Urine metabolic biomarkers for mouse ischemic acute kidney injury and nephrotoxic acute kidney injury

Metabolomics:Open Access

ISSN: 2153-0769

Open Access

Urine metabolic biomarkers for mouse ischemic acute kidney injury and nephrotoxic acute kidney injury

4th International Conference and Exhibition on Metabolomics & Systems Biology

April 27-29, 2015 Philadelphia, USA

Tafadzwa Chihanga, Qing Ma, Prasad Devarajan and Michael A Kennedy

Posters-Accepted Abstracts: Metabolomics

Abstract :

Acute Kidney Injury (AKI) previously known as acute renal failure, refers to abrupt reduction in renal function or urine output, occurring over hours or days, caused by kidney damage due to sepsis, respiratory failure, heart failure, trauma, major surgery, burns, toxic insult caused by medications and contrast agents used for imaging. AKI accounts for 1% of all hospital admissions, complicates 7% of hospitalizations and is present in up to 20% of critically ill patients. Overall mortality associated with AKI is estimated at 45-70% mortality associated with AKI in intensive care unit patients requiring renal replacement therapy is 50-60% and more than 2 million die from AKI each year. The aim of the present study was to examine the effects of Ischemia and Nephrotoxin induced AKI on the urine metabolomic profile. Two groups of Swiss-Webster mice were injected with cisplatin or renal ischemia reperfusion injuies (IRI) were performed, respectively, on the mice to induce AKI. Serum creatinine and urine neutrophil gelatinase-associated lipocalin levels were tested to confirm AKI after the injection and the surgery. After analysis of NMR data, significant metabolic differences were found. Metabolic differences could result in the discovery of new biomarkers for AKI. Comparison of the differences between the IRI and cisplatin treated mice could give insight to a common biomarker for AKI.

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