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Hyperglycaemia, inflammation, RAS activation: Three culprits to blame for acute kidney injury emerging in healthy rats during general anaesthesia
Author(s) -
EFRATI SHAI,
BERMAN SYLVIA,
ABU HAMAD RAMZIA,
EL NAKIB RANIN,
CHANIMOV MICHAEL,
SIMANTOV YARIV,
WEISSGARTEN JOSHUA
Publication year - 2012
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2012.01638.x
Subject(s) - medicine , general anaesthesia , renal function , inflammation , acute kidney injury , insulin , angiotensin ii , anesthesia , endocrinology , blood pressure
Aim: Major surgery under general anaesthesia might evoke acute kidney injury (AKI), sometimes culminating in end stage renal disease. We investigated the roles of hyperglycaemia, inflammation and renin‐angiotensin system (RAS) activation in induction of AKI following anaesthesia by different anaesthetic drugs and/or regimens. Methods: Ninety‐four Sprague‐Dawley rats underwent 1 h‐anaesthesia by various protocols, including repeated blood glucose and insulin measurements. Blood samples and kidneys were allocated at sacrifice, for evaluation of renal function, inflammatory status and Angiotensin‐II availability. Results: Hyperglycaemia emerged in unconscious rats irrespective of anaesthetic drug choice or anaesthesia regimen. Insulin increase correlated with hyperglycaemia levels. Levels of Cystatin‐C, as well as serum and urine neutrophil gelatinase‐associated lipocain (NGAL), were significantly augmented. Serum transforming growth factor beta (TGF‐β) and interleukins (IL)‐1β, ‐4, ‐6, and ‐10 were significantly increased. Intra‐renal Angiotensin‐II, TGF‐β, IL‐6 and‐10 were significantly increased. IL‐1 was decreased. IL‐4 remained unaltered. Conclusions: Acute hyperglycaemia, systemic and intra‐renal inflammation and RAS activation were independently triggered by induction of anaesthesia. Each confounder aggravated the impacts of the others, bringing about concomitant deterioration of renal function. Increased insulin secretion attenuated but did not abolish hyperglycaemia. Systemic inflammation was counterforced by anti‐inflammatory cytokines, whereas intra‐renal inflammation persisted, so that AKI progressed unopposed.