Display options
Cite
Perrone RD, Mouksassi MS, Romero K, et al. Total Kidney Volume Is a Prognostic Biomarker of Renal Function Decline and Progression to End-Stage Renal Disease in Patients With Autosomal Dominant Polycystic Kidney Disease. Kidney Int Rep. 2017;2(3):442-450doi: 10.1016/j.ekir.2017.01.003.
Perrone, R. D., Mouksassi, M. S., Romero, K., Czerwiec, F. S., Chapman, A. B., Gitomer, B. Y., Torres, V. E., Miskulin, D. C., Broadbent, S., & Marier, J. F. (2017). Total Kidney Volume Is a Prognostic Biomarker of Renal Function Decline and Progression to End-Stage Renal Disease in Patients With Autosomal Dominant Polycystic Kidney Disease. Kidney international reports, 2(3), 442-450. https://doi.org/10.1016/j.ekir.2017.01.003
Perrone, Ronald D, et al. "Total Kidney Volume Is a Prognostic Biomarker of Renal Function Decline and Progression to End-Stage Renal Disease in Patients With Autosomal Dominant Polycystic Kidney Disease." Kidney international reports vol. 2,3 (2017): 442-450. doi: https://doi.org/10.1016/j.ekir.2017.01.003
Perrone RD, Mouksassi MS, Romero K, Czerwiec FS, Chapman AB, Gitomer BY, Torres VE, Miskulin DC, Broadbent S, Marier JF. Total Kidney Volume Is a Prognostic Biomarker of Renal Function Decline and Progression to End-Stage Renal Disease in Patients With Autosomal Dominant Polycystic Kidney Disease. Kidney Int Rep. 2017 Jan 16;2(3):442-450. doi: 10.1016/j.ekir.2017.01.003. eCollection 2017 May. PMID: 29142971; PMCID: PMC5678856.
Copy Download .nbib Format: NLM
Share it on

Kidney Int Rep. 2017 Jan 16;2(3):442-450. doi: 10.1016/j.ekir.2017.01.003. eCollection 2017 May.

Total Kidney Volume Is a Prognostic Biomarker of Renal Function Decline and Progression to End-Stage Renal Disease in Patients With Autosomal Dominant Polycystic Kidney Disease.

Kidney international reports

Ronald D Perrone, Mohamad-Samer Mouksassi, Klaus Romero, Frank S Czerwiec, Arlene B Chapman, Berenice Y Gitomer, Vicente E Torres, Dana C Miskulin, Steve Broadbent, Jean F Marier

Affiliations

  1. Division of Nephrology, Department of Medicine, Tufts Medical Center, Boston, Massachusetts, USA.
  2. Pharsight, Montreal, Quebec, Canada.
  3. Critical Path Institute, Tucson, Arizona, USA.
  4. Otsuka Pharmaceutical Development and Commercialization Inc., Global Clinical Development, Rockville, Maryland, USA.
  5. Division of Nephrology, University of Chicago, Chicago, Illinois, USA.
  6. Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
  7. Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, Minnesota, USA.

PMID: 29142971 PMCID: PMC5678856 DOI: 10.1016/j.ekir.2017.01.003

Abstract

INTRODUCTION: Autosomal dominant polycystic kidney disease is the most common hereditary kidney disease. TKV is a promising imaging biomarker for tracking and predicting the natural history of autosomal dominant polycystic kidney disease. The prognostic value of TKV was evaluated, in combination with age and eGFR, for the outcomes of 30% decline in eGFR and progression to ESRD. Observational data including 2355 patients with TKV measurements were available.

METHODS: Multivariable Cox models were developed to assess the prognostic value of age, TKV, height-adjusted TKV, eGFR, sex, race, and genotype for the probability of a 30% decline in eGFR or ESRD.

RESULTS: TKV was the most important prognostic term for 30% decline in eGFR in autosomal dominant polycystic kidney disease patients with and without preserved baseline eGFR. For a 40-year-old subject with preserved eGFR (70 ml/min per 1.73 m

DISCUSSION: The capability to predict 30% decline in eGFR is a novel aspect of this study. TKV was formally qualified, both by FDA and EMA, as a prognostic enrichment biomarker for selecting patients at high risk for a progressive decline in renal function for inclusion in interventional clinical trials.

Keywords: end-stage renal disease; prognostic biomarker; renal function decline; total kidney volume

References

  1. Clin Chem Lab Med. 2009;47(9):1017-9 - PubMed
  2. Lancet. 2013 Nov 2;382(9903):1485-95 - PubMed
  3. Am J Kidney Dis. 2002 Feb;39(2 Suppl 1):S1-266 - PubMed
  4. J Am Soc Nephrol. 2016 Sep;27(9):2872-84 - PubMed
  5. N Engl J Med. 2014 Dec 11;371(24):2267-76 - PubMed
  6. Kidney Int Rep. 2017 Feb 21;2(3):451-460 - PubMed
  7. J Am Soc Nephrol. 2016 Mar;27(3):942-51 - PubMed
  8. Am J Kidney Dis. 2005 Dec;46(6):1058-64 - PubMed
  9. Transl Res. 2015 Apr;165(4):488-98 - PubMed
  10. Ann Intern Med. 2007 Oct 16;147(8):573-7 - PubMed
  11. Kidney Int. 2008 Jan;73(1):108-16 - PubMed
  12. Clin J Am Soc Nephrol. 2006 Jan;1(1):148-57 - PubMed
  13. Am J Kidney Dis. 2009 Aug;54(2):205-26 - PubMed
  14. J Am Soc Nephrol. 2006 Nov;17(11):3013-9 - PubMed
  15. J Am Soc Nephrol. 2014 Jan;25(1):18-32 - PubMed
  16. N Engl J Med. 2006 May 18;354(20):2122-30 - PubMed
  17. JAMA. 2014 Jun 25;311(24):2518-2531 - PubMed
  18. PLoS One. 2015 Jul 15;10(7):e0132927 - PubMed
  19. J Am Soc Nephrol. 2015 Jan;26(1):160-72 - PubMed
  20. Clin J Am Soc Nephrol. 2012 Mar;7(3):479-86 - PubMed
  21. Nat Rev Nephrol. 2011 Aug 23;7(10):556-66 - PubMed
  22. Biometrics. 2000 Jun;56(2):337-44 - PubMed
  23. Am J Kidney Dis. 2015 Oct;66(4):583-90 - PubMed

Publication Types

Grant support