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• W2137879965 abstract "Although glomerulonephritis and renal failure have been observed after allogenic stem cell transplantation, only a few such reports were published about patients undergoing autologous stem cell transplantation. We report a case of mesangial proliferative glomerulonephritis developing 4 months after autologous stem cell transplantation for chronic lymphatic leukemia. Serological test results, together with histological, immunohistochemical, and electronic microscopic findings of a kidney biopsy specimen, confirmed the diagnosis of mesangial proliferative glomerulonephritis in our patient. Complement and immunoglobulin A were not present in the kidney biopsy specimen. An abnormal clone, not previously reported, with the translocation t(5;11)(q31;q13) in blood and bone marrow was observed. The reason for and whether progenitor cells in stem cell transplantations could contribute to the development of glomerulonephritis remain open questions. Kidney biopsy should be performed in patients with microscopic hematuria and/or proteinuria after autologous stem cell transplantation. Although glomerulonephritis and renal failure have been observed after allogenic stem cell transplantation, only a few such reports were published about patients undergoing autologous stem cell transplantation. We report a case of mesangial proliferative glomerulonephritis developing 4 months after autologous stem cell transplantation for chronic lymphatic leukemia. Serological test results, together with histological, immunohistochemical, and electronic microscopic findings of a kidney biopsy specimen, confirmed the diagnosis of mesangial proliferative glomerulonephritis in our patient. Complement and immunoglobulin A were not present in the kidney biopsy specimen. An abnormal clone, not previously reported, with the translocation t(5;11)(q31;q13) in blood and bone marrow was observed. The reason for and whether progenitor cells in stem cell transplantations could contribute to the development of glomerulonephritis remain open questions. Kidney biopsy should be performed in patients with microscopic hematuria and/or proteinuria after autologous stem cell transplantation. RENAL FAILURE with nephrotic syndrome, membranous glomerulonephritis (GN), crescentic immunoglobulin A (IgA) GN, minimal change GN, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome have been reported after allogenic bone marrow or stem cell transplantation.1Gomez-Garcia P. Herrera-Arroyo C. Torres-Gomez A. et al.Renal involvement in chronic graft-versus-host disease A report of two cases.Bone Marrow Transplant. 1988; 3: 357-362PubMed Google Scholar, 2Rao P.S. Nephrotic syndrome in patients with peripheral blood stem cell transplantation.Am J Kidney Dis. 2005; 45: 780-785Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar, 3Miralbell R. Sancho G. Bieri S. et al.Renal insufficiency in patients with hematologic malignancies undergoing total body irradiation and bone marrow transplantation A prospective assessment.Int J Radiat Oncol Biol Phys. 2004; 58: 809-816Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar, 4Hiesse C. Goldschmidt E. Santelli G. Charpentier B. Machover D. Fries D. Membranous nephropathy in a bone marrow transplant recipient.Am J Kidney Dis. 1988; 11: 188-191Abstract Full Text PDF PubMed Scopus (57) Google Scholar, 5Müller G.A. Müller C.A. Markovic-Lipkowski J. et al.Membranous nephropathy after bone marrow transplantation in cyclosporine treatment.Nephron. 1989; 51: 555-556Crossref PubMed Scopus (41) Google Scholar, 6Barbara J.A. Thomas A.C. Smith P.S. Gillis D. Ho J.O.K. Woodroffe A.J. Membranous nephropathy with graft-versus-host disease in a bone marrow transplant recipient.Clin Nephrol. 1992; 37: 115-158PubMed Google Scholar, 7Yorioka N. Taniguchi Y. Shimote K. et al.Membranous nephropathy with chronic graft-versus-host disease in a bone marrow transplant recipient.Nephron. 1998; 80: 371-372Crossref PubMed Scopus (36) Google Scholar, 8Nergizoğlu G. Keven K. Ateş K. et al.Chronic graft-versus-host disease complicated by membranous glomerulonephritis.Nephrol Dial Transplant. 1999; 14: 2461-2463Crossref PubMed Scopus (45) Google Scholar, 9Rossi L. Cardarelli F. Vampa M.L. Buzio C. Olivetti G. Membranous glomerulonephritis after haematopoietic cell transplantation for multiple myeloma.Nephron. 