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PubMed2002

Hyponatraemia and hypokalaemia due to indapamide.

OBJECTIVES: To review Australian adverse drug reaction reports describing hyponatraemia and hypokalaemia attributed to indapamide and compare the characteristics of the patients with those in Australian reports implicating two other diuretic products (hydrochlorothiazide and amiloride hydrochloride; chlorothiazide). DESIGN: Descriptive analysis using reports from the database of the Adverse Drug Reactions Advisory Committee (ADRAC). MAIN OUTCOME MEASURES: Numbers of reports of hyponatraemia and hypokalaemia; proportion of such reports in total reports of adverse reactions to each drug; severity of electrolyte disturbances. RESULTS: Between August 1984 and September 2000, 84 Australian reports of hyponatraemia and 87 reports of hypokalaemia, in which indapamide was the sole suspected drug, were submitted to ADRAC. Most reports involved an indapamide dose of 2.5 mg daily. There was a significantly greater proportion of reports of hyponatraemia with indapamide and with the hydrochlorothiazide and amiloride combination than with chlorothiazide; hypokalaemia was significantly more common for indapamide than for the other two drugs. Of the 87 reports of hypokalaemia with indapamide, 35 patients also had hyponatraemia. For all three drugs, at least 80% of reports of hyponatraemia were in people aged 65 or over, and electrolyte disturbance was most commonly reported in elderly women. CONCLUSIONS: Hyponatraemia and hypokalaemia have been described in 20.9% and 21.7%, respectively, of reports to ADRAC in which indapamide was the sole suspected drug. The electrolyte disturbances can be severe.

Amiloride↗

PubMedDate not supplied

Spectrophotometric, spectrofluorimetric, and densitometric methods for the determination of indapamide.

Three sensitive spectrophotometric, spectrofluorimetric, and densitometric methods are described for the determination of indapamide. The first and second methods are based on the oxidative coupling reaction of indapamide with 3-methyl-2-benzothiazolinone hydrazone HCl (MBTH) in the presence of cerium(IV) ammonium sulfate in an acidic medium. The absorbance of the reaction product is measured at the lambdamax, 601 nm. With the same reaction, indapamide is determined by its quenching effect on the fluorescence of excess cerous ions at the emission lambdamax, 350 nm, and the excitation at lambdamax, 300 nm. The reaction conditions were optimized, and Beer's law was obeyed for indapamide at 1.2-9.6 microg/mL with mean recoveries of 99.92 +/- 0.83 and 99.97 +/- 1.11%, respectively. The third method, a stability-indicating densitometric assay, was developed for the determination of indapamide, using toluene-ethyl acetate-glacial acetic acid (69 + 30 + 1, v/v/v) as the developing system and scanning at the lambdamax, 242 nm, in the presence of the degradation product and related substance; for the indapamide concentration range of 0.6-6 microg/spot, the mean recovery was 99.73 +/- 0.71%. The proposed methods were successfully applied to the determination of indapamide in bulk powder and commercial tablets, and the results of the analysis agreed statistically with those obtained with the official method. Furthermore, the methods were validated according to the guidelines of the U.S. Pharmacopeia and also assessed by applying the standard additions technique.

Antihypertensive Agents↗

PubMed1990

[Role of prostaglandins in the mechanism of action of indapamide].

