CD59 protects rat kidney from complement mediated injury in collaboration with Crry

Abstract

In rats, CD59 maintains normal integrity of the kidney in collaboration with Crry in rats against complement-mediated damage in vivo.

Urine protein markers distinguish stone-forming from non-stone-forming relatives of calcium stone formers

“…Little is known about the relationship of CD59 to stone disease. CD59 is an 18-to 20-kDa glycoprotein inhibitor of the membrane attack complex of complement that is thought to play a role in protecting the kidney from complement-mediated injury (47). CD59 deficiency and increased urinary excretion of CD59 have been linked to renal tissue damage (18,24,45).…”

Anti-C5a complementary peptide ameliorates acute peritoneal injury induced by neutralization of Crry and CD59

“…Uncontrolled C activation can induce peritoneal damage, and membrane C regulators (CRegs) play important roles in controlling activation of C as shown in our previous reports (24 -26). We previously showed that neutralization of the CRegs Crry and CD59 in rat peritoneum caused development of acute peritoneal injury (25), and in relevant models it also triggered arthritis and nephritis (20,39). The animal model described here can be used to develop antiComplement agents for prevention of acute peritoneal injury associated with C activation in the peritoneum.…”

C5b-9 does not mediate chronic tubulointerstitial disease in the absence of proteinuria

“…Irreversible damage to the glomerular capillary wall and ultrafiltration of serum-derived proteins into the tubular lumen is one of the nonimmunologic mechanisms that evoke secondary tubulointerstitial disease, a process that is independent of the original inciter(s) of glomerular injury [2, 3]. Over the last two decades, substantial clinical [4-12] and experimental [12][13][14][15][16][17][18][19][20][21] evidence has accumulated to support the hypothesis that the abnormal presence of serum-derived complement components in the tubular lumen during proteinuric states leads to the assembly of the sublytic terminal membrane attack complex (C5b-9) on the brush border of tubular epithelial cells (TECs), and this is an important factor in the causation of tubulointerstitial damage in proteinuric renal diseases [22,23].In previous studies, we examined the progression of tubulointerstitial damage in three animal models of nonimmune-mediated chronic proteinuric renal disease (puromycin aminonucleoside, the remnant kidney model, and adriamycin nephropathy) using rats unable to generate C5b-9 due to the absence of the C6 complement component [19,21,24]. In these models, C5b-9 was localized to the lumen and brush border of TECs [19,21].…”