Propensity score-matched analysis of long-term outcomes for living kidney donation in alternative complement pathway diseases: a pilot study.


Journal

Journal of nephrology
ISSN: 1724-6059
Titre abrégé: J Nephrol
Pays: Italy
ID NLM: 9012268

Informations de publication

Date de publication:
05 2023
Historique:
received: 07 09 2022
accepted: 15 01 2023
medline: 31 5 2023
pubmed: 23 2 2023
entrez: 22 2 2023
Statut: ppublish

Résumé

Atypical hemolytic syndrome (aHUS) and C3 glomerulopathy (C3G) are complement-mediated rare diseases with excessive activation of the alternative pathway. Data to guide the evaluation of living-donor candidates for aHUS and C3G are very limited. The outcomes of living donors to recipients with aHUS and C3G (Complement disease-living donor group) were compared with a control group to improve our understanding of the clinical course and outcomes of living donation in this context. Complement disease-living donor group [n = 28; aHUS(53.6%), C3G(46.4%)] and propensity score-matched control-living donor group (n = 28) were retrospectively identified from 4 centers (2003-2021) and followed for major cardiac events (MACE), de novo hypertension, thrombotic microangiopathy (TMA), cancer, death, estimated glomerular filtration rate (eGFR) and proteinuria after donation. None of the donors for recipients with complement-related kidney diseases experienced MACE or TMA whereas two donors in the control group developed MACE (7.1%) after 8 (IQR, 2.6-12.8) years (p = 0.15). New-onset hypertension was similar between complement disease and control donor groups (21.4% vs 25%, respectively, p = 0.75). There were no differences between study groups regarding last eGFR and proteinuria levels (p = 0.11 and p = 0.70, respectively). One related donor for a recipient with complement-related kidney disease developed gastric cancer and another related donor developed a brain tumor and died in the 4th year after donation (2, 7.1% vs none, p = 0.15). No recipient had donor-specific human leukocyte antigen antibodies at the time of transplantation. Median follow-up period of transplant recipients was 5 years (IQR, 3-7). Eleven (39.3%) recipients [aHUS (n = 3) and C3G (n = 8)] lost their allografts during the follow-up period. Causes of allograft loss were chronic antibody-mediated rejection in 6 recipients and recurrence of C3G in 5. Last serum creatinine and last eGFR of the remaining patients on follow up were 1.03 ± 038 mg/dL and 73.2 ± 19.9 m/min/1.73 m2 for aHUS patients and 1.30 ± 0.23 mg/dL and 56.4 ± 5.5 m/min/1.73 m2 for C3G patients. The present study highlights the importance and complexity of living related-donor kidney transplant for patients with complement-related kidney disorders and motivates the need for further research to determine the optimal risk-assessment for living donor candidates to recipients with aHUS and C3G.

Sections du résumé

BACKGROUND
Atypical hemolytic syndrome (aHUS) and C3 glomerulopathy (C3G) are complement-mediated rare diseases with excessive activation of the alternative pathway. Data to guide the evaluation of living-donor candidates for aHUS and C3G are very limited. The outcomes of living donors to recipients with aHUS and C3G (Complement disease-living donor group) were compared with a control group to improve our understanding of the clinical course and outcomes of living donation in this context.
METHODS
Complement disease-living donor group [n = 28; aHUS(53.6%), C3G(46.4%)] and propensity score-matched control-living donor group (n = 28) were retrospectively identified from 4 centers (2003-2021) and followed for major cardiac events (MACE), de novo hypertension, thrombotic microangiopathy (TMA), cancer, death, estimated glomerular filtration rate (eGFR) and proteinuria after donation.
RESULTS
None of the donors for recipients with complement-related kidney diseases experienced MACE or TMA whereas two donors in the control group developed MACE (7.1%) after 8 (IQR, 2.6-12.8) years (p = 0.15). New-onset hypertension was similar between complement disease and control donor groups (21.4% vs 25%, respectively, p = 0.75). There were no differences between study groups regarding last eGFR and proteinuria levels (p = 0.11 and p = 0.70, respectively). One related donor for a recipient with complement-related kidney disease developed gastric cancer and another related donor developed a brain tumor and died in the 4th year after donation (2, 7.1% vs none, p = 0.15). No recipient had donor-specific human leukocyte antigen antibodies at the time of transplantation. Median follow-up period of transplant recipients was 5 years (IQR, 3-7). Eleven (39.3%) recipients [aHUS (n = 3) and C3G (n = 8)] lost their allografts during the follow-up period. Causes of allograft loss were chronic antibody-mediated rejection in 6 recipients and recurrence of C3G in 5. Last serum creatinine and last eGFR of the remaining patients on follow up were 1.03 ± 038 mg/dL and 73.2 ± 19.9 m/min/1.73 m2 for aHUS patients and 1.30 ± 0.23 mg/dL and 56.4 ± 5.5 m/min/1.73 m2 for C3G patients.
CONCLUSION
The present study highlights the importance and complexity of living related-donor kidney transplant for patients with complement-related kidney disorders and motivates the need for further research to determine the optimal risk-assessment for living donor candidates to recipients with aHUS and C3G.

Identifiants

pubmed: 36808609
doi: 10.1007/s40620-023-01588-x
pii: 10.1007/s40620-023-01588-x
doi:

Substances chimiques

Complement System Proteins 9007-36-7

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

979-986

Subventions

Organisme : Ulusal Metroloji Enstitüsü, Türkiye Bilimsel ve Teknolojik Araştirma Kurumu
ID : 114S261

Informations de copyright

© 2023. The Author(s) under exclusive licence to Italian Society of Nephrology.

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Auteurs

Yasar Caliskan (Y)

Saint Louis University Transplant Center, SSM-Saint Louis University Hospital, 1201 S. Grand Blvd., St. Louis, MO, 63104, USA. yasar.caliskan@health.slu.edu.
Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey. yasar.caliskan@health.slu.edu.

Seda Safak (S)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Ozgur Akin Oto (OA)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Arzu Velioglu (A)

Division of Nephrology, Marmara University School of Medicine, Istanbul, Turkey.

Berna Yelken (B)

Organ Transplantation Center, Koc University Hospital, Istanbul, Turkey.

Safak Mirioglu (S)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.
Division of Nephrology, Bezmialem Vakif University School of Medicine, Istanbul, Turkey.

Ahmet Burak Dirim (AB)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Abdulmecit Yildiz (A)

Division of Nephrology, Bursa Uludag University School of Medicine, Bursa, Turkey.

Nurana Guller (N)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Halil Yazici (H)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Alparslan Ersoy (A)

Division of Nephrology, Bursa Uludag University School of Medicine, Bursa, Turkey.

Aydin Turkmen (A)

Division of Nephrology, Istanbul University Istanbul School of Medicine, Istanbul, Turkey.

Krista L Lentine (KL)

Saint Louis University Transplant Center, SSM-Saint Louis University Hospital, 1201 S. Grand Blvd., St. Louis, MO, 63104, USA.

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