R Haridian Sosa Barrios, María García Vallejo, Víctor M Burguera Vion, Milagros Fernández Lucas, Maite E Rivera Gorrín
Graft renal vein pulsatility was associated with systemic venous congestion, supporting the transplanted vein as a functional equivalent of the native one. Retrograde pressure transmission into a rigid capsule is a plausible but unproven mechanism. Abnormal pulsatility rules congestion in but, because sensitivity is low, does not rule it out; interventional studies are needed before it guides management.
BACKGROUND: Bedside volume assessment after kidney transplantation is unreliable, and whether pulsatility of the graft renal vein in the denervated, encapsulated allograft reflects systemic venous congestion was unknown. We tested its association with the Venous Excess Ultrasound Score (VExUS).
METHODS: Prospective study of adult kidney transplant recipients assessed on days 1,7 and months 1,3. Pulsatility was categorised from continuous to discontinuous or reversed flow (≥30% threshold) and tested against VExUS-defined congestion by Fisher exact test, with exact confidence intervals and Cohen kappa; secondary analyses addressed bioimpedance (BIA), examination, delayed graft function and tacrolimus.
RESULTS: Eighty-eight recipients were transplanted, 80 completing follow-up; denominators were 86, 85, 82 and 80. Pulsatility was associated with VExUS on days 1 and 7 and month 1 (all p<0.05), not month 3. On day 1, the ≥30% threshold gave specificity 88% (95% CI 78-95) and low sensitivity 42% (20-67) for VExUS ≥1; at >50%, 94% (85-98) and 26% (9-51). Chance-corrected agreement was the highest of any method pair (kappa 0.32, day 1). Discontinuous or reversed flow occurred in only three recipients on day 1, too few to estimate. Pulsatility was unrelated to BIA and tacrolimus.
CONCLUSIONS: Graft renal vein pulsatility was associated with systemic venous congestion, supporting the transplanted vein as a functional equivalent of the native one. Retrograde pressure transmission into a rigid capsule is a plausible but unproven mechanism. Abnormal pulsatility rules congestion in but, because sensitivity is low, does not rule it out; interventional studies are needed before it guides management.