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Background/Aims: The c-Jun amino-terminal kinase (JNK) signaling pathway is activated in human kidney diseases and promotes renal injury in experimental glomerulonephritis. In this study, we examined whether JNK signaling plays a role in the development of diabetic nephropathy or in regulating hypertension, which exacerbates diabetic renal injury. Methods: Diabetes was induced in spontaneously hypertensive rats (SHR) using streptozotocin. At week 16 of diabetes, rats with equivalent hyperglycemia and albuminuria were randomized into groups which received no treatment, vehicle alone or a selective JNK inhibitor (CC-930, 60 mg/kg/bid) for 10 weeks. These rats were assessed for hypertension and progression of renal damage. Results: At week 16, diabetic rats showed increased kidney JNK activation compared with nondiabetic controls. Effective JNK inhibition was demonstrated at week 26 by reductions in c-Jun phosphorylation. CC-930 did not affect blood pressure, kidney hypertrophy, glomerular hyperfiltration, podocyte loss, glomerular fibrosis or tubulointerstitial injury in diabetic SHR. However, CC-930 reduced macrophages and ccl2 mRNA levels in diabetic kidneys. In contrast, CC-930 exacerbated albuminuria at week 26, which was associated with reduced glomerular mRNA levels of the podocyte-specific molecules, nephrin and podocin. Conclusion: JNK inhibition does not prevent the progression of early diabetic renal injury in hypertensive rats, which contrasts with the ability of JNK inhibition to suppress albuminuria and injury in experimental glomerulonephritis. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Currently, no large, nationwide studies have been conducted to analyze the demographic factors, underlying comorbidities, clinical outcomes, and health care utilization in rhabdomyolysis patients with and without acute kidney injury (AKI). Methods: We queried the National Inpatient Sample of Healthcare Cost and Utilization Project (HCUP) with patients with rhabdomyolysis from 2016 to 2018. The chi-squared test was used to compare categorical variables, and the adjusted Wald test was employed to compare quantitative variables. The logistic regression model was applied to calculate adjusted odds ratios (ORs) with 95% confidence intervals (95% CIs) to estimate the impact of AKI on outcomes in patients with rhabdomyolysis. Results: Among 111,085 rhabdomyolysis-related hospitalizations, a higher prevalence of AKI was noticed in older patients (mean age ± SD, 58.2 ± 21.6 vs. 53.8 ± 22.2), Medicare insurance (48.5% vs. 43.2%), and patients with a higher Charlson Comorbidity Index score (CCI 3–5, 15.1% vs. 5.5%). AKI was found to be independently associated with higher mortality (adjusted odds ratio [aOR] 3.33, 95% CI 2.33–4.75), longer hospital stays (adjusted difference 1.17 days, 95% CI: 1.00−1.34), and higher cost of hospital stay (adjusted difference $11,315.05, 95% CI: $9493.02–$13,137.07). Conclusions: AKI in patients hospitalized with rhabdomyolysis is related to adverse clinical outcomes and significant economic and survival burden. [ABSTRACT FROM AUTHOR]

Hyponatremia can occur with central nervous system (CNS) infections, but the frequency and severity may depend on the organism and nature of CNS involvement. In this cross-sectional study at a large Australian hospital network from 2015 to 2018, we aimed to determine the prevalence and severity of hyponatremia associated with CNS infection clinical syndromes, and the association with specific organisms. We examined the results of cerebrospinal fluid analysis from lumbar punctures performed in 184 adult patients with a serum sodium below 135 mmol/L who had abnormal cerebrospinal fluid analysis and a clinical syndrome consistent with an acute CNS infection (meningitis or encephalitis). Hyponatremia affected 39% of patients and was more severe and frequent in patients with encephalitis compared to meningitis (odds ratio = 3.03, 95% CI: 1.43–6.39, after adjusting for age). Hyponatremia was present on admission in 85% of cases. Herpes simplex virus infection was associated with the highest odds of hyponatremia (odds ratio = 3.25, 95% CI: 1.13–7.87) while enterovirus infection was associated with the lowest (odds ratio = 0.36, 95% CI: 0.14–0.92), compared to cases without an isolated organism. We concluded that the risk of hyponatremia may vary by the organism isolated but the clinical syndrome was a useful surrogate for predicting the probability of developing hyponatremia. [ABSTRACT FROM AUTHOR]