Clinical InvestigationIncidence, Correlates, and Consequences of Acute Kidney Injury in Patients With Pulmonary Arterial Hypertension Hospitalized With Acute Right-Side Heart Failure
Section snippets
Study Design
We reviewed medical records of patients with a diagnosis of PAH (World Health Organization class I) followed at Stanford Hospital between June 1999 and June 2009. We identified patients by accessing Stanford’s Institution Review Board–approved pulmonary hypertension database assembled by the Vera Moulton Wall Center (VMWC) for Pulmonary Vascular Disease. At the time of the study, the VWMC database contained clinical information on 495 patients with PAH, many followed for >5 years. These data
Baseline and Hospitalization Characteristics
The final cohort included 105 patients who experienced 184 episodes of acute right-side heart failure. Table 1 summarizes the baseline clinical characteristics of the patient population at cohort entry. The mean age at initial clinical visit was 42 ± 13 years, the majority of patients were women (81%) and most patients were caucasian (81%). The etiologies of PAH were idiopathic or heritable (28%), connective tissue disease (33%), drug- and/or toxin-related (31%), and congenital heart disease
Discussion
There have been numerous reports describing the natural history and consequences of developing AKI in the setting of decompensated left-side heart failure.1, 2, 22, 23, 24, 25, 26 In contrast, few studies have explored the incidence, correlates, and consequences of AKI in the setting of PAH and decompensated right-side heart failure. In the present study, we found that AKI is relatively common in patients with PAH hospitalized with acute right-side heart failure. Furthermore, AKI was strongly
Conclusion
Acute kidney injury is a strong predictor of early death in patients with PAH hospitalized with acute right-side heart failure. Chronic kidney disease, higher central venous pressure, and tachycardia on admission were independently associated with the risk of AKI. Future studies are needed to validate these findings in larger diverse populations and to determine the mechanisms leading to AKI in patients with PAH.
Acknowledgments
The authors thank the Vera Moulton Wall Center for their support and Dr André Denault, MD PhD, and Manisha Desai, PhD, for their advice.
Disclosures
Ramona Doyle, MD, is the Director of Clinical Development at Genentech. Roham Zamanian, MD, is a recipient of a 2006 Entelligence Actelion Career Development Award and is a consultant for Gilead and United Therapeutic Pharmaceuticals.
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