Intermediate and Long-term Outcomes of Survivors of Acute Kidney Injury Episodes: A Large Population-Based Cohort Study

Abstract

BackgroundThe long-term prognosis after acute kidney injury (AKI) is variable. It is unclear how the prognosis of AKI and its relationship to prognostic factors (baseline kidney function, AKI severity, prior AKI episodes, and recovery of kidney function) change as follow-up progresses.Study DesignObservational cohort study.Setting & ParticipantsThe Grampian Laboratory Outcomes Morbidity and Mortality Study II (GLOMMS-II) is a large regional population cohort with complete serial biochemistry and outcome data capture through data linkage. From GLOMMS-II, we followed up 17,630 patients hospitalized in 2003 through to 2013.PredictorsAKI identified using KDIGO (Kidney Disease: Improving Global Outcomes) serum creatinine criteria, characterized by baseline kidney function (estimated glomerular filtration rate [eGFR] ≥ 60, 45-59, 30-44, and <30 mL/min/1.73 m2), AKI severity (KDIGO stage), 90-day recovery of kidney function, and prior AKI episodes.OutcomesIntermediate- (30-364 days) and long-term (1-10 years) mortality and long-term renal replacement therapy.MeasurementsPoisson regression in time discrete intervals. Multivariable Cox regression for those at risk in the intermediate and long term, adjusted for age, sex, baseline comorbid conditions, and acute admission circumstances.ResultsOf 17,630 patients followed up for a median of 9.0 years, 9,251 died. Estimated incidences of hospital AKI were 8.4% and 17.6% for baseline eGFRs ≥ 60 and <60 mL/min/1.73 m2, respectively. Intermediate-term (30-364 days) adjusted mortality HRs for AKI versus no AKI were 2.48 (95% CI, 2.15-2.88), 2.50 (95% CI, 2.04-3.06), 1.90 (95% CI, 1.51-2.39), and 1.63 (95% CI, 1.20-2.22) for eGFRs ≥ 60, 45 to 59, 30 to 44, and <30 mL/min/1.73 m2, respectively. Among 1-year survivors, long-term HRs were attenuated: 1.44 (95% CI, 1.31-1.58), 1.25 (95% CI, 1.09-1.43), 1.21 (95% CI, 1.03-1.42), and 1.08 (95% CI, 0.85-1.36), respectively. The excess long-term hazards in AKI were lower for lower baseline eGFRs (P for interaction = 0.01).LimitationsNonprotocolized observational data. No adjustment for albuminuria.ConclusionsThe prognostic importance of a discrete AKI episode lessens over time. Baseline kidney function is of greater long-term importance.

Post-discharge kidney function is associated with subsequent ten-year renal progression risk among survivors of acute kidney injury

“…Indeed, a step 30% eGFR drop during admission was particularly common among those with AKI and low post-episode eGFR, indicating that nonrecovery with low subsequent progression was common. The interaction between AKI and eGFR on progression also complements previous studies, which have demonstrated a similar interaction between AKI and eGFR on mortality 11, 12. Finally, a complementary explanation for the poorer outcomes among those with a normal post-episode eGFR could be that AKI indicates a “failed stress test” unmasking subclinical renal disease.…”

“…However, in sensitivity analyses, we also estimated “subdistribution HRs” according to the Fine and Gray model (in which those who died without progression remain in the “risk set”) 25, 26. Because it is not possible to distinguish whether acute diagnoses recorded during the index admission were a cause or consequence of AKI, we did not adjust for acute diagnoses in the primary multivariable analysis, but in a sensitivity analysis, we compared the findings after acute hospital diagnoses (extracted from ICD-10 codes) were added to the models 12, 27. Because the most recent available post-episode eGFR was at discharge for 20% of the patients, we also repeated the analysis excluding these patients.…”

A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine

“…This means that, in the setting of stress or load of any type, the kidneys have a reduced ability to adapt to and manage a filtered load of solute and are at risk of creating volume overload and azotemia [9]. Small episodes of acute decompensation or superimposed ischemic events may unveil a latent CKD and cause further damage in a highly susceptible kidney, leading to a rise in serum creatinine, proteinuria, and CKD progression [31]. In these patients, it is quintessential to coordinate a treatment that combines the clinical demand for neurohormonal modulation, maintenance of diuresis, control of blood pressure, management of potassium and the acid base, and maintenance of adequate body hydration.…”

Acute Kidney Injury Masked by Malnutrition: A Case Report and the Problem of Protein

“…AKI is associated with significant morbidity and mortality among hospitalized patients, and management is generally aimed at reducing renal injury and preserving remaining kidney function . The kidney damage incurred with AKI is potentially reversible; however, the relationship between AKI and long‐term prognosis is complex, and, because of a number of factors, clinical outcomes vary widely …”