Membranoproliferative Glomerulonephritis Associated with Coeliac Disease and Autoimmune Thyroiditis
- Glomerular Diseases: From Inflammation to Fibrosis - II
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: From Inflammation to Fibrosis
- Randhay, Ashveer, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Sit, Shu Yin, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Tan, Mei Ying, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
- Dukka, Hari, University Hospitals of Derby and Burton NHS Foundation Trust, Derby, United Kingdom
Membranoproliferative glomerulonephritis (MPGN) is a pattern of glomerular injury which can be related to immune complex deposition from infections, paraproteinemia and autoimmune diseases. Rarely, there has been associations between MPGN and coeliac disease and MPGN and autoimmune thyroiditis described in literature. We present a case of a patient who had all three diagnoses and treated with a Sodium/glucose cotransporter-2 inhibitor (SGLT2i).
A 21 year old female presented with four month history of leg oedema, and subsequently confirmed nephrotic syndrome. She had recent diagnosis of hypothyroidism and coeliac disease prior to this presentation, and was established on gluten free diet and levothyroxine. At presentation, urine protein creatine ratio was 403.4mg/mmol with serum albumin of 2.9 g/dL. Complements C3 and C4 were normal, with no detected paraprotein and negative immunology (ANA, cryoglobulins, ANCA) and virology screen. Thyroglobulin and TSH receptor antibody levels were raised. Percutaneous kidney biopsy was performed which showed immune complex glomerulonephritis with MPGN pattern.
She was commenced on maximally tolerated Angiotensin-converting enzyme inhibitor (ACEi) and SGLT2i. After 8 months, there was resolution of oedema, and marked improvement of proteinuria (123.5 mg/mmol) without need for immunosuppressive therapy.
There have been five case reports of MPGN with nephrotic syndrome, associated with autoimmune thyroiditis. There have been biopsy studies showing thyroid antibody deposition in glomeruli, supporting this association. There have been four case reports of MPGN associated with coeliac disease. In these cases, a mix of pediatric and adult patients, hypocomplementemia was observed. In all the cases, gluten-free diet was sufficient to improve gastrointestinal symptoms, resolution of oedema and reduction in proteinuria.
As we did in this case, we believe supportive therapy for MPGN associated with coeliac disease and/or autoimmune thyroiditis should include management of the associated conditions with gluten-free diet and maintaining euthyroid state. In addition, ACEi and SGLT2i have a role in managing MPGN, and may help avoid need for immunosuppression in such cases.