Cardiorenal Syndrome in Acute Kidney Injury

Abstract

Varying degrees of cardiac and kidney dysfunction commonly are observed in hospitalized patients. As a demonstration of the significant interplay between the heart and kidneys, dysfunction or injury of one organ often contributes to dysfunction or injury of the other. The term cardiorenal syndrome (CRS) was proposed to describe this complex organ cross-talk. Type 3 CRS, also known as acute renocardiac syndrome, is a subtype of CRS that occurs when acute kidney injury contributes to or precipitates the development of acute cardiac dysfunction. Acute kidney injury may directly or indirectly produce acute cardiac dysfunction by way of volume overload, metabolic acidosis, electrolyte disorders such as hyperkalemia and hypocalcemia, and other mechanisms. In this review, we examine the definition, epidemiology, pathophysiology, and treatment options for CRS with an emphasis on type 3 CRS.

Distant organ dysfunction in acute kidney injury

“…49 In patients undergoing cardiac surgery, post-surgical AKI was found to be associated with an increased five-year risk for myocardial infarction and heart failure 50 (1.4 times hazard), as well as increased all-cause mortality, even when kidney function had recovered (1.3 times hazard) (Figure 3). [52][53][54][55] However, even in the absence of these conditions, cardiac dysfunction may still occur in the context of AKI. Traditional factors include fluid overload contributing to cardiac myocyte stretch, acidaemia, uraemia, the activation of renin-angiotensin-aldosterone and the sympathetic nervous system, which results in cardiac dysfunction, pericarditis and hyperkalaemia, which gives rise to arrhythmias.…”

“…Traditional factors include fluid overload contributing to cardiac myocyte stretch, acidaemia, uraemia, the activation of renin-angiotensin-aldosterone and the sympathetic nervous system, which results in cardiac dysfunction, pericarditis and hyperkalaemia, which gives rise to arrhythmias. [52][53][54][55] However, even in the absence of these conditions, cardiac dysfunction may still occur in the context of AKI. Perhaps the most compelling evidence for the close interrelated connection between the heart and kidney is that AKI increases the risk of CKD development and progression.…”

An Update on the Pathophysiology and Treatment of Cardiorenal Syndrome

“…In order to oxygenate the kidney, the difference between the arterial driving pressure and venous outflow pressures must remain large enough to allow for adequate renal blood flow and glomerular filtration rate [1]. In HF, increased central venous pressure (CVP) leads to a reduction of both perfusion gradient across the glomerular capillary bed and renal function [4,5].…”

“…Neurohormonal systems such as the RAAS and the SNS are homeostatic systems responsible for proper blood flow during periods of hypotension. Activation of RAAS occurs in response to decreased cardiac output or decreased perfusion within the renal system [4]. RAAS leads to increased production of angiotensin II, which causes systemic vasoconstriction and extracellular volume expansion via sodium retention.…”

“…Fluid overload can lead to the development of pulmonary edema and increased mortality. These patients are often at higher risk for needing renal replacement therapy [4]. AKI can lead to the development of hyperkalemia, disrupting electrolyte balance and causing arrhythmias, resulting in cardiac arrest.…”