TY - JOUR
T1 - A Systematic Review of Clinical Characteristics and Histologic Descriptions of Acute Tubular Injury
AU - Wen, Yumeng
AU - Yang, Chen
AU - Menez, Steven P.
AU - Rosenberg, Avi Z.
AU - Parikh, Chirag R.
N1 - Funding Information:
CRP was supported by the National Institutes of Health grants R01DK-93770 and R01HL-085757. He is also participating in the NIDDK sponsored Kidney Precision Medicine Project UH3DK114866. We appreciate the assistance from the librarians in the Icahn School of Medicine at Mount Sinai and Johns Hopkins University School of Medicine in obtaining study report with unavailable abstract or full text. YW, CY, and CRP participated in the study design. YW, CY, and SPM participated in abstract and full text review. YW carried out statistical analysis. YW, CY, SPM, AZR, and CRP drafted and revised the paper, and all authors approved the final version.
Funding Information:
CRP was supported by the National Institutes of Health grants R01DK-93770 and R01HL-085757 . He is also participating in the NIDDK sponsored Kidney Precision Medicine Project UH3DK114866. We appreciate the assistance from the librarians in the Icahn School of Medicine at Mount Sinai and Johns Hopkins University School of Medicine in obtaining study report with unavailable abstract or full text.
Publisher Copyright:
© 2020 International Society of Nephrology
PY - 2020/11
Y1 - 2020/11
N2 - 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, and immunohistochemistry. We compared ATI histology as a function of tissue procurement type, timing, and etiologies. Results: We included 292 studies comprising a total of 1987 patients. The majority of studies (222 of 292, 76%) were single-center case reports. The mean age of included patients was 47 years. 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 performed mostly after peak creatinine (86.7%, 391 of 451). We identified 16 histologic descriptions of tubular injury, including tubular cell sloughing (115 of 292, 39.4%), tubular epithelial flattening/simplification (110 of 292, 37.7%), tubular dilatation (109 of 292, 37.3%), and tubular cell necrosis (93 of 292, 31.8%). There was no difference in tubular injury histology among different tissue procurement types (native kidney biopsy, transplant kidney biopsy, and autopsy), among different etiologies, or between different tissue procurement timing (before or after creatinine peaks in native kidneys). Electron microscopy and immunohistochemistry were used in a minority of studies. Conclusion: ATI manifests with diverse histologic changes. Efforts to establish protocols to harmonize biopsy practices, to handle kidney biopsy for tissue interrogation, and to report results across clinical practice are needed to improve our understanding of this complex disease.
AB - 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, and immunohistochemistry. We compared ATI histology as a function of tissue procurement type, timing, and etiologies. Results: We included 292 studies comprising a total of 1987 patients. The majority of studies (222 of 292, 76%) were single-center case reports. The mean age of included patients was 47 years. 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 performed mostly after peak creatinine (86.7%, 391 of 451). We identified 16 histologic descriptions of tubular injury, including tubular cell sloughing (115 of 292, 39.4%), tubular epithelial flattening/simplification (110 of 292, 37.7%), tubular dilatation (109 of 292, 37.3%), and tubular cell necrosis (93 of 292, 31.8%). There was no difference in tubular injury histology among different tissue procurement types (native kidney biopsy, transplant kidney biopsy, and autopsy), among different etiologies, or between different tissue procurement timing (before or after creatinine peaks in native kidneys). Electron microscopy and immunohistochemistry were used in a minority of studies. Conclusion: ATI manifests with diverse histologic changes. Efforts to establish protocols to harmonize biopsy practices, to handle kidney biopsy for tissue interrogation, and to report results across clinical practice are needed to improve our understanding of this complex disease.
KW - acute kidney injury
KW - acute tubular injury
KW - acute tubular necrosis
KW - histology
KW - pathology
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U2 - 10.1016/j.ekir.2020.08.026
DO - 10.1016/j.ekir.2020.08.026
M3 - Article
C2 - 33163720
AN - SCOPUS:85092938304
SN - 2468-0249
VL - 5
SP - 1993
EP - 2001
JO - Kidney International Reports
JF - Kidney International Reports
IS - 11
ER -