Vol.64 No.2 March 2016
Review of studies for mechanisms of pyelonephritis and renal scarring
University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, Japan
Abstract
Pyelonephritis is a common bacterial infection in children, young women, elderly patients and patients who have underlying diseases. Renal scarring after pyelonephritis is problematic because of subsequent hypertension, impaired renal function or end-stage renal failure. Inflammatory processes in the kidney are responsible for renal tissue damage and scarring. Uropathogenic Escherichia coli(UPEC) is the common cause of pyelonephritis and the ability of UPEC to induce pyelonephritis is associated with the expression of various virulence factors including adhesive molecules, such as P- or Type 1-fimbriae which have adhesins at the very tip of their structure. UPEC facilitates a host innate immunity response through specific binding to receptors in uroepithelial cells. Several signal transduction pathways are activated resulting in the production of inflammatory cytokines which lead to the accumulation of polymorphonuclear leukocytes, macrophages and other inflammatory cells in the kidney tissue. The urinary concentration of these cytokines represents a possible biomarker of the severity of the inflammatory response or the degree of tissue damage resulting in renal scarring. Prevention of renal scarring after pyelonephritis depends on an early diagnosis, and rapid and effective antimicrobial treatment. Animal and clinical studies revealed various anti-inflammatory modalities including steroids, COX-2 inhibitors, antioxidants, angiotensin II receptor inhibitors and others to prevent renal scarring after pyelonephritis. Further studies are necessary to find more effective and safer drugs to prevent renal scarring during the treatment of pyelonephritis.
Key word
pyelonephritis, renal scarring, P pili, type 1 pili, innate immunity
Received
December 7, 2015
Accepted
December 16, 2015
Jpn. J. Chemother. 64 (2): 233-238, 2016
