Clinical and Presentation and Pathology Spectrum of Kidney Damage in Non-Hodgkin Lymphoma/Leukemia and Lymphoplasmacytic Lymphomas
Non-Hodgkin lymphoma / leukaemia (NHL / CLL) and lymphoplasmacytic lymphoma (LPCL) renal damage is caused by many mechanisms: tumour mass localization; clonal cell expansion; secretion of hormones, cytokines and growth factors; metabolic, electrolyte and coagulation disorders; paraprotein deposition; and complications of care. Kidney damage symptoms can overshadow and even exclude overt NHL / CLL or LPCL, and the diagnosis is indicated only by renal pathology findings. In patients with NHL / CLL or LPCL, the goal was to assess the clinical appearance and pathology of kidney damage. We searched for data for 158 patients with lymphoproliferative disorders (LPD) and pathology-proven kidney lesions using an electronic database and intentionally built graph. Further research omitted patients with multiple myeloma, Hodgkin’s lymphoma, Castleman ‘s disease, “primary” AL amyloidosis and “primary” light chain deposition illness. The study group consisted of 24 patients, 14 (58.3 percent) of whom were male and 10 (48.3 percent) of whom were male. NHL / CLL was diagnosed in 16 patients (66.6 percent), Waldenström’s Macroglobulinemia (WM) in 7 patients (29.1 percent) and Franklin ‘s disease (FD) in 1 (4.1 percent). 10 (41.7%) of patients had nephrotic syndrome (NS), 17 (70.8%) had reduced kidney function and 6 (25.2%) had both NS and renal dysfunction. Glomerulonephritis (GN) was observed in 11 (45.8%) of patients by pathology, GN trend was associated with monoclonal paraproteins in 4 cases, and paraneoplastic GN was considered in 7 cases. Interstitial nephritis was seen in 10 (41.6 percent) patients, 8 of them attributable to specific lymphoid infiltration; and only 3 (12.5 percent) cases were complicated by amyloidosis. Patients with NHL / CLL or LPCL that have renal defects exhibit a number of patterns of pathology that are hardly clinically predictable. Specific lymphoid interstitial infiltration and paraneoplastic glomerulonephritis with MN and MPGN patterns were most commonly present in our patient sequence. In certain instances of NS and/or acute damage to the kidney (A) For the diagnosis of NHL / CLL and LPCL, renal biopsy, precluded or accompanied by scrutinous haematological work-up, is critical in many cases of nephrotic syndrome and/or acute kidney injury.
E. V. Zakharova
Department of Nephrology, City Clinical Hospital n.a. S.P. Botkin, Moscow, Russian Federation.
E. S. Stolyarevich
Department of Pathology, City Nephrology Centre, Moscow, Russian Federation.
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