Abstract: PUB131
From Gut to Glomerulus: IgAN in Crohn Disease
Session Information
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Author
- Wieczorek, Peter, NYU Langone Health, New York, New York, United States
Introduction
Secondary IgA nephropathy has been increasingly associated with chronic inflammatory conditions, including inflammatory bowel disease (IBD). Crohn’s disease, a relapsing inflammatory disorder of the gastrointestinal tract, has been linked to several extraintestinal manifestations; however, renal involvement remains relatively uncommon and underrecognized. Chronic intestinal inflammation and mucosal immune dysregulation may contribute to aberrant IgA production and deposition within the glomeruli, highlighting a potential gut–kidney axis
Case Description
A 37 year old male with a history of crohn’s disease complicated by complex perianal disease and small bowel obstruction resulting in diverting ileostomy who presented to clinic for an elevated serum creatinine 1.3 - 1.5 of several years duratiin accompanied by recent minimal proteinuria UPCR 0.3 g/g and evidence of microhematuria. No family history of renal disease, recent or significant NSAID use. His only medication is Infliximab.
Vital signs: BP 126/78, Pulse 86/min, Temp 98.3, Resp 16, Spo2 98% on RA.
Physical exam is largely unremarkable. No extremity edema or swelling. Normal ostomy output. Abdomen soft and nontender to palpation. Lungs clear to auscultation. Regular rate and rhythm of heart.
Given proteinuria, hematuria, and evidence of CKD a renal biopsy was pursued which revealed IgA nephropathy with oxford classification score of M0 E0 S1 T0 C0, no proliferative glomerular lesions, mild IFTA, 4 of 17 glomeruli globally sclerosed. Given indolent course, he was started on RAAS blockade to address proteinuria.
Discussion
IgA pathogenesis follows a "4-hit" hypothesis. These hits include production of abberant galactose-deficient IgA, creation of auto-antibiodies against this abberant IgA, formation of pathogenic immune complexes between Gd-IgA and autoantibodies, and deposition of these complexes in the glomerular mesangium. Crohn's disease can increase the likelihood of developing IgA nephropathy; chronic intestinal inflammation disrupts mucosa and lead to abberant IgA production.