NaV Channels

These complement pathway abnormalities may induce PIG via a related process to that causing PIG in autoimmune diseases

These complement pathway abnormalities may induce PIG via a related process to that causing PIG in autoimmune diseases. the cause of the proteinuria and kidney dysfunction. Histological examination of the biopsy specimen showed glomeruli with an irregularly thickened GBM and bubble-like constructions in the capillary walls. Immunofluorescence staining did not display glomerular deposition of immunoglobulins, TAK-901 light chains, or complement parts. Congo reddish staining did not show amyloid deposition. Electron microscopy showed an irregularly thickened GBM with unusual constructions in the glomerular capillary walls including podocytic infolding and microspheres, suggesting PIG. There were no electron-dense TAK-901 deposits in the GBM, while numerous findings indicating podocyte injury were detected. Summary We present here the 1st reported case of PIG in a patient with multiple myeloma. The mechanisms underlying the development of PIG in multiple myeloma are unfamiliar, but may be associated with podocyte injury. strong class=”kwd-title” Keywords: Podocytic infolding glomerulopathy, Multiple myeloma, Microspheres Background Podocytic infolding glomerulopathy (PIG) was recently explained by Joh et al. [1] and offers attracted considerable attention because of the characteristic pathological changes to the glomeruli. The glomerular SFN changes are characterized by specific lesions of the thickened glomerular basement membrane (GBM) including microspheres, microtubular constructions, and podocytic infolding [1]. Individuals with PIG constantly present with proteinuria, and often possess kidney dysfunction [1]. PIG is not included in the current World Health Corporation classification of glomerular diseases. Only a small number of instances of PIG have been reported to day, and these have all been TAK-901 in Japan. These reports show that PIG tends to be associated with autoimmune abnormalities, such as systemic lupus erythematosus (SLE). Although some professionals consider that PIG should be classified as a new disease entity, it is also possible that PIG displays a transient morphological switch in individuals with conditions such as SLE and membranous nephropathy. In addition, the medical features and pathogenesis of PIG are TAK-901 still unclear. To elucidate these issues, it is important to accumulate info from reported instances. We present here the first reported case of PIG in a patient with multiple myeloma. Case demonstration A 79-year-old Japanese man presented with proteinuria, hypoalbuminemia, and increasing kidney dysfunction, and was admitted to his local hospital. He had a 3-yr history of hypertension, hyperlipidemia, and TAK-901 hyperuricemia with slight kidney dysfunction (serum creatinine level 1.1?mg/dL at age 76?years). He had been treated with an angiotensin II receptor blocker, statin, and allopurinol for 3?years. His proteinuria and hypoalbuminemia experienced gradually worsened, with increasing serum creatinine levels. On admission, his blood pressure was 140/67?mmHg. Physical exam revealed no lower leg edema. Laboratory checks showed designated hypergammaglobulinemia with hypoalbuminemia (total protein 8.1?g/dL, albumin 3.3?g/dL), kidney dysfunction (blood urea nitrogen 28?mg/dL, serum creatinine 1.28?mg/dL), hyperuricemia (uric acid 9.8?mg/dL), high levels of beta-2 microglobulin (5.9?mg/L) and IgG (3076?mg/dL), and low levels of IgA (35?mg/dL) and IgM (24?mg/dL). Pancytopenia and autoimmune abnormalities, such as anti-nuclear antibody, rheumatoid element, and hypocomplementemia, were not detected. Urinalysis showed proteinuria without hematuria (total urine protein and albumin excretion, 1423 and 949?mg/day time, respectively), and a high concentration of a tubulointerstitial injury marker (N-acetyl-beta-D-glucosaminidase 35.9 U/L). Serum and urine immunofixation electrophoresis showed monoclonal IgG() M proteins in the serum and Bence-Jones proteins in the urine. Bone marrow aspiration showed plasma cell proliferation (plasma cell count 22%). Considering these findings, the patient was diagnosed with multiple myeloma. A renal biopsy was performed to determine the cause of the proteinuria and kidney dysfunction. The biopsy specimen experienced 30 glomeruli, including one with global sclerosis and three with adhesive lesions. Histological exam showed glomeruli with an irregularly thickened GBM and a bubble-like appearance in the capillary walls (Number?1A, B). Immunofluorescence and Congo reddish staining showed no glomerular deposition of immunoglobulins (IgG, IgA, IgM), light chains (, ), match components (C3,.