Characteristics of acute ischemic stroke in patients with Nephrotic syndrome

The incidence of ischemic stroke (IS) is higher in nephrotic syndrome (NS) patients compared to general population. However, there is limited information on the specific characteristics to stroke patients with NS. In this study, we aimed to examine the clinical manifestations of acute IS in a large group of NS patients, comparing to those without NS. We conducted a retrospective cohort study to compare the clinical presentations of acute IS in patients with and without NS. This study was a multi-institutional study and used data from Chang Gung Research Database of Taiwan from 1 January 2001, to 31 December 2017. A total of 233 IS patients with NS and 1358 IS patients without NS were enrolled. The median age of participants was 68 (range: 59–79) years. The risk of dependent functional status (modified Rankin Scale score≧3) after IS was higher in NS patients compared to those without NS (Odd ratio (OR) 4.02, 95% confidence interval (CI) 2.39 to 6.76, p p p = 037). The risks of mortality or stroke recurrence within 30 days were similar between the two groups for all stroke subtypes. In conclusion, NS was associated with a higher risk of functional dependence following IS. Intensive treatment and rehabilitation should be considered for IS patients with NS.</p

Comparison of clinical variables between patients living in Taipei Basin and living around Taipei Basin.

<p><i>Abbreviations:</i> nPCR, normalized protein catabolism rate; TAC_urea, time-averaged concentration of blood urea nitrogen; UF, ultrafiltration volume per hemodialysis period; C-calcium, corrected calcium; ALT, alanine aminotransferase; Na, serum sodium; K, serum potassium; HbA1c, glycated hemoglobin; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; log hs-CRP, logarithmic conversion of high-sensitivity C-reactive protein levels.</p><p>Besides nPCR, no significant difference was noted between basin and around basin groups.</p

Complications, living areas, and reasons for mortality in 256 elderly patients.

<p>Sixty-eight patients (26.5%) died within 2 years. Infection (50%) and cardiovascular events (44.1%) were the major causes of 2-year mortality. Complications such as stroke (OR: 3.814, 95% CI (1.56–9.30); p = 0.004) and coronary artery disease (OR: 3.069, 95% CI (1.21–7.74); p = 0.019) were positively associated with mortality. Cancer status, asthma, pulmonary tuberculosis, hepatitis, liver cirrhosis, and cardiomegaly were not significantly associated with 2-year mortality. <i>Abbreviations:</i> CAD, coronary artery disease; GI, gastrointestinal; Pul TB, pulmonary tuberculosis; CTS, carpal tunnel syndrome; CV, cardiovascular.</p

Kaplan–Meier analysis of survival data from patients living in Taipei Basin and those living around Taipei Basin.

<p>Patients living in Taipei Basin suffered higher cumulative mortality than patients living areas around Taipei Basin (log-rank test, chi-square test = 11.01; p = 0.001).</p

Terrain of northern Taiwan: The Taipei Basin (circle part, including most of Taipei City) which is surrounded by mountains and hills has 6 million people living in it.

<p>The map was cited from Google map with adjustment.</p

Binary univariate logistic regression and multivariate Cox regression analysis of variables on 2-year mortality.

<p><i>Abbreviations:</i> Cr, creatinine; CAD, coronary artery disease; log hs-CRP, logarithmic conversion of high-sensitivity C-reactive protein levels; OR, odds ratio; HR, hazard ratio; CI, confidence intervals.</p

Status of protein-energy wasting and inflammation in basin and around basin groups.

<p><i>Abbreviation:</i> hs-CRP, high-sensitivity C-reactive protein level.</p><p>High hs-CRP was defined as an hs-CRP level >3 mg/L.</p><p>Low albumin was defined as a serum albumin level <3.6 g/dL.</p><p>The basin group had a significantly higher proportion of combined low albumin levels and high hs-CRP levels (p = 0.041).</p

Analyzed the data base from the Taiwan Air Quality Monitoring Network (TAQMN) operated by the Environmental Protection Administration (EPA)and cited the report from the air quality status in Taiwan for the year 2009 to 2011.

<p>The mean concentrations of PM_2.5, NO₂ and CO were significantly high in Taipei Basin during these 3 years. *, significant difference, <i>P</i><0.05.</p

Baseline characteristics of the patients studied (n = 256).

<p><i>Abbreviations:</i> DM, diabetes mellitus; AV, arteriovenous; TCC, tunneled-cuffed catheter; HDF, hemodiafiltration; nPCR, normalized protein catabolism rate; C-calcium, corrected calcium; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; Hs-CRP, high-sensitivity C-reactive protein.</p

The AMPK Agonist AICAR Inhibits TGF-β1 Induced Activation of Kidney Myofibroblasts

<div><p>Activation of interstitial myofibroblasts and excessive production of extracellular matrix proteins are common pathways that contribute to chronic kidney disease. In a number of tissues, AMP-activated kinase (AMPK) activation has been shown to inhibit fibrosis. Here, we examined the inhibitory effect of the AMPK activator, 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), on renal fibrosis <i>in</i><i>vivo</i> and TGF-β1-induced renal fibroblasts activation <i>in</i><i>vitro</i>. A unilateral ureteral obstruction (UUO) model was induced in male BALB/c mice. Mice with UUO were administered AICAR (500 mg/Kg/day) or saline intraperitoneally 1 day before UUO surgery and daily thereafter. Both kidneys were harvested 7 days after surgery for further analysis. For the in vitro studies, NRK-49F rat fibroblasts were pre-incubated with AICAR before TGF-β1 stimulation. The inhibitory effects of AICAR on signaling pathways down-stream of TGF-β1 were analyzed. In UUO model mice, administration of AICAR attenuated extracellular matrix protein deposition and the expression of α-smooth muscle actin (α-SMA), type I collagen and fibronectin. Pre-incubation of NRK-49F cells with AICAR inhibited TGF-β1-induced myofibroblast activation. Silencing of AMPKα1 by siRNA or by blocking AMPK activation with Compound C diminished the inhibitory effect of AICAR. Moreover, the inhibitory effects of AICAR on TGF-β1-mediated myofibroblast activation were associated with down-regulation of ERK 1/2 and STAT3. Our results suggest that AICAR reduces tubulointerstitial fibrosis in UUO mice and inhibits TGF-β1-induced kidney myofibroblast activation. AMPK activation by AICAR may have therapeutic potential for the treatment of renal tubulointerstitial fibrosis.</p></div