Recent evidence indicates that reduced cardiac output is not always the main cause of eGFR decline in acute decompensated heart failure. Instead, baroreceptors in the aorta detect the low perfusion pressure due to arterial underfilling, triggering a series of neurohormonal signals. One neurohormonal signal is the Renin-Angiotensin-Aldosterone System (RAAS) system in the kidneys to compensate for arterial underfilling. In addition, the macula densa senses low chloride concentration in tubular filtrate, promoting the release of renin from the juxtaglomerular cells. Angiotensin II is also released which stimulates vasoconstriction and the secretion of aldosterone, leading to fluid retention by increasing sodium reabsorption in an effort to restore fluid volume. The release of arginine vasopressin (AVP) in response to decreased arterial pressure leads to increased water reabsorption and fluid retention. Moreover, the sympathetic nervous system is overactivated in response to low blood pressure,, driving even more sodium reabsorption.
At the same time, venous congestion plays a role in driving fluid avidity and has been associated with a decline in eGFR. In heart failure, elevated venous pressure backs up into the kidneys, reducing their ability to filter blood and causing decreased glomerular filtration rate (GFR). This reduction in renal blood flow promotes sodium reabsorption, while intrarenal hemodynamic changes caused by congestion further impair the kidneys' capacity to excrete sodium. Venous congestion can trigger the kidneys' fibrotic pathways, leading to scarring, and cause endothelial cells to release neurohormones and cytokines, which promote inflammation. In some patients with acute decompensated heart failure, venous congestion can manifest as ascites with increased intra-abdominal pressure which worsens kidney function. Reducing this pressure through fluid removal has been shown to improve kidney function, as evidenced by lower serum creatinine levels after invasive interventions.
Furthermore, elevated levels of inflammatory cytokines, including C-reactive protein, TNF-α, and IL-6 increase the risk of mortality in cardiorenal syndrome. These cytokines contribute to oxidative stress, reduce nitric oxide availability, and cause endothelial dysfunction, which plays a key role in the development of cardiorenal syndrome.
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