2001; 88: 260-263Crossref PubMed Scopus (35) Google Scholar, 10Kimura S. Horie A. Hiki Y. et al.Nephrotic syndrome with crescent formation and massive IgA deposition following allogenic bone marrow transplantation for natural killer cell leukemia/lymphoma.Blood. 2003; 101: 4219-4221Crossref PubMed Scopus (41) Google Scholar, 11Akar H. Keven K. Çelebi H. et al.Nephrotic syndrome after allogenic peripheral blood stem cell transplantation.J Nephrol. 2002; 15: 79-82PubMed Google Scholar, 12Ruutu T. Hermans J. Niederwieser D. et al.EBMT Chronic Leukemia Working PartyThrombotic thrombocytopenic purpura after allogenic stem cell transplantation A survey of the European Group for Blood and Marrow Transplantation (EBMT).Br J Haematol. 2002; 118: 1112-1119Crossref PubMed Scopus (94) Google Scholar, 13Juckett M. Perry E.H. Daniels B.S. Weisdorf D.J. Hemolytic uremic syndrome following bone marrow transplantation.Bone Marrow Transplant. 1991; 7: 405-409PubMed Google Scholar, 14Oursler D.P. Holley K.E. Wagoner R.D. Hemolytic uremic syndrome after bone marrow transplantation without total body irradiation.Am J Nephrol. 1993; 13: 167-170Crossref PubMed Scopus (16) Google Scholar Whereas renal dysfunction in patients after allogenic stem cell transplantation was found at a frequency of 53%,15Parikh C.R. McSweeney P.A. Korular D. et al.Renal dysfunction in allogenic hematopoietic cell transplantation.Kidney Int. 2002; 62: 566-573Crossref PubMed Scopus (123) Google Scholar, 16Zager R.A. O’Quigley J. Zager B.K. et al.Acute renal failure following bone marrow transplantation A retrospective study of 272 patients.Am J Kidney Dis. 1989; 13: 210-216PubMed Scopus (212) Google Scholar it was much less (21%) after autologous stem cell transplantation.16Zager R.A. O’Quigley J. Zager B.K. et al.Acute renal failure following bone marrow transplantation A retrospective study of 272 patients.Am J Kidney Dis. 1989; 13: 210-216PubMed Scopus (212) Google Scholar, 17Schrier R.W. Parikh C.R. Comparison of renal injury in myeloablative autologous, myeloablative allogenic and non-myeloablative allogenic haematopoietic cell transplantation.Nephrol Dial Transplant. 2005; 20: 678-683Crossref PubMed Scopus (29) Google Scholar The mortality rate in this category of patients requiring dialysis therapy was reportedly as high as 83% to 88%.16Zager R.A. O’Quigley J. Zager B.K. et al.Acute renal failure following bone marrow transplantation A retrospective study of 272 patients.Am J Kidney Dis. 1989; 13: 210-216PubMed Scopus (212) Google Scholar, 17Schrier R.W. Parikh C.R. Comparison of renal injury in myeloablative autologous, myeloablative allogenic and non-myeloablative allogenic haematopoietic cell transplantation.Nephrol Dial Transplant. 2005; 20: 678-683Crossref PubMed Scopus (29) Google Scholar, 18Gruss E. Bernis C. Tomas J.F. et al.Acute renal failure in patients following bone marrow transplantation Prevalence, risk factors and outcome.Am J Nephrol. 1995; 15: 473-479Crossref PubMed Scopus (98) Google Scholar, 19Hahn T. Rondeau C. Shaukat A. et al.Acute renal failure requiring dialysis after allogenic blood and marrow transplantation identifies very poor prognosis patients.Bone Marrow Transplant. 2003; 32: 405-410Crossref PubMed Scopus (59) Google Scholar After autologous stem cell transplantation, only a few reports described renal histopathologic characteristics.20Takeuchi M. Tamaoki A. Tada A. et al.Crescentic glomerulonephritis developing 3 months after autologous peripheral blood stem cell transplantation for non-Hodgkin’s lymphoma.Bone Marrow Transplant. 1998; 22: 725-727Crossref PubMed Scopus (10) Google Scholar, 21Sakarcan A. Neuberg R.W. McRedmond K.P. Islek I. Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant.Am J Kidney Dis. 2002; 40: 1-5Abstract Full Text Full Text PDF PubMed Google Scholar, 22El-Seisi S. Gupta R. Clase C.M. Forrest D.L. Milandinovic M. Couban S. Renal pathology at autopsy in patients who died after hematopoietic stem cell transplantation.Biol Blood Marrow Transplant. 2003; 9: 683-688Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar The development of crescentic GN, membranoproliferative GN, and membranous GN and impairment of kidney function after autologous bone marrow transplantation were reported.20Takeuchi M. Tamaoki A. Tada A. et al.Crescentic glomerulonephritis developing 3 months after autologous peripheral blood stem cell transplantation for non-Hodgkin’s lymphoma.Bone Marrow Transplant. 