Glomerular injury may occur as a result of immune dysfunction in patients with remote lymphoplasmacytic
neoplasms. Glomerular injury concurrent with direct infiltration of the kidney by lymphoplasmacytic
neoplasms has been reported but is not extensively characterized. We identified 18 patients, all presenting with elevated serum
creatinine and many with
proteinuria, whose renal biopsies showed direct involvement of kidney by a variety of
neoplasms, including chronic leukocytic
leukemia/
small lymphocytic lymphoma (n = 7),
diffuse large B-cell lymphoma (n = 6),
multiple myeloma (n = 4), or B-cell
lymphoblastic lymphoma (n = 1). In 10 cases (55%), there was coexistent glomerular pathology: 5 of these cases, including
glomerulonephritis with
membranoproliferative glomerulonephritis-like pattern of injury (n = 4) and
membranous nephropathy (n = 1), featured deposition of
immune complexes; 2 demonstrated deposition of monoclonal
immunoglobulin components: λ light chain
amyloidosis (n = 1) and light chain deposition disease (n = 1); 2 showed
minimal change disease; and, in 1 case, there was focal crescentic pauci-immune-type
glomerulonephritis. In addition, 1 biopsy revealed
diabetic nephropathy and 3 showed nonspecific ischemic changes. In the remaining 4 cases, there were no significant glomerular abnormalities. In 11 cases (61%), the diagnosis of lymphoproliferative disease was established following the kidney biopsy. Our study indicates that lymphoplasmacytic
neoplasms may be first diagnosed in renal biopsies performed for evaluation of renal dysfunction with or without
proteinuria. Concurrent glomerular injury may be a direct result of the lymphoplasmacytic disorder through a
paraprotein deposition process resulting in
amyloid or
monoclonal immunoglobulin deposition disease, or may be caused indirectly through immune-mediated mechanisms, as in the cases of
glomerulonephritis with
membranoproliferative glomerulonephritis-like pattern of injury,
membranous nephropathy, and possibly
minimal change disease.