Document Type

Article

Publication Date

9-1-2017

Identifier

PMCID: PMC5513797 DOI: 10.1016/j.prostaglandins.2017.01.003

Abstract

Hyperfiltration is a well-known risk factor in progressive loss of renal function in chronic kidney disease (CKD) secondary to various diseases. A reduced number of functional nephrons due to congenital or acquired cause(s) results in hyperfiltration in the remnant kidney. Hyperfiltration-associated increase in biomechanical forces, namely pressure-induced tensile stress and fluid flow-induced shear stress (FFSS) determine cellular injury and response. We believe the current treatment of CKD yields limited success because it largely attenuates pressure-induced tensile stress changes but not the effect of FFSS on podocytes. Studies on glomerular podocytes, tubular epithelial cells and bone osteocytes provide evidence for a significant role of COX-2 generated PGE2 and its receptors in response to tensile stress and FFSS. Preliminary observations show increased urinary PGE2 in children born with a solitary kidney. FFSS-induced COX2-PGE2-EP2 signaling provides an opportunity to identify targets and, for developing novel agents to complement currently available treatment.

Journal Title

Prostaglandins & other lipid mediators

Volume

132

First Page

59

Last Page

68

MeSH Keywords

Animals; Biomechanical Phenomena; Dinoprostone; Eicosanoids; Humans; Kidney Glomerulus; Mechanical Phenomena; Podocytes

Keywords

Fluid flow shear stress; Hyperfiltration; Podocytes; Prostaglandin E(2); Prostanoid receptors; Tensile stress

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