A 31-year-old patient with traumatic spinal cord injury at the age of 20 and a history of repeated urinary tract infections related to neurogenic bladder (self-catheterisation) and episodes of urinary obstruction. In 2009, he was referred to the nephrology department for stage 2 chronic kidney disease, with proteinuria in the nephrotic range (creatinine 1.3mg/dl, proteinuria 20g/24h). The patient refused to undergo a renal biopsy and in the same year stopped attending nephrology consultations.
In January 2012, he began to experience episodes of decreased level of consciousness. Cranial computed axial tomography and lumbar puncture were performed, both of which were normal. Electroencephalogram with diffuse slowing. Creatinine at that time was 3.3mg/dl. The symptoms were diagnosed as secondary to urinary tract infection.
In April 2012, the same symptoms recurred, accompanied by temporo-spatial disorientation. She presented a new episode in the same month, but this time with behavioural changes (infantilism, nervousness, aggressiveness). Magnetic resonance imaging of the brain was performed with no findings of interest. Following this episode, treatment was started with clonazepam.
In May 2012, due to laboratory tests and clinical signs of end-stage renal failure, haemodialysis was started via a temporary catheter in the right jugular vein.
The patient presented, approximately once a month, in the first two hours after starting haemodialysis, episodes of decreased level of consciousness, and on other occasions psychomotor agitation.
In November 2012, he was assessed by Neurology and Psychiatry, with no relevant findings. They classified the symptoms as secondary to hypoxic-metabolic encephalopathy.
Despite presenting with correct KT and Kt/V, we increased the number of dialysis sessions to 4/week, with no clinical improvement.
In January 2013, we decided to discontinue treatment with baclofen (Lioresal®), replacing it with tinazidine and diazepam. After two weeks of treatment with tinazidine, the patient discontinued the drug due to drowsiness, and the spasticity was only controlled with diazepam.
Ten months after drug withdrawal, the patient had no further neurological symptoms.