1998; 22: 725-727Crossref PubMed Scopus (10) Google Scholar, 21Sakarcan A. Neuberg R.W. McRedmond K.P. Islek I. Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant.Am J Kidney Dis. 2002; 40: 1-5Abstract Full Text Full Text PDF PubMed Google Scholar, 22El-Seisi S. Gupta R. Clase C.M. Forrest D.L. Milandinovic M. Couban S. Renal pathology at autopsy in patients who died after hematopoietic stem cell transplantation.Biol Blood Marrow Transplant. 2003; 9: 683-688Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar However, decreased renal function was observed mostly in patients who underwent total-body irradiation.23Frisk P. Bratteby L.E. Carlson K. Lonnerholm G. Renal function after autologous bone marrow transplantation in children A long-term prospective study.Bone Marrow Transplant. 2002; 29: 129-136Crossref PubMed Scopus (80) Google Scholar We report the case of a patient with onset of mesangial proliferative GN 4 months after autologous stem cell transplantation. The GN was resistant to combined treatment with corticosteroid and cyclosporine A, but responded to cyclophosphamide. A 48-year-old woman, previously healthy, was admitted to our hospital with suspicion of chronic lymphatic leukemia (CLL). Her mother had had rheumatoid arthritis, secondary amyloidosis, and renal failure leading to hemodialysis treatment. Our patient had visited Kenya during 3 weeks in 2001, for which reason she was given malaria prophylaxis with mefloquine hydrochloride and vaccinations against hepatitis A and B and meningococcus. Serological test results for hepatitis C were negative. In February 2003, enlarged lymph nodes were found in the jugular, inguinal, and neck regions. Peripheral-blood white blood cell counts showed 32.0 × 109 leukocytes, 91% lymphocytes. Bone marrow examination (Fig 1) showed increased number of small lymphocytes that expressed positivity to CD5, CD19, CD20, CD22, CD23, and CD45, with clonality to κ chain. Among normal 46,XX cells, cytogenetic analysis at the diagnosis of CLL showed a small abnormal clone with a translocation t(5;11)(q31;q13) in blood and bone marrow. Because this translocation is not a typical abnormality in patients with CLL, fluorescence in situ hybridization also was performed by using the probes harboring the most common aberrations in CLL. The used probes ATM (11q22.3), CEP12 (centromeric region of chromosome 12), 13qS319 (13q14), and p53 (17p13; Vysis, Downers Grove, IL) showed a normal signal pattern in cells of the bone marrow sample (200 interphase cells studied). The cyclin 1 gene probe (CCND1: 11q13; Vysis) was not rearranged, but was moved to the long arm of chromosome 5 by fluorescence in situ hybridization in the abnormal meta-phases. The normal female karyotype was found in 3 control bone marrow specimens obtained at different times after autologous stem cell transplantation. Although the patient had negative serological test results for hepatitis C, results were positive for hepatitis A (assumed to be vaccine-induced), Epstein-Barr, and cytomegalovirus (IgG class) antibodies. The initial leukemia treatment consisted of 3 courses of intravenous fludarabine and cyclophosphamide, together with oral allopurinol, followed by peripheral stem cell isolation. After BEAC pretreatment consisting of intravenous carmustine (BCNU; total dose, 550 mg), cytarabine (1.440 mg), cyclophosphamide (10.800 mg), and etoposide (1.440 mg), together with mesna (total dose, 17.600 mg), in September 2003, the autologous stem cell transplantation was performed. Irradiation treatment was not used. Prophylactic treatment against Pneumocystis carinii with pentamidine inhalations was administered. At this time, she had normal kidney function, with a serum creatinine (SCr) level of 0.9 mg/dL (80 μmol/L). Because blood pressure was elevated to about 160 to 180/100 mm Hg, treatment with candesartan cilexetil, 16 mg/d, and bisoprolol, 5 mg/d, was started. In January 2004, the patient’s 24-hour urinary protein excretion was 1.180 mg/24 h (previously not observed). Serum protein electrophoresis showed a small band of IgG κ chain