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Abstract: SA-PO682

A Pilot Study of Urinary Podocyte-Derived Microparticles (MP) as a Marker for Podocyte Injury in Youth with Type 1 Diabetes

Session Information

  • Pediatric Glomerular Disease
    November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pediatric Nephrology

  • 1700 Pediatric Nephrology

Authors

  • Sullivan, Katie, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Scholey, James W., University of Toronto, Toronto, Ontario, Canada
  • Moineddin, Rahim, University of Toronto, Toronto, Ontario, Canada
  • Elia, Yesmino, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Medeiros, Thalia, Kidney Research Centre, The Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada
  • Sadi, Pusha, University of Manitoba, Winnipeg, Manitoba, Canada
  • Wicklow, Brandy, University of Manitoba, Winnipeg, Manitoba, Canada
  • Sochett, Etienne Bertrand, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Burger, Dylan, Kidney Research Centre, The Ottawa Hospital Research Institute, University of Ottawa, Ottawa, Ontario, Canada
  • Mahmud, Farid H., The Hospital for Sick Children, Toronto, Ontario, Canada
  • Dart, Allison, University of Manitoba, Winnipeg, Manitoba, Canada
Background

Podocyte injury plays a crucial role in the development of diabetic nephropathy. Recent animal and clinical studies have shown that podocytes release microparticles under conditions of stress, and may be an early marker of podocyte injury. Our objectives were to assess MP in youth with Type 1 (T1DM) and healthy controls (HC), and investigate associations with clinical characteristics, including glycemia and renal function. We included youth with T1DM (n= 53), mean age of 14.7 ±1.6 years and age matched (12.9±1.9years) healthy control (HC) subjects, (n=52).

Methods

MP were extracted from first am urine , processed immediately and frozen. MP were identified as of podocyte origin by co-labelling with Annexin V and Podoplanin. ACR was measured on two sets of first morning samples, albuminuria defined as >3.5mg/mmol in males and >4mg/mmol females. eGFR was calculated using the Larsson Equation, previously validated in the Type 1 population. MP numbers were normalised to urinary creatinine (MP/umol Cr). Data distribution was skewed, so groups were compared using non parametric analyses, and expressed as median (IQR).

Results

There was no difference observed in MP number between T1DM with no albuminuria, T1DM with albuminuria and HC 8.28 (8.87), 6.39 (8.90), & 10.39 (8.93); p=0.1530.Unexpectedly, there was only a modest positive correlation between MP number and blood glucose levels (r=0.21, p=0.04) in the T1DM subjects, and trends for MP number and eGFR (r=0.25, p=0.07). A modest positive correlation was also seen for HDL level (r=0.30, p=0.03). There was a more robust negative correlation with serum uric acid (r= -0.46, p=0.0007). Finally, MP number correlated with the urinary albumin excretion rate (r = 0.48, p=0.0029 ) in T1DM, but only in subjects with normal albumin excretion rates.

Conclusion

Podocyte-derived MP numbers are similar in youth with early T1DM and age-matched healthy subjects, although within the T1DM cohort, MP numbers associate with both glycemia and ACR. These findings suggest that podocyte injury cannot be detected by MP enumeration in the urine at this early stage of diabetes. Future will be necessary to define changes in podocyte MPs over time and their relationship to long term kidney outcomes.