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Vanillin as a new modulator candidate for renal injury induced by cisplatin in experimental rats

Posted by M M.Elseweidy, S E.Elswefy, M Shawky, et al. on 2017-09-18 20:02:59


Cisplatin is commonly prescribed for the treatment of various solid tumors but its use is limited due to certain side effects and renal injury is a true example. Oxidative stress and inflammation may contribute to the cisplatin induced nephrotoxicity. Accordingly, we evaluated the effect of oral vanillin intake (100 mg/kg body weight) daily for 4 weeks to combat this hazard. The present results have demonstrated significant attenuation of oxidative stress and renal injury where reduced glutathione (GSH) showed significant increase along with malondialdehyde (MDA) decrease. Fibrotic markers like fibroblast growth factor-23 (FGF-23), transforming growth factor-β1 (TGF-β1), inflammatory mediators such as nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α) showed also significant decrease in vanillin treated rats as compared with the control group.

Renal function showed also significant improvement where urea and creatinine demonstrated significant decrease and the histopathological study presented a good support to the biochemical markers results. Our conclusion that vanillin is a potent antioxidant, anti-inflammatory and anti-fibrotic agent. Additionally, it is a good modulator candidate for the renal injury induced by cisplatin intake.


Insulin resistance is prevalent worldwide and is associated with many metabolic diseases, in particular, type 2 diabetes mellitus (T2DM), obesity, nonalcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS) and metabolic syndrome (MetS). Angiopoietin-like protein 8 (ANGPTL8), a newly-identified secreted protein composing of 198 amino acids, is enriched in the liver of human. Considering its promising potential for β-cell proliferation and therapeutic prospect for diabetes, ANGPTL8 has aroused extensive interests. However, a recent collaborative study confirmed that ANGPTL8 didn’t stimulate dramatic β-cell regeneration. At present, a controversial scientific discussion on whether and how ANGPTL8 regulate insulin resistance has been ongoing. Interestingly, several in vitro and in vivo studies have suggested the complex roles of ANGPTL8 in insulin resistance. Data resulting from cross-sectional and longitudinal researches in human individuals involving the influence of ANGPTL8 on the development of insulin resistance were controversial. We therefore summarize currently clinical literature to exploit whether this exciting hormone could be applied for clinical application as a potential clinical biomarker to predict insulin resistance and related disorders.


Calcineurin, a serine/threonine phosphatase is a calcium dependent protein which on activation triggers transcriptional up regulation of inflammatory genes associated with inflammation in the arteries and progressive formation of plaques in CAD. The present investigation is aimed to study the possible association of Calcineurin encoding gene PPP3R1 (CnB 5I/5D) polymorphism in correlation with serum levels of calcineurin in coronary artery disease (CAD). A total of 300 angiographically documented CAD patients and 300 age, gender ethnicity matched healthy controls were recruited for the study. Serum Calcineurin levels were estimated by enzyme-linked immunosorbent assay (ELISA) and genotypes were determined based on PCR-RFLP. The CnB 5I/5D variation was found to be significantly associated with CAD (p < 0.03), correlated to elevated serum calcineurin levels encoded by (< 0.01) 5I/5D allele authenticated by Insilco analysis. Multiple logistic regression analysis also confirmed these findings [adjusted OR for DD genotype was 3.19 (95% CI 1.40–7.24) and p = 0.001]. The results suggest that 5-base pair deletion results in increased serum calcineurin levels and may trigger up regulation of calcineurin which mediates vascular inflammation and atherosclerosis in CAD.


Introduction: Total pancreatectomy (TP) markedly improves quality of life in children with chronic pancreatitis (CP), but results in brittle, insulinopenic diabetes. TP with IAT (TPIAT) may preserve insulin secretion. Minimal data are available regarding TPIAT in pediatric patients (Pts).

Methods: Between 2009-2016, TPIAT was performed in 13 Pts (7 boys) with median age 10.3 yrs (range 7-17 yrs). Six (46%) had a PRSS1 (protease, serine, 1) mutation, 2 (15.4%) had a CFTR (Cystic fibrosis transmembrane conductance regulator) mutation, 2 (15.4%) had combined CFTR/SPINK1 (serine protease inhibitor, Kazal-type, 1) mutations. All were euglycemic prior to TPIAT (normal fasting glucose and HbA1c; normal response to mixed meal tolerance test in a subset). Islet cells, isolated after TP, were infused in the portal vein. Pts were kept on an insulin infusion for (average) 6.8 days, then switched to MDI, with tight glycemic control.

Results: Six months after TPIAT, 5 Pts (38%) did not require insulin (HbA1c 5.5-6.1%), 3 Pts (23%) were on basal insulin only (0.03-0.35 U/Kg/day), with HbA1c of 5.5-6.7%, and 5 Pts (39%) required basal/bolus insulin therapy (0.5-1 U/Kg/day, median 0.6) with a HbA1c of 6.8-10.2%, median 7.6. Insulin requirements did not correlate with BMI-SDS (r=0.18) or number of islets/kg infused (r=-0.21). Pts with PRSS1 mutation had borderline lower (p=0.05, t-test) insulin requirements (0.1 U/kg/day) than Pts with CFTR mutation (0.46 U/kg/day). Ten Pts (77%) discontinued pain medication with complete pain resolution within 3 months. Complications including pyloric stenosis, intraabdominal adhesions, and gastroparesis occurred in 3 Pts; Spontaneous/exercise-induced hypoglycemia in 2 Pts.

Conclusions: TPIAT is an effective treatment for CP in children and adolescents. Within 6 months, it provided pain resolution in 77% and allowed good glycemic control with no insulin or low dose basal insulin in 61% of patients in this series.

Renalase in Children with Glomerular Kidney Diseases

Posted by Pitor S, Joanna P, Urszula D, et al. on 2017-08-16 20:09:20


Studies suggest that renalase, a renal catecholamine-inactivating enzyme, plays a major role in the pathogenesis of kidney and cardiovascular diseases in adults. This study seeks to determine the role of renalase in children with glomerular kidney diseases. We evaluated the serum renalase, arterial stiffness, intima-media thickness, blood pressure, and clinical and biochemical parameters in 78 children (11.9 ± 4.6 years of age) with glomerulopathies such as idiopathic nephrotic syndrome (40 cases), IgA nephropathy (12 cases), Henoch-Schönlein nephropathy (12 cases), and other glomerulopathies (14 cases). The control group consisted of 38 healthy children aged 11.8 ± 3.3 years. The mean renalase was 25.74 ± 8.94 μg/mL in the glomerulopathy group, which was not significantly different from the 27.22 ± 5.15 in the control group. The renalase level did not differ among various glomerulopathies either. However, proteinuric patients had a higher renalase level than those without proteinuria (28.43 ± 11.71 vs. 24.05 ± 6.23, respectively; p = 0.03). In proteinuric patients, renalase correlated with daily proteinuria. In the entire glomerulopathy group, renalase correlated with age, systolic central blood pressure (BP), diastolic peripheral and central BP, mean peripheral and central BP; peripheral diastolic BP Z-score, glomerular filtration rate, cholesterol, triglycerides, and pulse wave velocity. We conclude that in children with glomerulopathies renalase, although basically not enhanced, may underlie blood pressure elevation and arterial damage.

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