paraprotein. Paraprotein and light chains were absent in urine. Cytosolic antinuclear and anti–glomerular basement membrane antibodies, as well as antineutrophil cytoplasmic antibodies and antibodies against proteinase 3 and myeloperoxidase, were negative. SCr level was 1.2 mg/dL (109 μmol/L), and cystatin-C concentration was 1.16 mg/L (reference values, <1.20 mg/L; Table 1). Blood pressure was 175/110 mm Hg, and retinal hypertensive changes (Keith-Wagener grades I to II) were found. Candesartan cilexetil dose was increased to 16 mg twice daily; bisoprolol, to 5 mg twice daily; and lercandipine, 10 mg, plus indapamide were added to the treatment regimen. Blood pressure decreased to 144/85 mm Hg. However, proteinuria was sustained (protein, 1.100 mg/24 h) and SCr level remained at 1.2 mg/dL (108 μmol/L).Table 1Laboratory Parameters Before and After Stem Cell Transplantation200320042005Mar 24Jan 28May 24Sep 14Nov 8Jan 10May 4May 25Aug 1SCr (mg/dL)0.81.11.61.11.21.21.31.41.2Fasting plasma urea (mg/dL)—2742312831343631Serum cystatin-C (mg/L)—1.16—1.411.341.371.1—1.12Plasma albumin (g/dL)4.54.13.93.73.83.93.84.23.9Serum protein (g/dL)7.86.7⁎Monoclonal κ component in serum gamma-fraction present.6.7⁎Monoclonal κ component in serum gamma-fraction present.6.76.7——6.96.7Urinary protein (mg/24 h)—1180242197118130242229Blood hemoglobin (g/dL)11.411.210.59.210.110.811.911.113.6Blood leukocytes (×109/L)7.14.97.93.72.63.93.55.85.4Blood thrombocytes (×109/L)258167215175181187197194240NOTE. To convert SCr in mg/dL to μmol/L, multiply by 88.4; albumin, protein, and hemoglobin in g/dL to g/L, multiply by 10; urea in mg/dL to mmol/L, multiply by 0.357. Monoclonal κ component in serum gamma-fraction present. Open table in a new tab NOTE. To convert SCr in mg/dL to μmol/L, multiply by 88.4; albumin, protein, and hemoglobin in g/dL to g/L, multiply by 10; urea in mg/dL to mmol/L, multiply by 0.357. A kidney biopsy specimen (February 2004) showed mesangial proliferative GN (Fig 2) and immunohistochemical glomerular positivity to κ light chain (Fig 3). Tubular morphological characteristics were within normal limits. Immunofluorescence examination of IgG, IgA, IgM, and complement fraction C3 and fibrinogen was negative. Electron microscopy of the kidney specimen from February 2004 showed increased amounts of mesangial basement membrane–like material (Fig 4). Visceral epithelial cells and foot processes had normal structures. Repeated bone marrow examination, as described previously, had normal findings. Left ventricular hypertrophy was absent, ejection fraction was 70%, and a small nonsignificant diastolic dysfunction was observed on echocardiogram. Computerized scan of kidneys, suprarenal glands, and renal arteries, together with ultrasound examination of the kidneys and urinary tract, were normal.Fig 3Kidney biopsy specimen with κ light-change precipitations along glomerular capillary walls. (Antibody dilution, 1:75,000; original magnification ×50.)View Large Image Figure ViewerDownload (PPT)Fig 4Electron micrograph (February 2004) shows increased amounts of mesangial basement membrane (mbm) material and obliteration of capillary loops (ocl). There were no electron-dense deposits in capillary loop basement membrane (clbm). Abbreviations: pc, podocyte; pcfp, podocyte foot processes. Bar = 2 μm.View Large Image Figure ViewerDownload (PPT) From April 1 to the end of June 2004, SCr, cholesterol, low-density cholesterol, and blood pressure values increased, and treatment was intensified by administering moxonidine and rosuvastatine. Immunosuppression was initiated with a 64-mg/d dose of methylprednisolone (later tapered to 4 mg/d) and cyclosporine A (200 to 100 mg/d). Despite this treatment, SCr level increased to 1.6 mg/dL (140 μmol/L), for which reason cyclosporine A was replaced by cyclophosphamide (150 mg/d). Because hemoglobin concentration decreased to 10.0 g/dL (100 g/L), cyclophosphamide dose was decreased to 50 mg/d, and subcutaneous injections with human recombinant erythropoietin, 6,000 U/wk, were initiated. Because of nonresponse, erythropoietin dose was increased to 10,000 U/wk, after which the patient’s hemoglobin level remained at greater than 13.5 g/dL (>135 g/L). During this treatment regimen, SCr level decreased to 1.1 mg/dL (98 μmol/L); urea, to 11 mg/dL (3.9 mmol/L); and urinary