Case Presentation: 54 years old man with a history of hypertension was hospitalized due to elevated BUN/creatinine of 33/4.6 mg/dL and Hb of 9.9 mg/dL (baseline 15). He endorsed dyspnea on exertion, anorexia and weight loss of 15 pounds in 6 months. One month ago, he was treated for acute bronchitis with levofloxacin and was noted to have a creatinine change from 0.9 to 1.5, attributed to dehydration. Physical exam was notable for normal vital signs and new holosystolic murmur at the apex. Additional labs revealed hypoalbuminemia (2.7), hematuria (143 RBC), random urine protein 120 mg/dl and ESR of 61mm/h. Further glomerulopathy work-up was negative. Electrophoresis with immunofixation revealed two monoclonal spikes (IgG-Kappa). Flow cytometry and bone marrow biopsy showed Kappa monoclonal B cell population with 11; 14 translocation and p53 deletion, diagnosis of Mantle Cell Lymphoma (MCL). A kidney biopsy revealed membranoproliferative glomerulonephritis with IgG and Kappa immune deposits, likely to be related to MCL. Concomitantly, blood cultures grew Group D enterococci. A transesophageal echocardiogram revealed severe mitral regurgitation and a small vegetation. Diagnosis of bacterial endocarditis was made and the patient underwent mitral valve replacement (MVR). Pathological examination of mitral valve confirmed the diagnosis. Post-surgical creatinine improved to 2.7 from a peak of 5. Treatment was continued as an outpatient with antibiotics and chemotherapy induction regimen with a plan for autologous stem cell transplantation.
Discussion: Membranoproliferative glomerulonephritis (MPGN) is a pattern of glomerular injury characterized by light microscopic changes on renal biopsy. It was recently reclassified as complement-mediated and immune complex-mediated (IC-MPGN). Damage in IC-MPGN results from glomerular immunoglobulin deposition and complement pathway activation as a result of infections, autoimmune diseases or monoclonal gammopathies. The rapid deterioration of kidney function with a decrease in the glomerular filtration rate >50% in <3 months in our patient, defined a rapidly progressive glomerulonephritis. Further results of kidney biopsy confirmed the diagnosis of MPGN with monoclonal IgG deposits. The degree of kidney impairment in MPGN varies and can present as rapidly progressive glomerulonephritis. Final workup in our patient revealed the presence of two entities associated with glomerular immune complex deposition: bacterial endocarditis and monoclonal gammopathy secondary to Non-Hodgkin’s lymphoma (Mantle cell lymphoma).
Conclusions: Non-Hodgkin’s lymphoma is a rare cause of IC-MPGN; furthermore, concomitant association with endocarditis, an infectious process capable of inducing a similar immune complex deposition, makes this case even more unique. Hospitalized patients with rapid progression of renal failure need a comprehensive and quick workup as delay in the underlying diagnosis can cause irreversible kidney damage.