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Uraemic Pruritus Pathophysiology — ESENeph MCQ

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HardElectrolyte DisordersUraemic Pruritus PathophysiologyESENeph

A 50-year-old man with CKD G5D develops severe pruritus. Initial assessment reveals calcium 2.65 mmol/L, phosphate 2.0 mmol/L, and PTH 90 pmol/L. His pruritus partly improves after optimising CKD-MBD parameters. What is the underlying pathophysiology of uraemic pruritus?

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Correct answer: B — Multifactorial: immune dysregulation, altered opioid receptor balance (mu/kappa), neuropathy, CKD-MBD derangement, and xerosis

Uraemic pruritus is multifactorial: (1) immune dysregulation (Th1/Th2 imbalance, elevated IL-31, mast cell activation); (2) altered opioid receptor balance (upregulated mu-opioid tone relative to kappa-opioid, explaining why kappa agonists like Difelikefalin work); (3) peripheral neuropathy; (4) CKD-MBD derangement (elevated calcium, phosphate, PTH); and (5) xerosis (dry skin). Treatment targets multiple pathways: emollients, optimised dialysis and CKD-MBD, Gabapentin/Pregabalin, UVB phototherapy, and Difelikefalin.

Reference: KDIGO 2017 – CKD-MBD; Verduzco and Welling 2020 – Uraemic Pruritus Pathophysiology