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Am J Kidney Dis. 2016 Feb;67(2):243-50. doi: 10.1053/j.ajkd.2015.09.019. Epub 2015 Nov 4.

Clinical Characteristics and Outcomes of Renal Infarction.

Author information

1
Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul, Korea.
2
Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, Seoul, Korea.
3
Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea.
4
Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
5
Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
6
Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea.
7
Department of Internal Medicine, Wonju Severance Christian Hospital, Wonju, Korea.
8
Department of Internal Medicine, Kyung Hee University College of Medicine, Seoul, Korea.
9
Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea.
10
Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul, Korea. Electronic address: cslimjy@snu.ac.kr.

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 ≥ 0.3mg/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)<60mL/min/1.73m(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<60mL/min/1.73m(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<60mL/min/1.73m(2), ESRD, and death.

KEYWORDS:

Renal infarction; acute kidney injury (AKI); cardiogenic etiology; case series; end-stage renal disease (ESRD); kidney function; mortality; outcomes; parenchymal perfusion defect; reduced glomerular filtration rate; renal blood flow

PMID:
26545635
DOI:
10.1053/j.ajkd.2015.09.019
[Indexed for MEDLINE]

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