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KMID : 0359919940130010100
Korean Journal of Nephrology
1994 Volume.13 No. 1 p.100 ~ p.107
Clinical and Pathological Comparision of the Patients with asymptomactic Hematuria
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Abstract
Since Baehr30 first describe the syndrome of asymptomatic hematuria with a reprot of 14 patientis in which asymptomatic gross hematuria was not assiciated with hypertension, edema or azotemia, its causative diseases have had been revealed as
Aloprt's
syndrome, benign familial hematuria, IgA nephropathy and idiopathi hematuria.
Many investigators have had electron of biopsy specimens from idiopathic hematuria ptients with no familial occurrences of hematuria, hearing loss and progressive renal disease. Yoshikawa et al.1) found normal on light and immunofluorescence
microscopy
but ultrastructural changes widespread attenuation of the logmeruiar basement membrane on electron microscopy in some patients and described s "thin glomerular basement membrane disease"
the purposes are to evaluate the causes of asymptomatic hematuria and to review and compared the clinical, laboratory and pathological features of the patients with thin GBMA 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 asymptomaitc hematuria were Idiopathic hematuria (63 cases); IgA nephropathy (20 cases0; Alport's syndrome (5 cases0; Benign familial hematurial (2 cases).
Idiopathic hematuria is composed of Thin GBM disease (31 cases) and Non-thin GBM disease (32 cases). The patints 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 C4 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¡¾20.5 nm in Thin GBM disease and 265.0¡¾58.1 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-chinical course and prognosis casrefully.
KEYWORD
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