ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO893

Intermittent Hematuria in a Patient with Crohn Disease: A Case Report

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Warner, David M., University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
  • Gudsoorkar, Prakash Shashikant, UC Health Medical Center, Cincinnati, Ohio, United States
  • Nysather, Jacob A., UC Health Medical Center, Cincinnati, Ohio, United States
Introduction

There are a variety of secondary causes of IgA vasculitis (IgAV) and glomerulonephritis in adults. We report a rare case of IgAV with crescentic glomerulonephritis in a patient with Crohn Disease (CD) treated with infliximab.

Case Description

A 30-year-old male with biopsy-proven CD on infliximab developed intermittent gross hematuria, elevated serum creatinine (SCr), and a palpable purpuric lesion. Genitourinary cancer, hemorrhagic cystitis, and infectious etiologies were ruled out and his infliximab was held.

He was referred to nephrology after 6 months of symptom onset. Glomerular serology work-up revealed polyclonal IgA and IgG on immunofixation with a protein gap of 5.1 g/dL; the rest was unremarkable. A kidney biopsy (Figure 1) showed focal fibrocellular crescents with diffuse mesangial expansion and hypercellularity. Immunofluorescence (IF) confirmed IgA glomerulonephritis M1, E1, S0, T1, C1. Pulse steroids with a slow taper and valsartan were started, with improvement in SCr and hematuria (Table 1).

Discussion

Secondary causes of IgA nephropathy (IgAN) include HIV, HBV, HCV, renal cell carcinoma, celiac disease, and lymphoma. Less common secondary causes include inflammatory bowel disease (IBD) and infliximab treatment.

CD is thought to cause IgAN through increased IgA glycosylation, which correlates with disease severity, and elevated levels of the apoptosis inhibitor of macrophages (AIM), leading to co-localization of IgA, IgG, and IgM in the glomeruli.

Infliximab has been shown to cause secondary IgAN; however, his intermittent hematuria and worsening SCr persisted despite discontinuing infliximab, suggesting CD progression linked to IgAV and nephritis.

A recent Japanese study showed patients with IBD have a higher cumulative incidence of IgAN compared to non-IBD (p=0.0028), with CD having a strong association compared to ulcerative colitis.

Pre- and Post-Treatment Labs
Lab ValuePre-BiopsyPost-TreatmentReference Value
Serum Cr1.84 mg/dL1.09 mg/dL0.60-1.30 mg/dL
Serum Cystatin C2.23 mg/dL1.77 mg/dL0.60-1.00 mg/dL
Urine Protein/Cr3.163.05<0.15
Urine RBC>100/HPF25/HPF0-3/HPF