AbstractRationale & Objective Quantifying the change in proteinuria after acute kidney injury (AKI) may shed light on the pathway through which AKI contributes to kidney disease progression. Study Design Prospective cohort study of patients with chronic kidney disease (CKD) Settings & Participants 3,197 participants who were enrolled in the multicenter, prospective Chronic Renal Insufficiency Cohort (CRIC) between 7/1/2013 and 12/1/2021 Exposure AKI was defined as ≥1.5 peak to nadir inpatient serum creatinine (SCr) ascertained during a hospital admission Outcome(s) Natural log-transformed urine protein to creatinine ratio (uPCR) ascertained at annual CRIC research study visits Analytical Approach Mixed effects regression Results Among 3,197 participants, the mean age was 65 years, 44% were female, and 42% self-identified as non-Hispanic Black. The median baseline estimated glomerular filtration rate (eGFR) was 52 mL/min/1.73m2 and uPCR was 0.14 g/g. 560 patients experienced 861 episodes of AKI over a median of 6 years with most being stage 1 (68%). In the multivariable model that adjusted for blood pressure and renin angiotensin system inhibitor (RASi) use, each AKI episode was associated with a 3% increase in uPCR (relative change ratio of 1.03, [95% CI 1.01-1.05, pLimitations Hospitalized AKI with baseline CKD only, predominance of stage 1 AKI, timing of proteinuria collection was limited to annual visits, residual confounding Conclusions Among CKD patients, AKI was independently associated with worsening proteinuria (independent of changes in blood pressure or RASi use) and may reflect residual structural damage to the kidneys. However, the increase in proteinuria among patients with CKD after AKI was small.
Kwong et al. (Thu,) studied this question.