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• W2072719500 abstract "Light chain deposition disease (LCDD) is characterized by the deposition of κ or λ immunoglobulin light chains in many organs, including the kidney.1Colombat M. Stern M. Groussard O. et al.Pulmonary cystic disorder related to light chain deposition disease.Am J Respir Crit Care Med. 2006; 173: 777-780Crossref PubMed Scopus (92) Google Scholar, 2Randall R.E. Williamson Jr, W.C. Mullinax F. Tung M.Y. Still W.J. Manifestations of systemic light chain deposition.Am J Med. 1976; 60: 293-299Abstract Full Text PDF PubMed Scopus (302) Google Scholar The disease frequently is associated with multiple myeloma or other lymphoplasmacytic proliferative disorders, although a significant number of patients with LCDD show no evidence of bone marrow abnormalities.3Ganeval D. Noel L.H. Preud'homme J.L. Droz D. Grunfeld J.P. Light-chain deposition disease: Its relation with AL-type amyloidosis.Kidney Int. 1984; 26: 1-9Crossref PubMed Scopus (169) Google Scholar LCDD frequently has been reported to recur after renal transplantation, inevitably followed by graft failure.3Ganeval D. Noel L.H. Preud'homme J.L. Droz D. Grunfeld J.P. Light-chain deposition disease: Its relation with AL-type amyloidosis.Kidney Int. 1984; 26: 1-9Crossref PubMed Scopus (169) Google Scholar Multiple myeloma also has been considered a major cause of light chain deposition in renal allografts and to show a high rate of recurrence.4Walker F. Bear R.A. Renal transplantation in light-chain multiple myeloma.Am J Nephrol. 1983; 3: 34-37Crossref PubMed Scopus (25) Google Scholar, 5Gerlag P.G. Koene R.A. Berden J.H. Renal transplantation in light chain nephropathy: Case report and review of the literature.Clin Nephrol. 1986; 25: 101-104PubMed Google Scholar The most characteristic feature of LCDD is nodular glomerulopathy resembling diabetic glomerulosclerosis. The mesangial nodules are composed of extracellular matrix proteins admixed with the monoclonal light chain deposits. Glomerular basement membranes (GBMs), tubular basement membranes (TBMs), and vessel walls are variably thickened as a consequence of subendothelial light chain deposition. Clinically, various degrees of proteinuria and renal insufficiency are common manifestations,2Randall R.E. Williamson Jr, W.C. Mullinax F. Tung M.Y. Still W.J. Manifestations of systemic light chain deposition.Am J Med. 1976; 60: 293-299Abstract Full Text PDF PubMed Scopus (302) Google Scholar and rapid deterioration in kidney function can occur as a consequence of disease progression. We report a case of LCDD progression more than 4 years after renal transplantation, with a retrospective analysis of serial biopsy specimens that showed gradual progression of κ light chain deposition in the renal allograft. A 61-year-old man received an HLA-identical, blood group type ABO–compatible renal transplant from his sister. The cause of his renal failure was unknown. Cyclosporine, mycophenolate mofetil, and methylprednisolone were administered as immunosuppressive therapy. A small amount of proteinuria, ± to + by dipstick (∼0.5 g/d), had been found 3 days after the transplantation (Fig 1). Renal biopsy was performed on postoperative days 18 and 43 because of a slight increase in serum creatinine level and showed no evidence of rejection and unremarkable glomerular changes (Fig 1). Two years later, serum creatinine level increased to 3 mg/dL (265 μmol/L; estimated glomerular filtration rate, 15.84 mL/min/1.73 m2 [0.26 mL/s/1.73 m2]), and renal biopsy was performed again on postoperative day 774. It showed very mild tubulointerstitial rejection without apparent glomerular changes. Although methylprednisolone therapy had been continued and the patient was additionally administered intravenous 15-deoxyspergualin (total, 1,750 mg), serum creatinine level remained high, and another renal biopsy was performed on postoperative day 913. The biopsy specimen showed chronic allograft nephropathy without apparent glomerular changes. To prevent further deterioration of graft function, cyclosporine therapy was replaced with tacrolimus, and the doses of mycophenolate mofetil and