ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: FR-PO198

Urinary PTH1R: Novel Predictor of Mineral Metabolism Disorder and Renal Outcome of CKD

Session Information

Category: CKD (Non-Dialysis)

  • 1901 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Qiu, Dandan, National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
  • Pan, Yu, National Clinical Research Center of Kidney Diseases, Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
  • Shi, Jingsong, National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
  • Zhou, Minlin, National Clinical Research Center of Kidney Diseases Jinling Hospital, Nanjing, China
  • Xu, Feng, Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
  • Liu, Zhihong, National Clinical Research Center of Kidney Diseases,, Nanjing, JIangSu, China
  • Jiang, Song, National Clinical Research Center of Kidney Diseases Jinling Hospital, Nanjing, China
Background

There is short of early predictor of mineral metabolism disorder and renal outcome in patients with chronic kidney disease (CKD). This study aimed to explore the association of urinary parathyroid hormone 1 receptor (PTH1R) with mineral metabolism markers, and the predictive value for renal outcome in CKD.

Methods

29 healthy controls and 140 diabetic nephropathy (DN) patientswere enrolled as discovery cohort and 200 general CKD patients were enrolled as an independent validation cohort. All patients were followed up for at least 1 year and measured the intact PTH (iPTH), fibroblast growth factor 23 (FGF23) in baseline serum and PTH1R in baseline urine.Urinary PTH1R was normalized to urine creatinine and log transformed [uPTH1R/Cr(log10)].The composite renal endpoint was defined as end-stage renal disease (ESRD) or 30% reduction of baseline eGFR during follow-up.

Results

In discovery cohort, DN patients had a significantly higher mean uPTH1R/Cr(log10) level compared with healthy control (2.53±0.61 pg/mg versus 1.89±1.14 pg/mg, P<0.01). uPTH1R/Cr(log10) was significantly increased in DN patients with eGFR of 60~75 ml/min/1.73m2, which was earlier than serum FGF23 and iPTH. Baseline uPTH1R/Cr(log10) was associated with serum calcium (r=-0.224, P<0.01), serum FGF23 (r=0.232, P<0.05), and eGFR slope (r=0.318, P<0.001). 59 patients in discovery cohort entered into composite renal endpoint during follow-up. Cox regression analysis showed that higher uPTH1R/Cr(log10) had a significantly higher risk for renal outcome [HR=2.190; 95%CI(1.048,4.575), P<0.05]. Validation cohort confirmed that uPTH1R/Cr(log10) was an independent risk factor for renal outcome [HR=1.573; 95%CI(1.094,2.263), P<0.05] in general CKD patients. Addition of uPTH1R/Cr(log10) to eGFR and proteinuria could significantly improve the prediction value for renal outcome (likelihood ratio test, P<0.001).

Conclusion

Urinary PTH1R was an independent risk factor for renal outcome in CKD patients, and was a novel biomarker of disordered mineral metabolism.