protein excretion, to 197 mg/24 h. Serum protein electrophoresis returned to normal, and the previous M-component disappeared. Bone marrow remained normal at reexamination. Clinical data and laboratory findings over time are listed in Table 1. Since then, SCr level has fluctuated from 1.2 to 1.5 mg/mL (129 to 110 μmol/L), and the clinical course has been uneventful. A repeated kidney biopsy performed in June 2005 (Fig 5) confirmed the finding of mesangial proliferative GN with more pronounced mesangial changes. In this biopsy, immunohistochemistry also remained negative. Decreased glomerular filtration rate has been observed after allogenic15Parikh C.R. McSweeney P.A. Korular D. et al.Renal dysfunction in allogenic hematopoietic cell transplantation.Kidney Int. 2002; 62: 566-573Crossref PubMed Scopus (123) Google Scholar, 16Zager R.A. O’Quigley J. Zager B.K. et al.Acute renal failure following bone marrow transplantation A retrospective study of 272 patients.Am J Kidney Dis. 1989; 13: 210-216PubMed Scopus (212) Google Scholar, 17Schrier R.W. Parikh C.R. Comparison of renal injury in myeloablative autologous, myeloablative allogenic and non-myeloablative allogenic haematopoietic cell transplantation.Nephrol Dial Transplant. 2005; 20: 678-683Crossref PubMed Scopus (29) Google Scholar, 18Gruss E. Bernis C. Tomas J.F. et al.Acute renal failure in patients following bone marrow transplantation Prevalence, risk factors and outcome.Am J Nephrol. 1995; 15: 473-479Crossref PubMed Scopus (98) Google Scholar, 19Hahn T. Rondeau C. Shaukat A. et al.Acute renal failure requiring dialysis after allogenic blood and marrow transplantation identifies very poor prognosis patients.Bone Marrow Transplant. 2003; 32: 405-410Crossref PubMed Scopus (59) Google Scholar and autologous bone marrow transplantation.23Frisk P. Bratteby L.E. Carlson K. Lonnerholm G. Renal function after autologous bone marrow transplantation in children A long-term prospective study.Bone Marrow Transplant. 2002; 29: 129-136Crossref PubMed Scopus (80) Google Scholar After autologous stem cell transplantation, biopsy-proven GN-like crescentic GN,20Takeuchi M. Tamaoki A. Tada A. et al.Crescentic glomerulonephritis developing 3 months after autologous peripheral blood stem cell transplantation for non-Hodgkin’s lymphoma.Bone Marrow Transplant. 1998; 22: 725-727Crossref PubMed Scopus (10) Google Scholar membranoproliferative GN,21Sakarcan A. Neuberg R.W. McRedmond K.P. Islek I. Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant.Am J Kidney Dis. 2002; 40: 1-5Abstract Full Text Full Text PDF PubMed Google Scholar and membranous GN22El-Seisi S. Gupta R. Clase C.M. Forrest D.L. Milandinovic M. Couban S. Renal pathology at autopsy in patients who died after hematopoietic stem cell transplantation.Biol Blood Marrow Transplant. 2003; 9: 683-688Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar were reported. In the latter case of membranous GN,22El-Seisi S. Gupta R. Clase C.M. Forrest D.L. Milandinovic M. Couban S. Renal pathology at autopsy in patients who died after hematopoietic stem cell transplantation.Biol Blood Marrow Transplant. 2003; 9: 683-688Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar the patient had metastatic breast cancer, which could point to a malignancy-related secondary membranous GN. Most cases of GN after stem cell transplantation were reported after allogenic transplantation. To our best knowledge, the development of mesangial proliferative GN after autologous stem cell transplantation has not been described before. Renal dysfunction in the course after stem cell transplantation was recognized years ago,3Miralbell R. Sancho G. Bieri S. et al.Renal insufficiency in patients with hematologic malignancies undergoing total body irradiation and bone marrow transplantation A prospective assessment.Int J Radiat Oncol Biol Phys. 2004; 58: 809-816Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar, 4Hiesse C. Goldschmidt E. Santelli G. Charpentier B. Machover D. Fries D. Membranous nephropathy in a bone marrow transplant recipient.Am J Kidney Dis. 1988; 11: 188-191Abstract Full Text PDF PubMed Scopus (57) Google Scholar, 5Müller G.A. Müller C.A. Markovic-Lipkowski J. et al.Membranous nephropathy after bone marrow transplantation in cyclosporine treatment.Nephron. 