LAUSR

the biochemical hallmarks for GS were confirmed. Hypokalemia of GS may be further aggravated by a poor general state, including dehydration possibly resulting in proximal renal tubular damage. Renal injury due to chronic hypokalemia is known as hypokalemic nephropathy, and is seen in various disorders, including diarrheal diseases. This nephropathy presents as chronic kidney disease (CKD) associated with renal tubular dysfunctions and pathologic abnormalities in the renal tubulointerstitium; clinical features include polyuria, low specific gravity of urine, and tubular proteinuria. Although CKD associated with tubulointerstitial injury has recently been noted in cases of GS, reports about proximal renal tubular damage are limited. A case-control study identified renal phosphate wasting in GS. Another report described a case of GS presenting with Fanconi syndrome and polyuria, in which tubular proteinuria was not measured. Our patient exhibited widespread but reversible proximal renal tubular damage, as determined by changes in several indicators, including BMG excretion. Thus, the findings from our patient and those reported by others suggest proximal renal tubular damage can potentially occur from early childhood in GS. Finally, we emphasize that further prospective studies for GS are needed to identify proximal renal tubular damage in view of dehydration and hypokalemic nephropathy in both stable and poor states, including all types of infections.