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—vaⅡ 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。
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.
