Background:Posterior reversible encephalopathy syndrome (PRES) describes a disorder of abrupt onset neurological symptoms due to potentially reversible lesions on brain imaging. Case reports of PRES in PD patients are scarce.Case presentation:A 42-year-old male presented to the emergency department (ED) with two weeks of worsening occipital headaches, nausea, vomiting and dizziness. The patient had a background of end-stage renal disease due to primary focal segmental glomerulosclerosis, and resistant hypertension. He had been receiving peritoneal dialysis (PD) for one month; hypertension was treated with torasemide 100 mg/day, perindopril 10 mg/day, amlodipine 10 mg/day, moxonidine 0.6 mg/day, doxazosin 8–16 mg/day. One week earlier, he was brought into ED due to hypertensive crisis (blood pressure (BP) was 190/120 mmHg); intravenous labetolol 20 mg, oral moxonidine 0.4 mg, doxazosin 8 mg were administered; afterwards he was released for outpatient treatment.On admission, BP was 187/114 mmHg, heart rate - 75 beats/minute, oxygen saturation - 98% on room air, and body temperature - 36.5°C. Laboratory tests revealed severe renal dysfunction (serum creatinine: 1478 mcmol/l, serum urea: 29.1 mmol/l) and normal inflammatory indicators (WBC: 4.51 x 109/l, CRP: 0.65 mg/l) (Table). Head CT showed no obvious intracranial hemorrhage, ischemia, or mass lesion; PRES was suspected. Due to hypervolemia, he was temporarily transferred to hemodialysis. On day 12, fundoscopy revealed flame-shaped hemorrhages, microaneurysms, cotton wool patches in the posterior pole surrounding the optic nerve. On day 14, he was transferred to the intensive care unit (ICU) due to uncontrollable hypertension (BP was 202/129 mmHg) and epileptic seizure; MRI showed bilateral subcortical occipital and frontoparietal hyperintensity with vasogenic edema typical of PRES. BP was decreased to approximately 155/90 mmHg using a combination of anti-hypertensive medication and ultrafiltration. Subsequently he was discharged on day 28. Two months later he underwent cadaveric kidney transplantation. After the transplantation, his BP control improved and he was left with bisoprolol 5 mg/day, amlodipine 10 mg/day, and doxazosine 4 mg/day (office BP one month after the transplantation: 124/90 mmHg, after two months: 135/95 mmHg, after three months: 135/95 mmHg).Conclusions:This is to the best of our knowledge the fifth report of PRES in an adult patient undergoing PD, and the first presenting a PD patient with history of PRES whose hypertension control improved after kidney transplantation. It is likely that the cause of described PRES episode was multifactorial, originating from the complications of ESRD, hypertension and poor compliance with PD.
