{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T04:04:38Z","timestamp":1779681878634,"version":"3.53.1"},"reference-count":12,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T00:00:00Z","timestamp":1778716800000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Persistent renal dysfunction after haematologic remission in monoclonal immunoglobulin deposition disease creates uncertainty regarding treatment intensity when clinical parameters do not distinguish reversible injury from established structural remodelling. We report a 34\u2010year\u2010old man with light\u2010 and heavy\u2010chain deposition disease who presented with serum creatinine 1.8\u2009mg\/dL and heavy proteinuria (urine protein\u2010to\u2010creatinine ratio 5.0\u2009g\/gCr). After cyclophosphamide, bortezomib and dexamethasone therapy, haematologic parameters improved and proteinuria decreased; however, renal function continued to worsen, and serum creatinine increased to 4.1\u2009mg\/dL before autologous stem cell transplantation. Despite a deep haematologic response after transplantation, serum creatinine remained elevated at 2.7\u2009mg\/dL. A second kidney biopsy demonstrated persistent proliferative glomerular lesions with limited global sclerosis (1\/56 glomeruli). Minimal residual disease remained detectable at 0.0029%, supporting additional clone\u2010directed therapy. Following CD38\u2010directed treatment, proteinuria resolved and minimal residual disease became undetectable, yet serum creatinine remained approximately 1.9\u2009mg\/dL with persistent microscopic haematuria. Because laboratory findings could not determine whether residual dysfunction reflected ongoing activity or fixed chronic change, a third kidney biopsy was performed. This biopsy revealed resolution of active glomerular lesions with predominance of chronic remodelling (5\/32 globally sclerotic glomeruli). Therapy was discontinued, and renal function subsequently improved gradually to 1.1\u2009mg\/dL, remaining stable for more than 5\u2009years without further therapy. Serial kidney biopsies informed two distinct therapeutic decisions\u2014treatment escalation and subsequent discontinuation\u2014when clinical parameters alone were insufficient to guide management.<\/jats:p>","DOI":"10.1111\/nep.70213","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T03:14:08Z","timestamp":1778814848000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Repeat Kidney Biopsy to Inform Escalation and Discontinuation of Therapy in Light\u2010 and Heavy\u2010Chain Deposition Disease"],"prefix":"10.1111","volume":"31","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2065-1957","authenticated-orcid":false,"given":"Seiji","family":"Kakiuchi","sequence":"first","affiliation":[{"name":"Department of Hematology Yodogawa Christian Hospital  Osaka 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