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Posterior reversible encephalopathy syndrome (PRES) is an uncommon but serious neurologic complication in end-stage kidney disease (ESKD). In peritoneal dialysis (PD), potential triggers include uncontrolled hypertension, fluid overload, and rapid osmotic shifts from hypertonic solutions. We report, to our knowledge, the first PD case of PRES in which icodextrin was deliberately used to deliver controlled, sustained ultrafiltration (UF) during recovery.
Case report.
A 43-year-old woman with newly diagnosed ESKD began automated PD alternating 1.5% and 2.5% dextrose(UF 600–1,000 mL/day). After 2 months she stopped PD and antihypertensives. One week later she developed acute cortical blindness and a generalized seizure, then recurrent convulsions, and received urgent hemodialysis locally before transfer.
On arrival she was febrile (38.30C), tachycardic (113/min), hypertensive (189/109 mmHg), and hypoxemic (SpO₂ 92% room air), with GCS 9 (E2V2M5) and bilateral leg edema. Chest radiograph showed pulmonary congestion with right pleural effusion. A 2-h dwell yielded PD effluent 59 white cells/mm³ (8.5% neutrophils),not consistent with peritonitis. Labs showed severe azotemia, anemia, and markedly elevated NT-proBNP (Table 1). Brain MRI revealed symmetric cortical–subcortical T2/FLAIR hyperintensities across both hemispheres and cerebellum without diffusion restriction (vasogenic edema) (Fig.1). EEG showed diffuse theta–delta slowing without epileptiform discharges. Abrupt visual loss and the bilateral, non-territorial MRI pattern argued against uremic encephalopathy and acute ischemic stroke; and minimal inflammatory markers made central nervous system infection was unlikely. Taken together, severe hypertension, volume overload, and imaging supported PRES.
Management focused on controlled blood pressure (IV then oral agents), stabilizing her at 120–130/70–90 mmHg, with strict volume control. Despite high-dose furosemide, residual urine was only 300 – 400 mL/day, so PD prescription was tailored. Given acute cerebral injury, renal replacement therapy needed balance solute and fluid removal with osmotic gentleness to avoid abrupt shifts in intracranial pressure, serum sodium, and plasma osmolality that might worsen neurologic injury. Accordingly, we minimized hypertonic dextrose and used 7.5% icodextrin for the long dwell to provide sustained UF without steep osmotic gradients. This strategy yielded 1.0–2.7 L/day of UF while maintaining serum sodium at 133–134 mmol/L (Table 2), with no further seizures and steady cardiopulmonary decongestion. Neurologic status normalized by day 3, and she was discharged on day 13 on the optimized prescription. To our knowledge, this is the first reported PD case of PRES in which icodextrin was deliberately used to achieve controlled, sustained ultrafiltration during recovery.
PRES may occur in PD after interruption of dialysis and antihypertensives. In this first reported PD-PRES case deliberately using icodextrin, pairing targeted blood-pressure control with an osmotically steady PD program enabled controlled ultrafiltration without steep osmotic shifts and resulted in full neurologic recovery.
