Slowing Progression of Chronic Kidney Disease

Paul Drawz, Thomas H. Hostetter, Mark E. Rosenberg

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations


Early identification of CKD provides an opportunity to implement therapies to improve kidney function and slow progression. To understand the epidemiology of progression, normal and CKD-related rates of decline in kidney function must be defined. Competing risks exist when occurrence of death and development of ESRD are considered. Common pathophysiologic mechanisms underlie the progression of most kidney diseases, including glomerular capillary hypertension, renal fibrosis, podocyte loss, proteinuria and activation of systems such as the RAAS and intrarenal activation of developmental and injury pathways. These pathophysiologic factors present potential targets for therapy. Controlling blood pressure may be critical in achieving clinically important outcomes. Therapy directed at inhibiting the RAAS remains the mainstay of treatment. Single agent inhibition of this system is as efficacious as dual blockade with fewer adverse effects. Other therapies include correction of metabolic acidosis, dietary protein restriction, and new models for delivering care to patients with CKD. Emerging therapies targeting endothelin, uric acid, kidney fibrosis, oxidant stress, and kidney augmentation hold promise for the future.

Original languageEnglish (US)
Title of host publicationChronic Renal Disease
PublisherElsevier Inc.
Number of pages15
ISBN (Electronic)9780124116160
ISBN (Print)9780124116023
StatePublished - 2015

Bibliographical note

Funding Information:
This work was supported in part by NIH grant K23DK087919 (PD).

Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.


  • Blood pressure target
  • Chronic kidney disease
  • Endothelin
  • Progression
  • Renin-angiotensin-aldosterone


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