1989; 51: 555-556Crossref PubMed Scopus (41) Google Scholar, 6Barbara J.A. Thomas A.C. Smith P.S. Gillis D. Ho J.O.K. Woodroffe A.J. Membranous nephropathy with graft-versus-host disease in a bone marrow transplant recipient.Clin Nephrol. 1992; 37: 115-158PubMed Google Scholar, 7Yorioka N. Taniguchi Y. Shimote K. et al.Membranous nephropathy with chronic graft-versus-host disease in a bone marrow transplant recipient.Nephron. 1998; 80: 371-372Crossref PubMed Scopus (36) Google Scholar, 8Nergizoğlu G. Keven K. Ateş K. et al.Chronic graft-versus-host disease complicated by membranous glomerulonephritis.Nephrol Dial Transplant. 1999; 14: 2461-2463Crossref PubMed Scopus (45) Google Scholar, 9Rossi L. Cardarelli F. Vampa M.L. Buzio C. Olivetti G. Membranous glomerulonephritis after haematopoietic cell transplantation for multiple myeloma.Nephron. 2001; 88: 260-263Crossref PubMed Scopus (35) Google Scholar and a decrease in glomerular filtration rate by more than 30% was observed in 54% and 49% of patients.3Miralbell R. Sancho G. Bieri S. et al.Renal insufficiency in patients with hematologic malignancies undergoing total body irradiation and bone marrow transplantation A prospective assessment.Int J Radiat Oncol Biol Phys. 2004; 58: 809-816Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar Kidney dysfunction and GN observed after allogenous stem cell transplantation has been related to the presence of graft rejection, graft-versus-host reaction, total-body irradiation, immunosuppression, antibiotic toxicity, and the freezing-thawing procedure, as well as the medium used for stem cell preservation.24Ohsawa I. Ohi H. Fujita T. et al.Glomerular and extraglomerular immune complex deposits in a bone marrow transplant recipient.Am J Kidney Dis. 2000; 36: 1-5Abstract Full Text Full Text PDF PubMed Google Scholar, 25Lin J. Markowitz G.S. Nicolaides M. et al.Membranous glomerulopathy associated with graft-versus-host disease following allogenic stem cell transplantation. Report of 2 cases and review of the literature.Am J Nephrol. 2001; 21: 351-356Crossref PubMed Scopus (62) Google Scholar, 26Suehiro T. Masutani Y. Yokoyama M. et al.Diffuse proliferative glomerulonephritis after bone marrow transplantation.Clin Nephrol. 2002; 58: 231-237Crossref PubMed Google Scholar, 27Miyazaki Y. Mori Y. Kishimoto N. et al.Membranous nephropathy associated with donor lymphocyte infusion following allogenic bone marrow transplantation.Int J Hematol. 2003; 78: 262-265Crossref PubMed Scopus (20) Google Scholar, 28Bernis C. Camara R. Garcia-Sánchez A. Martinez M.A. Selgas R. Nephrotic syndrome in a bone marrow transplant recipient after cyclosporine withdrawal.Nephrol Dial Transplant. 2003; 18: 2457Crossref PubMed Scopus (11) Google Scholar, 29Sato N. Kishi K. Yagisawa K. et al.Nephrotic syndrome in a bone marrow transplant recipient with chronic graft-versus-host disease.Bone Marrow Transplant. 1995; 16: 303-305PubMed Google Scholar, 30Lee G.-W. Lee J.-H. Kim S.-B. et al.Membranous glomerulopathy as a manifestation of chronic graft-versus-host disease after non-myeloablative stem cell transplantation in a patient with paroxysmal nocturnal hemoglobinuria.J Korean Med Sci. 2003; 18: 901-904PubMed Google Scholar, 31Tsutsumi C. Miyazaki Y. Fukushima T. et al.Membranous nephropathy after allogenic stem cell transplantation Report of 2 cases.Int J Hematol. 2004; 79: 193-197Crossref PubMed Scopus (22) Google Scholar However, total-body irradiation shielding did not prevent the development of renal dysfunction.3Miralbell R. Sancho G. Bieri S. et al.Renal insufficiency in patients with hematologic malignancies undergoing total body irradiation and bone marrow transplantation A prospective assessment.Int J Radiat Oncol Biol Phys. 2004; 58: 809-816Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar In our case, total-body irradiation was not given. The use of dimethylsulfoxide (DMSO; 10% at −80°C to −196°C) has been considered to be a safe method to preserve stem cells and is the most used preservation medium today.32Tzeng C.H. Hsieh R.K. Chuang M.W. et al.Bone marrow cryopreservation and clinical implications in autologous bone marrow transplantation.Proc Natl Sci Counc Repub China B. 1988; 12: 88-94PubMed Google Scholar, 33Galmes A. Besalduch J. Bargay J. et al.A simplified method for cryopreservation of haematopoietic stem cells with −80°C mechanical freezer with dimethyl sulfoxide as the sole cryoprotectant.Leuk Lymphoma. 