methylprednisolone were increased. However, despite these dose adjustments, kidney function gradually deteriorated. The final biopsy on postoperative day 1,543, when serum creatinine and blood urea nitrogen levels had increased to 6.0 mg/dL (530 μmol/L; estimated glomerular filtration rate, 7.12 mL/min/1.73 m2 [0.12 mL/s/1.73 m2]) and 90 mg/dL (32 mmol/L) accompanied by slight proteinuria, respectively. Light microscopic examination of the final biopsy specimen showed diffuse interstitial fibrosis with tubular atrophy, with no evidence of rejection (Fig 2A). One third of glomeruli were globally sclerotic, and residual glomeruli showed widening of the mesangial area with sclerosis (Fig 2B). The basement membrane of Bowman's capsule, TBM, and vessel walls were thickened and tortuous. Arteriolar hyalinosis was severe. Direct immunofluorescence examination showed diffuse linear deposition of κ light chains along the GBM, mesangial area, TBM, and Bowman's capsule (Fig 2C). However, staining for λ light chain was negative (Fig 2D), as well as immunoglobulin G, immunoglobulin M, and immunoglobulin A. Congo red staining for amyloid was negative. Electron microscopy showed band-like subendothelial electron-dense deposits along the GBM (Fig 2E). Electron-dense deposits were also present along the TBM (Fig 2F) and Bowman's capsule and showed deposition of granular to powdery electron-dense material. Pathological changes were mostly consistent with the diagnosis of LCDD. Staining for κ light chains was negative in the biopsy specimens from day 43 (Fig 3E). In biopsy specimens obtained on day 774, weak immunofluorescence staining for κ light chain was detected along the GBM, TBM, and Bowman's capsule basement membrane (Fig 3I), which had become more intense in the biopsy specimens obtained on day 913 (Fig 3M). Electron microscopy showed no deposits in the GBM or TBM on day 0 (Fig 3B and C) or 43 (Fig 3F and G). In the biopsy performed on day 774, electron-dense deposits were detected along the GBM and TBM, but the deposits were very fine and powdery, without continuity (Fig 3J and K). However, the deposits had become more apparent in the biopsy specimen from day 913 (Fig 3N and O). The intensity of κ light chain deposition was proportional to the amount of the electron-dense deposits. The patient needed to be started on hemodialysis therapy again 5 days after the final biopsy. Serum and urine immunoelectrophoresis showed neither the M spike nor Bence-Jones proteins. However, immunofixation electrophoresis of urine showed the κ type of Bence-Jones protein. Bone marrow biopsy showed a moderately hypocellular bone marrow with small collections of atypical plasmacytoid cells. The myelogram showed an increase in percentage of plasma cells (11.6%). Flow cytometric analysis of bone marrow specimens showed monoclonality of the plasmacytoid fraction gated by CD38 for cytoplasmic κ chain (86.4%). LCDD in renal allografts is uncommon and in general is associated in most patients with recurrent myeloma, rather than as a de novo disease.6Ecder T. Tbakhi A. Braun W.E. et al.De novo light-chain deposition disease in a cadaver renal allograft.Am J Kidney Dis. 1996; 28: 461-465Abstract Full Text PDF PubMed Scopus (17) Google Scholar, 7Howard A.D. Moore Jr, J. Tomaszewski M.M. Occurrence of multiple myeloma three years after successful renal transplantation.Am J Kidney Dis. 1987; 10: 147-150PubMed Scopus (36) Google Scholar Recurrence of LCDD in renal allografts has been reported to occur at an incidence of more than 50% within 4 years of renal transplantation and frequently is associated with graft failure.8Penn I. Occurrence of cancers in immunosuppressed organ transplant recipients.Clin Transpl. 1990; 4: 53-62Google Scholar, 9Sheil A.G.R. Cancer in Dialysis and Transplant Patients Kidney Transplantation.in: Saunders, Philadelphia, PA1994: 390-400Google Scholar, 10Leung N. Lager D.J. Gertz M.A. et al.Long-term outcome of renal transplantation in light-chain deposition disease.Am J Kidney Dis. 2004; 43: 147-153Abstract Full Text Full Text PDF PubMed Scopus (158) Google Scholar Conversely, de novo multiple myeloma or LCDD arising in a renal allograft is very rare, and only a few cases have been reported7Howard A.D. Moore Jr, J. Tomaszewski M.M. Occurrence of multiple myeloma three years after successful renal transplantation.Am J Kidney Dis. 1987; 10: 147-150PubMed Scopus (36) Google Scholar, 8Penn I. Occurrence of cancers in immunosuppressed organ transplant recipients.Clin Transpl. 