Journal
JOURNAL OF DIABETES AND ITS COMPLICATIONS
Volume 29, Issue 5, Pages 621-628Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jdiacomp.2015.04.014
Keywords
Acute hyperglycemia; Hyperglycemic clamp; Urinary microalbumin; Renal tubular impairment; Inflammation; Oxidative stress
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Funding
- National Natural Science Foundation of China [81173428, 81373864, 81200612]
- Medical Epigenetics Key Laboratory of Hormones and Development (Ministry of Health) Metabolic Diseases Hospital & Tianjin Institute of Endocrinology in Tianjin Medical University
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Aims: Growing evidences suggest that acute hyperglycemia is strongly related to kidney injury. Our study aimed to investigate the effects of acute hyperglycemia on kidney glomerular and tubular impairment in non-diabetic conscious rats. Methods: Non-diabetic conscious rats were randomly subjected to 6 h of saline (control group) or high glucose (acute hyperglycemia group) infusion. Blood glucose was maintained at 16.0-18.0 mmol/L in acute hyperglycemia group. Renal structure and function alterations, systemic/renal inflammation and oxidative stress markers were assessed, and apoptosis markers of renal inherent cells were evaluated. Results: Acute hyperglycemia caused significant injury to structure of glomerular filtration barrier, tubular epithelial cells and peritubular vascular endothelial cells. It increased urinary microalbumin (68.01 +/- 27.09 mu g/24 h vs 33.81 +/- 13.81 mu g/24 h, P = 0.014), beta 2-microglobulin, Cystatin C, urinary and serous neutrophil gelatinase-associated lipocalin levels (P < 0.05). Acute hyperglycemia decreased megalin and cubilin expression, activated systemic and renal oxidative stress as well as inflammation and promoted renal inherent cell apoptosis. Conclusions: Acute hyperglycemia causes significant injury to kidney function and structure. Compared with damages of glomerular filtration barrier, renal tubular injury may contribute more to acute hyperglycemia induced proteinuria. Activation of inflammation especially renal inflammation, oxidative stress and enhanced apoptosis may be the underlying mechanisms. (C) 2015 Elsevier Inc. All rights reserved.
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