The role of prostaglandins (PG) has been evoked in the mechanism of action of indapamide. Indeed, PG can act in the regulation of the blood pressure (BP) at different levels: vasodilatation, diuretic, natriuretic, antagonism of angiotensin II and vasopressin (VP), action on adrenergic system. To confirm this hypothesis, we studied the action of certain eicosanoids inhibitors on the antihypertensive action of indapamide in the SHR rat, anaesthetized with pentobarbital (40 mg/kg i.p.). Indapamide (3 mg/kg i.p.) induces significant decrease on BP over 60 min. Mepacrine (5 mg/kg i.p.), phospholipase A2 inhibitor, indomethacin (5 mg/kg i.p), cyclo-oxygenase inhibitor, and tranylcypromine (0,1 mg/kg i.p.), prostacyclin synthase inhibitor, antagonize the antihypertensive action of indapamide. In order to eliminate the importance of VP, we used Brattleboro rats (genetically depleted in VP): indapamide (3 mg/kg i.p.) maintains its hypotensive activity. To eliminate the role of kidney in PG synthesis, we have used cyclo-oxygenase extrarenal inhibitor (sulindac) and the bilateral nephrectomy. Sulindac (1,25 mg/kg i.p.) and the bilateral nephrectomy do not remove the hypotensive action of indapamide. These results, demonstrating the PG extrarenal role and probably that of PGI2, localized in the vascular wall, could explain part of the antihypertensive mechanism of indapamide.

Animals↗

PubMed1988

Effect of indapamide on phosphate metabolism and vascular reactivity.

The effect of indapamide, a nonthiazide diuretic, on urinary electrolytes, renal hemodynamics, and tissue inorganic phosphate was examined in normal anesthetized rats, as well as on vascular reactivity in vitro. Intravenous injections of 0.5 ml/kg of 1 x 10(-5), 1 x 10(-4), and 1 x 10(-3) M indapamide solutions reduced mean arterial pressure from 123 to 114, 130 to 113, and 128 to 114 mm Hg and the plasma phosphate concentrations from 6.4 to 4.2, 6.6 to 4.8, and 7.0 to 4.5 mg/dl, respectively. Similarly, there was a dose-dependent effect of indapamide on fractional excretion of phosphate, which increased from 17 to 44, 24 to 53, and 18 to 75 percent in animals receiving increasing doses of indapamide. This effect of indapamide on the external phosphate balance was associated with significant reduction of kidney cortex and skeletal muscle total inorganic phosphate. In contrast, fractional sodium excretion augmented by 2.6, 2.5, and 2.5 percent, respectively, at each dose of indapamide. This compound also reduced significantly the contractions of strips of rabbit aorta and mesenteric artery elicited by norepinephrine (0.01 to 1.0 micrograms/ml). These results suggest that indapamide-induced reduction of blood pressure could be mediated by an effect of this drug on phosphate balance, and probably on vascular reactivity.

Animals↗

PubMed1983

Effects of competitive red blood cell binding and reduced hematocrit on the blood and plasma levels of [14C]Indapamide in the rat.

The effects of chlorthalidone and acetazolamide on the red blood cell binding of indapamide were investigated. Both drugs caused a substantial decrease in the amount of indapamide bound to the erythrocytes in vitro. This effect was demonstrated by a change in the indapamide blood/plasma ratio from approximately 6 in control samples, to a value of 1 when either of the displacing agents was added. Coadministration of acetazolamide with 14C-labeled indapamide to rats, resulted in a 5-fold drop in the blood levels of total radioactivity, relative to rats dosed with [14C]indapamide alone. Concomitantly, there was a 2-fold increase in the plasma levels of total radioactivity after acetazolamide coadministration. In rats whose hematocrits had been reduced by extensive bleeding, there were only minor alterations in the blood/plasma partitioning of [14C]indapamide. Thus, chlorthalidone and acetazolamide were able to displace indapamide from erythrocytes in vitro and in vivo, possibly by competition at a carbonic anhydrase binding site. The pharmacokinetics of drugs which are extensively bound to erythrocytes may be significantly altered by the presence of other agents capable of competitive binding.

Acetazolamide↗

PubMedDate not supplied

Indapamide: clinical pharmacology, therapeutic efficacy in hypertension, and adverse effects.

