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[Aluminum poisoning caused by the phosphate binder in a non-dialysed child with chronic renal insufficiency]
B Feldmann1, D Färber, B F Pontz
1Kinderklinik der Technischen Universität München.
Insights
Aluminum accumulation from phosphate binders can cause severe bone disease in infants with chronic renal insufficiency. Avoiding aluminum-containing treatments is crucial for these young patients to prevent intoxication and bone malformations.
Area of Science:
- Pediatric Nephrology
- Bone Metabolism
- Toxicology
Context:
- Chronic renal failure impairs aluminum excretion.
- Aluminum accumulates in tissues, leading to intoxication.
- Phosphate binders and dialysate are common aluminum sources.
Purpose:
- To report a case of aluminum osteomalacia in an infant with chronic renal insufficiency.
- To highlight the risks of aluminum exposure in non-dialyzed children.
- To recommend avoiding aluminum-based therapies in this vulnerable population.
Summary:
- A non-dialyzed infant with chronic renal insufficiency developed osteomalacia after 6 months of aluminum-containing phosphate binders.
- Radiographic findings included subepiphyseal/metaphyseal changes, a "bone-within-bone" appearance, and pathological fractures.
- Therapy change led to resolution of bone alterations and decreased serum aluminum levels.
Impact:
- Demonstrates the direct link between aluminum exposure and bone disease in pediatric chronic renal insufficiency.
- Underscores the importance of careful medication selection in non-dialyzed children.
- Provides evidence for avoiding aluminum-containing phosphate binders in this patient group.
Abstract:
In patients with chronic renal failure, aluminium, which is included in the dialysate or released from phosphate binders, cannot be eliminated adequately. It forms a deposit in the tissues and leads to intoxication. After a 6-month therapy with aluminium-containing phosphate binders in a non-dialysed baby with chronic renal insufficiency, an osteomalacia arose with distinct subepiphyseal and metaphyseal changes attributable to disorders of mineralization. The consequence of this was a "bone-within-bone" appearance and pathological fractures. After a change of therapy, the bone alterations receded within a few months. Simultaneously, the distinctly elevated serum level of aluminium fell. Therefore, aluminium should be avoided in non-dialysed children with chronic renal insufficiency.