HAL (France)
open access
Calcineurin inhibitors treatment in kidney transplant recipients is frequently associated with hyperkalemia, acidosis and hypertension but not with increased expression or phosphorylation of the sodium chloride cotransporter
Background and hypothesis Calcineurin inhibitors (CNIs), widely used after kidney transplantation, may alter signaling pathways regulating the NaCl cotransporter (NCC), potentially causing an acquired form of pseudo-hypoaldosteronism type II (PHAII), characterized by hyperkalemia, metabolic acidosis
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