Document Detail

Soluble klotho and autosomal dominant polycystic kidney disease.
MedLine Citation:
PMID:  22193235     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND OBJECTIVES: Fibroblast growth factor 23 (FGF23) levels are elevated in patients with autosomal dominant polycystic kidney disease (ADPKD) and X-linked hypophosphatemia (XLH), but only the latter is characterized by a renal phosphate wasting phenotype. This study explored potential mechanisms underlying resistance to FGF23 in ADPKD.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: FGF23 and klotho levels were measured, and renal phosphate transport was evaluated by calculating the ratio of the maximum rate of tubular phosphate reabsorption to GFR (TmP/GFR) in 99 ADPKD patients, 32 CKD patients, 12 XLH patients, and 20 healthy volunteers. ADPKD and CKD patients were classified by estimated GFR (CKD stage 1, ≥90 ml/min per 1.73 m(2); CKD stage 2, 60-89 ml/min per 1.73 m(2)).
RESULTS: ADPKD patients had 50% higher FGF23 levels than did XLH patients; TmP/GFR was near normal in most ADPKD patients and very low in XLH patients. Serum klotho levels were lowest in the ADPKD group, whereas the CKD and XLH groups and volunteers had similar levels. ADPKD patients with an apparent renal phosphate leak had two-fold higher klotho levels than those without. Serum klotho values correlated inversely with cyst volume and kidney growth.
CONCLUSIONS: Loss of klotho might be a consequence of cyst growth and constrain the phosphaturic effect of FGF23 in most patients with ADPKD. Normal serum klotho levels were associated with normal FGF23 biologic activity in all XLH patients and a minority of ADPKD patients. Loss of klotho and FGF23 increase appear to exceed and precede the changes that can be explained by loss of GFR in patients with ADPKD.
Ivana Pavik; Philippe Jaeger; Lena Ebner; Diane Poster; Fabienne Krauer; Andreas D Kistler; Katharina Rentsch; Gustav Andreisek; Carsten A Wagner; Olivier Devuyst; Rudolf P Wüthrich; Christoph Schmid; Andreas L Serra
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-22
Journal Detail:
Title:  Clinical journal of the American Society of Nephrology : CJASN     Volume:  7     ISSN:  1555-905X     ISO Abbreviation:  Clin J Am Soc Nephrol     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-16     Completed Date:  2012-06-12     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  101271570     Medline TA:  Clin J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  248-57     Citation Subset:  IM    
Institute of Physiology and Zurich Center for Integrative Human Physiology, Zurich, Switzerland.
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MeSH Terms
Biological Transport
Case-Control Studies
Cross-Sectional Studies
Fibroblast Growth Factors / blood
Glomerular Filtration Rate
Glucuronidase / blood*
Hypophosphatemic Rickets, X-Linked Dominant / blood,  genetics
Kidney Tubules / metabolism,  physiopathology
Least-Squares Analysis
Linear Models
Middle Aged
Phosphates / metabolism
Polycystic Kidney, Autosomal Dominant / blood*,  genetics,  physiopathology
Renal Insufficiency, Chronic / blood,  genetics
Young Adult
Reg. No./Substance:
0/Phosphates; 0/fibroblast growth factor 23; 62031-54-3/Fibroblast Growth Factors; EC; EC protein

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