Clinical Characteristics and Outcomes of Renal Infarction
- Authors
- Oh, Yun Kuy; Yang, Chul Woo; Kim, Yong-Lim; Kang, Shin-Wook; Park, Cheol Whee; Kim, Yon Su; Lee, Eun Young; Han, Byoung Geun; Lee, Sang Ho; Kim, Su-Hyun; Lee, Hajeong; Lim, Chun Soo
- Issue Date
- Feb-2016
- Publisher
- W. B. Saunders Co., Ltd.
- Keywords
- Renal infarction; parenchymal perfusion defect; renal blood flow; acute kidney injury (AKI); mortality; kidney function; reduced glomerular filtration rate; end-stage renal disease (ESRD); cardiogenic etiology; outcomes; case series
- Citation
- American Journal of Kidney Diseases, v.67, no.2, pp 243 - 250
- Pages
- 8
- Journal Title
- American Journal of Kidney Diseases
- Volume
- 67
- Number
- 2
- Start Page
- 243
- End Page
- 250
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/9408
- DOI
- 10.1053/j.ajkd.2015.09.019
- ISSN
- 0272-6386
1523-6838
- Abstract
- Background: Renal infarction is a rare condition resulting from an acute disruption of renal blood flow, and the cause and outcome of renal infarction are not well established. Study Design: Case series. Setting & Participants: 438 patients with renal infarction in January 1993 to December 2013 at 9 hospitals in Korea were included. Renal infarction was defined by radiologic findings that included single or multiple wedge-shaped parenchymal perfusion defects in the kidney. Predictor: Causes of renal infarction included cardiogenic (n = 244 [55.7%]), renal artery injury (n = 33 [7.5%]), hypercoagulable (n = 29 [6.6%]), and idiopathic (n = 132 [30.1%]) factors. Outcomes: We used recurrence, acute kidney injury (AKI; defined as creatinine level increase >= 0.3 mg/dL within 48 hours or an increase to 150% of baseline level within 7 days during the sentinel hospitalization), new-onset estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m(2) (for >3 months after renal infarction in the absence of a history of decreased eGFR), end-stage renal disease (ESRD; receiving hemodialysis or peritoneal dialysis because of irreversible kidney damage), and mortality as outcome metrics. Results: Treatment included urokinase (n = 19), heparin (n = 342), warfarin (n = 330), and antiplatelet agents (n = 157). 5% of patients died during the initial hospitalization. During the median 20.0 (range, 1-223) months of follow-up, 2.8% of patients had recurrent infarction, 20.1% of patients developed AKI, 10.9% of patients developed new-onset eGFR, 60 mL/min/1.73 m(2), and 2.1% of patients progressed to ESRD. Limitations: This was a retrospective study; it cannot clearly determine the specific causal mechanism for certain patients or provide information about the causes of mortality. 16 patients were excluded from the prognostic analysis. Conclusions: Cardiogenic origins were the most important causes of renal infarction. Despite aggressive treatment, renal infarction can lead to AKI, new-onset eGFR < 60 mL/min/1.73 m(2), ESRD, and death. (C) 2016 by the National Kidney Foundation, Inc.
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