When Waldenström macroglobulinemia hits the kidney: Description of a case series and management of a "rare in rare" scenario.


Journal

Cancer reports (Hoboken, N.J.)
ISSN: 2573-8348
Titre abrégé: Cancer Rep (Hoboken)
Pays: United States
ID NLM: 101747728

Informations de publication

Date de publication:
Apr 2024
Historique:
revised: 29 02 2024
received: 23 10 2023
accepted: 09 03 2024
medline: 25 4 2024
pubmed: 25 4 2024
entrez: 25 4 2024
Statut: ppublish

Résumé

Renal injury related to Waldenström macroglobulinemia (WM) occurs in approximately 3% of patients. Kidney biopsy is crucial to discriminate between distinct histopathological entities such as glomerular (amyloidotic and non-amyloidotic), tubulo-interstitial and non-paraprotein mediated renal damage. In this context, disease characterization, management, relationship between renal, and hematological response have been poorly explored. We collected clinical, genetic and laboratory data of seven cases of biopsy-proven renal involvement by WM managed at our academic center and focused on three cases we judged paradigmatic discussing their histopathological patterns, clinical features, and therapeutic options. In this illustrative case series, we confirm that serum creatinine levels and 24 h proteinuria are parameters that when altered should prompt the clinical suspicion of WM-related renal involvement, even if at present there are not precise cut-off levels recommending the execution of a renal biopsy. In our series AL Amyloidosis (n = 3/7) and tubulo-interstitial infiltration by lymphoma cells (n = 3/7) were the two more represented entities. BTKi did not seem to improve renal function (Case 1), while bortezomib-based regimens demonstrated a beneficial activity on the hematological and organ response, even when used as second-line therapy after chemoimmunotherapy (Case 3) and also with coexistence of anti-MAG neuropathy (Case 2). In case of poor response to bortezomib, standard chemoimmunotherapy (CIT), such as rituximab-bendamustine, represents an effective option (Case 1, 6, and 7). In our series, CIT generates durable responses more frequently in cases with amyloidogenic renal damage (Case 1, 5, and 7). In this illustrative case series, we confirm that serum creatinine levels and 24 h proteinuria are parameters that when altered should prompt the clinical suspicion of WM-related renal involvement, even if at present there are not precise cut-off levels recommending the execution of a renal biopsy. Studies with higher numerosity are needed to better clarify the pathological and clinical features of renal involvement during WM and to determine the potential benefit of different therapeutic regimens according to the histopathological subtypes.

Sections du résumé

BACKGROUND BACKGROUND
Renal injury related to Waldenström macroglobulinemia (WM) occurs in approximately 3% of patients. Kidney biopsy is crucial to discriminate between distinct histopathological entities such as glomerular (amyloidotic and non-amyloidotic), tubulo-interstitial and non-paraprotein mediated renal damage. In this context, disease characterization, management, relationship between renal, and hematological response have been poorly explored. We collected clinical, genetic and laboratory data of seven cases of biopsy-proven renal involvement by WM managed at our academic center and focused on three cases we judged paradigmatic discussing their histopathological patterns, clinical features, and therapeutic options.
CASE METHODS
In this illustrative case series, we confirm that serum creatinine levels and 24 h proteinuria are parameters that when altered should prompt the clinical suspicion of WM-related renal involvement, even if at present there are not precise cut-off levels recommending the execution of a renal biopsy. In our series AL Amyloidosis (n = 3/7) and tubulo-interstitial infiltration by lymphoma cells (n = 3/7) were the two more represented entities. BTKi did not seem to improve renal function (Case 1), while bortezomib-based regimens demonstrated a beneficial activity on the hematological and organ response, even when used as second-line therapy after chemoimmunotherapy (Case 3) and also with coexistence of anti-MAG neuropathy (Case 2). In case of poor response to bortezomib, standard chemoimmunotherapy (CIT), such as rituximab-bendamustine, represents an effective option (Case 1, 6, and 7). In our series, CIT generates durable responses more frequently in cases with amyloidogenic renal damage (Case 1, 5, and 7).
CONCLUSION CONCLUSIONS
In this illustrative case series, we confirm that serum creatinine levels and 24 h proteinuria are parameters that when altered should prompt the clinical suspicion of WM-related renal involvement, even if at present there are not precise cut-off levels recommending the execution of a renal biopsy. Studies with higher numerosity are needed to better clarify the pathological and clinical features of renal involvement during WM and to determine the potential benefit of different therapeutic regimens according to the histopathological subtypes.

Identifiants

pubmed: 38662353
doi: 10.1002/cnr2.2062
doi:

Substances chimiques

Bortezomib 69G8BD63PP

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2062

Informations de copyright

© 2024 The Authors. Cancer Reports published by Wiley Periodicals LLC.

Références

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Auteurs

Nicolò Danesin (N)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Greta Scapinello (G)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Dorella Del Prete (D)

Nephrology, Dialysis and Transplantation Unit, Department of Medicine, University of Padova, Padova, Italy.

Elena Naso (E)

Nephrology, Dialysis and Transplantation Unit, Department of Medicine, University of Padova, Padova, Italy.

Tamara Berno (T)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Andrea Visentin (A)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Laura Bonaldi (L)

Immunology and Molecular Oncology Diagnostic Unit, Veneto Institute of Oncology, IOV-IRCCS, Padova, Italy.

Annalisa Martines (A)

Immunology and Molecular Oncology Diagnostic Unit, Veneto Institute of Oncology, IOV-IRCCS, Padova, Italy.

Roberta Bertorelle (R)

Immunology and Molecular Oncology Diagnostic Unit, Veneto Institute of Oncology, IOV-IRCCS, Padova, Italy.

Fabrizio Vianello (F)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.
Veneto Institute of Molecular Medicine, Fondazione per la Ricerca Biomedica Avanzata, Padova, Italy.

Carmela Gurrieri (C)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Renato Zambello (R)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.
Veneto Institute of Molecular Medicine, Fondazione per la Ricerca Biomedica Avanzata, Padova, Italy.

Chiara Castellani (C)

Cardiovascular Pathology Unit, Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Marny Fedrigo (M)

Cardiovascular Pathology Unit, Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Stefania Rizzo (S)

Cardiovascular Pathology Unit, Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Annalisa Angelini (A)

Cardiovascular Pathology Unit, Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padova, Padova, Italy.

Livio Trentin (L)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.

Francesco Piazza (F)

Hematology Unit, Department of Medicine, University of Padova, Padova, Italy.
Veneto Institute of Molecular Medicine, Fondazione per la Ricerca Biomedica Avanzata, Padova, Italy.

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