1995; 17: 181-184Crossref PubMed Scopus (31) Google Scholar Because DMSO could decrease proteinuria in experimental Heymann nephritis,34Lotan D. Kaplan B.S. Fong J.S. Goodyer P.R. de Chadarevian J.P. Reduction of protein excretion by dimethyl sulfoxide in rats with passive Heymann nephritis.Kidney Int. 1984; 25: 778-788Crossref PubMed Scopus (28) Google Scholar it seems unlikely that DMSO would contribute to the development of GN. DMSO also decreased glomerular damage in experimental lupus nephritis.35Milner L.S. de Chadarevian J.P. Goodyer P.R. Mills M. Kaplan B.S. Amelioration of murine lupus nephritis by dimethyl sulfoxide.Clin Immunol Immunopathol. 1987; 45: 259-267Crossref PubMed Scopus (2) Google Scholar The different nature in immunologic responses after autologous and allogenic stem cell transplantation may explain divergences in renal pathological states in bone marrow and stem cell transplant recipients. Cellular components of renal glomeruli are derived from the mesenchyme. Experimental GN showed that bone marrow carries stem cells or progenitor cells for mesangial cells and may have functions in glomerular remodeling.36Ito T. Suzuki A. Imai E. Okabe M. Hori M. Bone marrow is a reservoir of repopulating mesangial cells during glomerular remodeling.J Am Soc Nephrol. 2001; 12: 2625-2635PubMed Google Scholar Moreover, numerous cells (CD34+, CD68+, c-kit+), cytokines, and growth factors were implicated in the pathogenesis of transplantation-associated GN.37El Kossi M.M. El Nahas A.M. Stem cell factor and crescentic glomerulonephritis.Am J Kidney Dis. 2003; 41: 785-795Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, 38Imasawa T. Roles of bone marrow cells in glomerular diseases.Clin Exp Nephrol. 2003; 7: 179-185Crossref PubMed Scopus (12) Google Scholar Whether stem cells (CD34+ and others) might induce responses of immunologic regulators (such as interleukin 6, among many others), thereby contributing to the development of GN, remains a matter of debate. The chromosomal abnormality found in our patient is new and was not reported previously, but we regarded the translocation t(5;11)(q31;q13) to be causing the CLL in our patient. In later bone marrow examinations, recurrence of this chromosome abnormality was not found in our patient. The previously observed monoclonal κ chain in serum disappeared during treatment for GN. According to Hovenga et al,39Hovenga S. de Wolf J. ThM. Guikema J.E.J. et al.Autologous stem cell transplantation in multiple myeloma after VAD and EDAP courses A high incidence of oligoclonal serum Igs post transplantation.Bone Marrow Transplant. 2000; 25: 723-728Crossref PubMed Scopus (49) Google Scholar it is not unusual to observe small monoclonal bands after autologous stem cell transplantation as the immune system is reconstituted, disappearing spontaneously as immunologic diversity develops. This also could be the case in our patient. However, although we could not draw a clear conclusion, it still is possible that our GN treatment with cyclophosphamide contributed to its disappearance. Adenovirus-related nephritis was described after hematopoietic stem cell transplantation.40Bruno B. Zager R.A. Boeckh M.J. et al.Adenovirus nephritis in hematopoietic stem-cell transplantation.Transplantation. 2004; 77: 1049-1057Crossref PubMed Scopus (80) Google Scholar However, prodromal signs were not present in our patient, and the dominant findings of interstitial changes with normal glomeruli seen in patients with adenovirus-related nephritis were absent in our patient. The possibility that hepatitis C virus, increasingly found in association with autoimmune phenomena, could have a role in the development of GN in our patient was excluded by negative serological test results. We also consider the vaccine-induced positive test result for hepatitis A not to be responsible for the GN in our patient. As put forward by almost all previous investigators, pretransplantation treatments (such as antibiotics) could participate in the pathophysiological process of the GN in our patient. A moderate dose of fludarabine was administered to our patient, not reaching the dose known to cause renal dysfunction.41Macheta M.P. Parapia L.A. Gouldesbrough D.R. Renal failure in a patient with chronic lymphocytic leukaemia treated with fludarabine J.Clin Pathol. 