Prevention of post procedural acute kidney injury in the catheterization laboratory in a real-world population.

BACKGROUND: Radiologists and cardiologists have a remarkably different approach to the clinical importance and to the need for prophylactic treatment of contrast-induced acute kidney injury (CI-AKI). OBJECTIVES: To evaluate the efficacy of forced diuresis with matched controlled hydration (FMH) in a real-world, high risk population. METHODS: This is an investigator-driven, single-center, retrospective analysis of prospectively collected data. A total of 150 consecutive patients undergoing coronary angiography, angioplasty or TAVR who were treated with FMH were compared to a matched historical control cohort. RESULTS: In the FMH treated patients, eGFR improved following the procedure from 37ml/min per 1.73m2 at baseline to 39ml/min per 1.73m2 (p<0.001); the net creatinine decreased from 1.85mg/dl to 1.78mg/dl (p<0.001). Among the matched control group, eGFR deteriorated from a baseline value of 36.7ml/min per 1.73m2 to 33.2ml/min per 1.73m2 post procedurally (p<0.001); the net creatinine increased from 1.88mg/dl to 2.14mg/dl (p<0.001). The incidence of post procedural AKI was substantially lower in the FMH treated group (2.7%) compared to the control group (26.7%). By multivariable analysis FMH treatment was independently correlated with reduced incidence of post procedural AKI compared with the control group (OR 0.06, p<0.001). Contrast volume did not correlate with AKI in neither univariate nor multivariate analyses. CONCLUSIONS: In patients undergoing coronary angiography, angioplasty or TAVR, who are considered high risk to develop post procedural AKI, forced diuresis with matched controlled hydration resulted in a significant net creatinine decrease, eGFR increase and a decrease in the incidence of AKI.

Cardiac Hypertrophy and Cardiac Cell Death in Chronic Kidney Disease.

BACKGROUND: Chronic kidney disease (CKD) is a prevalent clinical condition affecting 15% of the general population. Cardiorenal syndrome (CRS) type 4 is characterized by an underlying CKD condition leading to impairment of cardiac function and increased risk for major cardiovascular events. To date, the mechanisms leading from CKD to CRS are not completely understood. In particular, it is unclear whether the pathological changes that occur in the heart in the setting of CKD involve enhanced cell death of cardiac cells. OBJECTIVES: To assess whether CKD may mediate loss of cardiac cells by apoptosis. METHODS: We established rat models for CKD, acute myocardial infarction (acute MI), left ventricular dysfunction (LVD), and sham. We measured the cardiac-to-body weight as well as kidney-to-body weight ratios to validate that renal and cardiac hypertrophy occur as part of disease progression to CRS. Cardiac cells were then isolated and the percent of cell death was determined by flow cytometry following staining with annexin-FITC and propidium iodide. In addition, the levels of caspase-3-dependent apoptosis were determined by Western blot analysis using an anti-cleaved caspase-3 antibody. RESULTS: CKD, as well as acute MI and LVD, resulted in significant cardiac hypertrophy. Nevertheless, unlike the increased levels of cell death observed in the acute MI group, in the CKD group, cardiac hypertrophy was not associated with induction of cell death of cardiac cells. Caspase-3 activity was even slightly reduced compared to sham-operated controls. CONCLUSIONS: Our data show that while CKD induces pathological changes in the heart, it does not induce cardiac cell death.