Indapamide will soon be marketed in the United States as an oral antihypertensive agent and diuretic. Its molecular structure includes both a polar sulfamoyl chlorobenzamide moiety and a lipid-soluble methylindoline moiety. It differs chemically from the thiazides in that it does not possess the thiazide ring system and it contains only one sulfonamide group. Indapamide is rapidly and well absorbed after oral ingestion, and it has a long terminal half-life in whole blood which permits once daily administration. Indapamide is extensively metabolized by the liver with excretion of unchanged drug accounting for approximately 5% of the total dose. Although indapamide is thought to exert its antihypertensive effect by its diuretic action, several investigations employing laboratory animal preparations have documented a direct vascular action. It has been categorized as a calcium channel blocking agent and this may account for a portion of its antihypertensive effectiveness. In both the treatment of edema and as an antihypertensive agent, indapamide appears to be comparable to hydrochlorothiazide, chlorthalidone and furosemide and seems to have no clinically important advantage over these agents. Side effects associated with indapamide are minimal and appear to be comparable to those observed with other antihypertensive diuretics. Based on few published studies, indapamide appears to be a useful long acting antihypertensive and diuretic agent that is well tolerated and associated with minimal biochemical abnormalities or side effects.

Blood Proteins↗

PubMed1993

Randomized prospective study of a nonthiazide diuretic, indapamide, in preventing calcium stone recurrences.

We examined the biochemical changes and the efficacy of indapamide in the prevention of calcium stone recurrences. Seventy-five patients with calcium nephrolithiasis and hypercalciuria were randomly assigned to three different therapies: diet and fluid (group A), diet and fluid plus indapamide 2.5 mg/day (group B), and diet and fluid plus indapamide 2.5 mg/day plus allopurinol 300 mg/day (group C). Before treatment and after 6, 12, 24, and 36 months of therapy, we evaluated blood pressure, serum and urine risk parameters (including relative supersaturations of calcium oxalate, calcium phosphate and uric acid), stone rate, and the proportion of calculi-free patients. During the 3 years of treatment, urinary calcium greatly decreased in groups B and C, dropping to 50% of the pretreatment values; urinary oxalate also significantly declined in group B (-24%) and group C (-27%). Relative supersaturations of calcium oxalate and calcium phosphate decreased to the same extent in groups B and C (about one-half of the pretreatment value), and relative supersaturation of uric acid was particularly reduced in group C (-65% of the pretreatment value). The stone rate improved in all three groups (p < 0.005), but using actuarial analysis in the evaluation of calculi-free patients, indapamide, and indapamide plus allopurinol groups were found to have a significantly more favorable effect than diet and fluid treatment (p < 0.02), without any difference between the two drug groups. Because indapamide has fewer side effects than thiazide diuretics, we conclude that indapamide could be an interesting alternative to thiazides in the prevention of calcium stones in hypercalciuric patients.

Adult↗

PubMed1975

Antihypertensive activity of a new agent, indapamide: a double-blind study.

In a double-blind trail in 22 patients with mild to moderate essential hypertension, indapamide was compared with chlorathiazide and placebo. Dosage levels were set at 5 mg. indapamide and 500 mg. chlorothiazide daily, for 5 days out of 7, and patients were treated alternately, in random sequence, with each drug for a month over a 3-month period. Blood pressure readings and blood chemistry investigations were carried out before and after each treatment period and a careful history was kept of subjective symptoms and patients' tolerance of therapy. The results show that both active treatments produced drops in systolic and diastolic pressures, but were only statisically significant and different from placebo in the case of indapamide. Indapamide also produce much greater subjective improvement (74%) in patients with functional symptoms compared with chlorothiazide (15%). In an overall assessment, indapamide produced an excellent to good response to treatment in 57% of patients. Comparable responses for chlorotiazide and placebo were 25% and 20% respectivlely. Using patients as their own controls to compare the relative effectiveness of the three periods of treatment, indapamide was shown to be more effective than placebo in 65% of cases and more effective han chlorothiazide in 60%. Although patient tolerance of indapamide was slightly better, both drugs were well accepted and no significant changes from baseline levels were noted in any of the laboratory parameters investigated.

Adult↗

PubMed1983

Effect of indapamide on the baroreceptor reflex in essential hypertension.

