Endothelin-1 and angiotensin II work in tandem to drive disease progression1-3

ET-1 and Ang II play a key role in the mechanisms of disease in IgA nephropathy and FSGS.

Elevated levels of endothelin-1 and angiotensin II result in:

Mesangial proliferation and the inflammatory response
Icon showing cross-section of Bowman's capsule, with emphasis on mesangial cell proliferation, inflammation, and proteinuria in IgA nephropathy
in IgA nephropathy1,4-6
Podocyte injury and loss
Icon showing cross-section of Bowman's capsule, with emphasis on podocyte injury, matrix accumulation, and fibrosis in FSGS
in FSGS1,3,7

Identifying patients at high risk of progression in IgA nephropathy

FSGS=focal segmental glomerulosclerosis; IgA=immunoglobulin A.


1. Komers R, et al. Am J Physiol Regul Integr Comp Physiol. 2016:R877-R884. 2. Kohan DE, et al. Kidney Int. 2014;86:896-904. 3. Raina R, et al. Kidney Dis. 2020;6:22-34. 4. Dhaun N, et al. Br J Pharmacol. 2012;167:720-731. 5. Ebefors K, et al. Kidney Int. 2019;96:957-970. 6. Wyatt RJ, et al. New Engl J Med. 2013;368:2402-2414. 7. Maguire JJ, et al. Semin in Nephrol. 2015;35:125-136.

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