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Abstract: SA-PO138

Crescents: An Eclipsed Presentation of Multiple Myeloma

Session Information

Category: Onconephrology

  • 1600 Onconephrology

Authors

  • Bajaj, Arrsh, Mercy Health St Elizabeth Youngstown Hospital, Youngstown, Ohio, United States
  • Castillo, Kathleen, Mercy Health St Elizabeth Youngstown Hospital, Youngstown, Ohio, United States
  • Sarac, Erdal, Mercy Health St Elizabeth Youngstown Hospital, Youngstown, Ohio, United States
  • Negrete, Hilmer O., Mercy Health St Elizabeth Youngstown Hospital, Youngstown, Ohio, United States
Introduction

Kidney involvement is common in multiple myeloma (MM) and is associated with increased mortality. Light chain cast nephropathy, monoclonal immunoglobulin deposition disease and light chain amyloidosis are the most frequent presentations. Very few cases are reported of MM presenting as crescentic glomerulonephritis (CGN). Here, we present a case of a female with rapidly progressive loss of renal function and proteinuria who was found to have MM and CGN.

Case Description

A 45-year old woman with h/o hypertension, diabetes mellitus, GERD, iron deficiency anemia, nephrolithiasis and COVID infection six months presented with worsening renal function. Her baseline creatinine three months prior was 0.88 mg/dL eGFR >60 and had recently increased to 2.81 mg/dL eGFR of 22. Laboratory investigations revealed a hemoglobin 8.3 g/dL, platelet count 404 x 10x9/L. Serum calcium and uric acid levels were within normal limits. Urinalysis showed proteinuria without hematuria with a urine protein/creatinine ratio 1.9 g/g, urine albumin/creatinine ratio 506 mg/g and urine albumin/protein ratio of 0.27. Complement levels, ANCA, Anti-GBM, ANA, RF and hepatitis serology were all unrevealing. Serum Kappa and Lambda free light chains were elevated with ratio being of 0.09. Bone marrow was done which demonstrated approximately 10% lambda restricted plasma cell clones. In view of progressive renal dysfunction she was admitted with the suspicious of light chain nephropathy for consideration of plasma exchange therapy. Kidney biopsy was obtained which showed findings consistent with crescentic GN, with weak linear IgG staining along glomerular basement membranes without evidence of cast nephropathy, monoclonal immunoglobulin deposition or amyloidosis. The patient was started on Cyclophosphamide-Bortezomib-Dexamethasone regimen and since then her kidney function has remained stable.

Discussion

Rare kidney findings in patients with MM include membranoproliferative GN, cryoglobulinemia, immunotactoid and fibrillary glomerulopathy. MM associated Crescentic GN is extremely rare. Its etiology and pathophysiology is unclear but it seems that treatment of MM may temporarily halt its progression as in this case.