Estimated GFR in autosomal dominant polycystic kidney disease: errors of an unpredictable method.
ADPKD
Chronic kidney disease
Glomerular filtration rate
Journal
Journal of nephrology
ISSN: 1724-6059
Titre abrégé: J Nephrol
Pays: Italy
ID NLM: 9012268
Informations de publication
Date de publication:
11 2022
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
2109-2118Subventions
Organisme : Instituto de Salud Carlos III
ID : PI19/01220
Informations de copyright
© 2022. The Author(s).
Références
Martínez V, Comas J, Arcos E, Díaz JM, Muray S, Cabezuelo J, Ballarín J, Ars E, Torra R (2013) Renal replacement therapy in ADPKD patients: a 25-year survey based on the Catalan registry. BMC Nephrol 14:186. https://doi.org/10.1186/1471-2369-14-186
doi: 10.1186/1471-2369-14-186
pubmed: 24007508
pmcid: 3844422
Chebib FT, Torres VE (2016) Autosomal dominant polycystic kidney disease: core curriculum. Am J Kidney Dis 67:792–810. https://doi.org/10.1053/j.ajkd.2015.07.037
doi: 10.1053/j.ajkd.2015.07.037
pubmed: 26530876
Cornec-Le Gall E, Alam A, Perrone RD (2019) Autosomal dominant polycystic kidney disease. Lancet 393:919–935. https://doi.org/10.1016/S01406736(18)32782-X
doi: 10.1016/S01406736(18)32782-X
pubmed: 30819518
Bergmann C, Guay-Woodford LM, Harris PC, Horie S, Peters DJM, Torres VE (2018) Polycystic kidney disease. Nat Rev Dis Primers 4:50. https://doi.org/10.1038/s41572-018-0047-y
doi: 10.1038/s41572-018-0047-y
pubmed: 30523303
pmcid: 6592047
Grantham JJ (2008) Clinical practice. Autosomal dominant polycystic kidney disease. N Engl J Med 359:1477–1485. https://doi.org/10.1056/NEJMcp0804458
doi: 10.1056/NEJMcp0804458
pubmed: 18832246
Cornec-Le Gall E, Marie-Pierre Audrézet MP, Rousseau A, Hourmant M, Renaudineau E, Charasse C et al (2016) The PROPKD score: a new algorithm to predict renal survival in autosomal dominant polycystic kidney. J Am Soc Nephrol 27:942–951. https://doi.org/10.1681/ASN.2015010016
doi: 10.1681/ASN.2015010016
pubmed: 26150605
Porrini E, Ruggenenti P, Luis-Lima S, Carrara F, Jiménez A, de Vries APJ et al (2019) Estimated GFR: time for a critical appraisal. Nat Rev Nephrol 15:177–190. https://doi.org/10.1038/s41581-018-0080-9
doi: 10.1038/s41581-018-0080-9
pubmed: 30518813
Torres VE, Chapman AB, Devuyst O, Gansevoort RT, Perrone RD, Dandurand A et al (2018) Multicenter, open-label, extension trial to evaluate the long-term efficacy and safety of early versus delayed treatment with tolvaptan in autosomal dominant polycystic kidney disease: the TEMPO 4:4 trial for the TEMPO 4:4 trial investigators. Nephrol Dial Transplant 33:477–489. https://doi.org/10.1093/ndt/gfx043
doi: 10.1093/ndt/gfx043
pubmed: 28379536
https://www.aemps.gob.es/medicamentosUsoHumano/informesPublicos/docs/IPT-tolvaptan-Jinarc-PQRAD.pdf?x42633 ; accessed 02 Dec 2021
Gansevoort RT, Arici M, Benzing T, Birn H, Capasso G, Covic A et al (2016) Recommendations for the use of tolvaptan in autosomal dominant polycystic kidney disease: a position statement on behalf of the ERA-EDTA working groups on inherited kidney disorders and European Renal Best Practice. Nephrol Dial Transplant 31:337–348. https://doi.org/10.1093/ndt/gfv456
doi: 10.1093/ndt/gfv456
pubmed: 26908832
pmcid: 4762400
Luis-Lima S, Gaspari F, Negrín-Mena N, Carrara F, Díaz-Martín L, Jiménez-Sosa A et al (2018) Iohexol plasma clearance simplified by dried blood spot testing. Nephrol Dial Transplant 33:1597–1603. https://doi.org/10.1093/ndt/gfx323
doi: 10.1093/ndt/gfx323
pubmed: 29211858
https://lfr.ecihucan.es/en/renal-function-lab ; accessed 02 Dec 2021
Krutzén E, Bäck SE, Nilsson-Ehle I, Nilsson-Ehle P (1984) Plasma clearance of a new contrast agent, iohexol: a method for the assessment of glomerular filtration rate. J Lab Clin Med 104:955–961
pubmed: 6438261
Magistronia R, Corsib C, Martí T, Torra R (2018) A review of the imaging techniques for measuring kidney and cyst volume in establishing autosomal dominant polycystic kidney disease progression. Am J Nephrol 48:67–78. https://doi.org/10.1159/000491022
doi: 10.1159/000491022
