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Diabetic nephropathy (DN) is the most frequent cause of end-stage renal disease. The activation of the renin-angiotensin system (RAS) and lipid disorders are major risk factors in progressive chronic kidney disease. Inhibition of the RAS is one of the most widely used therapies to treat chronic kidney disease. But its effect is not sufficient, and lowered hyperlipidemia is required. Most of medications for hypertension have effects only on the blood pressure in DN. This study is to evaluate the influence of irbesartan on blood lipid, kidney function, and the pathological change of kidney, liver, and adipose tissue.
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Focal brain ischemia resulted in a strong induction of c-Fos and c-Jun proteins in the cortex, which positively correlated with the degree of neurological deficits. Treatment of rats with irbesartan significantly improved neurological outcome of focal cerebral ischemia when compared with the vehicle-treated group and markedly reduced the expression of c-Fos and c-Jun proteins in the cortex on the ligated side of the brain. Irbesartan pretreatment completely abolished the ischemia-induced c-Fos expression in the hippocampus.
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Persistent reduction of microalbuminuria after withdrawal of all antihypertensive treatment suggests that high-dose irbesartan treatment confers long-term renoprotective effects.
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The early addition of irbesartan during microalbuminuria was cost-saving and more effective than both delaying irbesartan treatment until advanced overt nephropathy (AON) (0.45 LYG, Can $54,100 saved) and conventional antihypertensive use (0.62 LYG, $68,400 saved). This was due to the increased drug costs associated with the use of irbesartan being offset by savings arising from delays in the development of overt nephropathy and the subsequent delay to end-stage renal disease (ESRD). Sensitivity analyses confirmed the robustness of the study results.
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These results indicate that ANG II expression is increased in the liver of these animals with steatohepatitis. Furthermore, RAS control by either angiotensin-converting enzyme inhibition or AT1 receptor blockade seems to provide a beneficial modulation concerning the inflammatory response to liver injury in this model. Consequently, blockade of RAS could be a new approach to prevent or to treat patients with NASH.
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This is a randomized, controlled and double-blinded intervention study. A total of 82 HD patients from six Danish HD centres will be treated for a year with an ARB (irbesartan) or placebo. The inclusion criteria are urine output > 300 ml/day, dialysis vintage < 1 year and LV ejection fraction > 30%. The primary outcomes are change in RRF, LV hypertrophy, arterial stiffness and intra-dialytic haemodynamics.
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All clinical trials published in English that reported both subjective and objective outcomes of efficacy were reviewed.
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Electronic databases up until January 2002.
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Gender and obesity may influence response to pharmacological modulation of the renin-angiotensin system. We used SHHF/Mcc-fa(cp) rats to study effect of obesity and gender on the ability of an AT1 receptor antagonist to decrease blood pressure. After 2 weeks treatment with irbesartan (50 mg/kg), only lean and obese males showed significant decreases in blood pressure, while obese females were completely resistant. Lean females showed a trend toward lowering of pressure (p=0.06). However, irbesartan similarly shifted angiotensin II dose response curves to the right in all groups. Twelve weeks of irbesartan also failed to decrease blood pressure, but did significantly reduce heart weight in obese females. In untreated rats, obese females had lower plasma renin activity and serum angiotensin converting enzyme activity compared to lean males, while lean and obese females had increased urinary endothelin excretion. Despite an otherwise similar genetic background contributing to hypertension and heart failure, obese females have different patterns of humoral activation compared to lean males, which may contribute to their resistance to the depressor effects of irbesartan.
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Adult male diabetic (mRen2)27 rats were followed for 5 or 12 weeks. Treatment with vehicle, irbesartan (ARB), or ARB combined with the neprilysin inhibitor thiorphan (irbesartan+thiorphan [ARNI]) occurred during the final 3 weeks. Retinal cell death, gliosis, and capillary loss were evaluated. Real-time polymerase chain reaction (RT-PCR) analyses were performed to quantify the retinal level of inflammatory cell markers.
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By finding no independent correlation between proteinuria (or albuminuria) and tHcy levels, this study improves the external validity of previous negative findings. Therefore, it is unlikely that the observed positive association between proteinuria and cardiovascular disease is directly related to hyperhomocysteinemia.
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A sensitive, specific and selective liquid chromatography/tandem mass spectrometric method has been developed and validated for the simultaneous determination of irbesartan and hydrochlorothiazide in human plasma. Plasma samples were prepared using protein precipitation with acetonitrile, the two analytes and the internal standard losartan were separated on a reverse phase C(18) column (50mmx4mm, 3microm) using water with 2.5% formic acid, methanol and acetonitrile (40:45:15, v/v/v (%)) as a mobile phase (flow rate of 0.70mL/min). Irbesartan and hydrochlorothiazide were ionized using ESI source in negative ion mode, prior to detection by multiple reaction monitoring (MRM) mode while monitoring at the following transitions: m/z 296-->269 and m/z 296-->205 for hydrochlorothiazide, 427-->175 for irbesartan. Linearity was demonstrated over the concentration range 0.06-6.00microg/mL for irbesartan and 1.00-112.00ng/mL for hydrochlorothiazide. The developed and validated method was successfully applied to a bioequivalence study of irbesartan (300mg) with hydrochlorothiazide (12.5mg) tablet in healthy volunteers (N=36).
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To verify if the acute hypertension that occurs after reversal of complete renal ischaemia is related to the duration of ischaemia, is different in one-kidney (1K) and two-kidney (2K) rats, and is prevented by angiotensin receptor blockade.
