Abstract: SA-PO489
Pattern of Urinary Inflammatory Markers in Longstanding Type 1 Diabetes with and Without Diabetic Kidney Disease: Results from the Canadian Study of Longevity in Type 1 Diabetes
Session Information
- Diabetic Kidney Disease: Basic - III
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 601 Diabetic Kidney Disease: Basic
Authors
- Ambinathan, Jaya Prakash Nath, University of Toronto, Toronto, Ontario, Canada
- Lovblom, Leif Erik, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada
- Sridhar, Vikas, University of Toronto, Toronto, Ontario, Canada
- Lytvyn, Yuliya, University of Toronto, Toronto, Ontario, Canada
- Bjornstad, Petter, University of Colorado School of Medicine, Aurora, Colorado, United States
- Perkins, Bruce A., University of Toronto, Toronto, Ontario, Canada
- Lovshin, Julie A., University of Toronto, Toronto, Ontario, Canada
- Cherney, David, University of Toronto, Toronto, Ontario, Canada
Background
Diabetic kidney disease (DKD) contributes to significant mortality and morbidity in type 1 diabetes (T1D). Inflammation is a contributing factor to the pathogenesis of DKD, even during its early stages. Urinary inflammatory markers have been used to determine distinct urinary secretion phenotypes in different stages of DKD in T1D. The nature of urinary inflammatory markers in longstanding T1D is, however, unknown. Our objective was to study changes in urine inflammatory markers within the normal range of albuminuria in longstanding T1D, and to quantify the differential urinary excretion of inflammatory markers in participants with DKD versus those without DKD (resistors).
Methods
A 42-plex human urinary inflammatory markers was analyzed from participants of Canadian study of longevity in T1D of more than 50 years duration (n=74) and compared to age and sex matched comparators (n=73). Normoalbuminuric T1D participants (n=44) were categorized into tertiles of albumin:creatinine ratio (<0.8, 0.8-1.2, 1.2-2 mg/mmol). T1D subjects were grouped as those with and without DKD (n=25 vs. n=49).
Results
A stepwise increase was observed in 27 of 42 urine inflammatory markers across tertiles of normoalbuminuria. Urinary inflammatory marker excretion was lower in both DKD and DKD-resistors vs. controls. When comparing participants with DKD vs. DKD-resistors, IL-6, a potent inflammatory cytokine, was significantly different, with higher urinary excretion in DKD versus resistors (0.24±0.25 vs 0.13±0.16, P=0.03).
Conclusion
Urinary excretion of inflammatory markers increases with the degree of albuminuria within the normal range in participants with longstanding T1D. This is consistent with our previous observation in an adolescent T1D cohort with shorter disease duration. Lower urine inflammatory marker excretion in longstanding T1D versus comparators may represent as yet unidentified protective factors in these long-term survivors, irrespective of DKD status, and needs further exploration. DKD participants had higher urinary excretion of IL-6 compared to resistors, highlighting a possible role of inflammation in DKD risk.