血管收縮素受體阻斷劑對糖尿病或高血壓病人尿中

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血管收縮素受體阻斷劑對糖尿病或高血壓病人尿中D- 乳酸濃度之影響

中文摘要

根據我們之前的動物實驗結果,尿中 D- 乳酸濃度( μM/mM creatinine )可能可以作為偵測早期腎

臟損傷之指標;人體實驗結果,糖尿病與高血壓病患尿中 D- 乳酸濃度在腎臟損傷之生化指標微白 蛋白尿( microalbuminuria )尚未出現前,即顯著高於正常人( P < 0.05 )。因此,本研究進一步 探討:糖尿病與高血壓病患服用具有腎保護功能及降低蛋白尿之 Angiotensin receptor blocker—va lsartan ,對病患尿中 D- 乳酸、 N-acetyl-β-D-glucosaminidase ( NAG )及 microalbumin 濃度之影響

,以及尿中 D- 乳酸與腎臟病變之相關性。

本試驗採收 39 位健康成年人之尿液做為對照組,並且將糖尿病( n = 74 )與高血壓( n = 81 )患

者分別分為三組:未服用 valsartan ,服用 valsartan 12 週,以及服用 valsartan 24 週。患者服用 valsa rtan 之劑量依照醫師之診斷,其範圍為 40-120 mg/day 。結果顯示,未服用 valsartan 之糖尿病患者 尿中 D- 乳酸濃度( 31.69 ± 8.83 μM/mM cr )皆顯著高於服用 valsartan12 週( 9.08 ± 2.12 μM/mM c r )或服用 valsartan 24 週( 4.03 ± 0.90 μM/mM cr )之患者;未服用 valsartan 之高血壓患者尿中 D- 乳酸濃度( 12.57 ± 3.85 μM/mM cr )皆顯著高於服用 valsartan12 週( 8.85 ± 1.50 μM/mM cr )或服 用 valsartan 24 週( 3.73 ± 1.11 μM/mM cr )之患者。值得注意的是,糖尿病或高血壓患者尿中 D- 乳酸、 NAG 及 microalbumin 濃度下降之趨勢與病患服用 valsartan 週數有明顯正相關性,而且服用 valsartan 24 週之糖尿病或高血壓患者,其尿中 D- 乳酸、 NAG 及 microalbumin 濃度與正常人比較 皆無統計之差異。

綜合上述,糖尿病患者尿中 D- 乳酸與微白蛋白尿具有相同之特性—確實會因患者服用 valsartan 之

影響而下降,而且在微白蛋白尿出現之前,尿中 D- 乳酸濃度即顯著升高。因此,我們建議可以偵 測尿中 D- 乳酸濃度作為早期腎臟損傷之指標。

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The Effect of Angiotensin Type 1 Receptor Blocker on Urinary D-Lactate Concentrations in Diabetic or Hypertensive Patients Ⅱ

英文摘要

According to our previous research, there was a significant increase in urine levels of D-lactate (μM/mM cr eatinine) in diabetic rats compared to normal rats (P < 0.01). We further demonstrated the urine levels of D-lactate in diabetic or hypertensive patients were prominently elevated before the appearance of microalb uminuria (P < 0.05). In this study, we investigated an angiotensin II receptor blocker, valsartan, with prove n effect on microalbuminuria on the clinical effects of urinary D-lactate concentrations in diabetic or hyper tensive patients.

We studied three groups in diabetic or hypertensive patients who were not receiving valsartan, receiving 1 2-week, and 24-week valsartan. Valsartan dosage ranged from 40-120 mg/day according to doctor’s diagno sis. Urine levels of D-lactate, NAG (N-acetyl-β-D-glucosaminidase), and microalbumin were measured in 74 diabetic patients, 81 hypertensive patients, and 39 healthy subjects as controls.

In diabetic patients, the levels of urinary D-lactate were significantly lower in patients receiving either 24- week (4.03 ± 0.90 μM/mM cr) or 12-week (9.08 ± 2.12 μM/mM cr) valsartan compared with those not rece iving valsartan (31.69 ± 8.83 μM/mM cr). In hypertensive patients, the levels of urinary D-lactate were sig nificantly lower in patients receiving either 24-week (3.73 ± 1.11 μM/mM cr) or 12-week (8.85 ± 1.50 μM/

mM cr) valsartan compared with those not receiving valsartan (12.57 ± 3.85 μM/mM cr). The descending t endency of urinary D-lactate, NAG, and microalbumin all had a positive relationship with the duration of p atients receiving valsartan. Notably, there were no difference in urine levels of D-lactate, NAG, and microa lbumin between 24-week valsartan group of diabetic or hypertensive patients and healthy subjects.

In conclusion, the significant reduction of urinary D-lactate was similar with the proven effect on microalb uminuria by valsartan in diabetic or hypertensive patients. We suggest that urinary D-lactate may be a usef ul indicator for early diagnosis of diabetic or hypertensive nephropathy, serving in the assessment of therap eutic effects.

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