Bhutani H, Smith V, Rahbari-Oskoui F, Mittal A, Grantham JJ, Torres VE et al (2015) A comparison of ultrasound and magnetic resonance imaging shows that kidney length predicts chronic kidney disease in autosomal dominant polycystic kidney disease. Kidney Int 88:146–151. https://doi.org/10.1038/ki.2015.71
doi: 10.1038/ki.2015.71
pubmed: 25830764
pmcid: 4490113
López-Martínez M, Luis-Lima S, Morales E, Navarro-Díaz M, Negrín-Mena N, Folgueras T et al (2020) The estimation of GFR and the adjustment for BSA in overweight and obesity: a dreadful combination of two errors. Int J Obes (Lond) 44:1129–1140. https://doi.org/10.1038/s41366-019-0476-z
doi: 10.1038/s41366-019-0476-z
pubmed: 31641213
Lin L, Hedayat AS, Wu W (2012) Statistical tools for measuring agreement. Springer, New York
doi: 10.1007/978-1-4614-0562-7
Gaspari F, Ruggenenti P, Porrini E, Motterlini N, Cannata A, Carrara F et al (2013) The GFR and GFR decline cannot be accurately estimated in type 2 diabetics. Kidney Int 84:164–173. https://doi.org/10.1038/ki.2013.47
doi: 10.1038/ki.2013.47
pubmed: 23447062
Knight EL, Verhave JC, Spiegelman D, Hillege HL, de Zeeuw D, Curhan GC et al (2004) Factors influencing serum cystatin-C levels other than renal function and the impact on renal function measurement. Kidney Int 65:1416–1421. https://doi.org/10.1111/j.1523-1755.2004.00517.x
doi: 10.1111/j.1523-1755.2004.00517.x
pubmed: 15086483
Stevens LA, Schmid CH, Greene T, Li L, Beck GJ, Joffe MM et al (2009) Factors other than glomerular filtration rate affect serum cystatin-C levels. Kidney Int 75:652–660. https://doi.org/10.1038/ki.2008.638
doi: 10.1038/ki.2008.638
pubmed: 19119287
Reutens AT, Bonnet F, Lantieri O, Roussel R, Balkau B, Epidemiological Study on the Insulin Resistance Syndrome Study Group (2013) Epidemiological study on the insulin resistance syndrome study group. The association between cystatin-C and incident type 2 diabetes is related to central adiposity. Nephrol Dial Transplant 28:1820–1829. https://doi.org/10.1093/ndt/gfs561
doi: 10.1093/ndt/gfs561
pubmed: 23291367
Naour N, Fellahi S, Renucci JF, Poitou C, Rouault C, Basdevantet A et al (2009) Potential contribution of adipose tissue to elevated serum cystatin-C in human obesity. Obesity (Silver Spring) 17:2121–2126. https://doi.org/10.1038/oby.2009.96
doi: 10.1038/oby.2009.96
pubmed: 19360013
Reaven GM (1988) Role of insulin resistance in human disease. Diabetes 37:1595–1607. https://doi.org/10.2337/diab.37.12.1595
doi: 10.2337/diab.37.12.1595
pubmed: 3056758
Luis-Lima S, Escamilla-Cabrera B, Negrín-Mena N, Estupiñán S, Delgado-Mallén P, Marrero-Miranda D et al (2019) Chronic kidney disease staging with cystatin C or creatinine-based formulas: flipping the coin. Nephrol Dial Transplant 34:287–294. https://doi.org/10.1093/ndt/gfy086
doi: 10.1093/ndt/gfy086
pubmed: 29762739
https://www.ema.europa.eu/en/documents/product-information/jinarc-epar-product-information_en.pdf ; accessed 02 Dec 2021
https://senefro.org/contents/webstructure/APKD/Guias_Sociedad_Otsuka_V03.pdf ; accessed 02 Dec 2021
Orskov B, Borresen ML, Feldt-Rasmussen B, Østergaard O, Laursen I, Strandgaard S et al (2010) Estimating glomerular filtration rate using the new CKD-EPI equation and other equations in patients with autosomal dominant polycystic kidney disease. Am J Nephrol 31:53–57. https://doi.org/10.1159/000256657
doi: 10.1159/000256657
pubmed: 19887788
Spithoven EM, Meijer E, Boertien WE, Sinkeler SJ, Tent H, de Jong PE et al (2013) Tubular secretion of creatinine in autosomal dominant polycystic kidney disease: consequences for cross-sectional and longitudinal performance of kidney function estimating equations. Am J Kidney Dis 62:531–540. https://doi.org/10.1053/j.ajkd.2013.03.030
doi: 10.1053/j.ajkd.2013.03.030
pubmed: 23714171
Ruggenenti P, Gaspari F, Cannata A, Carrara F, Cella C, Ferrari S et al (2012) GFR-ADPKD Study Group. Measuring and estimating GFR and treatment effect in ADPKD patients: results and implications of a longitudinal cohort study. PLoS One 7:e32533. https://doi.org/10.1371/journal.pone.0032533
doi: 10.1371/journal.pone.0032533
pubmed: 22393413
pmcid: 3291245