Yun Kuy Oh1, Chul Woo Yang2, Yong-Lim Kim3, Shin-Wook Kang4, Cheol Whee Park2, Yon Su Kim5, Eun Young Lee6, Byoung Geun Han7, Sang Ho Lee8, Su-Hyun Kim9, Hajeong Lee5, Chun Soo Lim10. 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.
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.
Authors: Jihyun Yang; Jun Yong Lee; Young Ju Na; Sung Yoon Lim; Myung-Gyu Kim; Sang-Kyung Jo; Wonyong Cho Journal: Kidney Res Clin Pract Date: 2016-05-11