Dendrobium officinale Kimura & Migo polysaccharide inhibits hyperglycaemia-induced kidney fibrosis via the miRNA-34a-5p/SIRT1 signalling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Fibrosis is a fundamental change occurring in impaired renal function and plays an important role in the progression of diabetic kidney disease (DKD). Dendrobium officinale Kimura & Migo polysaccharide (DOP), a primary active component of Dendrobium officinale Kimura & Migo, is reported to act on reducing blood glucose, suppressing inflammation. However, the anti-fibrosis effect of DOP in the treatment of DKD is still unclear. AIM OF THE STUDY: To explore the therapeutic effect of DOP on renal fibrosis in DKD. MATERIALS AND METHODS: We used db/db mice as a DKD model and administered DOP by oral gavage. The expression of miRNA-34a-5p, SIRT1, and fibrosis molecules (TGF-ß, CTGF, and a-SMA) were detected in renal tissue. Human renal tubular epithelium cells (HK-2) were cultured with 5.5 mM glucose (LG) or 25 mM glucose (HG), and intervened with 100-400 µg/ml DOP. The changes of the above indicators were observed in vitro. RESULTS: MiRNA-34a-5p was mainly localised in the nucleus and increased expression in the DKD mice. Inhibition or excitation of miRNA-34a-5p is involved in renal fibrosis by regulating SIRT1. DOP could depress the miRNA-34a-5p/SIRT1 signalling pathway to relieve renal fibrosis. Moreover, DOP has outstanding results in the treatment of DKD through hypoglycaemic action and weight reduction. CONCLUSIONS: DOP plays a protective role in arresting or slowing the progression of fibrosis, which may provide a novel clinical treatment strategy for DKD.

Effects of calcitriol on peripheral endothelial progenitor cells and renal renovation in rats with chronic renal failure.

BACKGROUND: The role of calcitriol (1,25-dihydroxyvitamin D3 or 1,25-(OH)2D3) in physiological processes, such as anti-fibrosis, anti-inflammation, and immunoregulation is known; however, its role in the remodeling of the glomerular capillary endothelium in rats with chronic renal failure (CRF) remains unclear. METHODS: Here, we analyzed the role/number of endothelial progenitor cells (EPCs), renal function, and pathological alterations in rats with CRF, and compared the results before and after supplementation with calcitriol in vivo. RESULTS: Amongst the three experimental groups (sham group, CRF group, and calcitriol-treated group (0.03 µg/kg/d), we observed substantially elevated cell adhesion and vasculogenesis in vivo in the calcitriol-treated group. Additionally, lower levels of serum creatinine (Scr) and blood urea nitrogen (BUN) was recorded in the calcitriol-treated group than the CRF group (p > 0.05). Calcitriol treatment also resulted in an improvement in renal pathological injury. CONCLUSIONS: Thus, calcitriol could ameliorate the damage of glomerular arterial structural and renal tubules vascular network integrity, maybe through regulating the number and function of EPCs in the peripheral blood of CRF rats. Treatment with it may improve outcomes in patients with renal insufficiency or combined cardiac insufficiency. Calcitriol could ameliorate CRF-induced renal pathological injury and renal dysfunction by remodeling of the glomerular capillary endothelium, thus, improving the function of glomerular endothelial cells.

Blood pressure variability is independent of systolic pressure in adolescent and young adult patients undergoing hemodialysis.

BackgroundPre-dialysis blood pressure variability (BPV) in adolescent and young-adult maintenance hemodialysis (MHD) patients remains unknown. This study aimed to show the degree of 44-h BPV and to explore its related risk factors in adolescent and young-adult MHD patients.MethodsOne hundred and fifty-three hemodialysis patients aged from 14 to 29 were selected from 11 medical facilities in Guizhou, China. Variability independent of the mean BP (VIM) obtained by 44-h ambulatory BP monitoring was used to calculate BPV. Baseline characteristics, physical measurement, and laboratory parameters were compared between different groups categorized by quartiles of VIM of systolic BP (VIMSBP).ResultsVIMSBP levels were found to be positively related to interdialytic weigh growth rate (IDWG), serum phosphorus, and serum intact parathyroid hormone (iPTH; Spearman correlation coefficients 0.474, 0.229, and 0.437, respectively; P<0.05 for all) and negatively related to hemoglobin (Hb) and albumin (-0.317, P<0.001, and -0.166, P=0.04, respectively) in all adolescent and young-adult MHD patients. In multiple linear regression analysis, IDWG, Hb, serum phosphorus, and serum iPTH had an independent association with VIMSBP.ConclusionOur analysis revealed an independent association of BPV with IDWG, Hb, serum phosphorus, and serum iPTH among adolescent and young-adult patients undergoing dialysis. This observation warrants further study.

Serum Phosphorus and Progression of CKD and Mortality: A Meta-analysis of Cohort Studies.

BACKGROUND: Recent studies have indicated that phosphorus may play an independent pathogenic role in chronic kidney disease (CKD) progression, but some of those studies were underpowered and yielded inconsistent results. STUDY DESIGN: Systematic review and meta-analysis. SETTING & POPULATION: Non-dialysis-dependent patients with CKD (transplant recipients were excluded). SELECTION CRITERIA FOR STUDIES: Studies assessing the risk ratio of serum phosphorus level on kidney failure and mortality for non-dialysis-dependent patients with CKD published from January 1950 to June 2014 were included following systematic searching of MEDLINE, EMBASE, and the Cochrane Library. PREDICTOR: Serum phosphorus level. OUTCOME: Kidney failure, defined as doubled serum creatinine level, 50% decline in estimated glomerular filtration rate, or end-stage kidney disease. RESULTS: In 12 cohort studies with 25,546 patients, 1,442 (8.8%) developed kidney failure and 3,089 (13.6%) died. Overall, every 1-mg/dL increase in serum phosphorus level was associated independently with increased risk of kidney failure (hazard ratio, 1.36; 95% CI, 1.20-1.55) and mortality (hazard ratio, 1.20; 95% CI, 1.05-1.37). LIMITATIONS: Existence of potential residual confounding could not be excluded. CONCLUSIONS: This meta-analysis suggests an independent association between serum phosphorus level and kidney failure and mortality among non-dialysis-dependent patients with CKD and suggests that large-scale randomized controlled trials should target disordered phosphorus homeostasis in CKD.