In experimental septic acute renal failure, urinary analysis is used to help diagnose and classify renal injury. However, the scientific basis for such use has not been systematically evaluated. Thus, we appraised the value of common urinary findings for the diagnosis and classification of experimental septic acute renal failure.
Academic medical center and university-based research laboratory.
Experimental studies describing urinary biochemistry, derived indexes, and microscopy in septic acute renal failure.
Twenty-seven articles fulfilled all inclusion criteria. Due to heterogeneity, no formal quantitative analysis was possible. The methods for induction of sepsis and models were variable. The urinary sodium, fractional excretion of sodium, and urine osmolality were reported in only four (15%), 21 (78%), and seven (26%) studies, respectively. The fractional excretion of sodium exhibited a decrease, no change, or an increase from baseline in 11 (52%), five (24%), and five (24%) studies, respectively. The urine osmolality decreased from baseline in all endotoxin-induced models but showed an early transient increase in six (22%) studies of cecal-ligation perforation. Proteinuria or urinary enzymuria was reported in only seven (26%) studies. Urinary microscopy was described in one study. Only ten studies (37%) simultaneously reported on histopathology. In all these studies, histology either was normal or showed minor ultrastructural changes on electron microscopy.
No conclusions are possible on how several urinary tests perform in diagnosing or classifying acute renal failure or in predicting the presence of acute tubular necrosis in experimental sepsis. Additional research is necessary to define the diagnostic and prognostic value of urinalysis in experimental sepsis.
From the Division of Critical Care Medicine, University of Alberta Hospital, University of Alberta, Edmonton, AB, Canada (SMB); Department of Intensive Care, Austin Hospital, Melbourne, Australia (SMB, CL, LW, RB); Department of Medicine, Melbourne University, Melbourne, Australia (RB); Howard Florey Institute, University of Melbourne, Melbourne, Australia (CL, LW, CNM); and Department of Nephrology, Charité Campus Mitte, Berlin, Germany (CL).
Supported, in part, by clinical fellowships from the Canadian Institutes for Health Research and the Alberta Heritage Foundation for Medical Research Clinical Fellowship (SMB), a Royal College of Physicians and Surgeons of Canada Detweiler Traveling Fellowship (SMB), and a grant from the Else Kröner-Fresenius Foundation (CL).
The authors have not disclosed any potential conflicts of interest.
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