Dear Sir,

Berlyn first described aluminum toxicity due to using aluminum hydroxide for peptic ulcer. After that physicians recognized its phosphate absorption properties caused serum phosphor decline and calcium level increase. All these effects introduced aluminum as a principle drug for uremic patients by the early 70s. Berlyn found aluminum deleterious effects without measuring of serum aluminum level.[1] Acute aluminum toxicity has been less described although children with hyperparathyroidism and preexisting developmental delaying are more prone to aluminum toxicity.[2,3]

Acute aluminum neurotoxicity is related to accumulation of aluminum in the gray matter of the brain.[4] Aluminum toxicity in acute form can present from days to weeks, and chronic forms happen insidiously over a period of months to years.[5–8] A wide range of complaints, mainly in cognition and speech disorders, lead to motor seizure, coma, and death.[9,10] The reports mainly described acute aluminum toxicity in adults,[11] while in this case report, we present an 18-month-old boy with secondary hyperparathyroidism due to CRF, who developed acute encephalopathy following short-term aluminum hydroxide as a phosphor binder.

An 18-month-old boy affected with congenital nephrotic syndrome, who was under medical therapy with enalapril as an antiproteinuric agent and nutritional supplements, was controlled up to age of one; he presented with CRF in 18^th month of age and needed renal replacement therapy because of refractory acidosis (pH 7.03, Base: 6 meq/L), hyperphosphatemia (17 mg/dl), and severe hypocalcemia (5 mg/dl). Hyperphosphatemia, in this case, obligated us using aluminum hydroxide to remove phosphor which led to severe symptomatic convulsion due to hypocalcemia. We initiate aluminum hydroxide therapy (at a dose of 150 mg/kg/daily in four divided doses) and chronic peritoneal dialysis catheter insertion simultaneously. After 4 days, episodes of tics reported by mother in head and neck progressed to persistent head tremor at 5^th day with decreased cognition (indifference to environmental stimuli and his mother′s face) with nonsense speech [Video 1]. At first step, we held onto aluminum hydroxide and continued peritoneal dialysis. His electroencephalograph (EEG) shows abnormal sleep pattern (sleep spindle has not formed) and brain imaging was unremarkable in spite of his developmental delay. His serum aluminum level was not accessible. After discharge (3 days later), his tremor resolved a bit and his face was not masked but he was agitated with noise and trigger; gradually, he could recognize his parents as prior to the usage of aluminum by the end of first month, as reported by his mother.

Aluminum toxicity occurs in patients with Glomerular filtration rate (GFR) <30 ml/min/1.73 m². In these patients, aluminum absorption may occur from the gut, the dialysate fluid, or from parenteral infusions which are inadequately excreted in kidney failure.[12] Long-term use of aluminum phosphate binders as aluminum contaminated dialysate can result in progressive encephalopathy with symptoms of agitation, speech disorder, confusion, myoclonus, coma, and/or seizures,[8] while aluminum level is not a sensitive test for detecting or predicting aluminum toxicity in these patients.[13,14]

Children, who developed chronic renal insufficiency before the age of one and who are not under renal replacement therapy, can develop a progressive encephalopathy with a clinical picture similar to dialysis dementia characterized by developmental delay, the evolution of microcephaly, seizures, hypotonia, and involuntary movements, including chorea and tremor,[15,16] whereas acute toxicity by aluminum is a rare event especially in children.[17] In adult with kidney disease, aluminum acute toxicity can be symptomatic 10 days after aluminum usage with confusion, deliriium, tremors, hallucinations, slurred speech, and dis-orientation and symptoms were reversible in 60 days.[11]

Our case showed signs of aluminum neurotoxicity soon after 5 days following use of aluminum hydroxide (150 mg/kg/d) although his complaints started on 4^th day with head tics and grimace. These complaints progressed to full blown picture with symptoms of declining of cognition (unresponsive to mother face and voice), head tremor, incoherent speech progressing to speechless state which resolved after discontinuation of drug and continuous dialysis over 1 month. This case shows that young children with CRF and preexisting developing retardation, acidosis, and hyperparathyroidism are so prone to developing acute encephalopathy as soon as 5 days following ingestion of aluminum hydroxide (150 mg/kg/daily). The early complaints may be so subtle like as tics and grimace can be recognized only by parents. It progresses rapidly to persistent head tremor, speech arrest, and incognition that obviate aluminum usage in young children with CRF.

Brain imaging is not diagnostic and EEG shows nonspecific findings. The main key to the diagnosis is clinical findings and the parents′ report about baby′s complaints.

This case shows for the first time that without measuring aluminum serum level, aluminum cannot be a safe drug for children who are affected with CRF even for 5 days usage. Aluminum can cause head tremor, incognesia, and speech arrest in children affected with CRF shortly (before 5 days) after usage, a reversible event, that abates slowly over 1 month after holding it.

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