Arch Gen Intern Med 2018 Volume 2 Issue 3 5 http://www.alliedacademies.org/archives-of-general-internal-medicine/ Review Article Although newer pharmacologic and interventional therapies for the treatment of Heart failure continue to evolve, the optimum strategy of management for the patients with cardio renal syndrome is still unanswered. Various pathophysiologic mechanisms have been proposed including the low output hypothesis and the raised renal venous pressure hypothesis. These mechanisms have been tested and challenged in many trials. Although, modest beneft has been achieved with management strategies targeting these hypotheses. Role of biomolecules and neurohormones such as BNP, adenosine has provided newer insights in mechanisms of Cardio- renal syndrome (CRS). However, when studied in clinical trials, drugs targeting these pathways did not have signifcant clinical outcomes. Diuretics remain cornerstone of management. But their propensity to cause AKI and electrolyte disturbances when used at higher dosages limits their use. Vasodilator proves of clinical beneft in raised CVP states. But risk of hypotension and constant hemodynamic monitoring preclude their use in many clinical situations. Ultrafltration had modest success in the initial studies, but recent trials have questioned their role in patients with ADHF. Pharmacologic therapies such as nesiritide, adenosine antagonists and vasopressin antagonists are still in trial phases and beneft has not yet been proved. Thus, our knowledge of CRS still needs depth and understanding of pathophysiologic mechanisms which when achieved may result in improved clinical outcomes and patient care. This review article on focuses on pathophysiology and management strategies of patients with CRS. Abstract Introduction Understanding the interaction between heart and the kidneys has been the age-old question in the practice of medicine. Many theories have been postulated to solve this enigmatic problem and few have supportive evidences. Since decades, it has been known that the presence of renal dysfunction in settings of heart failure purports poor prognosis. Hence, over these years there has been a continuous effort to unfold the various mechanisms behind the complex interplay of heart and renal axis. Defnition and Classifcation In 2004, the NHLB Institute tried in defning the CRS. It stated CRS a condition in which therapy to relieve congestive symptoms of HF is limited by a decline in renal function as manifested by a reduction in GFR [1]. Cardio renal syndrome (CRS) is an umbrella term that defnes disorders of the heart and kidneys whereby “acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other organ. Worsening renal function is most commonly defned as an absolute increase in serum creatinine of ≥ 0.3 mg/dl [2]. In 2010, at a consensus conference of the Acute Dialysis Quality Initiative (ADQI), the CRS was classifed into fve subtypes primarily based upon the organ that initiated the insult as well as the acuity of disease (Table 1) [3]. Many others including Braam et al. [4] had their individual opinions regarding this classifcation. They said this classifcation based on a time frame is too simplistic. They viewed CRS in a more integrated manner. They defned the cardio renal syndrome as a pathophysiological condition in which combined heart and kidney dysfunction amplifes progression of failure of the individual organ, by inducing similar pathophysiological mechanisms. Therefore, regardless of which organ fails frst, the same neurohormonal systems are activated causing accelerated cardiovascular disease, and progression of damage and failure of both organs. These systems are broken down into two broad categories of "hemodynamic factors" and non-hemodynamic factors or "cardio renal connectors". Problem Statement Presence of renal dysfunction in heart failure has reported in numerous studies. An overall prevalence of 30-60% is mentioned [5]. In a study by Ezkowitz et al., [6] in 6,427 patients with cardiologist-diagnosed HF and angiographically proven coronary artery disease (mean age 69 years; 65% men; one-year mortality, 10%), 39% had creatinine clearances <60 ml/min. In the ADHERE study, The Acute Decompensated Heart Failure National Registry (ADHERE) database reported data on over 100,000 patients with HF requiring hospitalization, approximately 30 percent had a diagnosis of chronic kidney disease (defned as a serum creatinine greater than 2.0 mg/ dL. Over 60% of patients admitted in this registry with acute decompensated HF (ADHF) had stage 3 (GFR<60 ml/min per 1.73 m 2 ) or worse CKD. One study showed echo evidence of LVH in 45% patients with creatinine clearance of <24 ml/min and in 70% of those planning to initiate haemodialysis [7]. The prevalence of CKD (type 2 CRS) is seen in 32%-50% of patients in the large chronic HF trials [7]. Cardio-renal syndrome. Dhiraj Kumar*, Abhijeet Yelale, Girish Sabnis, Hetan Shah, Charan Lanjewar, Prafulla Kerkar King Edward Memorial Hospital, Mumbai, Maharashtra, India Accepted on April 16, 2018 Keywords: Cardio renal syndrome, Heart failure, RAAS. ISSN: 2591-7951