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Editor,—Akçay et alreported urinary glycosaminoglycan (GAG) excretion to be significantly diminished in children with idiopathic urolithiasis compared with controls, and proposed that urinary GAG may play an important role in the prevention and reduction of calculi in children.1 Our findings do not fully support this hypothesis.2 We evaluated urinary GAG excretion in 22 children with calcium oxalate stones (eight with absorptive hypercalciuria, six with renal hypercalciuria, eight with normocalciuria) and in 20 age matched controls. There was no significant difference in total urinary GAG between the two groups. In terms of the various GAG fractions, patients with renal hypercalciuria excreted considerably less keratan sulphate and considerably more dermatan sulphate than the other patients and healthy controls. There was no difference between the two groups in chondroitin sulphate, heparan sulphate, and hyaluronic acid excretion. We conclude that there is no significant correlation between the formation of calcium oxalate stones and urinary GAG excretion.
These conflicting data can be reconciled if the degree of sulphation (that is, the number of negatively charged sites on the surface) is of primary importance in the prevention of stone formation rather than the amount of total or individual GAGs.3 Although we did not investigate this in our study, it is likely to influence the inhibitory potency of GAGs, and may explains the finding of Suzukiet al that heparan sulphate, which is highly sulphated, is incorporated into calcium oxalate crystals precipitated from urine in preference to chondroitin sulphate, despite the fact the urinary concentration of chondroitin sulphate is many times greater than that of heparan sulphate.4 With the exception of our paper, no study has ever examined in detail individual GAGs in children's urine and attempted to relate them to the occurrence of stones; the routine measurement of total GAG excretion in the investigation of children with idiopathic urolithiasis is irrational and should be discontinued.5
In summary, we were unable to detect any difference in the urinary GAG excretion of children with idiopathic urolithiasis and healthy subjects. On the basis of these and similar findings, as well as the lack of any unequivocal experimental evidence that urinary GAGs are significant inhibitors of calcium oxalate crystallisation in vitro, the role of urinary GAGs in the formation of renal calculi is a matter for debate requiring further study.
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