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: TH-PO0551

A Toothache with a Twist: Dental Abscess Unmasking IgAN

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Lorenzo Capps, Maria Jose, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States
  • Vega Batista, Franklyn, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States
  • El-Charabaty, Elie, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States
Introduction

IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Its pathogenesis is linked to mucosal immune dysregulation and production of galactose-deficient IgA1, typically triggered by respiratory or gastrointestinal stimulation. Odontogenic infection remains an underrecognized potential mucosal trigger.

Case Description

A 31-year-old woman with no significant past history presented with one day of bilateral ankle edema and arthralgias, in the setting of a partially treated right mandibular periapical abscess managed nine weeks earlier with amoxicillin-clavulanate and NSAIDs. She denied fever, gross hematuria, or upper respiratory symptoms. The examination revealed facial flushing, a dental abscess, and 1+ ankle edema. Blood pressure was 204/106 mmHg. Creatinine was 1.55 mg/dL, albumin 3.3 g/dL, and urine protein-to-creatinine ratio 5.7 g/g; urinalysis showed 2+ protein, 3+ blood, and 15 RBC/hpf. C3 was normal with mildly elevated C4. ANA, anti-dsDNA, ANCA, anti-GBM, and PLA2R were negative; Strep A throat PCR was negative. Serum free light chains showed an elevated kappa/lambda ratio. Renal vein duplex was patent. CT of the facial bones confirmed a periapical abscess at the right second mandibular premolar; no organism was isolated. Kidney biopsy demonstrated mesangioproliferative, crescentic, necrotizing glomerulonephritis with one necrotic glomerulus and no endocapillary proliferation, consistent with IgAN. She received intravenous antibiotics with planned tooth extraction at discharge and eventual steroid therapy initiation.

Discussion

Negative serologies, normal C3, patent renal veins, and biopsy findings argued against postinfectious, lupus, ANCA-associated, anti-GBM, and membranous disease, supporting primary IgAN. The temporal link between a persistent odontogenic infection and new nephritic-nephrotic crescentic IgAN aligns with the four-hit model, in which sustained mucosal antigenic stimulation drives galactose-deficient IgA1 production, immune complex deposition, and glomerular injury. The oral cavity is increasingly recognized as a relevant mucosal site, though microbiologic confirmation was not obtained. Persistent dental infection may act as a mucosal trigger or amplifier of IgAN activity. Glomerular disease should be considered in patients with concurrent odontogenic infection and new hypertension, edema, or proteinuria, with prompt source control alongside nephrology evaluation.