*Purpose: Living kidney donation (LKD) is associated with increased long-term risk of CKD/ESRD. Post donation DM/HTN are associated with this increased risk. However, the remaining kidney is rarely biopsied and thus mechanisms behind progression remain unproven. Parallel data from uninephrectomized rat models shows podocyte hypertrophic stress and depletion driving ESRD. We used nephron segment specific urine mRNA markers to identify injury patterns post donation to see if similar mechanisms operate in humans.

*Methods: 2 podocyte markers mRNA (podocin,nephrin), a distal tubular/collecting duct marker (aqp2) were measured in urine pellet of spot samples normalized to Cr. Podocyte Stress was measured as the ratio of the two podocyte markers podocin and nephrin (UPod:Neph). Podocyte injury/stress leads to downregulation of nephrin expression leading to higher UPod:Neph. Ratio of podocin to aqp2 (UPod:Aqp2)was used to assess preferential glomerular vs. tubular injury. Assessment of post donation hyperfiltration: Using difference in eGFR (CKD-EPI) before (day 0) and after donation (day14) we estimated delta value.

*Results: Table 1 highlights characteristics of 87 donors

In a multivariable linear regression model the change in eGFR by 14 days post donation was associated with increased podocyte stress and preferential glomerular over tubular injury.

.

Figure below demonstrates relationship of increasing hyperfiltration with two outcomes adjusted for other factors.

.

Separate analysis with proteinuria showed no relation of early hyperfiltration with proteinuria.

*Conclusions: Early post donation hyperfiltration is associated with podocyte injury/ stress and preferential glomerular vs. tubular injury but not proteinuria. Longer follow up is required to study relationship of hyperfiltration, podocyte stress and progressive kidney dysfunction after LKD.

« Back to 2020 American Transplant Congress