The effect of chronic treatment with indapamide on blood pressure (BP), baroreceptor sensitivity (BRS) and vascular reactivity (VR) were investigated in 10 patients with essential hypertension. After 3 months of therapy with indapamide 2.5 mg/d the mean arterial pressure (MAP) had decreased from 135 +/- 6 to 112 +/- 2 mmHg (p less than 0.001); the heart rate (HR) had not changed, VR had decreased from 6.1 +/- 1.2 to 4.8 +/- 1.8 (pg . min . kg)-1 (p less than 0.05), and BRS had increased from 8.3 +/- 3.7 to 12.2 +/- 5.3 ms/mmHg (p less than 0.005), with a leftshift of the relationship between BP and heart period. An inverse correlation was found between the pre-treatment systolic blood pressure and the change in baroreceptor sensitivity after indapamide (r = 0.59; p less than 0.05). In conclusion, chronic treatment with indapamide enhances BRS and resets the reflex. The resetting may account for the lack of tachycardia at rest observed after treatment with indapamide. The mechanism by which indapamide interferes with the baroreceptor reflex requires further investigations.

Adult↗

PubMed1982

Effects of once daily indapamide and pindolol on blood pressure, plasma aldosterone concentration and plasma renin activity in a general practice setting.

Sixteen patients with essential hypertension completed a double blind factorial trial comparing the effects of indapamide (2.5 mg daily) and pindolol (10 mg daily) on blood pressure, heart rate, plasma renin activity and plasma aldosterone concentration. There were four randomised test phases of eight weeks each during which patients received indapamide alone, pindolol alone, indapamide plus pindolol and no active treatment (placebo). Blood pressure and heart rate were measured every two weeks. Supine mean arterial pressure fell from 117 mm Hg in the placebo phase to 111 mm Hg in the indapamide phase, 106 mm Hg in the pindolol phase and 103 mm Hg in the combined indapamide plus pindolol phase. Factorial analysis confirmed that the hypotensive effects of the two drugs were additive, without evidence of potentiation or antagonism. Indapamide caused significant reductions in plasma potassium and chloride, and increases in plasma bicarbonate and urate concentrations; it also caused increases in plasma renin activity and aldosterone concentration. These changes are similar to those observed with thiazide diuretics.

Adult↗

PubMed1990

Cardiovascular protective properties of indapamide.

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoprotein-cholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.

Blood Vessels↗

PubMed1990

Beneficial effects of indapamide on lipoproteins and apoproteins in ambulatory hypertensive patients.

Among the numerous risk factors for atherosclerosis, 2 are particularly important: hypertension and primary or secondary abnormalities of plasma lipids and lipoproteins. Antihypertensive treatments significantly decrease the risk of cerebrovascular accidents, renal failure or hypertensive cardiomyopathy, but they have little influence on coronary artery disease. It has been suggested that some antihypertensive agents may have deleterious effects by altering serum lipoproteins and this may override the benefit of blood pressure reduction. Diuretics increase the blood concentration of total cholesterol, low-density lipoproteins and triglycerides. Indapamide, a methylindoline agent with vasodilator activity, has no adverse lipid effects. Twenty-six studies have clearly demonstrated that indapamide appears to be unique among diuretics because of an absence of adverse lipid effects. In some studies indapamide significantly increased high-density lipoprotein cholesterol, apoproteins A1, A2 and apoprotein E. When a thiazide diuretic had been given previously, indapamide treatment normalized the lipid and lipoprotein profiles. The reason for the lack of adverse lipid effects of indapamide is discussed. Thus indapamide, 2.5 mg once daily, is effective and safe for the control of mild to moderate hypertension, both in young and older patients. It may be an optimal diuretic for use in normolipidemic or hyperlipidemic patients, as it increases high-density lipoprotein but not low-density lipoprotein cholesterol.

Apoproteins↗

PubMed1988

Binding of indapamide to serum proteins and erythrocytes.

