Figure 4.

Mechanisms of venous congestion at the level of the kidney. Venous congestion can result from venous vascular hypertonia with subsequent venous hypertension, from volume stasis arising from (sub-)obstructed outflow, and/or from external compression. At the level of the kidneys, this congestion induces a retrograde dysfunction of the peritubular and glomerular capillaries. Reflex arteriolar constriction and activation of the renin–angiotensin–aldosterone system prevents further microcirculatory deterioration at the cost of reduced organ perfusion and subsequent parenchymal hypoxia. An oxidative stress response induces immunological, neurological, and metabolic protection mechanisms by activating the autonomic nervous system and the intravascular distribution of cytokines, endocrines, and vasoactive mediators, causing endothelial activation and a generalized state of inflammation. In non-pregnant individuals, this sequence of events unfolds in the kidneys as part of the pathophysiology of renocardial syndrome but can also occur in other internal organs as in cardiohepatic or hepatorenal syndromes. In pregnancy, this mechanism may unfold in the uterus and placenta as well as in internal organs. In this picture, the kidney may serve as a proxy for other maternal organs, such as uterus-placenta, heart, etc.