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To summarize the (1) economic impact of the increased prevalence and costs associated with ESRD secondary to diabetes, (2) major evidence in diabetic nephropathy associated with the use of agents that block the renin-angiotensin-aldosterone system (RAAS) to delay the progression to ESRD, and (3) results of a recent pharmacoeconomic analysis on the economic impact of the use of the angiotensin receptor blocker (ARB) irbesartan to block the RAAS in diabetic nephropathy.
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We enrolled 43 individuals with type 2 diabetes mellitus. All individuals were on a high-salt diet to minimize the contribution of the systemic renin-angiotensin system. After an acute exposure to captopril (25 mg), they were randomized to treatment with either irbesartan (300 mg) or aliskiren (300 mg) for 2 weeks.
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Plasma renin activity (PRA), measured under controlled conditions, is a marker of the degree and persistence of renin-angiotensin system blockade.
Most patients considered both devices to be reliable reminders (IDAS II: 75%;MEMS: 84%, p = ns). Ten patients (42%) preferred the MEMS, while 11 (46%) preferred the IDAS II; three (12%) expressed no preference. Patients found the MEMS device easier to use than the IDAS device (p < 0.001) but appreciated the IDAS blister packs better than the MEMS bulk packaging (p < 0.01). Over the 4-month period, the median "taking adherence" was excellent (99.2%) and comparable with both devices. However, the regularity of drug intake timing was higher with the IDAS II (p < 0.01).
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The antihypertensive and diuretic effects of the aqueous extract of Lepidium sativum L. (LS) were studied both in normotensive (WKY) and spontaneously hypertensive rats (SHR). Daily oral administration of the aqueous LS extract (20mg/kg for 3 weeks) exhibited a significant decrease in blood pressure (p<0.01) in SHR rats while in WKY rats, no significant change was noted during the period of treatment. The systolic blood pressure was decreased significantly from the 7th day (p<0.05) to the end of treatment (p<0.01) in SHR rats. The aqueous LS extract enhanced significantly the water excretion in WKY rats (p<0.001) but no statistically significant change was observed in SHR rats. Furthermore, oral administration of aqueous LS extract at a dose of 20mg/kg produced a significant increase of urinary excretion of sodium (p<0.05), potassium (p<0.01) and chlorides (p<0.01) in WKY rats. In spontaneously hypertensive rats, the aqueous LS extract administration induced a significant increase of urinary elimination of sodium (p<0.01), potassium (p<0.001) and chlorides (p<0.001). Glomerular filtration rate showed a significant increase after oral administration of LS in normal rats (p<0.001) while in SHR rats, no significant change was noted during the period of treatment. Furthermore, no significant changes were noted on heart rate after LS treatment in SHR as well as in WKY rats. Our results suggest that daily oral administration of aqueous LS extract for 3 weeks exhibited antihypertensive and diuretic activities.
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To perform a health economic analysis on treatment with irbesartan in patients with type 2 diabetes and hypertension. A Markov model was adapted to the Hungarian setting to simulate renal deterioration from the development of microalbuminuria to nephropathy, doubling of serum creatinine, end-stage renal disease (ESRD) and all-cause mortality. Outcomes for two treatments were evaluated: (1) a placebo regimen of standard antihypertensive medications, and (2) the addition of irbesartan 300 mg administered daily, with both treatment initiated after developing microalbuminuria. Outcomes were discounted at 5% annually to correspond with national guidelines. Treatment with irbesartan was estimated to improve undiscounted life expectancy by 0.98 +/- 0.05 years, reduce the cumulative incidence of ESRD by 7.5 +/- 0.4%, and reduce lifetime costs by Hungarian Forints (HUF) 519,993 +/- 70,814, compared to placebo. Irbesartan was projected to improved life expectancy and reduce costs compared to placebo in the Hungarian setting in hypertensive patients with type 2 diabetes and microalbuminuria.
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The blood-pressure lowering activity, tolerability, and safety of irbesartan was evaluated in 52 hypertensive patients with chronic renal insufficiency. After a 3-week placebo period, once-daily irbesartan was administered for 12 weeks at a daily dose of 150 mg titrated to 300 mg. A second, non-angiotensin-converting enzyme inhibitor, antihypertensive drug was added after 8 weeks as needed. Twenty-four-hour creatinine clearance was determined and renal clearance studies of inulin and para-aminohippurate were done in a subset of 11 patients. Trough sitting blood pressures were reduced at the end of the first week in all groups. At weeks 4, 8, and 12 the reductions in systolic blood pressure/diastolic blood pressure averaged -11.9/-8.7, -10.8/-9.4, and -14.7/-12.1 mm Hg in patients with mild renal insufficiency and -7.7/-6.3, -13.1/-11.8, and -14.1/-10.6 mm Hg in patients with moderate-to-severe renal insufficiency. Creatinine clearance, glomerular filtration rate, and effective renal plasma flow were stable. Irbesartan was withdrawn in only five patients because of adverse clinical or laboratory experience. Hyperkalemia (>6 mEq/l) requiring discontinuation of irbesartan occurred in only one patient. Once-daily irbesartan given as monotherapy at dose of 150-300 mg or in combination with other antihypertensive drugs is effective in reducing blood pressure in hypertensive patients with chronic renal disease. Irbesartan regimens are well tolerated in all groups. In addition, the blood pressure-lowering effect of irbesartan is accompanied by a significant reduction in proteinuria in patients with chronic renal insufficiency.