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Abstract: PO1857

Proliferative Glomerulonephritis with Monoclonal IgG Deposits (PGNMID): A Report of Two Cases Managed with Renin-Angiotensin-Aldosterone System (RAAS) Inhibition Alone

Session Information

Category: Trainee Case Report

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials


  • Vynnyk, Marianna, Lenox Hill Hospital, New York, New York, United States
  • DeVita, Maria V., Lenox Hill Hospital, New York, New York, United States
  • Rosenstock, Jordan L., Lenox Hill Hospital, New York, New York, United States

PGNMID is a relatively rare disorder with monoclonal immunoglobulins (Ig) deposition in glomeruli that resembles immune complex glomerulonephritis (GN), after exclusion of other related disorders such as amyloidosis and cryoglobulinemia. The pathogenesis and management of PGNMID remains uncertain, especially if no systemic clonal disorder is found, which is frequently the case. Some groups have recommended anti-plasma cell or anti-B cell therapy in most if not all cases, even if a clone is not identified. We present two cases of PGNMID that were managed with RAAS blockade alone and whose renal disease remained stable over 6 and 10 years of follow up.

Case Description

Two cases were identified who had prolonged follow up with PGNMID and no immunosuppressive treatment. Charts were reviewed retrospectively and data collected from time of biopsy until most recent follow up.
Case 1 is a 25 year old obese black woman with recent onset of hypertension who presented with serum creatinine (sCr) 1.4mg/dl. Urinalysis (UA) showed 1+ protein and no blood. 24hr urine protein was 296mg. Renal biopsy (done as she had positive antiphospholipid antibodies) revealed PGNMID (IgG kappa) with diffuse mesangial proliferation and focal sclerosing GN with focal fibrous crescents. There was no evidence of thrombotic microangiopathy. Serum and urine immunofixation (IF) were negative for monoclonal protein. Bone marrow biopsy was unremarkable. The patient was treated with angiotensin-receptor blocker (ARB) without immunosuppressive therapy. Six years later the most recent sCr was 1.5mg/dl and urine protein-creatinine ratio (PCR) was 1100mg/g.
Case 2 is a 41 year old white woman who presented with sCr 0.6mg/dl. UA had 3+ protein and no blood. 24hr urine protein was 2.3g. Renal biopsy showed PGNMID (IgG kappa) with mesangial and endocapillary proliferation. Serum and urine IF were negative for monoclonal proteins. Bone marrow biopsy was not done. The patient was treated with an angiotensin-converting enzyme inhibitor (ACEI) alone. After ten years of follow up, her sCr was 0.7mg/dl, and urine PCR was 632mg/g.


We report 2 cases of PGNMID with stable renal function and proteinuria after 6 and 10 years of RAAS therapy alone. This suggests that not all patients with PGNMID may require immunosuppression.