Key result
In renal transplant recipients with postischemic injury, elevated endogenous ANP levels and adequate glomerular ANP receptors failed to alleviate renal vasoconstriction or hypofiltration.
Observational (n=23)
Absolute Event Rate: 140% vs 114%
p-value: p=NS
Endogenous ANP elevation and adequate receptor density fail to alleviate renal vasoconstriction and hypofiltration in postischemic acute renal allograft failure.
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Persistent hypofiltration despite ANP elevation cautions against ANP-centric management in delayed graft function; leaves open mechanisms of postischemic vasoconstriction.
Vinot et al. (1995) conducted an observational in Renal transplantation with postischemic acute renal allograft failure (n=23). Delayed allograft function (postischemic injury) vs. Prompt allograft function was evaluated on Median plasma ANP levels at 60 to 180 min after graft reperfusion (pg/ml) (p=NS). In renal transplant recipients with postischemic injury, elevated endogenous ANP levels and adequate glomerular ANP receptors failed to alleviate renal vasoconstriction or hypofiltration.
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