Does acute kidney injury lead to CKD progression?

Mild to moderate acute kidney injury (AKI) is slightly associated with worsening subsequent kidney function in patients with chronic kidney disease (CKD) following adjustments for pre-AKI estimated glomerular filtration rate (eGFR), proteinuria, and other covariables, with the possibility of no correlation, suggests a study.

A total of 3,150 CKD patients were included in this multicentre prospective cohort study. Hospitalized AKI was defined by a ≥50-percent increase in inpatients serum creatinine (SCr) level from nadir to peak. The investigators evaluated the trajectory of kidney function using eGFR based on SCr level (eGFRcr) or cystatin C level (eGFRcys) measured at annual study visits.

Of the patients, 433 had at least one AKI episode over a median follow-up of 3.9 years, most of which (92 percent) had stage 1 or 2 severity. After AKI, reductions were observed in eGFRcr (‒2.30 mL/min/1.73 m², 95 percent confidence interval [CI], ‒3.70 to ‒0.86) and in eGFRcys (‒3.61 mL/min/1.73 m², 95 percent CI, ‒6.39 to ‒0.82).

In fully adjusted models, however, these reductions went down to just ‒0.38 mL/min/1.73 m² (95 percent CI, ‒1.35 to 0.59) for eGFRcr and ‒0.15 mL/min/1.73 m² (95 percent CI, ‒2.16 to 1.86) for eGFRcys. Notably, the CI bounds indicated the possibility of no effect.

Likewise, estimates of changes in eGFR slope following AKI as determined by either SCr level (0.04 mL/min/1.73 m² per year, 95 percent CI, ‒0.30 to 0.38) or cystatin C level (‒0.56 mL/min/1.73 m² per year, 95 percent CI, ‒1.28 to 0.17) also had CI bounds that indicated the possibility of no effect.

“Few cases of severe AKI, no adjudication of AKI cause, and lack of information about nephrotoxic exposures after hospital discharge,” the investigators said.