1990; 4: 53-62Google Scholar, 9Sheil A.G.R. Cancer in Dialysis and Transplant Patients Kidney Transplantation.in: Saunders, Philadelphia, PA1994: 390-400Google Scholar despite the high frequency of monoclonal gammopathy in transplant recipients.11Radl J. Valentijn R.M. Haaijman J.J. Paul L.C. Monoclonal gammapathies in patients undergoing immunosuppressive treatment after renal transplantation.Clin Immunol Immunopathol. 1985; 37: 98-102Crossref PubMed Scopus (76) Google Scholar In the native kidney, LCDD is associated with various degrees of renal insufficiency in most patients, and rapid deterioration of kidney function could also occur during the advanced stage of the disease.12Markowitz G.S. Dysproteinemia and the kidney.Adv Anat Pathol. 2004; 11: 49-63Crossref PubMed Scopus (70) Google Scholar However, acute renal failure could be present at the time of diagnosis in approximately 30% of patients with LCDD.13Korbet S.M. Schwartz M.M. Multiple myeloma.J Am Soc Nephrol. 2006; 17: 2533-2545Crossref PubMed Scopus (119) Google Scholar Other paraprotein-related kidney diseases, including heavy chain deposition disease,14Buxbaum J. Gallo G. Nonamyloidotic monoclonal immunoglobulin deposition disease Light-chain, heavy-chain, and light- and heavy-chain deposition diseases.Hematol Oncol Clin North Am. 1999; 13: 1235-1248Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar cryoglobulinemia,15Dussol B. Tsimaratos M. Lerda D. et al.[Viral hepatitis C and membranoproliferative glomerulonephritis in a renal transplant patient].Nephrologie. 1995; 16: 223-226PubMed Google Scholar immunotactoid glomerulopathy,16Rosenstock J.L. Markowitz G.S. Valeri A.M. et al.Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features.Kidney Int. 2003; 63: 1450-1461Crossref PubMed Scopus (253) Google Scholar, 17Pronovost P.H. Brady H.R. Gunning M.E. Espinoza O. Rennke H.G. Clinical features, predictors of disease progression and results of renal transplantation in fibrillary/immunotactoid glomerulopathy.Nephrol Dial Transplant. 1996; 11: 837-842Crossref PubMed Scopus (111) Google Scholar, 18Alpers C.E. Rennke H.G. Hopper Jr, J. Biava C.G. Fibrillary glomerulonephritis: An entity with unusual immunofluorescence features.Kidney Int. 1987; 31: 781-789Crossref PubMed Scopus (141) Google Scholar, 19Korbet S.M. Rosenberg B.F. Schwartz M.M. Lewis E.J. Course of renal transplantation in immunotactoid glomerulopathy.Am J Med. 1990; 89: 91-95Abstract Full Text PDF PubMed Scopus (35) Google Scholar and amyloidosis16Rosenstock J.L. Markowitz G.S. Valeri A.M. et al.Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features.Kidney Int. 2003; 63: 1450-1461Crossref PubMed Scopus (253) Google Scholar, 17Pronovost P.H. Brady H.R. Gunning M.E. Espinoza O. Rennke H.G. Clinical features, predictors of disease progression and results of renal transplantation in fibrillary/immunotactoid glomerulopathy.Nephrol Dial Transplant. 1996; 11: 837-842Crossref PubMed Scopus (111) Google Scholar, 18Alpers C.E. Rennke H.G. Hopper Jr, J. Biava C.G. Fibrillary glomerulonephritis: An entity with unusual immunofluorescence features.Kidney Int. 1987; 31: 781-789Crossref PubMed Scopus (141) Google Scholar, 19Korbet S.M. Rosenberg B.F. Schwartz M.M. Lewis E.J. Course of renal transplantation in immunotactoid glomerulopathy.Am J Med. 1990; 89: 91-95Abstract Full Text PDF PubMed Scopus (35) Google Scholar also have been reported after renal transplantation. One transplant patient with heavy chain deposition disease developed recurrent disease approximately 1.5 years after transplantation.14Buxbaum J. Gallo G. Nonamyloidotic monoclonal immunoglobulin deposition disease Light-chain, heavy-chain, and light- and heavy-chain deposition diseases.Hematol Oncol Clin North Am. 1999; 13: 1235-1248Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar Cryoglobulinemic nephropathy may develop either de novo or as recurrent cryoglobulinemic nephropathy in patients with active hepatitis.15Dussol B. Tsimaratos M. Lerda D. et al.