A 31-year-old patient with traumatic spinal cord injury at 20 years of age and a history of recurrent urinary tract infections in relation to neurogenic bladder (self-sleep) and episodes of urinary obstruction.
In 2009, she was referred to the nephrology service for stage 2 chronic kidney disease with proteinuria in nephrotic range (creatinine 1.3 mg/dl, proteinuria 20g/24h).
The patient refuses to undergo renal biopsy and in the same year he stops attending nephrology consultations.
In January 2012 began with episodes of decreased level of consciousness.
Cranial computerized axial tomography and lumbar puncture were performed, both being normal.
Electroencephalogram with diffuse slowing.
Creatinine at that time was 3.3mg/dl. The patient was referred for urinary tract infection.
In April 2012, the same picture was repeated, accompanied by temporo-spatial disorientation.
He had a new episode in the same month, but this time with behavioral change (infantilism, nervousness, aggressiveness).
Magnetic resonance imaging of the brain showed no relevant findings.
After this episode, treatment with clonazepam is started.
In May 2012, by laboratory and clinical analysis of end-stage renal failure, hemodialysis was initiated through a provisional catheter in the right jugular vein.
The patient presented, approximately once a month, in the first two hours after starting hemodialysis, episodes of decreased level of consciousness, and sometimes psychomotor agitation.
In November 2012 he was assessed by Neurology and Psychiatry, without detecting relevant findings.
They refer the condition as secondary to hypoxic-metabolic encephalopathy.
Despite presenting correct KT and Kt/V, we increased the number of dialysis sessions to 4/week, without evidence of clinical improvement.
In January 2013, we stopped treatment with baclofen (Liophene), sustitures due to tinazidine and diazepam.
After two weeks of treatment with tinazidine, the patient stopped taking the drug due to somnolence, controlling for seizures only with diazepam.
Ten months after drug withdrawal, the patient has not presented neurological symptoms.
