TY - JOUR
T1 - Relationship of copeptin, a surrogate marker for arginine vasopressin, with change in total kidney volume and gfr decline in autosomal dominant polycystic kidney disease
T2 - Results from the crisp cohort
AU - Boertien, Wendy E.
AU - Meijer, Esther
AU - Li, Jie
AU - Bost, James E.
AU - Struck, Joachim
AU - Flessner, Michael F.
AU - Gansevoort, Ron T.
AU - Torres, Vicente E.
N1 - Funding Information:
Support: The CRISP Study is supported by cooperative agreements from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (DK056943, DK056956, DK056957, and DK056961) and by the National Center for Research Resources (NCRR) GCRCs at each institution ( RR000039 Emory, RR00585 Mayo, RR23940 Kansas, and RR000052 UAB) and the NCRR CTSAs at each institution ( RR025008 Emory, RR024150 Mayo, RR033179 Kansas, RR025777 UAB, and RR024153 Pittsburgh).
PY - 2013/3
Y1 - 2013/3
N2 - Background: Experimental studies indicate that arginine vasopressin (AVP) may have deleterious effects in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). However, the significance of AVP in human ADPKD is unclear. Study Design: Longitudinal observational study with 8.5 (IQR, 7.7-9.0) years' follow-up (CRISP [Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease]). Setting & Participants: 241 patients with ADPKD with creatinine clearance >70 mL/min. Predictor: Plasma copeptin concentration, a surrogate marker for AVP. Outcomes: Change in measured glomerular filtration rate (mGFR, assessed by iothalamate clearance) and total kidney volume (measured by magnetic resonance imaging). Measurements: Baseline copeptin level, plasma and urinary osmolality, and measurements of total kidney volume and mGFR during follow-up. Results: In these patients (median age, 34 [IQR, 25-40] years; 38% men; median mGFR, 94 [IQR, 79-145] mL/min/1.73 m 2; median total kidney volume, 859 [IQR, 577-1,299] mL), median copeptin level was 2.9 (IQR, 1.8-5.1) pmol/L. Copeptin was not associated with plasma osmolality (P = 0.3), the physiologic stimulus for AVP release, but was associated significantly with change in total kidney volume during follow-up (P < 0.001). This association remained significant after adjusting for sex, age, cardiovascular risk factors, and diuretic use (P = 0.03). Copeptin level was associated borderline significantly with change in mGFR after adjusting for these variables (P = 0.09). Limitations: No standardization of hydration status at time of copeptin measurement. Conclusions: These data show that in ADPKD, copeptin level, as a marker for AVP, is not correlated with plasma osmolality. Most importantly, high copeptin levels are associated independently with disease progression in early ADPKD. This is in line with experimental studies that indicate a disease-promoting role for AVP.
AB - Background: Experimental studies indicate that arginine vasopressin (AVP) may have deleterious effects in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD). However, the significance of AVP in human ADPKD is unclear. Study Design: Longitudinal observational study with 8.5 (IQR, 7.7-9.0) years' follow-up (CRISP [Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease]). Setting & Participants: 241 patients with ADPKD with creatinine clearance >70 mL/min. Predictor: Plasma copeptin concentration, a surrogate marker for AVP. Outcomes: Change in measured glomerular filtration rate (mGFR, assessed by iothalamate clearance) and total kidney volume (measured by magnetic resonance imaging). Measurements: Baseline copeptin level, plasma and urinary osmolality, and measurements of total kidney volume and mGFR during follow-up. Results: In these patients (median age, 34 [IQR, 25-40] years; 38% men; median mGFR, 94 [IQR, 79-145] mL/min/1.73 m 2; median total kidney volume, 859 [IQR, 577-1,299] mL), median copeptin level was 2.9 (IQR, 1.8-5.1) pmol/L. Copeptin was not associated with plasma osmolality (P = 0.3), the physiologic stimulus for AVP release, but was associated significantly with change in total kidney volume during follow-up (P < 0.001). This association remained significant after adjusting for sex, age, cardiovascular risk factors, and diuretic use (P = 0.03). Copeptin level was associated borderline significantly with change in mGFR after adjusting for these variables (P = 0.09). Limitations: No standardization of hydration status at time of copeptin measurement. Conclusions: These data show that in ADPKD, copeptin level, as a marker for AVP, is not correlated with plasma osmolality. Most importantly, high copeptin levels are associated independently with disease progression in early ADPKD. This is in line with experimental studies that indicate a disease-promoting role for AVP.
KW - Autosomal dominant polycystic kidney disease
KW - arginine vasopressin
KW - copeptin
KW - disease progression
KW - glomerular filtration rate
KW - kidney function
KW - polycystic kidney disease
KW - total kidney volume
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U2 - 10.1053/j.ajkd.2012.08.038
DO - 10.1053/j.ajkd.2012.08.038
M3 - Article
C2 - 23089511
AN - SCOPUS:84874117983
SN - 0272-6386
VL - 61
SP - 420
EP - 429
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 3
ER -