Community-Acquired Acute Kidney Injury as a Risk Factor of de novo Heart Failure Hospitalization

Abstract

Objectives: Because patients with hospital-acquired acute kidney injury (AKI) are at risk for subsequent development of heart failure (HF) and little is known about the relation between community-acquired AKI (CA-AKI) and HF, we sought to determine if CA-AKI is a risk factor for incident HF hospitalization. Methods: We utilized Baylor Scott & White Health databases at the primary care and inpatient hospitalization levels to identify adults without a prior history of HF who had 2 or more serum creatinine measurements within 13 months in the primary care setting. We defined CA-AKI as a serum creatinine increase ≥0.3 mg/dL or ≥1.5 times the baseline for consecutive values within a 13-month period. We created a flag for de novo HF hospitalization at 90, 180, and 365 days following CA-AKI evaluation. Results: In the analyses, 210,895 unique adults were included, of whom 5,358 (2.5%) had CA-AKI. Those with CA-AKI had higher rates of comorbidities, higher rate of males (48 vs. 42%, p < 0.001), and were older (61.5 [50.3, 73.1] vs. 54.1 [42.8, 64.7] years, p < 0.001) than those who did not have CA-AKI. In total, 607 (0.3%), 833 (0.4%), and 1,089 (0.5%) individuals had an incident HF hospitalization in the 90, 180, and 365 days following the CA-AKI evaluation, respectively. After adjusting for demographic and clinical characteristics, patients with CA-AKI had >2 times the risk of de novo HF hospitalization compared with patients who did not have CA-AKI (90 days: 2.35 [1.83–3.02], p < 0.001; 180 days: 2.52 [2.04–3.13], p < 0.001; 365 days: 2.16 [1.77–2.64], p < 0.001). These multivariable models yielded strong predictive abilities, with the areas under the receiver-operating characteristic curve >0.90. Conclusion: After controlling for baseline and clinical characteristics, patients with CA-AKI were at approximately twofold the risk of de novo HF hospitalization (within 90, 180, and 365 days) compared with those who did not have CA-AKI. Hence, detecting CA-AKI may provide an opportunity for early intervention at the primary care level to possibly delay HF development.

From cardiorenal syndromes to cardionephrology: a reflection by nephrologists on renocardiac syndromes

“…There was a 58% increase in the risk of CHF during 2.9 years of follow-up, a 40% increase in the risk of acute myocardial infarction during 2.3 years of follow-up, and a 15% increase in the risk of stroke over a period of 2.7 years [ 34 ]. Other studies have shown that the increased risks did not differ between AKI patients with and without previous CKD and neither status with respect to recovery of renal function nor severity of AKI [ 35–37 ]; there are also no differences between patients with and without previous cardiovascular conditions, including CHF [ 38 , 39 ], suggesting that the long-term risk of cardiovascular events is associated with AKI itself.…”

Cardiovascular risk associated with serum potassium in the context of mineralocorticoid receptor antagonist use in patients with heart failure and left ventricular dysfunction

“…27 Importantly, a recent US study showed that patients with community acquired acute kidney injury (CA-AKI: 2.5% among 210 895 adults) -as defined by a serum creatinine increase ≥0.3 mg/dL or ≥ 1.5 times the baseline for consecutive values -were at approximately twofold the risk of de novo HF hospitalization (within 90, 180, and 365 days) compared with those who did not have CA-AKI. 28 There are guideline recommendations for the frequency of K + monitoring in patients with HF administered a RAAS inhibitor 29 as well as suggestions regarding the frequency of K + monitoring in patients with hyperkalaemia receiving a K + -lowering agent. 30 Importantly, the present results stemmed from trials where K + was monitored serially (median number of K + measurements was 8.2 per patient per year in EPHESUS and 4.5 in EMPHASIS-HF).…”

“…Of note, the combined use of RAAS inhibitors, loop diuretics and non‐steroidal anti‐inflammatory drugs in the community increases the risk of developing acute kidney injury . Importantly, a recent US study showed that patients with community acquired acute kidney injury (CA‐AKI: 2.5% among 210 895 adults) – as defined by a serum creatinine increase ≥0.3 mg/dL or ≥ 1.5 times the baseline for consecutive values – were at approximately twofold the risk of de novo HF hospitalization (within 90, 180, and 365 days) compared with those who did not have CA‐AKI …”

The Role of Gut-Derived, Protein-Bound Uremic Toxins in the Cardiovascular Complications of Acute Kidney Injury

“…Moreover, in a prospective study of 968 patients undergoing cardiac surgery, AKI stage and duration were linked to cardiovascular events during the five years of follow-up [ 32 ]. AKI was also shown to be associated with a risk of readmission for heart failure within the first two years of hospital discharge for patients who had experienced an AKI episode, independently of cardiovascular risk factors and a history of heart failure [ 33 , 34 , 35 ]. Patients who recovered from dialysis-requiring AKI also had a higher long-term risk of global coronary events, major adverse cardiovascular events (MACE) (nonfatal myocardial infarction (MI), cardiac revascularization, and acute ischemic stroke events), and cardiovascular mortality, regardless of subsequent progression to CKD [ 36 , 37 ].…”