To the Editor:
Renal infarction (RI) is a rare condition resulting from the acute disruption of renal blood flow in the renal arteries or their branches. Heart disease, renal artery injury, hypercoagulability, and idiopathic origins are the causes of renal infarction. Despite urokinase, heparin, warfarin, and antiplatelet treatment, RI can lead to acute kidney injury (AKI), chronic kidney disease (CKD), end-stage renal disease, and death [1], [2], [3].
In the previous issue of this journal, Yang et al [4] presented a retrospective single-center study for risk factors and outcome of RI. In their study, AKI was found in 34.8% of patients. Diabetes mellitus and high C-reactive protein were independent predictors for AKI on multivariate analysis. RI progressed to CKD in 27.4% of patients, and old age was an independent risk factor for CKD. Surprisingly, AKI history was inversely proportional to the development of CKD [4].
In contrast, the previous large meta-analysis showed that patients with AKI had a higher risk for developing CKD (pooled adjusted hazard ratio, 8.8; 95% confidence interval, 3.1–25.5) [5]. Yang et al [4] explained that the inverse association between AKI and CKD progression probably resulted from wrong patient selection because the long-term analysis was conducted only from the patients who survived. They stated that excluded patients had higher incidence of AKI, diabetes mellitus and malignancy. These patients also had higher Charlson comorbidity index score and C-reactive protein level.
In conclusion, Cox regression analyses of risk factors associated with the estimated glomerular filtration rate decreasing to < 60 mL/min/1.73 m2 after 1 year in RI had selection bias [4]. The authors may need to further analyze long-term outcomes of RI using not only CKD but also other composite outcomes such as death, increasing creatinine more than 2 times, or hospitalization.
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