A Systematic Review of Clinical Characteristics and Histologic Descriptions of Acute Tubular Injury

Abstract Introduction The term acute tubular injury (ATI) represents histopathologic renal tubular injury and often manifests clinically as acute kidney injury (AKI). Studies systematically summarizing the clinical presentation and histological changes in human ATI are limited. Methods We used a comprehensive search strategy to search human studies of ATI from 1936 to July 2019. We extracted study characteristics, clinical characteristics and histologic descriptions of ATI by bright field, immunofluorescence, electron microscopy (EM) and by immunohistochemistry. We compared ATI histology as a function of tissue procurement type, timing and etiologies. Results We included 292 studies comprising of 1987 patients. The majority of studies (222/292, 76%) were single-center case reports. The mean age of included patients was 47 years old. In native kidney biopsy cases, baseline, peak and latest creatinine were 1.3 mg/dL, 7.19 mg/dL and 1.85 mg/dL respectively, and biopsy was mostly performed after peak creatinine (86.7%, 391/451). We identified 16 histologic descriptions of tubular injury, including tubular cell sloughing (115/292, 39.4%), tubular epithelial flattening/simplification (110/292, 37.7%), tubular dilatation (109/292, 37.3%) and tubular cell necrosis (93/292, 31.8%). There was no difference in tubular injury histology between different tissue procurement types (native kidney biopsy, transplant kidney biopsy and autopsy), between different etiologies or between different tissue procurement timing (before or after creatinine peaks in native kidneys). EM and immunohistochemistry were used in minority of studies. Conclusions ATI manifests with diverse histologic changes. Efforts to establish protocols to harmonize biopsy practices, handle kidney biopsy for tissue interrogation and report results across clinical practice are needed to improve our understanding of this complex disease.