inhibition of the terminal complement pathway which would ultimately give rise to the assembly of the membrane attack complex. CONCLUSION: There is a lack of information in literature regarding renal involvement in PNH, albeit it is possible to state that the pathophysiological mechanisms of acute and chronic impairment differ. Despite not being a curative therapy, Eculizumab is able to ease kidney lesions in these patients.

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ObjectiveTo investigate prognostic factors among critically ill patients with community-acquired bacterial meningitis and acute kidney injury.MethodsA retrospective study including patients admitted to a tertiary infectious disease hospital in Fortaleza, Brazil diagnosed with community-acquired bacterial meningitis complicated with acute kidney injury. Factors associated with death, mechanical ventilation and use of vasopressors were investigated.ResultsForty-one patients were included, with a mean age of 41.6 ± 15.5 years; 56% were males. Mean time between intensive care unit admission and acute kidney injury diagnosis was 5.8 ± 10.6 days. Overall mortality was 53.7%. According to KDIGO criteria, 10 patients were classified as stage 1 (24.4%), 18 as stage 2 (43.9%) and 13 as stage 3 (31.7%). KDIGO 3 significantly increased mortality (OR = 6.67; 95%CI = 1.23 - 36.23; p = 0.028). Thrombocytopenia was not associated with higher mortality, but it was a risk factor for KDIGO 3 (OR = 5.67; 95%CI = 1.25 - 25.61; p = 0.024) and for mechanical ventilation (OR = 6.25; 95%CI = 1.33 - 29.37; p = 0.02). Patients who needed mechanical ventilation by 48 hours from acute kidney injury diagnosis had higher urea (44.6 versus 74mg/dL, p = 0.039) and sodium (138.6 versus 144.1mEq/L; p = 0.036).ConclusionMortality among critically ill patients with community-acquired bacterial meningitis and acute kidney injury is high. Acute kidney injury severity was associated with even higher mortality. Thrombocytopenia was associated with severer acute kidney injury. Higher urea was an earlier predictor of severer acute kidney injury than was creatinine.