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. 2021 Oct 5;15(4):624–634. doi: 10.1093/ckj/sfab194

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© The Author(s) 2021. Published by Oxford University Press on behalf of the ERA.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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FIGURE 1: — Paradigm shift of the pathophysiological mechanisms of oedema formation in NS. Historically Starling's Principle was thought to be the main mechanism, but due to observations from clinical and experimental studies this was rejected. More recent studies show a role for urinary protein-activated plasmin promoting ENaC activation in the cortical collecting duct.

J _v, trans-endothelial filtration volume; L_p, hydraulic conductivity of the membrane; S, surface area; P, hydrostatic pressure; π, oncotic pressure; ACE, angiotensin-converting enzyme; uPA(R), urokinase (receptor).