Urine Fetuin-A is a biomarker of autosomal dominant polycystic kidney disease progression
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Published on: June 23, 2015
Nathalie Piazzon1,2, Florian Bernet3, Linda Guihard4
1Ecole Polytechnique Fédérale de Lausanne (EPFL), Bâtiment SV ISREC, Station 19, Lausanne, Switzerland. nathalie.piazzon@unil.ch.
Insights
Urinary Fetuin-A shows promise as a biomarker for diagnosing autosomal dominant polycystic kidney disease (ADPKD). Elevated levels in ADPKD patients indicate disease progression and correlate with kidney function decline.
Area of Science:
- Nephrology
- Biochemistry
- Genetics
Background:
- Autosomal dominant polycystic kidney disease (ADPKD) is a genetic kidney disorder leading to end-stage renal disease.
- Early diagnosis and monitoring of ADPKD are challenging despite developing treatments.
Purpose of the Study:
- To evaluate the diagnostic utility of urinary Fetuin-A as a novel biomarker for ADPKD.
- To assess the correlation of urinary Fetuin-A levels with ADPKD progression and renal function.
Main Methods:
- Analyzed renal and urinary Fetuin-A levels in ADPKD mouse models (Pkd1, Bicc1).
- Measured urinary Fetuin-A in ADPKD patients, healthy volunteers, and control patients using ELISA.
- Utilized Receiver Operating Characteristic (ROC) analysis to determine diagnostic accuracy.
Main Results:
- Renal Fetuin-A was upregulated in ADPKD mouse models.
- Urinary Fetuin-A levels were significantly higher in ADPKD patients compared to controls.
- Urinary Fetuin-A showed 94% sensitivity and 60% specificity for ADPKD detection (AUC 0.74).
- Levels correlated with renal insufficiency and increased over two years in patients with preserved function.
Conclusions:
- Urinary Fetuin-A serves as a sensitive biomarker for ADPKD progression.
- Further research is needed to elucidate the role of Fetuin-A in ADPKD pathogenesis.
Background:
Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by numerous fluid-filled cysts that frequently result in end-stage renal disease. While promising treatment options are in advanced clinical development, early diagnosis and follow-up remain a major challenge. We therefore evaluated the diagnostic value of Fetuin-A as a new biomarker of ADPKD in human urine.
Results:
We found that renal Fetuin-A levels are upregulated in both Pkd1 and Bicc1 mouse models of ADPKD. Measurement by ELISA revealed that urinary Fetuin-A levels were significantly higher in 66 ADPKD patients (17.5 ± 12.5 μg/mmol creatinine) compared to 17 healthy volunteers (8.5 ± 3.8 μg/mmol creatinine) or 50 control patients with renal diseases of other causes (6.2 ± 2.9 μg/mmol creatinine). Receiver operating characteristics (ROC) analysis of urinary Fetuin-A levels for ADPKD rendered an optimum cut-off value of 12.2 μg/mmol creatinine, corresponding to 94% of sensitivity and 60% of specificity (area under the curve 0.74 ; p = 0.0019). Furthermore, urinary Fetuin-A levels in ADPKD patients correlated with the degree of renal insufficiency and showed a significant increase in patients with preserved renal function followed for two years.
Conclusions:
Our findings establish urinary Fetuin-A as a sensitive biomarker of the progression of ADPKD. Further studies are required to examine the pathogenic mechanisms of elevated renal and urinary Fetuin-A in ADPKD.
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