Search

To investigate the role of neutrophil gelatinase-associated lipocalin in the evaluation of renal function, nutrition, anemia and inflammation in patients with chronic kidney diseases. A total of 302 patients with chronic kidney diseases were selected, and their clinical data, blood neutrophil gelatinase-associated lipocalin levels, renal function, nutrition, anemia, inflammation and calcium, and phosphorus metabolism were analyzed. Serum neutrophil gelatinase-associated lipocalin level increased with the progression of chronic kidney diseases. Higher neutrophil gelatinase-associated lipocalin levels were observed in patients with chronic kidney diseases stage 3b compared with healthy individuals (P < 0.05), while the patients with chronic kidney diseases stage 5 showed higher levels compared with other chronic kidney diseases stages (P < 0.01). Moreover, the ROC curve showed that neutrophil gelatinase-associated lipocalin had a better diagnostic performance from the chronic kidney diseases stage 3b to 5 (P < 0.05). In addition, the serum neutrophil gelatinase-associated lipocalin levels in patient with chronic kidney diseases were negatively correlated with body mass index, number of red blood cells, hemoglobin, transferrin, the estimatedglomerular filtration rate (eGFR), serum calcium (P < 0.01); and were positively correlated with mean arterial blood pressure, blood BUN, SCr and alpha 1 microglobulin, beta 2 microglobulin, urinary inhibition C, homocysteine, PTH levels, neutrophils ratio, free serum ferritin and c-reactive protein (P < 0.01); while no significant correlation was found with gender, and age (P > 0.05). Serum neutrophil gelatinase-associated lipocalin levels are closely related to renal function injury, inflammatory response and anemia-related indicators in patients with chronic kidney diseases, and thus could be used as a diagnostic biomarker for evaluating the degree of renal injury and related complications in patients with chronic kidney diseases. [ABSTRACT FROM AUTHOR]

Aims: Type 2 diabetes mellitus (T2DM) is commonly complicated by renal impairment. Polyethylene glycol loxenatide (PEX168) is a novel long‐acting glucagon‐like peptide‐1 receptor agonist for T2DM. PEX168 pharmacokinetics was studied to identify requirements for dose‐modification in T2DM complicated by renal impairment. Methods: This was a single‐centre, open‐labelled, parallel‐group, single‐dose, phase I clinical trial of patients with mild and moderate renal impairment, and with or without T2DM. Age‐, sex‐ and body mass index‐matched subjects with normal renal function, and with or without T2DM were recruited as controls. Subjects received a single abdominal subcutaneous injection of PEX168 200 μg. Pharmacokinetic samples were taken at 0, 24, 48, 72, 96, 120, 144, 216, 312, 480, 648 and 720 hours. Results: Twenty‐three patients were included in the pharmacokinetics analysis. Vz/F and CL/F were lower in the moderate impairment group than in the other groups. The mean t1/2 (163 hours) in the moderate impairment group was prolonged compared to the mild impairment (117 hours) and normal (121 hours) groups. AUC0–inf increased by 13 and 100.7% in patients with mild and moderate renal impairment, respectively. Most adverse events were mild gastrointestinal disorders, with only 1 serious adverse event observed. Conclusion: A single dose of 200 μg of PEX168 was in general well tolerated in patients with renal impairment. The in vivo clearance rate of PEX168 in patients with moderate renal impairment is slower than in patients with mild renal impairment and normal renal function and dose adjustment might be required (ClinicalTrials.org #NCT02467790). [ABSTRACT FROM AUTHOR]

Purpose: To investigate whether Niban protein plays a role in renal interstitial fibrosis by regulating renal tubular epithelial cell apoptosis and explore the underlying mechanism. Methods: Unilateral ureteral obstruction (UUO) model was performed in C57B/6J mice, and divided into sham operation group and groups of days 3, days 7, and days 14. Niban expression was detected by immunohistochemistry and Western blot. TUNEL assays were used to detected apoptosis. Niban siRNA and overexpression Niban plasmid were transfected in HK-2 cells respectively to explore apoptosis related mechanisms of Niban during angiotensin II (AngII) – and endoplasmic reticulum (ER) stress-induced injury. Results: With the development of obstruction, Niban's expression decreased gradually while apoptosis increased. Silencing of Niban not only increased the AngII- and ER stress-induced apoptosis, but also promoted the expression of caspase 8, caspase 9, Bip, and Chop. Overexpression of Niban reduced AngII-induced apoptosis and the expression of caspase 8 and caspase 9. Conclusions: Niban protein is involved in apoptosis regulation in HK-2 cells, and most likely via caspase-dependent pathway. [ABSTRACT FROM AUTHOR]