CRIC study: Chronic kidney disease progression after acute kidney injury

It is often accepted that acute kidney injury (AKI) is an independent risk factor for accelerated loss of kidney function. Studies pointing to this association have, however, had methodological limitations, such as inadequate control for differences between patients who had AKI and those who did not.

The present study set out to address whether AKI is independently associated with subsequent kidney function trajectory in people with chronic kidney disease (CKD). Data from CRIC (Chronic Renal Insufficiency Cohort), a multicentre, prospective cohort study of adults with CKD in the US, were included. CRIC participants had their serum creatinine (SCr), cystatin C and urine protein–creatinine ratio measured annually.

3150 participants were included at baseline. Mean age was 65 years, 44% were female, 54% of participants had diabetes and 11% a history of heart failure. Mean eGFR based on SCr level (eGFRcr) was 52 mL/min/1.73 m², mean eGFR based on cystatin C level (eGFRcys) was 51 mL/min/1.73 m² and median uPCR was 0.13 g/g (14.7 mg/mmol).  

Over a median follow-up of 3.9 years, 612 episodes of AKI (defined by a ≥50% increase in inpatient SCr level from nadir to peak) occurred among 433 participants. Most episodes (92%) were stage 1 or 2 in severity. Each episode of AKI was associated with a decrease in eGFRcr of –2.30 (95% CI, –3.70 to –0.86) mL/min/1.73 m2 and in eGFRcys of –3.61 (–6.39 to –0.82) mL/min/1.73 m².

After adjusting for pre-AKI eGFR, proteinuria and other covariables, the decreases were attenuated to –0.38 (–1.35 to –0.59) mL/min/1.73 m² for eGFRcr and –0.15 (–2.16 to –1.86) mL/min/1.73 m² for eGFRcys. The CI bounds included the possibility of no effect.

Estimates of changes in eGFR slope after AKI determined by either SCr (0.04 [–0.30 to 0.38] mL/min/1.73 m2) or cystatin C (–0.56 [–1.28 to 0.17] mL/min/1.73 m²) also included the possibility of no effect. 

These findings suggest that the small association between mild to moderate AKI and subsequent worsening of kidney function in people with CKD is due to much of the kidney disease being present before AKI. The authors suggest that a greater impact on overall CKD burden may be achieved by efforts to flatten the eGFR slope and treat proteinuria before AKI, rather than focusing on ameliorating the effects of each individual AKI episode.

The full article can be read here.