Abstract
Inflammatory bowel disease (IBD) is profoundly associated with extraintestinal manifestations (EIM) that can involve almost every organ in our body. Although the exact etiology of IBD is still poorly understood, it is generally characterized by an overly aggressive inflammatory response in the intestinal mucosa. Renal damage is one of the manifestations encountered in Crohn’s disease (CD) and ulcerative colitis (UC) and it accounts for 4% - 23% of IBD patients. The common renal complications of IBD include: glomerulonephritis, tubulointerstitial nephritis, nephrolithiasis, amyloidosis and iatrogenic complications of IBD treatment. Several hypotheses have emerged to explain the pathogenic mechanisms underlying the prevalence of IBD-induced kidney injuries. The present work aims to elucidate the pathological principles that drive secondary renal injury in individuals with IBD and highlight the currently used therapeutic strategies for evaluating, monitoring and treating kidney complications-related IBD.
Highlights
Inflammatory bowel disease (IBD) is an idiopathic disease characterized by severe inflammation of the gastrointestinal tract
IL-17 was absent in renal tissue with primary IgA Nephropathy (IgAN). These findings suggest the simultaneous involvement of IL-17 in both worsening intestinal inflammation and enhancing rapidly progressive IgAN development in Crohn’s disease (CD) patients [24]
The extraintestinal manifestations (EIM) of IBD involves a range of renal complications including nephrolithiasis, tubulointerstitial nephritis, glomerulonephritis, amyloidosis and drug-related nephrotoxicity
Summary
Inflammatory bowel disease (IBD) is an idiopathic disease characterized by severe inflammation of the gastrointestinal tract. Renal complication is considered as one of the EIMs and accounts for 4% - 23% of IBD patients [3]. The association of kidney diseases with IBD has been reported in many clinical and experimental studies; the underlying mechanism(s) are not fully elucidated. Several hypotheses have been postulated to explore the nature of this involvement whether kidney injury occurs as a secondary complication to IBD, shares the same patho-immunological origin, is an autoimmune disease by itself, or it is provoked as side-effect to therapy.
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