Failure is not an Alternative: A Systematic Review of the Prognostic Factors of Cardiorenal Syndrome

Abstract

Cardiorenal syndrome (CRS) is a pathophysiological condition of the heart and kidneys. Cardiac and renal illnesses are prevalent and commonly overlap to substantial increase mortality, morbidity, and cost. Smoking, hypertension, coronary artery disease, diabetes, sepsis, and labs of blood urea, serum creatinine, eGFR, and LVEF were identified as death risk factors. Up to 40% of decompensated HF patients exhibit with CRS 1. Just 9% of patients with acute HF had normal renal function. Those with type 4 CRS have a 49% higher mortality risk.

Increasing AKI severity was related with worse outcomes, including a higher fatality rate and longer stay in the critical care unit. Anemia predicted rehospitalization in individuals with renal failure. Reduced basic eGFR, lower serum albumin, and the use of diuretics were risk factors for the development of CRS1 in senior AHF patients. Spironolactone was emonstrated to be a safe and effective therapy option for patients with acute heart failure at risk for CRS.

Diabetes and hypertension were found as the two most important risk factors in patients with CRS. Acute renal functional impairments were particularly connected to obesity (increased leptin levels and anthropometric variables) and high blood pressure. The extent to which this hyperfiltration results in glomerular and tubulointerstitial fibrosis and progressive renal disease may rely on various factors including systemic and renal inflammation. Insulin-induced hyperinsulinemia can reduce the quantity of uric acid excreted by the kidneys due to its ability to stimulate urate-anion exchanger and/or sodium-dependent anion co-transporter in the renal proximal tubule. Increased circulating norepinephrine is associated with increased vasoconstriction (or lower compliance) and impaired heart rate response in elderly individuals with CHF.

Cardiorenal syndrome Type 1 is typically associated with Acute Decompensated Heart Failure. This is caused by a diuresis-induced stimulation of the RAAS, which results in sodium retention and precipitates CRS via renovascular processes. Numerous resistance mechanisms to diuretics have been examined. Cardiopulmonary bypass and renal ischemia-reperfusion injury initiate a sequence of events that leads in cellular damage and organ failure. Both the kidney and the heart release Tumor Necrosis Factor (TNF), a potent proinflammatory cytokine. Anti-TNF medication can minimize these consequences.

Studies have shown that NT-pro BNP maintains a favorable prognosis for individuals with heart failure and renal impairment. Increased troponins in CKD patients are indicative of continued myocardial injury, left ventricular dilatation, and reduced left ventricle systolic and diastolic function