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Abstract: TH-PO403

Systemic Inflammation and Kidney Stone Disease in Autosomal Dominant Polycystic Kidney Disease

Session Information

Category: Genetic Diseases of the Kidneys

  • 1101 Genetic Diseases of the Kidneys: Cystic


  • Gitomer, Berenice Y., University of Colorado, Denver, Colorado, United States
  • You, Zhiying, University of Colorado, Denver, Colorado, United States
  • Brosnahan, Godela M., University of Colorado, Denver, Colorado, United States
  • Wang, Wei, University of Colorado, Denver, Colorado, United States
  • Hopp, Katharina, University of Colorado, Denver, Colorado, United States
  • Nowak, Kristen L., University of Colorado, Denver, Colorado, United States
  • Chapman, Arlene B., University of Chicago Pritzker School of Medicine, Chicago, Illinois, United States
  • Perrone, Ronald D., Tufts Medical Center, Boston, Massachusetts, United States
  • Torres, Vicente E., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Yu, Alan S.L., The University of Kansas Medical Center, Kansas City, Kansas, United States
  • Chonchol, Michel, University of Colorado, Denver, Colorado, United States

In preliminary studies, we have shown that autosomal dominant polycystic kidney disease (ADPKD) patients with kidney stone disease (KSD) experience faster decline in kidney function compared to those with no kidney stone disease (NKSD). Kidney stone disease affects ~ 20 to 30% of patients with ADPKD, a much higher prevalence compared to the general population. As KSD is associated with increased inflammation in non-ADPKD patients, we assessed whether KSD, also associates with increased inflammation in ADPKD patients with KSD.


Baseline serum levels of a panel of pro-inflammatory biomarkers (OLINK, Boston MA) were determined among participants in the HALT PKD clinical trials. Levels were compared between 40 ADPKD patients with self-reported KSD and 46 age, sex and estimated glomerular filtration rate (eGFR) matched NKSD ADPKD patients. Elevated IL-6 levels wereconfirmed by ELISA (Meso Scale Diagnostic Inc., Rockville, MD).


Mean age and eGFR was 40 ± 11 years and eGFR 75 ± 27 ml/min/1.73m2 in KSD patients and 41 ± 9 years and eGFR 80 ± 26 ml/min/1.73m2 in NKSD. Six pro-inflammatory biomarkers in serum were significantly increased in ADPKD patients with KSD compared to ADPKD patients with no NKSD these included interleukin 6 (IL6), fibroblast growth factor 23 (FGF23), monocyte chemotactic protein 3 (MCP3), chemokine C-C motif ligand 20 (CCL20), osteoprotogerin (OPG) and interleukin 24 (IL24). Higher IL6 levels in KSD patients were confirmed by ELISA (KSD (N= 50) 1.58 ± 2.01 vs NKSD (N = 75) 0.97 ± 1.07 pg/ml; P = 0.03).


ADPKD patients with KSD have evidence of increased inflammation based on higher circulating levels of pro-inflammatory cytokines. Increased inflammation associated with KSD may represent a further injury to the cystic kidney. In the literature, it has been shown that further injury to the cystic kidney exacerbates disease progression. Thus, it is intriguing to speculate that KSD may be a risk factor for kidney disease progression in patients with ADPKD. Further studies will be required to determine the effects of inflammation on disease progression in ADPKD.


  • NIDDK Support