Abstract

Background Renal dysfunction after acute kidney injury (AKI) is common, potentially modifiable, but poorly understood. Acute kidney disease (AKD) describes renal dysfunction 7 to 90 days after AKI and is determined by percentage change in creatinine from baseline. Chronic kidney disease (CKD) is defined as the estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m2 persisting for more than 90 days. We compared CKD incidence using both creatinine- and cystatin C-based GFR with AKD incidence at 90 days in AKI survivors. Methods A prospective cohort study was conducted in a Swedish intensive care unit (ICU) between 2008 and 2010. We included AKI patients alive at 90 days. We excluded patients <18 and >100 years, death before follow-up, CKD prior to admission, and follow-up before 60 days or beyond 270 days. Creatinine and cystatin C were measured at 90 days and converted to eGFR (mL/min/1.73 m2). Results We included 274 patients. At 90-day follow-up, the median creatinine eGFR (MDRD) was 81.6 (IQR 58.6–106.8) and median cystatin C eGFR was 51.5 (IQR 35.8–70.7). The incidence of CKD (eGFR < 60) was 25.8% based on creatinine but 63.7% using cystatin C estimates. AKD was present in 47 patients (18.9%). Age, discharge cystatin C, creatinine at discharge, and female gender predicted creatinine-defined CKD at follow-up. Age, discharge cystatin C, CRRT on ICU, and diabetes were associated with cystatin C-based CKD. Conclusions In AKI survivors followed up at 3 months, CKD criteria were met in a quarter of patients using creatinine and in two-thirds using cystatin C eGFR. Less than one-fifth of patients fulfilled AKD criteria. The application of AKD criteria may underestimate renal dysfunction in AKI survivors.

Highlights

  • Acute kidney injury (AKI) in the critically ill is associated with an increased risk of chronic kidney disease (CKD), endstage renal disease (ESRD), and elevated long-term mortality [1,2,3,4]

  • Chronic kidney disease according to the KDIGO 2012 definition is an impairment of renal function or structure persisting for more than 90 days and corresponding to an estimated glomerular filtration rate (GFR) under 60 ml/min/1.73 m2. e use of creatinine as an endogenous marker of GFR is confounded in intensive care unit (ICU) patients due to fluid overload and importantly sarcopenia [9, 10]

  • Details of the entire ICU cohort are given in Table S2. e median follow-up was 101.5 days (IQR 89.5–126)

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Summary

Introduction

Acute kidney injury (AKI) in the critically ill is associated with an increased risk of chronic kidney disease (CKD), endstage renal disease (ESRD), and elevated long-term mortality [1,2,3,4]. Cystatin C may be a superior marker in critical illness because it is not affected by muscle mass [11] It is uncertain whether creatinine and cystatin C give similar estimates of the glomerular filtration rate (eGFR) in the months following discharge. Acute kidney disease (AKD) describes renal dysfunction 7 to 90 days after AKI and is determined by percentage change in creatinine from baseline. Chronic kidney disease (CKD) is defined as the estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m2 persisting for more than 90 days. We compared CKD incidence using both creatinine- and cystatin C-based GFR with AKD incidence at 90 days in AKI survivors. In AKI survivors followed up at 3 months, CKD criteria were met in a quarter of patients using creatinine and in two-thirds using cystatin C eGFR. Less than one-fifth of patients fulfilled AKD criteria. e application of AKD criteria may underestimate renal dysfunction in AKI survivors

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