Renal tubular damage may contribute more to acute hyperglycemia induced kidney injury in non-diabetic conscious rats

Abstract 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 μg/24 h vs 33.81 ± 13.81 μg/24 h, P = 0.014), β2-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.