Prevention of Cardiorenal Syndromes

Abstract

The cardiorenal syndromes (CRS) are composed of five recently defined syndromes which represent common clinical scenarios in which both the heart and the kidney are involved in a bidirectional injury process leading to dysfunction of both organs. Common to each subtype are multiple complex pathogenic factors, a precipitous decline in function and a progressive course. Most pathways that lead to CRS involve acute injury to organs which manifest evidence of chronic disease, suggesting reduced ability to sustain damage, maintain vital functions, and facilitate recovery. Prevention of CRS is an ideal clinical goal, because once initiated, CRS cannot be readily aborted, are not completely reversible, and are associated with serious consequences including hospitalization, complicated procedures, need for renal replacement therapy, and death. Principles of prevention include identification and amelioration of precipitating factors, optimal management of both chronic heart and kidney diseases, and future use of multimodality therapies for end-organ protection at the time of systemic injury. This paper will review the core concepts of prevention of CRS with practical applications to be considered in today's practice.

The Role of Congestion in Cardiorenal Syndrome Type 2: New Pathophysiological Insights into an Experimental Model of Heart Failure

“…Therefore, animal studies may provide important insights into the pathogenesis of CRS2 by mimicking human phenotypes. The predominant mechanisms proposed include neurohormonal activation, hemodynamic factors such as renal hypoperfusion and venous congestion as well as inflammation and oxidative stress [2,3,4,5]. …”

“…A high venous pressure is an alternative and important cause of worsening kidney function; in this case, tubular damage plays a major role [6] and simultaneously constitutes a stimulus for peripheral synthesis and the release of inflammatory mediators [7]. Moreover, inflammation could be an additional nonhemodynamic mechanism for the progression of chronic kidney disease [5,8] triggered by local kidney factors or by increased gut absorption of endotoxin [9,10]. In fact, patients with severe HF feature high levels of tumor necrosis factor (TNF)-α and interleukins (IL) [11].…”

Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

“…Its presence is associated with a worse prognosis following cardiovascular diseases. 2 Although preventing this condition includes identification and amelioration of the precipitating factors and connections, 3 the pathophysiological mechanisms of the syndrome remain to be elucidated. It is also known that the presence of CKD increases severity, worsens the response to treatment, and is associated with poor cardiac and renal outcomes in cardiorenal syndrome.…”

10.5937/mckg48-4232 = Secondary hyperparathyroidism and cardiorenal syndrome type IV: Etiopathogenesis, clinical significance and treatment

“…kardiorenalni sindrom je patofiziološki poremećaj funkcije srca i bubrega, gde akutni ili hronični poremećaj funkcije jednog organa podstiče akutni ili hronični poremećaj funkcije drugog organa (1)(2)(3)(4)(5)(6)(7)(8). razlikujmo pet tipova kardiorenalnog sindroma, a u kardiorenalnom sindromu tip 4 (hronični renokardijalni sindrom) nedostatak vitamina d i sekundarni hiperparatireoidizam dovode do poremećaja funkcije srca i bubrega (1)(2)(3)(4)(5)(6)(7)(8).…”

“…razlikujmo pet tipova kardiorenalnog sindroma, a u kardiorenalnom sindromu tip 4 (hronični renokardijalni sindrom) nedostatak vitamina d i sekundarni hiperparatireoidizam dovode do poremećaja funkcije srca i bubrega (1)(2)(3)(4)(5)(6)(7)(8). Bolesnici koji boluju od hronične bolesti bubrega izloženi su brojnim tradicionalnim (hipertenzija, hiperlipidemija, dijabetes melitus, gojaznost, pušenje cigareta, fizička neaktivnost) i netradicionalnim (anemija, mikroinflamacija, hiperhomocisteinemija, oksidativni stres, nedostatak vitamina d, sekundarni hiperparatireoidizam) faktorima rizika, koji ubrzavaju opadanje funkcije bubrega i doprinose razvoju kardiovaskularnih bolesti (1)(2)(3)(4)(5)(6)(7)(8).…”