Abstract

Ultrasound-measured renal resistive index (RRI) has been suggested to predict allograft survival in renal transplant recipients. Based on experimental and clinical data, we objected to the theory that RRI specifically mirrors allograft characteristics. Instead, we hypothesized that RRI rather represents a marker of systemic vascular damage than an organ-specific marker. In order to refute this hypothesis, RRI should override the resistive index measured in other abdominal parenchymatous organs-such as the spleen-as predictor of allograft outcome. We therefore set out to simultaneously measure renal and splenic ultrasound resistive index in kidney allograft recipients. Eighty-seven stable transplant recipients were recruited. We measured RRI, splenic resistive index (SRI) and an established marker of systemic vascular damage, namely common carotid intima-media thickness (IMT). During a follow-up of 4.9 ± 0.5 years, the occurrence of the combined primary end point, defined as a decrease of ≥ 50% in estimated glomerular filtration rate (eGFR), need for dialysis treatment or death, was recorded. At baseline, both RRI and SRI correlated with common carotid IMT [RRI: r = 0.203 (P = 0.006); SRI: r = 0.315 (P < 0.001)], but not with allograft-specific markers such as eGFR or proteinuria. Elevated RRI was a weak non-significant predictor of the combined primary end point. Notably, RRI did not surpass SRI as outcome predictor. When analysing individual components of the combined primary end point separately, elevated RRI failed to predict strictly renal events (decrease of ≥ 50% in eGFR/need for dialysis treatment), while it predicted total mortality. Our findings support the notion that RRI is not a specific indicator of allograft damage. Similar to SRI, RRI is rather associated with systemic vascular damage markers and mortality.

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