2018
DOI: 10.1016/j.kint.2018.01.028
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Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits is associated with high rate of early recurrence in the allograft

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Cited by 57 publications
(39 citation statements)
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“…For example, monoclonal immunoglobulin-related diseases tend to be progressive and are unlikely to undergo spontaneous remission [21][22][23][24][25] . Monoclonal immunoglobulin-related diseases also show higher rates of recurrence after kidney transplantation (often >80%) than their nonmonoclonal counterparts [26][27][28] . Monoclonal diseases are poorly responsive to conventional immunosuppression and instead require clone-directed therapy 25,[29][30][31][32] .…”
Section: E X P E Rt C O N S E N S U S D O C U M E N Tmentioning
confidence: 99%
See 1 more Smart Citation
“…For example, monoclonal immunoglobulin-related diseases tend to be progressive and are unlikely to undergo spontaneous remission [21][22][23][24][25] . Monoclonal immunoglobulin-related diseases also show higher rates of recurrence after kidney transplantation (often >80%) than their nonmonoclonal counterparts [26][27][28] . Monoclonal diseases are poorly responsive to conventional immunosuppression and instead require clone-directed therapy 25,[29][30][31][32] .…”
Section: E X P E Rt C O N S E N S U S D O C U M E N Tmentioning
confidence: 99%
“…Owing to differences in clinical characteristics and therapy, it is essential to distinguish MGRS-associated disorders from kidney diseases that are unrelated to monoclonal immunoglobins 10,12,24,28,94,95 . In patients suspected of having MGRS, the evaluation starts with a kidney biopsy.…”
Section: Evaluation Of Suspected Mgrsmentioning
confidence: 99%
“…7 Thus, only 9%-32% PGNMID-IgG patients have a detectable nephropathic clone. 7,18,26,27 In contrast, the nephropathic clone was detected in the bone marrow in 88% (14 of 16) of our PGNMID-LC patients. Further, 29% of PGNMID-LC patients had symptomatic multiple myeloma, which is exceedingly rare in PGNMID-IgG.…”
Section: Discussionmentioning
confidence: 64%
“…This could be due to the higher level of circulating MIg in PGNMID-LC than PGNMID-IgG and/or may also reflect differences in the mechanisms of complement activation and glomerular inflammation induced by the deposition of monoclonal LCs. (iv) In more than two-thirds of PGNMID-IgG patients, no monoclonal gammopathy or bone marrow B-cell clone are detected at diagnosis or on follow up, 2,7,18,26 and it has been suggested that an oligoclonal response with the same IgG light-and heavy-chain isotype could be involved in the development of glomerulonephritis, at least in some cases. 7 Thus, only 9%-32% PGNMID-IgG patients have a detectable nephropathic clone.…”
Section: Discussionmentioning
confidence: 99%
“…Unlike in MGRS (such as Proliferative Glomerulonephritis with Monoclonal Immunoglobulin Deposits, monoclonal immunoglobulin deposition disease, and C3 glomerulopathy with monoclonal gammopathy) in which the risk for recurrence and graft lost is high, the 3 patients with FGN with MGUS were not at increased risk for early recurrence. [16][17][18] However, if the monoclonal gammopathy was involved in the pathogenesis of FGN (monotypic deposits), perhaps early recurrence could occur as seen in other MGRS-related diseases. 15,18 DNAJB9 is an excellent marker of FGN and its utility in the evaluation of the allograft in those with native disease of FGN has several benefits.…”
Section: Discussionmentioning
confidence: 99%