Review of renal compression in heart failure

 The following are key points to remember from this state-of-the-art review on renal compression in heart failure (HF):

Key points

1. Previous studies have linked poor renal function in HF to both decreases in perfusion (due to low cardiac output) and increases in renal congestion (due to increases in central venous pressure). The latter is believed to play a significant role in worsening renal function (WRF) in HF.
2. The authors hypothesize that three important mechanisms, alone or in combination, may contribute to renal congestion in HF: increased intracapsular, perirenal, and intra-abdominal pressures. These increases in pressure can lead to compression of the kidney and renal vasculature.
3. Increased intracapsular pressure: As central venous pressures in HF increase, this leads to an increase in interstitial fluid in the renal parenchyma. Given that the kidneys are surrounded by a rigid capsule, volume expansion does not occur, which means increased interstitial fluid causes an increase in intracapsular pressure. This causes compression of renal veins, glomeruli, and tubules, which subsequently may lead to WRF.
4. Increased perirenal pressure: Just outside of the renal capsule but within the renal fascia is the perirenal space, comprised mostly of adipose tissue. While not fully understood, increases in perirenal adipose tissue, as well as renal sinus fat within the kidney, may lead to renal vein compression and exacerbation of WRF in an already congested kidney.
5. Increased intra-abdominal pressure: In patients with significant HF, increases in intra-abdominal pressure can be a result of many processes, which include development of ascites or retention of fluid in the splanchnic system. This leads to compression of renal vasculature and can contribute to WRF in HF. A similar effect can be seen in patients with significant obesity leading to increased intra-abdominal pressure.
6. The authors suggest that renal decapsulation in HF patients may possibly lead to improved renal outcomes. Data from rat and piglet animal models suggest that decapsulation reduced renal tubular damage and ischemic acute kidney injury.
7. The authors introduce the “renal tamponade” hypothesis to explain why significant WRF is present when central venous pressures are high in HF. Intra- and extra-renal compression of the kidney and renal vasculature through the above three mechanisms are major contributors.
8. More research is needed to better define these mechanisms and to explore the possible benefit of renal decapsulation in managing WRF in HF.

Marty Tam MD., FACC,

6 March 2022