Korean Journal of Nephrology 1994;13(1):100-107.

무증상 혈뇨환아의 임상 및 병리학적 비교

박승모 , 권민중 , 이재승 , 김병길 , 성순희 , 정현주 , 최인준

Abstract

Since Baehr first described the syndrome of asymptomatic hematuria with a report of 14 patients in which asymptomatic gross hematuria was not associat- ed with hypertension, edema or azotemia, its causative diseases have had been revealed as Alports syndrome, benign familial hematuria, IgA nephropathy and idiopathic hematuria. Many investigators have had electron microscopic examination of biopsy specimens from idiopathic hematuria patients with no familial occurrences of hematuria, hearing loss and progressive renal disease. Yoshikawa et al." found normal on light and immuno@- fluorescence microscopy but ultrastructural changes -widespread attenuation of the glomerular basement membrane- on electron microscopy in some patients and described as thin glomerular basement membrane dis- The purposes are to evaluate the causes of asymptomatic hematuria and to review and compare the clinical, laboratory and pathological features of the patients with thin GBM disease and non-thin GBM disease. We investigated the clinical reports of 90 patients, which were admitted for the evaluation of asymptomatic hematuria to the department of pediatrics in Severance hospital over the period Jan. 1988 to Jun. 1993. The results are as follows. The causative diseases of the patients with asymptomatic hematuria were Idiopathic hematuria (63 cases); IgA nephropathy (20 cases); Alports syndrome (5 cases); Benign familia1 hematuria (2 cases). Idiopathic hematuria is composed of Thin GBM disease (31 cases) and Non-thin GBM disease(32 cases). The patients with Thin GBM disease are younger and more frequent in microscopic hematuria than ones with Non-thin GBM disease statistically in the clinical features (p<0 01 and p<0 05 respectively). The patients with Thin GBM disease are lower in GFR and higher in C level than ones with Non-thin GBM disease statistically (p<0.05 in both), but both were within normal range. The thickness of GBM is 171.2±20.5 nm in Thin GBM disease and 265.0±58.1 nm in Non-thin GBM disease and it is significant (p<0.01). Both group cannot be differentiated by clinical findings, laboratory results and light or immunofluorescence microscopy but only by electron microscopy and they are expected to follow-up their clinical course and prognosis carefully.