The results of the present study demonstrated that ACZ has a potent vasodilatory effect on the renal circulation of patients with essential hypertension, leading to an obvious decrease in RVR and an increase in RBF.
Aim: To assess the relation between intima-media thickness (IMT) of the common carotid artery and atherosclerotic renal artery stenosis (ARAS) ≧50% (one or both renal arteries) in type 2 diabetic patients with hypertension. Methods: We performed a retrospective study of type 2 diabetic patients with hypertension who underwent magnetic resonance angiography or digital subtraction angiography for renal artery stenosis at the National Cardiovascular Center or at the Nagasaki Municipal Medical Center between May 1999 and May 2001. Renal artery stenosis was defined as a narrowing of the artery to at least 50% of normal. Thirty type 2 diabetic patients with hypertension (17 men and 13 women, mean age 65.4 ± 7.6 years) were identified and divided into two groups: those with ARAS in one or both renal arteries (n = 15) and those without ARAS (n = 15). We used high-resolution B-mode ultrasonography to measure the IMT of the common carotid artery. Results: With and without ARAS were 9 men and 6 women (mean age 65.0 ± 7.6 years) and 8 men and 7 women (mean age 65.7 ± 6.8 years), respectively. The IMT of the carotid artery was significantly greater in patients with ARAS than in patients without ARAS (1.07 ± 0.10 vs. 0.84 ± 0.12 mm, p < 0.01). However, the only clinical findings that statistically significantly differed were systolic blood pressure and plasma renin activity. Conclusion: Our findings suggest that the measurement of the IMT of the carotid artery may be useful as a noninvasive screening method for the defection of ARAS even in asymptomatic type 2 diabetic patients.
We describe a 39-year-old Japanese man with post-streptococcal acute glomerulonephritis (PSAGN) super-imposed on long-term immunoglobulin A nephropathy (IgA-N). The histological findings of the first renal biopsy, done at 21 years of age, revealed mild mesangial proliferative glomerulonephritis with mesangial IgA deposition. Nineteen years later, acute nephritic syndrome with hypocomplementemia and an increasing anti-streptolysin O (ASO) titer developed 2 weeks after the onset of an upper respiratory infection. A second renal biopsy revealed severe segmental endocapillary proliferative and exudative glomerulonephritis, with fibrocellular crescents in about 40% of the glomeruli. Immunofluorescence showed that more C3 than IgA was deposited in the mesangium and that the IgA deposits had decreased. Electron microscopy revealed "hump" electron-dense deposits on the epithelial side of the glomerular basement membrane. These features were consistent with PSAGN superimposed on IgA-N. After 2 weeks of observation, blood pressure, C3 level, and ASO titer had returned to normal, although the persisting nephritic syndrome necessitated steroid therapy. Six months after the onset of the acute nephritic syndrome, the patient remained asymptomatic, except for microhematuria.
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