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Kidney Week

Abstract: PO0092

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

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Wen, Yumeng, Johns Hopkins Medicine, Baltimore, Maryland, United States
  • Yang, Chen, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Menez, Steven, Johns Hopkins Medicine, Baltimore, Maryland, United States
  • Rosenberg, Avi Z., Johns Hopkins Medicine, Baltimore, Maryland, United States
  • Parikh, Chirag R., Johns Hopkins Medicine, Baltimore, Maryland, United States
Background

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 histologic changes in human ATI are limited.

Methods

We comprehensively searched human studies of ATI from 1936 to July 2019. We extracted study characteristics, clinical characterstics and histologic descriptions of ATI by bright field, immunofluorescence or electron microscopy (EM) and by immunohistochemistry. We also compared histology of tubular cell injury as a function of tissue procurement timing and etiologies.

Results

We included 292 studies comprising of 1987 patients. The majority of studies (76%) were single center case reports. The mean age of patients included was 47 years old. 39.3% of patients had hypertension and 24.9% of them had diabetes mellitus. Baseline, peak and latest creatinine were 1.29 mg/dL, 7.04 mg/dL and 1.86 mg/dL respectively. 48.9% of studies were native kidney biopsy cases, of which 86.7% were performed after serum creatnine peaked. There were significant amount of missing data in these clinical characteristics reported across studies. We identified 16 histologic descriptions used to report tubular injury (shown in Figure 1), including tubular cell sloughing (39.4%), tubular epithelial flattening/simplification (37.7%), tubular dilatation (37.3%), tubular cell necrosis (31.9%), regenerative changes (28.1%) and tubular cell vacuolization (26.4%). There was no difference in tubular injury histology either before or after creatinine peaked or between etiologies. EM and immunohistochemistry were used in minority of studies.

Conclusion

Tubular injury manifests with diverse histological changes. Efforts to establish protocols to harmonize biopsy practices, handle kidney biopsy and report results across clinical practice are needed to improve our understanding of this complex disease.