Tamm-Horsfall protein (THP) is produced exclusively by the kidney, where it is released into both the urine and the circulation. Although the primary form of circulating THP is nonpolymerizing, urinary THP exists as a mix of polymerizing and nonpolymerizing forms. Urinary THP has been shown to play roles in such disparate processes as prevention of urinary tract infections and kidney stone formation, along with the regulation of multiple ion channels within the kidney. The generation of THP knockout mouse models has allowed the investigation of these phenomena and shown a prospective role for circulating THP in ischemia-reperfusion acute kidney injury as well as sepsis. Recent studies have suggested that THP is protective in ischemic injury owing to its inhibition of oxidative stress via the calcium channel transient receptor potential cation channel, subfamily M, member 2 t(TRPM2), and protection in sepsis is at least partially due to THP's promotion of macrophage function.
Keywords: Tamm-Horsfall protein; kidney injury; oxidative stress; sepsis; uromodulin.
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