Kidney Week

Abstract: FR-PO186

Effect of Periodontal Therapy on CKD: Findings of the Kidney and Periodontal Disease (KAPD) Pilot Randomized Controlled Trial

Session Information

• CKD: Epidemiology, Risk Factors, Prevention - II
  October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

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

Authors

• Grubbs, Vanessa, San Francisco General Hospital Renal Center, San Francisco, California, United States

Vanessa Grubbs,

• Vittinghoff, Eric, University of California, San Francisco, San Francisco, California, United States

Eric Vittinghoff,

• Garcia, Faviola M., University of California, San Francisco, San Francisco, California, United States

Faviola M. Garcia,

• Powe, Neil R., Priscilla Chan and Mark Zuckerberg San Francisco Gen Hosp & UCSF, San Francisco, California, United States

Neil R. Powe,

Background

CKD and periodontal disease (PD) disproportionately affect poor and minority populations. Observational studies suggest PD may be a modifiable CKD risk factor. The KAPD study (NCT01802216) was a pilot RCT to assess the feasibility of recruiting and retaining patients from a diverse, public hospital setting and to determine the variability of kidney and inflammatory biomarkers in response to PD treatment.

Methods

We randomly enrolled 51 adult patients with moderate/severe PD and CKD to immediate PD treatment (whole mouth deep cleaning + local minocycline to deep pockets, n=34) or delayed treatment with rescue (deep cleaning for worsening tooth sites, n=17) every 4 months for a 12-month protocol, with biomarkers assessed at baseline, 4-month, and 12-month study visits.

Results

Of enrolled patients, 82% were non-white; 47% had seen a dentist within the last 2 years; and 80% completed all 4 visits of the 12-month protocol (28 intervention, 13 rescue). 6 delayed treatment patients (35%) required rescue treatment. For intervention group, biomarkers of vascular injury (ADMA), and inflammation (IL-6) improved; tubular injury (urine NGAL) worsened; and UACR improved while serum NGAL worsened (markers of glomerular injury). Changes among UACR and serum NGAL in the rescue group were opposite, but similar otherwise.

Conclusion

KAPD demonstrated enrolling and retaining patients from a diverse, public hospital setting in a 12-month trial is feasible. There was variability in kidney and inflammatory biomarkers in response to PD treatment. Rescue treatment may have obscured decisive treatment effect. A larger trial is needed to determine the extent to which PD treatment may slow CKD progression.

eGFR, estimated glomerular filtration rate; ADMA, asymmetrical dimethylarginine; UACR, urine albumin/creatinine ratio; NGAL, neutrophil gelatinase-associated lipocalin; IL-6, Interleukin-6

Funding

• NIDDK Support –