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A2145 - Type-1 Cardiorenal Syndrome in Isolated Right Heart Failure: A Retrospective Analysis
Author Block: G. S. Thind; Internal Medicine, WMU SCHOOL OF MEDICINE, Kalamazoo, MI, United States.
Introduction
Type-1 cardiorenal syndrome is an inadequately defined disease process characterized by acute kidney injury (AKI) due to reduced renal perfusion in the setting of worsening heart failure. Reduced cardiac output causing lower renal blood flow has been traditionally considered to be the major mechanism involved. Recently, the role of renal venous congestion has been highlighted. Furthermore, focused analysis of renal injury with worsening right heart failure has not been made. We did a retrospective analysis to inspect this.
Methods
Data from the Multiparameter Intelligent Monitoring in Intensive Care-III database was queried. ICD-9 codes for cor pulmonale, pulmonary hypertension, and AKI were used to identify potential patients. Notes, laboratory data, and intake/output data of all potential de-identified patients were reviewed. Inclusion criteria included AKI in the setting of isolated right heart failure or severe pulmonary hypertension (confirmed with echocardiogram or right heart catheterization), evidence of fluid overload, and improvement of AKI with diuresis. Exclusion criteria were evidence of left heart failure and other causes of AKI.
Results
A total of seven patients were recognized. All patients had evidence of severe pulmonary hypertension with no evidence of left heart failure. Six of these had echocardiographic evidence of right heart systolic dysfunction. All seven patients had underlying lung disease as the cause of pulmonary hypertension. Right heart catheterization was performed in three of these patients. Cardiac index was normal in one, marginally reduced in the second, and higher than normal in the third. Two patients had liver profile available - one had elevation of aspartate transaminase, alanine transaminase, and alkaline phosphatase; the other had elevation of aspartate transaminase and bilirubin. Renal electrolytes were available for five patients and they all showed pre-renal physiology.
Discussion
Our analysis highlights the importance of right heart dysfunction in the pathogenesis of cardiorenal syndrome. Right heart failure should be considered an independent risk factor for the development of cardiorenal syndrome. This study also explores its various mechanisms. There has been a shift in focus on the effect of renal venous congestion as the cause of reduced renal perfusion. At least one patient in our study had evidence of normal cardiac output; the development of cardiorenal syndrome in this patient can only be explained from renal venous congestion. Signs of congestive hepatopathy in the setting of right heart dysfunction were also seen in our study. This study provides valuable insights into the mechanisms of this underappreciated disease entity.