INFLAMMATION AND FIBROSIS

CKD IN T2D: INFLAMMATION AND FIBROSIS ARE DAMAGING YOUR PATIENTS' KIDNEYS AND INCREASING THE RISK OF CV EVENTS1-5

There are 3 major drivers that contribute to CKD progression and related CV events

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MR_OVERACTIVATION_FLOWCHART VIDEO


MR overactivation may lead to inflammation and fibrosis, thus contributing to damage in the kidneys and CV system.1-5

Even with current treatment regimens addressing metabolic and haemodynamic drivers, patients remain at high risk of CKD progression and CV events with inflammation and fibrosis being largely unaddressed1,2

Inflammation and fibrosis in CKD and T2D as driven by MR overactivation video

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Inflammation and fibrosis in CKD and T2D as driven by MR overactivation video


Rajiv Agarwal, MD, takes us through how MR overactivation impacts inflammation and fibrosis and leads to CKD progression and CV events1-5

Normal MR function
Normal MR function in the kidneys
MR overactivation
MR overactivation within kidneys

MR overactivation contributes to the risk of CV dysfunction4,6

Both preclinical and clinical trials provide evidence of the connection between MR overactivation and CV dysfunction. As CKD progresses, there is an increased chance that a patient with CKD and T2D might experience a CV event like a myocardial infarction or stroke.

Read more about the effects of MR overactivation on a cellular level

Together, these effects elevate the risk of CKD progression and cardiovascular events.11

UACR testing can reveal albuminuria as a consequence of inflammation and fibrosis12,13
Learn more

BP=blood pressure; CKD=chronic kidney disease; CV=cardiovascular; MR=mineralocorticoid receptor; T2D=type 2 diabetes; UACR=urine albumin-to-creatinine ratio.

References:

  • Alicic RZ, et al. Clin J Am Soc Nephrol. 2017;12:2032–2045. Return to content
  • Alicic RZ, et al. Adv Chronic Kidney Dis. 2018;25:181–191. Return to content
  • Black LM, et al. J Histochem Cytochem. 2019;67(9):663–681. Return to content
  • Tesch GH, et al. Front Pharmacol. 2017;8. doi:10.3389/fphar.2017.00313. Return to content
  • Toth-Manikowski S, et al. J Diabetes Res. 2015;2015. doi:10.1155/2015/697010. Return to content
  • Agarwal R, et al. Eur Heart J. 2021;42:152–162. Return to content
  • Kolkhof P, et al. Mol Cell Endocrinol. 2012;350(2):310-317. Return to content
  • Thomas C, et al. Nat Rev. 2015;1:15018. doi:10.1038/nrdp.2015.18. Return to content
  • Bauersachs J, et al. Hypertension. 2015;65:257-263. Return to content
  • Buonafine M, et al. Am J Hypertension. 2018;31:1165–1174. Return to content
  • Bakris GL, et al; FIDELIO-DKD Investigators. N Engl J Med. 2020;383(23):2219-2229. Return to content
  • American Diabetes Association Professional Practice Committee. Diabetes Care. 2022;45(suppl 1):S1-S264. Return to content
  • Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int Suppl. 2013;3(1):1–150. Return to content