The Histopathologic Spectrum of Kidney Biopsies in Patients with Inflammatory Bowel Disease

Ambruzs, Josephine M.; Walker, Patrick D.; Larsen, Christopher P.

doi:10.2215/cjn.04660513

Cited by 164 publications

(172 citation statements)

References 49 publications

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“…Glomerular disease is very rare. In a series of 83 patients with inflammatory bowel disease who had received a renal biopsy for various reasons, IgAN was the most common finding (24% of the cases), followed by proliferative glomerulonephritis (7%) and minimal-change disease (5%); the remaining cases exhibited vascular and/or tubular diseases 81 . In single cases, successful treatment of inflammatory colitis led to clinical remission of IgAN and a second renal biopsy revealed disappearance of glomerular IgA deposits and mesangial proliferative changes 82 .…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

The mucosa–kidney axis in IgA nephropathy

2015

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Links between IgA nephropathy (IgAN) and the mucosa have been recognized since the 1970s. In particular, the observation of visible haematuria induced by respiratory infections in patients with IgAN and the association of IgAN with diseases in which the mucosa plays a part, especially coeliac disease, have been taken as evidence of a mucosa-kidney axis. Here, we review current evidence that links the mucosa, in particular the gastrointestinal mucosa, and IgA produced by the bone marrow with IgAN. Genome-wide association studies in patients with IgAN have identified risk loci in genes involved in the intestinal mucosal integrity and immune network. Furthermore, the systemic immune response to mucosal antigens in IgAN is increased. Moreover, patients with IgAN have an increased reactivity to dietary proteins associated with subclinical intestinal mucosal inflammation. Associations between IgAN and gastrointestinal diseases have also been reported in a small number of patients, but whether these diseases share a common pathogenesis or whether gastrointestinal inflammation exacerbates IgAN is uncertain. Indeed, mucosal alterations such as infections could activate the innate immune system, aggravate a pre-existing IgAN and promote disease manifestations such as macrohaematuria. Various clinical interventions and trials targeting the mucosa or presumed mucosa-associated mechanisms have so far not yielded consistent findings and the results of ongoing trials are eagerly awaited.

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Section: Inflammatory Bowel Diseasementioning

confidence: 99%

The mucosa–kidney axis in IgA nephropathy

2015

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“…TIN has a strong association with IBD [65]. Other renal conditions in IBD patients include nephrolithiasis/urolithiasis, fistulas, glomerulonephritis, and renal amyloidosis [46, 66].…”

Section: Introductionmentioning

confidence: 99%

“…Other renal conditions in IBD patients include nephrolithiasis/urolithiasis, fistulas, glomerulonephritis, and renal amyloidosis [46, 66]. These manifestations may be secondary to systemic inflammation, susceptibility to autoimmunity, nutritional deficits, medication use, genetic predisposition, and infectious agents [65, 67]. One study reviewing renal biopsies in adults with IBD showed that TIN was present in 19 % of kidney biopsies [65].…”

Section: Introductionmentioning

confidence: 99%

Tubulointerstitial nephritis: diagnosis, treatment, and monitoring

et al. 2016

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Tubulointerstitial nephritis (TIN) is a frequent cause of acute kidney injury (AKI) that can lead to chronic kidney disease (CKD). TIN is associated with an immune-mediated infiltration of the kidney interstitium by inflammatory cells, which may progress to fibrosis. Patients often present with non-specific symptoms, which can lead to delayed diagnosis and treatment of the disease. Etiology of TIN can be drug-induced, infectious, idiopathic, genetic, or related to a systemic inflammatory condition such as tubulointerstitial nephritis and uveitis (TINU) syndrome, inflammatory bowel disease, or IgG4-associated immune complex multiorgan autoimmune disease (MAD). It is imperative to have a high clinical suspicion for TIN in order to remove potential offending agents and treat any associated systemic diseases. Treatment is ultimately dependent on underlying etiology. While there are no randomized controlled clinical trials to assess treatment choice and efficacy in TIN, corticosteroids have been a mainstay of therapy and recent studies have suggested a possible role for mycophenolate mofetil. Urinary biomarkers such as alpha1-microglobulin and beta2-microglobulin may help diagnose and monitor disease activity in TIN. Screening for TIN should be implemented in children with inflammatory bowel disease, uveitis, or IgG4-associated MAD.

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“…In addition, there were several reports about glomerulonephritis associated with Crohn's disease. According to a retrospective review of 83 kidney biopsies from patients with inflammatory bowel diseases, the frequency of immunoglobulin (Ig)A nephropathy was significantly higher in those patients than in control cases with renal biopsy specimens during the same period (24% vs. 8%) (Ambruzs et al 2014). Hence, it is also necessary to exclude the secondary glomerular diseases and vascular lesions originating from Crohn's disease by renal biopsy.…”

Section: Discussionmentioning

confidence: 99%