Estimated GFR in autosomal dominant polycystic kidney disease: errors of an unpredictable method.


Journal

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

Informations de publication

Date de publication:
11 2022
Historique:
received: 18 10 2021
accepted: 16 02 2022
pubmed: 1 4 2022
medline: 25 10 2022
entrez: 31 3 2022
Statut: ppublish

Résumé

Autosomal dominant polycystic kidney disease (ADPKD) causes about 10% of cases of end stage renal disease. Disease progression rate is heterogeneous. Tolvaptan is presently the only specific therapeutic option to slow kidney function decline in adults at risk of rapidly progressing ADPKD with chronic kidney disease (CKD) stages 1-4. Thus, a reliable evaluation of kidney function in patients with ADPKD is needed. We evaluated the agreement between measured (mGFR) and estimated glomerular filtration rate (eGFR) by 61 formulas based on creatinine and/or cystatin-C (eGFR) in 226 ADPKD patients with diverse GFR values, from predialysis to glomerular hyperfiltration. Also, we evaluated whether incorrect categorization of CKD using eGFR may interfere with the indication and/or reimbursement of Tolvaptan treatment. No formula showed acceptable agreement with mGFR. Total Deviation Index averaged about 50% for eGFR based on creatinine and/or cystatin-C, indicating that 90% of the estimations of GFR showed bounds of error of 50% when compared with mGFR. In 1 out of 4 cases with mGFR < 30 ml/min, eGFR provided estimations above this threshold. Also, in half of the cases with mGFR between 30 and 40 ml/min, formulas estimated values < 30 ml/min. The evaluation of renal function with formulas in ADPKD patients is unreliable. Extreme deviation from real renal function is quite frequent. The consequences of this error deserve attention, especially in rapid progressors who may benefit from starting treatment with tolvaptan and in whom specific GFR thresholds are needed for the indication or reimbursement. Whenever possible, mGFR is recommended.

Sections du résumé

BACKGROUND
Autosomal dominant polycystic kidney disease (ADPKD) causes about 10% of cases of end stage renal disease. Disease progression rate is heterogeneous. Tolvaptan is presently the only specific therapeutic option to slow kidney function decline in adults at risk of rapidly progressing ADPKD with chronic kidney disease (CKD) stages 1-4. Thus, a reliable evaluation of kidney function in patients with ADPKD is needed.
METHODS
We evaluated the agreement between measured (mGFR) and estimated glomerular filtration rate (eGFR) by 61 formulas based on creatinine and/or cystatin-C (eGFR) in 226 ADPKD patients with diverse GFR values, from predialysis to glomerular hyperfiltration. Also, we evaluated whether incorrect categorization of CKD using eGFR may interfere with the indication and/or reimbursement of Tolvaptan treatment.
RESULTS
No formula showed acceptable agreement with mGFR. Total Deviation Index averaged about 50% for eGFR based on creatinine and/or cystatin-C, indicating that 90% of the estimations of GFR showed bounds of error of 50% when compared with mGFR. In 1 out of 4 cases with mGFR < 30 ml/min, eGFR provided estimations above this threshold. Also, in half of the cases with mGFR between 30 and 40 ml/min, formulas estimated values < 30 ml/min.
CONCLUSIONS
The evaluation of renal function with formulas in ADPKD patients is unreliable. Extreme deviation from real renal function is quite frequent. The consequences of this error deserve attention, especially in rapid progressors who may benefit from starting treatment with tolvaptan and in whom specific GFR thresholds are needed for the indication or reimbursement. Whenever possible, mGFR is recommended.

Identifiants

pubmed: 35357684
doi: 10.1007/s40620-022-01286-0
pii: 10.1007/s40620-022-01286-0
pmc: PMC9584992
doi:

Substances chimiques

Tolvaptan 21G72T1950
Creatinine AYI8EX34EU

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2109-2118

Subventions

Organisme : Instituto de Salud Carlos III
ID : PI19/01220

Informations de copyright

© 2022. The Author(s).