[Viral hepatitis C and membranoproliferative glomerulonephritis in a renal transplant patient].Nephrologie. 1995; 16: 223-226PubMed Google Scholar Although recurrent immunotactoid glomerulopathy after renal transplantation has been reported to occur in approximately half the cases, graft function has been reported to remain adequate after 5 to 11 years of follow-up in most cases.16Rosenstock J.L. Markowitz G.S. Valeri A.M. et al.Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features.Kidney Int. 2003; 63: 1450-1461Crossref PubMed Scopus (253) Google Scholar, 17Pronovost P.H. Brady H.R. Gunning M.E. Espinoza O. Rennke H.G. Clinical features, predictors of disease progression and results of renal transplantation in fibrillary/immunotactoid glomerulopathy.Nephrol Dial Transplant. 1996; 11: 837-842Crossref PubMed Scopus (111) Google Scholar, 18Alpers C.E. Rennke H.G. Hopper Jr, J. Biava C.G. Fibrillary glomerulonephritis: An entity with unusual immunofluorescence features.Kidney Int. 1987; 31: 781-789Crossref PubMed Scopus (141) Google Scholar, 19Korbet S.M. Rosenberg B.F. Schwartz M.M. Lewis E.J. Course of renal transplantation in immunotactoid glomerulopathy.Am J Med. 1990; 89: 91-95Abstract Full Text PDF PubMed Scopus (35) Google Scholar Several cases of de novo immunotactoid glomerulopathy in renal allografts have been reported.16Rosenstock J.L. Markowitz G.S. Valeri A.M. et al.Fibrillary and immunotactoid glomerulonephritis: Distinct entities with different clinical and pathologic features.Kidney Int. 2003; 63: 1450-1461Crossref PubMed Scopus (253) Google Scholar, 20Calls Ginesta J. Torras A. Ricart M.J. et al.Fibrillary glomerulonephritis and pulmonary hemorrhage in a patient with renal transplantation.Clin Nephrol. 1995; 43: 180-183PubMed Google Scholar, 21Rao K.V. Hafner G.P. Crary G.S. Anderson W.R. Crosson J.T. De novo immunotactoid glomerulopathy of the renal allograft: Possible association with cytomegalovirus infection.Am J Kidney Dis. 1994; 24: 97-103Abstract Full Text PDF PubMed Scopus (26) Google Scholar However, the recurrence rate of amyloidosis after renal transplantation has been reported to be 10% to 20% for AL amyloidosis22Hartmann A. Holdaas H. Fauchald P. et al.Fifteen years' experience with renal transplantation in systemic amyloidosis.Transpl Int. 1992; 5: 15-18Crossref PubMed Google Scholar, 23Pasternack A. Ahonen J. Kuhlback B. Renal transplantation in 45 patients with amyloidosis.Transplantation. 1986; 42: 598-601Crossref PubMed Scopus (102) Google Scholar and 4% for AA amyloidosis,24Sherif A.M. Refaie A.F. Sobh M.A. et al.Long-term outcome of live donor kidney transplantation for renal amyloidosis.Am J Kidney Dis. 2003; 42: 370-375Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar and the graft loss rate from recurrent amyloidosis was only 3%.22Hartmann A. Holdaas H. Fauchald P. et al.Fifteen years' experience with renal transplantation in systemic amyloidosis.Transpl Int. 1992; 5: 15-18Crossref PubMed Google Scholar The accumulated experiences of LCDD in renal transplantation suggest that transplantation is not a valid option for patients with LCDD because of the high frequency of recurrence and progression to graft failure. However, in some recipients in whom the original kidney disease remains uncertain, such as in this case, recurrent LCDD can be a possible reason for graft dysfunction. Immunohistochemical analysis for light chains and careful electron microscopic observation to identify inconspicuous light chain deposition can be helpful for the diagnosis of LCDD, which should prompt further examination to detect an underlying plasma cell disorder in the course of patient management. We gratefully acknowledge the technical assistance of Hideki Nakayama and Mayuko Ohno. Support: None. Financial Disclosure: None." @default.
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• W2072719500 title "Light Chain Deposition Disease After Renal Transplantation" @default.
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