Cardiorenal Syndrome Type 1

Abstract

Cardiorenal syndrome (CRS) type 1 is characterized as the development of acute kidney injury (AKI) and dysfunction in the patient with acute cardiac illness, most commonly acute decompensated heart failure (ADHF). There is evidence in the literature supporting multiple pathophysiological mechanisms operating simultaneously and sequentially to result in the clinical syndrome characterized by a rise in serum creatinine, oliguria, diuretic resistance, and in many cases, worsening of ADHF symptoms. The milieu of chronic kidney disease has associated factors including obesity, cachexia, hypertension, diabetes, proteinuria, uremic solute retention, anemia, and repeated subclinical AKI events all work to escalate individual risk of CRS in the setting of ADHF. All of these conditions have been linked to cardiac and renal fibrosis. In the hospitalized patient, hemodynamic changes leading to venous renal congestion, neurohormonal activation, hypothalamic-pituitary stress reaction, inflammation and immune cell signaling, systemic endotoxemic exposure from the gut, superimposed infection, and iatrogenesis all contribute to CRS type 1. The final common pathway of bidirectional organ injury appears to be cellular, tissue, and systemic oxidative stress that exacerbate organ function. This review explores in detail the pathophysiological pathways that put a patient at risk and then effectuate the vicious cycle now recognized as CRS type 1.

Excessively High Hydration Volume May Not Be Associated With Decreased Risk of Contrast‐Induced Acute Kidney Injury After Percutaneous Coronary Intervention in Patients With Renal Insufficiency

“…When kidney function is normal, the contrast medium is excreted relatively quickly (within a few hours); however, in patients with chronic kidney disease, the excretion half‐life might be more than 10 hours 29. In addition, excessive hydration may increase risk of heart failure, consequently leading to volume overload or increased preload, lower cardiac output, and inadequate renal perfusion, such as cardiorenal syndrome, which, in turn, may increase venous pressure, leading to kidney congestion, activation of the renin angiotensin aldosterone system, and marked alterations of immune and somatic cell signaling 30, 31. These are likely the reasons that higher hydration volumes at the average speed did not show any benefits in preventing CI‐AKI in the present study.…”

Effect of Estimated Plasma Volume Reduction on Renal Function for Acute Heart Failure Differs Between Patients With Preserved and Reduced Ejection Fraction

“…1,3,5 The main underlying mechanism is thought to be related to plasma volume reduction (PVR) with the subsequent reduction of renal perfusion and activation of the renin-angiotensin-aldosterone system. 6 Previous studies have shown that PVR, represented by hemoconcentration, is associated with WRF. 7,8 Therefore, the maintenance of optimal PV without the resultant impairment of renal function is essential for AHF management.…”

De Novo Acute Heart Failure and Acutely Decompensated Chronic Heart Failure

“…The acute cardiorenal syndrome (type 1), defined as a worsening of renal function in patients with acutely decompensated heart failure, arises in 25-33% of patients with ADCHF (20). To determine the appropriate treatment, patients with this syndrome should be classified on pathophysiologic grounds as suffering from either prerenal renal failure with predominant left-heart failure (forward failure) or intrarenal renal failure due to renal venous congestion (backward failure) (20,21).…”