Invasive Hemodynamic Predictors of Renal Outcomes after Percutaneous Coronary Interventions

Abstract

Objectives: To determine the association of right heart invasive hemodynamic parameters with post-percutaneous coronary intervention (PCI) acute kidney injury (AKI). Background: AKI after PCI is associated with a high morbidity and mortality. Various mechanisms are implicated in AKI after PCI. However, the association between filling pressures and invasive hemodynamic measures of right heart function with post-PCI AKI has not been described. Methods: This is a retrospective single-center analysis of patients of who underwent simultaneous right heart catheterization (RHC) and left heart catheterization with PCI at the Einstein Medical Center, Philadelphia, between January 2010 and December 2016. We included patients who had hemodynamic parameters from the concomitant RHC as well as measurements of kidney function up to 1 month after the procedure. We excluded patients with ST elevation myocardial infarction, end-stage renal disease, cardiogenic shock, and PCI with a need for mechanical circulatory device support. Multivariate linear regression analysis was used to analyze the association between the various right ventricular hemodynamic parameters and eGFR within 1 week and 1 month after catheterization after adjusting for age, race, gender, diabetes and hypertension, contrast volume, cardiac index, and baseline eGFR. Results: Right atrial (RA) pressure was inversely associated with eGFR within 1 week (β = –1.66; 95% CI –3.06 to –0.25; p = 0.021) and 1 month after PCI (β = –2.14; 95% CI –4.08 to –0.20; p = 0.031). Conclusion: Elevated RA pressure is associated with a worsening kidney function after cardiac catheterization and PCI.

Acute Kidney Injury in Cardiogenic Shock: An Updated Narrative Review

“…This is supported by animal studies in which increasing renal venous pressure, mediated by a decreased renal perfusion leads to a reduction in glomerular filtration [19,45]. Local hypertension in the glomerulus and resultant tubulointerstitial hypoxia cause loss of glomerular integrity and tubular damage giving rise to cardiorenal syndrome [46,47]. Secondarily, venous congestion also stimulates the release of proinflammatory cytokines such as TNF (tumor necrosis factor) and IL-6.…”

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“…117 • In patients with evidence of congestion, appropriate decongestive therapies must be instituted before PCI and TAVR to achieve euvolemia, given the association between elevated right atrial pressures and AKI after PCI. 118 In this context, the use of bioimpedance plethysmography-based volume management may play a role in contrast-induced AKI reduction and can be considered in high-risk patients. 119 • Iodinated contrast media minimization has not been demonstrated to be associated with a reduction in AKI after TAVR.…”

NGAL in trans-catheter aortic valve implantation on and off RenalGuard

“…In the past, contrast material was considered the main culprit. In recent years, AKI has been attributed to a multifactorial cause including inflammation, embolization, contrast material, bleeding, nephrotoxic drugs, hypo-perfusion and cardio-renal syndrome [2]. The implications include prolonged hospitalization, the need for renal replacement therapy and even death.…”