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.
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.
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.
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 m2 (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.
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 m2, and 2.1% of patients progressed to ESRD.
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.
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 m2, ESRD, and death.