Journal article
Subclinical chronic kidney disease modifies the diagnosis of experimental acute kidney injury
L Succar, TJ Pianta, T Davidson, JW Pickering, ZH Endre
Kidney International | ELSEVIER SCIENCE INC | Published : 2017
Abstract
Extensive structural damage within the kidney must be present before serum creatinine increases. However, a subclinical phase of chronic kidney disease (CKD) usually goes undetected. Here we tested whether experimental subclinical CKD would modify functional and damage biomarker profiles of acute kidney injury (AKI). Subclinical CKD was induced in rats by adenine or aristolochic acid models but without increasing serum creatinine. After prolonged recovery (three to six weeks), AKI was induced with a subnephrotoxic dose of cisplatin. Urinary levels of kidney injury molecule-1 (KIM-1), cytochrome C, monocyte chemotactic protein-1 (MCP-1), clusterin, and interleukin-18 increased during CKD indu..
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Awarded by Australian National Health and Medical Research Council (NHMRC)
Funding Acknowledgements
We are grateful to the late Associate Professor Philip Wallace Peake for his mentorship and contribution to this study. We also thank the Anatomical Pathology Unit at South East Sydney Laboratory Services, at the Prince of Wales Hospital, for assistance with processing tissue histology. We gratefully acknowledge funding for LS by the Australian National Health and Medical Research Council (NHMRC) Grant APP1079502, for the Chronic Kidney Disease Centre of Research Excellence (CKD.CRE).