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Asymptomatic low molecular weight proteinuria: a report on 5 cases
Insights
Low molecular weight (LMW) proteinuria in children can indicate kidney tubular malfunction. Early detection of LMW proteinuria in asymptomatic children may predict future progressive tubular dysfunction, necessitating long-term monitoring.
Area of Science:
- Pediatric Nephrology
- Clinical Biochemistry
Background:
- Asymptomatic proteinuria in children can signify tubular malfunction.
- Low molecular weight (LMW) proteins in urine are key indicators of this dysfunction.
Purpose of the Study:
- To investigate the long-term outcomes of children with asymptomatic LMW proteinuria.
- To determine if LMW proteinuria predicts progressive tubular dysfunction.
Main Methods:
- Analysis of a 15-year screening program data involving 280,000 children (ages 3-19).
- Identification and clinical follow-up of 5 boys with LMW proteinuria.
- Renal biopsy and biochemical assessments (serum creatinine, urinalysis) during follow-up.
Main Results:
- Four out of five boys had normal renal histology initially.
- Over 4-16 years, 2 patients developed glycosuria, hypophosphatemia, and/or aminoaciduria.
- One patient showed only elevated serum creatinine; two remained with persistent LMW proteinuria.
Conclusions:
- Early identification of LMW proteinuria in children may indicate a risk for developing progressive tubular dysfunction.
- Long-term, indefinite follow-up is recommended for these patients to monitor for evolving renal abnormalities.
Abstract:
In children with asymptomatic proteinuria, a high proportion of low molecular weight (LMW) proteins is an indicator of tubular malfunction. In a routine screening program covering the last 15 years and involving 280,000 children, aged between 3 and 19 years, we have identified 5 boys with LMW proteinuria. In 4 of these, renal biopsy was histologically normal on the first presentation. Follow-up for 4-16 years showed normal growth curves, but further evidence of tubular dysfunction appeared: glycosuria and hypophosphatemia in 2 patients; one of them had also aminoaciduria and rising serum creatinine (greater than 1.2 mg/100 ml). Another patient had only increased serum creatinine. The other two, still less than 13 years old, show so far no other abnormality than persistent LMW proteinuria. It is suggested that early identification of LMW proteinuria may presage gradual development of progressive tubular dysfunction with age and that such patients should be followed up indefinitely.