Purpose: Phase contrast microscopy method is useful in the examination of urine sediment to differentiate glomerular (Gl) hematuria from non-glomerular (nonGl) hematuria. In this study, we compared the diagnostic value of optical microscopy with that of phase contrast microscopy.
Method: One hundred and sixty fresh urine samples of microscopic hematuria (5/HPF or more) from 118 patients with renal disease and 42 patients with urologic disease were analyzed. The erythrocytes referred to as Gl, are defined to have acanthocytes, target configuration, or finger ring shape, and a Gl cell/total erythrocyte ratio greater than 3% is defined as reliable marker for Gl bleeding.
Result: Sensitivity and specificity of this criteria for Gl bleeding were 50.9% and 94.9% in acanthocytes, 69.6% and 89.1% in the target configuration, and 88.4% and 89.1% in the finger ring, respectively. As for the microscopic observation methods, the sensitivity and specificity of this criteria for Gl bleeding were 88.1% and 81.0% with phase contrast microscopy, 74.6% and 90.9% with optical microscopy with no dyeing, and 74.6% and 88.6% with optical microscopy with dyeing, respectively.
Conclusion: Gl and nonGl hematuria were correctly diagnosed by counting the urinary Gl cells not only by phase contrast microscopy, but also by optical microscopy. This method seems to have important clinical usefulness by offering information on urinary bleeding.

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Background: Urinary excretion of some low molecular weight proteins (LMWPs) is used as an indicator of tubular dysfunction, since they are increased by the damage of tubular reabsorption. Although serum cystatin C is known to be a sensitive marker for GFR, the property of urinary cystatin C as a LMWP has not been fully observed. We evaluated the clinical utility of urinary cystatin C.
Methods: Urine samples were collected from 130 patients with various degree of renal dysfunction, 62 healthy subjects, and 2 patients with acute renal failure, one with renal acute renal failure, the other with prerenal acute renal failure. Urine levels of cystatin C, β₂-microglobulin (β₂mG), and α₁-microglobulin (α₁mG) were measured by immunonephelometry. Creatinine clearance (Ccr) tests were conducted on 130 patients with renal dysfunction. Creatinine (CRE) was measured by enzyme assay.
Results: The daily urinary excretions of cystatin C and α₁mG were increased significantly in patients with Ccr<30ml/min (group I), compared to those in patients with 30≤Ccr<70ml/min (II), and Ccr≥70ml/min (III). Although the mean daily excretion of β₂mG increased as Ccr decreased, the significant difference was not observed. The rate of increase in the mean value between III and I was extremely high in cystatin C. Fractional excretions of cystatin C and β₂mG calculated in the same groups increased significantly in I compared to II and III. The rate of increase in the mean value was higher in cystatin C. Regression analyses between urine CRE and each three LMWP gave the best correlation coefficient for cystatin C in healthy subjects. While in one patient with renal acute renal failure, the rate of increase in urine cystatin C was higher than that of other LMWPs, in another patient with prerenal acute renal failure, the rate of increase in urine cystatin C was low.
Conclusions: Although details of urinary movement of LMWPs in nephrons have not been clearly elucidated, the urinary cystatin C seems to have distinctive properties, and to be useful for the evaluation of renal injury.

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Cholesterol crystal embolism (CCE) is a multivisceral disease caused by occlusion of small arteries with cholesterol crystal emboli deriving from eroded atherosclerotic plaques of the aorta and/or large feeder arteries. The factors precipitating CCE are manipulation of the aorta or other large arteries during arteriography or surgery, and anticoagulant or thrombolytic therapy. CCE has been reported to be a life-threatening condition involving multiple vital organ dysfunction, including renal failure, cardiac failure, skin ischemic lesions such as livedo reticularis, patchy skin necrosis, and purple toes, gastrointestinal ischemia, and/or visual disturbance.
We report a 63-year-old male patient of CCE after percutaneous transluminal coronary angioplasty, who contracted severe pneumonia of Pneumocystis carinii and Cytomegalo virus during steroid therapy (prednisolone 20mg for 3 months). He was treated successfully with mechanical ventilation, hemodialysis, and appropriate antibiotic therapy.
Although corticosteroid therapy has been reported to be effective in some CCE patients, the indications of steroid therapy, dosage of corticosteroids, duration of the treatment, or efficacy of prophylactic administration of antibiotics are not yet established. Further interventional studies are required in order to evaluate the benefit of corticosteroid therapy for CCE.

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We report two cases of heterozygous Fabry disease with severe organ damage. Case 1 was a 47-yearold woman. In April 1977, at the age of 27 years, she had proteinuria and edema around the 26th week of her second pregnancy and was diagnosed as toxicosis of pregnancy. She had proteinuria after the delivery. In 1990, a renal biopsy showed zebra bodies under electron microscopic findings, and the patient was diagnosed as Fabry disease. In 1998, a myocardial biopsy showed identical findings. The patient developed severe hypertension and decreased renal function, and α-galactosidase enzyme replacement therapy was initiated. However, despite treatment, she was started on dialysis in 2004. Case 2 was a 40-year-old woman. In March 2003, the patient presented with severe hypertension. The patient had cerebral infarction, cardiac hypertrophy, old myocardial infarction and renal failure without diabetes mellitus, hyperlipidemia and collagen disease. The patient was diagnosed as Fabry disease from persistent numbness and pain in the four extremities, a family history of mortality due to heart disease, and skin biopsy findings. She is currently undergoing enzyme replacement therapy. It is generally known that female Fabry disease patients are asymptomatic or mildly symptomatic, as were the present two patients, but some can have marked organ disorders. Hence, even in female patients, it is necessary to consider Fabry disease as a causative disease of chronic renal failure.

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