Renal function at hospital admission and mortality due to acute kidney injury after myocardial infarction

Abstract

Background: The role of an impaired estimated glomerular filtration rate (eGFR) at hospital admission in the outcome of acute kidney injury (AKI) after acute myocardial infarction (AMI) has been underreported. The aim of this study was to assess the influence of an admission eGFR<60 mL/min/1.73 m(2) on the incidence and early and late mortality of AMI-associated AKI.

Methods: A prospective study of 828 AMI patients was performed. AKI was defined as a serum creatinine increase of ≥ 50% from the time of admission (RIFLE criteria) in the first 7 days of hospitalization. Patients were divided into subgroups according to their eGFR upon hospital admission (MDRD formula, mL/min/1.73 m(2)) and the development of AKI: eGFR ≥ 60 without AKI, eGFR<60 without AKI, eGFR ≥ 60 with AKI and eGFR<60 with AKI.

Results: Overall, 14.6% of the patients in this study developed AKI. The admission eGFR had no impact on the incidence of AKI. However, the admission eGFR was associated with the outcome of AMI-associated AKI. The adjusted hazard ratios (AHR, Cox multivariate analysis) for 30-day mortality were 2.00 (95% CI 1.11-3.61) for eGFR<60 without AKI, 4.76 (95% CI 2.45-9.26) for eGFR ≥ 60 with AKI and 6.27 (95% CI 3.20-12.29) for eGFR<60 with AKI. Only an admission eGFR of <60 with AKI was significantly associated with a 30-day to 1-year mortality hazard (AHR 3.05, 95% CI 1.50-6.19).

Conclusions: AKI development was associated with an increased early mortality hazard in AMI patients with either preserved or impaired admission eGFR. Only the association of impaired admission eGFR and AKI was associated with an increased hazard for late mortality among these patients.

Figure 1. Hospital admission eGFR, AKI development and 30-day mortality rates after acute myocardial infarction.

Hazard ratio (Cox multivariate analysis, left) and crude mortality (right).

Figure 2. Hospital admission eGFR, AKI development and 30-day to 1-year mortality rates after acute myocardial infarction.

Hazard ratio (Cox multivariate analysis, left) and crude mortality (right). Note that only the combination of an admission eGFR<60 mL/min/1.73 m² with AKI was associated with a higher late mortality. * 30-day to 1-year mortality rates were estimated for patients who survived for 30 days after AMI.

Figure 3. COX curve for 30-day survival among the four groups divided into admission eGFR and AKI development.

Admission eGFR, estimated glomerular filtration rate upon admission (mL/min/1.73 m²); AKI, acute kidney injury. For the comparison between admission eGFR≥60 without AKI and admission eGFR<60 without AKI, p = 0.020; between admission eGFR≥60 without AKI and admission eGFR≥60 with AKI, p<0.001; for admission eGFR≥60 without AKI and admission eGFR<60 with AKI, p<0.001.

Figure 4. COX curve for 30-day to 1-year survival among the four groups divided into admission eGFR and AKI development.

Admission eGFR, estimated glomerular filtration rate upon admission (mL/min/1.73 m²); AKI, acute kidney injury. P = 0.002 for the comparison between admission eGFR≥60 without AKI and admission eGFR<60 with AKI, while the differences between the others groups with an admission eGFR≥60 without AKI were non-significant. * 30-day to 1-year mortality rates were estimated for patients who survived for 30 days after AMI.