1996; 48: 181-182Crossref Scopus (14) Google Scholar Although mesangiocapillary or crescentic GN41Macheta M.P. Parapia L.A. Gouldesbrough D.R. Renal failure in a patient with chronic lymphocytic leukaemia treated with fludarabine J.Clin Pathol. 1996; 48: 181-182Crossref Scopus (14) Google Scholar, 42Tisler A. Pierratos A. Lipton J.H. Crescentic glomerulonephritis associated with p-ANCA positivity in fludarabine-treated chronic lymphocytic leukaemia.Nephrol Dial Transplant. 1996; 11: 2306-2308Crossref PubMed Scopus (16) Google Scholar were described in association with fludarabine treatment,41Macheta M.P. Parapia L.A. Gouldesbrough D.R. Renal failure in a patient with chronic lymphocytic leukaemia treated with fludarabine J.Clin Pathol. 1996; 48: 181-182Crossref Scopus (14) Google Scholar, 42Tisler A. Pierratos A. Lipton J.H. Crescentic glomerulonephritis associated with p-ANCA positivity in fludarabine-treated chronic lymphocytic leukaemia.Nephrol Dial Transplant. 1996; 11: 2306-2308Crossref PubMed Scopus (16) Google Scholar mesangial proliferative GN was not. Moreover, the fibrillary GN and immunotactoid (microtubular) glomerulopathic lesions observed in patients with CLL also belonged to a different class of immune-mediated GN43Bridoux F. Hugue V. Coldefy O. et al.Fibrillary glomerulonephritis and immunotactoid (microtubular) glomerulopathy are associated with distinct immunologic features.Kidney Int. 2002; 62: 1764-1775Crossref PubMed Scopus (170) Google Scholar than that of our patient. Whether fludarabine could affect CD4/CD8 and T helper subtype 1/T helper subtype 2 cell ratios and thus precipitate or exacerbate immune-mediated events was not examined in our patient and remains unanswered. Hemolytic uremic syndrome and thrombotic thrombocytopenic purpura after stem cell transplantation12Ruutu T. Hermans J. Niederwieser D. et al.EBMT Chronic Leukemia Working PartyThrombotic thrombocytopenic purpura after allogenic stem cell transplantation A survey of the European Group for Blood and Marrow Transplantation (EBMT).Br J Haematol. 2002; 118: 1112-1119Crossref PubMed Scopus (94) Google Scholar, 13Juckett M. Perry E.H. Daniels B.S. Weisdorf D.J. Hemolytic uremic syndrome following bone marrow transplantation.Bone Marrow Transplant. 1991; 7: 405-409PubMed Google Scholar, 14Oursler D.P. Holley K.E. Wagoner R.D. Hemolytic uremic syndrome after bone marrow transplantation without total body irradiation.Am J Nephrol. 1993; 13: 167-170Crossref PubMed Scopus (16) Google Scholar seem to occur after both allogenic12Ruutu T. Hermans J. Niederwieser D. et al.EBMT Chronic Leukemia Working PartyThrombotic thrombocytopenic purpura after allogenic stem cell transplantation A survey of the European Group for Blood and Marrow Transplantation (EBMT).Br J Haematol. 2002; 118: 1112-1119Crossref PubMed Scopus (94) Google Scholar, 13Juckett M. Perry E.H. Daniels B.S. Weisdorf D.J. Hemolytic uremic syndrome following bone marrow transplantation.Bone Marrow Transplant. 1991; 7: 405-409PubMed Google Scholar and autologous transplantation14Oursler D.P. Holley K.E. Wagoner R.D. Hemolytic uremic syndrome after bone marrow transplantation without total body irradiation.Am J Nephrol. 1993; 13: 167-170Crossref PubMed Scopus (16) Google Scholar and may develop regardless of treatment with total-body irradiation or cyclosporine. Immune-mediated hemolysis, known to occur in patients with CLL, did not seem likely because no signs of hemolysis were present in our patient. According to Stevenson et al,44Stevenson W.S. Nankivell B.J. Hertzberg M.S. Nephrotic syndrome after stem cell transplantation.Clin Transplant. 2005; 19: 141-144Crossref PubMed Scopus (36) Google Scholar it seems justified to perform kidney biopsy for histological confirmation of the diagnosis in patients with microscopic hematuria and/or proteinuria after stem cell transplantation. The observation in our case report might indicate that some unidentified cells used in stem cell transplantation may contribute to the development of de novo GN. It still remains that the mesangial proliferative GN in our patient might have occurred by coincidence." @default.
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