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עמוד בית
Thu, 21.11.24

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November 2024
Anna Rozenfeld MD, Aliza Goldman RN MSC, Tal Stern BS, Shmuel Banai MD, Yacov Shacham MD

Background: One-third of patients with acute decompensated heart failure (ADHF) develop worsening kidney function, known as type I cardiorenal syndrome (CRS). CRS is linked to higher mortality rates, prolonged hospital stays, and increased readmissions.

Objectives: To explore the impact of real-time monitoring of urinary output (UO) trends on personalized pharmacologic management, fluid balance, and clinical outcomes of patients with ADHF admitted to a cardiac intensive care unit.

Methods: Our study comprised 35 patients who were hospitalized with ADHF and continuously monitored for UO (UOelec). Standard diuretic and fluid protocols were implemented after 2 hours of oliguria, and patient outcomes were compared to a historical matched control (HMC) group. Patients were assessed for daily and cumulative fluid balance (over 72 hours) as well as for the occurrence of acute kidney injury (AKI).

Results: Significantly more patients in the UOelec group demonstrated negative fluid balance daily and cumulatively over time in the intensive care unit compared to the HMC group: 91% vs. 20%, respectively (P < 0.0001 for 72-hour cumulative fluid balance). The incidence of AKI was significantly lower in the UOelec monitoring cohort compared to the HMC: 23% vs. 57%, respectively (P = 0.003). Moreover, higher AKI resolution, and lower peak serum creatinine levels were demonstrated in the UOelec group vs. the HMC group.

Conclusions: Implementing real-time monitoring of UO in ADHF patients allowed for early response to oliguria and goal-directed adjustment to treatment. This finding ultimately led to reduced congestion and contributed to early resolution of AKI.

March 2021
Moran Slavin MD, Shmuel Avital MD, Yael Einbinder MD, Barak Benjamin MD, and Roye Inbar MD

Background: Peritoneal dialysis (PD) is a treatment option for patients with end-stage renal disease (ESRD) and cardiorenal syndrome (CRS).

Objectives: To evaluate the outcome of this patient population.

Methods: A retrospective study was conducted of patients who underwent an open or laparoscopic insertion of a PD catheter at our institution between 2009 and 2017. Data included demographics, peri-operative parameters, and long-term outcome. Patient and technique survival curves are presented, including subgroup analysis by method of catheter insertion and techniques for infection prevention.

Results: The study population included 95 men and 42 women, aged 65.7 ± 12.4 years. Mean follow-up was 34.6 ± 27.3 months. Open insertion was performed in 113 cases, while 24 underwent laparoscopic insertion. There was no difference in technique survival between these groups (P = 0.943). Removal of the catheter was required in 66% of patients. Median technique survival was 12.1 months. Two-year technique survival was 37% and 5-year technique survival was 12%. The leading cause for catheter removal was infection (69%). Application of measures for prevention of infections were significantly associated with prolonged technique survival (P = 0.001). Technique survival after 2 years was 38% with the application of a single measure and 57% with the application of two measures (P = 0.001). CRS patients (n=24) had a significantly lower overall survival rate (2-year survival 20% vs. 74%, P = 0.001).

Conclusions: The method of catheter insertion has no effect on technique survival. Prevention of infections is the most significant factor for improving the technique survival rates.

December 2015
May-Tal Rofe MD, Ran Levi PhD, Einat Hertzberg-Bigelman MSc, Pavel Goryainov MSc, Rami Barashi MD, Jeremy Ben-Shoshan MD PhD, Gad Keren MD and Michal Entin-Meer PhD
 

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. 


 

 
November 2013
O. Havakuk, M. Entin-Meer, J. Ben-Shoshan, P. Goryainov, S. Maysel-Auslender, E.l Joffe and G. Keren
 Background: Vitamin D has been shown to induce beneficial effects on cardiovascular and renal morbidity by regulating inflammation and tissue fibrosis.

Objectives: To evaluate the effect of vitamin D analogues on cardiac function and fibrosis in an animal model of cardiorenal syndrome.

Methods: Unilateral nephrectomy was performed and myocardial infarction induced in rats. Rats were treated with vitamin D receptor activator (VDRA, paricalcitol, 40 ng/250 g x 3/week) versus a vehicle. A third group of animals, which served as the control, underwent sham surgery and received no treatment. After 4 weeks of treatment, cardiac function and fibrosis were assessed by trans-thoracic echo and histology, respectively. As a parameter of systemic inflammation, previously shown to be altered in acute coronary syndrome, T regulatory (Treg) cell levels were measured by flow cytometry. Renal dysfunction was documented by standard laboratory tests.

Results: After 4 weeks of treatment, no significant improvement in cardiac function parameters was noted following VDRA administration. VDRA treatment did not significantly alter Treg cell systemic levels. Consistently, despite a trend toward less extent of myocardial fibrosis, we found no clear beneficial effects of VDRA on myocardial tissue inflammation and remodeling.

Conclusions: Vitamin D treatment showed no beneficial effects on cardiac function parameters and fibrosis in an animal model of cardiorenal syndrome. 

September 2012
J. Ben-Shoshan, M. Entin-Meer, H. Guzner-Gur and G. Keren

Heart failure (HF) accompanied by renal failure, termed cardiorenal syndrome (CRS), encompasses both the development and worsening of renal insufficiency secondary to HF as well as the harmful effects of impaired renal function on the cardiovascular system, and remains a universal clinical challenge. CRS was recently classified into subtypes depending on the etiologic and chronologic interactions between cardiac and renal dysfunctions. The mechanisms underlying the CRS are multifactorial, including hemodynamic alterations, neurohormonal effects, and inflammatory components. However, despite enhanced understanding and awareness of CRS, further elucidation of the mechanisms involved and the appropriate treatment approaches are clearly warranted. CRS is a difficult condition to manage, as treatment to relieve congestive symptoms of HF is limited by a further decline in renal functions, itself a major independent predictor of long-term cardiac morbidity. In order to perform a proper clinical investigation and implement appropriate treatment that will minimize subsequent progression of heart and kidney injury, a comprehensive approach to these two pathologies is crucial. In the present review we discuss current theories behind the mechanistic evolution of the CRS as well as therapeutic issues regarding this multifaceted condition.
 

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