Renal involvement in paediatric inflammatory bowel disease

Mohamed Mutalib

doi:10.1007/s00467-019-04413-5

Abstract

Inflammatory bowel disease (IBD), which includes Crohn’s disease, ulcerative colitis and inflammatory bowel disease unclassified, is a chronic inflammatory disorder that predominantly affects the gastrointestinal (GI) tract and has a rising incidence in both children and adults. Symptoms are caused by inappropriate inflammatory response triggered by interaction between the environment, gut microbiome and host immune system in a genetically susceptible individual. Extranintestinal manifestations of IBD are common and can affect any body system outside the gut; they can precede or run parallel to GI inflammation. Renal involvement in IBD is uncommon and can be part of extraintestinal manifestation or metabolic complications of IBD. Many medications used to treat IBD can cause renal damage. Renal manifestation in children with IBD can range from asymptomatic biochemical abnormalities to variable stages of renal impairment with significant morbidity and even mortality burden.

Highlights

Inflammatory bowel disease (IBD) is a chronic, relapsing and remitting inflammatory condition predominantly affecting the gastrointestinal (GI) tract that results from complex interplay of the individual’s genetic makeup, the environment, the gut microbiota and the host immune response [1]
Crohn’s disease is characterised by transmural inflammation that can affect any part of the GI tract with characteristic skip lesions of healthy tissues, while ulcerative colitis is a continuous mucosal inflammation largely confined to the colon
Extraintestinal manifestations of IBD are disorders linked to IBD and can affect virtually any body system outside the GI tract [3]

Summary

Introduction

Inflammatory bowel disease (IBD) is a chronic, relapsing and remitting inflammatory condition predominantly affecting the gastrointestinal (GI) tract that results from complex interplay of the individual’s genetic makeup, the environment, the gut microbiota and the host immune response [1]. Secondary tubulointerstitial nephritis can result from hypokalaemia (due to GI losses, in patients with stomas and extensive bowel surgery), hyperoxaluria and renal amyloidosis Such a diverse aetiology may explain the discrepancy in treatment outcome: some authors have reported improvement in renal function with optimisation of IBD treatment, while others have found no such correlation [36]. They are frequently used in isolation or combined with other immune modulators such as azathioprine [52]. Apart from a single case report of an adult patient who developed lupus nephritis after using golimumab (a new anti TNFα), there is no data on the renal effects of golimumab [57]. The renal injury recovered completely with systemic steroids and the authors were able to reintroduce Vedolizumab with pre- and postadministration steroid cover with no further effects on renal function [63]

Conclusion

Summary points

Findings

Compliance with ethical standards