Renal Compression in Heart Failure: The Renal Tamponade Hypothesis

State-of-the-Art Review

Eva M. Boorsma, MD; Jozine M. ter Maaten, MD, PHD; Adriaan A. Voors, MD, PHD; Dirk J. van Veldhuisen, MD, PHD


JACC Heart Fail. 2022;10(3):175-183. 

In This Article

Increased Perirenal Pressure

Increased volume of adipose tissue within the perirenal fascia may lead to increased perirenal pressure (Central Illustration). Both the thickness of the perirenal adipose tissue surrounding the kidney and accumulation of fat in the renal sinus have been associated with chronic kidney disease, arteriosclerosis, hypertension, and the onset of diabetes.[24–27] This association can be explained by perirenal adipose tissue compressing the renal vasculature, leading to pathologic activation of the renin-angiotensin-aldosterone system (RAAS) and reduced renal perfusion (Central Illustration), as well as venous compression, (further) congesting the renal interstitium.[28,29] Alternatively, perirenal adipose tissue can cause RAAS activation through its inflammatory properties and increased local levels of TNF-α.[29,30] Renal sinus fat is of interest in relation to the renal capsule, inasmuch as the renal sinus is not protected from outside compression by the renal capsule (Figure 1, number 4). This means that increases in renal sinus fat volume directly increase pressures within the renal capsule.

Indeed, renal sinus volume has been correlated to both GFR and intrarenal perfusion in patients with type 2 diabetes.[31] Although this is not an acute mechanism, altered intrarenal hemodynamics resulting from perirenal fat may contribute to a decrease of renal function in the setting of interstitial congestion. Whether increases in perirenal fat and/or renal sinus fat contribute to renal congestion in HF is yet to be established.