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Auteurs

Rosa Miquel Rodríguez (RM)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.

Sergio Luis-Lima (S)

Department of Nephrology and Hypertension, IIS-Fundación Jimenez Díaz, UAM, Madrid, Spain.

Juan Manuel Fernandez (JM)

Nephrology Department, Hospital Universitario Dr Negrín, Las Palmas, Spain.

María Vanesa Pérez Gómez (MVP)

Department of Nephrology and Hypertension, IIS-Fundación Jimenez Díaz, UAM, Madrid, Spain.

Beatriz González Toledo (BG)

Department of Nephrology and Hypertension, IIS-Fundación Jimenez Díaz, UAM, Madrid, Spain.

Marian Cobo (M)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.

Patricia Delgado-Mallén (P)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.

Beatriz Escamilla (B)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.

Cristina Oramas Marco (CO)

Laboratory of Renal Function, Faculty of Medicine, University of La Laguna, La Laguna, Spain.

Sara Estupiñán (S)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.

Coriolano Cruz Perera (CC)

Research Unit, Hospital Universitario de Canarias, Calle Ofra s/n 38023 La Laguna, Tenerife, Spain.

Natalia Negrín Mena (NN)

Research Unit, Hospital Universitario de Canarias, Calle Ofra s/n 38023 La Laguna, Tenerife, Spain.

Laura Díaz Martín (LD)

Laboratory of Renal Function, Faculty of Medicine, University of La Laguna, La Laguna, Spain.
Red de Investigación Renal (REDINREN), Instituto Carlos III-FEDER, 28040, Madrid, Spain.

Sergio Pitti Reyes (SP)

Radiology Unit, Hospital Universitario de Canarias, Tenerife, Spain.

Ibrahim Hernández González (IH)

Radiology Unit, Hospital Universitario de Canarias, Tenerife, Spain.

Federico González-Rinne (F)

Research Unit, Hospital Universitario de Canarias, Calle Ofra s/n 38023 La Laguna, Tenerife, Spain.

Alejandra González-Delgado (A)

Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.

Carmen Ferrer-Moure (C)

Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.

Begoña López-Botet Zulueta (BL)

Department of Nephrology and Hypertension, IIS-Fundación Jimenez Díaz, UAM, Madrid, Spain.

Armando Torres (A)

Nephrology Department, Hospital Universitario de Canarias, Tenerife, Spain.
Internal Medicine Department, Faculty of Medicine, Universidad de La Laguna, Tenerife, Spain.
Instituto de Tecnología Biomédicas, ITB, Universidad de La Laguna, La Laguna, Spain.

Jose Carlos Rodriguez Pérez (JC)

Nephrology Department, Hospital Universitario Dr Negrín, Las Palmas, Spain.
University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain.

Flavio Gaspari (F)

Laboratory of Renal Function, Faculty of Medicine, University of La Laguna, La Laguna, Spain.

Alberto Ortiz (A)

Department of Nephrology and Hypertension, IIS-Fundación Jimenez Díaz, UAM, Madrid, Spain.
Red de Investigación Renal (REDINREN), Instituto Carlos III-FEDER, 28040, Madrid, Spain.

Esteban Porrini (E)

Research Unit, Hospital Universitario de Canarias, Calle Ofra s/n 38023 La Laguna, Tenerife, Spain. esteban.l.porrini@gmail.com.
Internal Medicine Department, Faculty of Medicine, Universidad de La Laguna, Tenerife, Spain. esteban.l.porrini@gmail.com.
Instituto de Tecnología Biomédicas, ITB, Universidad de La Laguna, La Laguna, Spain. esteban.l.porrini@gmail.com.
Laboratory of Renal Function, Faculty of Medicine, University of La Laguna, La Laguna, Spain. esteban.l.porrini@gmail.com.

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