The binding of indapamide to isolated serum proteins and erythrocytes was studied in order to understand its blood distribution. In serum, indapamide was mainly bound to alpha 1-acid glycoprotein with a high affinity (K = 73.4/mM), and to albumin and lipoproteins. Indapamide was bound to erythrocytes via a saturable process with a high affinity (K = 385/mM and N = 57 microM for an hematocrit value of 0.48), and erythrocytes were the main binding component in blood (more than 80% of indapamide was associated to erythrocytes in blood). The binding to serum proteins affected indapamide distribution in blood, and alpha 1-acid glycoprotein was shown to be the more effective protein in decreasing the amount of indapamide associated to erythrocytes.

Blood Platelets↗

PubMed1993

Effects of indapamide on contractile responses and 45Ca2+ movements in various isolated blood vessels.

The effects of indapamide on contractile responses in various isolated artery rings and on spontaneous mechanical activity in portal vein segments were investigated. Arteries used were: rabbit aorta, mesenteric (fifth branch), femoral and basilar, and sheep coronary arteries. 45Ca2+ uptake was also analysed in rabbit mesenteric arteries. Indapamide (10(-10)-3 x 10(-4) M) produced a concentration-dependent inhibition of the contractile responses induced by high K+ (80 mM), 5-hydroxytryptamine (10(-5) M), and noradrenaline (10(-6) or 10(-4) M) in all the arteries studied. The inhibitory effect was greater in mesenteric (fifth branch) the IC50 values being 9.2 +/- 3.0 x 10(-6) and 5.5 +/- 4.0 x 10(-8) M for depression of high K(+)- and agonist-induced contractions, respectively. Indapamide inhibited in a concentration-dependent manner the contractile responses elicited by the addition of Ca2+ (1-5 mM) to Ca(2+)-free high K+ solution as well as the spontaneous mechanical activity of rat portal vein. Indapamide also reduced the 45Ca2+ uptake in rabbit mesenteric arteries stimulated by noradrenaline (10(-4) M) or by high K+ (80 mM) without affecting the Ca2+ influx in resting tissues. Our results indicate that indapamide blocked both depolarization-and noradrenaline-induced Ca2+ influx while it did not modify passive Ca2+ entry. Peripheral resistance vessels were demonstrated to be the arteries most sensitive to indapamide vascular effects.

Animals↗

PubMed1993

Comparison of indapamide and hydrochlorothiazide on spontaneous contraction of cardiomyocytes in culture: the effect on alterations of extracellular calcium or potassium.

1. The purpose of this study was to determine whether indapamide or hydrochlorothiazide had a direct action on the heart, specifically to determine whether either diuretic affected spontaneous contractile function of cardiomyocytes in culture or altered the response to increases in extracellular potassium or calcium. 2. Chick embryonic ventricular cells were cultured from 7-day-old chick embryo and myocardial cell aggregates were prepared. Spontaneous cardiac contractile frequency of ventricular myocyte aggregates was monitored. Indapamide [chloro-4-N-(methyl-2-indolinyl-1)-sulfamoyal-3-benzamide] over a concentration range of 10(-9)-10(-6) M did not alter cardiac contractile frequency. 3. Indapamide, in a dose dependent manner, significantly (P < 0.05) antagonized the effect of increases in extracellular potassium [K+]0 that produced a concentration dependent reduction in cardiac contractile frequency. In contrast, hydrochlorothiazide accentuated the effect of increased [K+]0 while hydrochlorothiazide did not alter spontaneous contractile frequency at the usual [K+]0 of 2.0 mM. 4. Indapamide produced a significant (P < 0.05) reduction in the effect of increases in extracellular calcium [Ca2+]0 on cardiac contractility while hydrochlorothiazide was associated with a slight accentuation of the effect of increased [Ca2+]0. Indapamide also slightly reduced the effect of the calcium agonist Bay K 8644, which increases intracellular calcium through voltage operated calcium channels. 5. These data indicate that diuretics modulate a cardiac response to changes in extracellular potassium and calcium. Indapamide antagonizes the effects of increases in extracellular potassium and calcium while hydrochlorothiazide has the opposite effect on the cardiac response to increases in [K+]0 or [Ca2+]0.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1996

Regression of left ventricular hypertrophy in patients with essential hypertension. Results of 6 month treatment with indapamide.

Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity in hypertensive patients. The effects of diuretics on LVH have raised controversies, but recent studies suggest that diuretics are able to reduce LVH in hypertensive patients, mainly through a reduction in ventricular diameter. The present multicenter open study was designed to test the effects of indapamide, a widely used nonthiazide diuretic, on LVH in patients with essential hypertension. Patients had to have mild-to-moderate essential hypertension (supine diastolic blood pressure [sDBP] 95 to 115 mm Hg) with echocardiographic evidence of LVH (left ventricular mass index [LVMI] > 130 g/m2 for men and > 110 g/m2 for women). After a 2 week placebo run-in period, eligible patients underwent a 6 month treatment with 2.5 mg indapamide daily. All echograms were performed by the same investigator before and after 6 months of indapamide. Clinical and biological acceptability and quality of life (visual analog scale) were also studied. One hundred and thirty patients were included in the study and 112 completed the trial. Indapamide induced a significant reduction i systolic and diastolic blood pressures. Indapamide induced a marked reduction in posterior wall thickness (from 12.1 +/- 2.0 to 11.2 +/- 1.6 mm) and in interventricular wall thickness (from 12.7 +/- 1.7 to 11.8 +/- 1.9 mm; each P < .001) and a slight decrease in left ventricular diameter (P = .049). This resulted in a 13% reduction in LVMI (from 161.9 +/- 37.9 to 140.7 +/- 33.8 g/m2, P < .001). Left ventricular fractional shortening remained unchanged. There was no significant relation between changes in LVMI and changes in systolic, diastolic, or mean blood pressure. No significant adverse clinical or biological effects were reported during the study. The increased score of the visual analog scale indicated that overall well-being was improved (P < .001). Our study indicates that indapamide, in addition to blood pressure control, is able to reduce LVH. This effect was achieved mainly through a reduction in wall thicknesses rather than in internal cavity diameter.

Adult↗

PubMed2006

Indapamide SR versus candesartan and amlodipine in hypertension: the X-CELLENT Study.

BACKGROUND: Reducing systolic blood pressure (BP) is of major benefit to patients with isolated systolic hypertension, but lowering normal diastolic BP may be harmful in terms of cardiovascular risk. Effects of different drugs on systolic BP, diastolic BP, and pulse pressure are therefore of interest. METHODS: The NatriliX SR versus CandEsartan and amLodipine in the reduction of systoLic blood prEssure in hyperteNsive patienTs study (X-CELLENT) was a randomized, double-blind, placebo-controlled study comparing the effects of three drugs on these BP components. Patients with systolic-diastolic or isolated systolic hypertension (n = 1758) received indapamide (1.5 mg) sustained release (SR), candesartan (8 mg), amlodipine (5 mg), or placebo once daily for 12 weeks. RESULTS: Compared to placebo all active treatments reduced all BP components significantly (P < .001). For the patients with isolated systolic hypertension (n = 388), the three treatments significantly reduced systolic BP, but only indapamide SR did not change diastolic BP and thus reduced pulse pressure significantly relative to placebo (P = .005). In an ancillary study using ambulatory BP monitoring (n = 576), all three treatments significantly reduced BP components during 24 h relative to placebo. Changes in systolic BP and pulse pressure were similar with the three treatments, but the reduction in diastolic BP was significantly smaller, and therefore more favorable, with indapamide SR compared with candesartan (P = .039). In patients with isolated systolic hypertension (n = 106), indapamide SR reduced 24-h systolic BP significantly more than amlodipine (P = .037), and only indapamide SR reduced 24-h pulse pressure significantly relative to placebo (P = .03). All three drugs were well tolerated. CONCLUSIONS: This distinctive BP-lowering profile of indapamide SR seems highly beneficial when compared to the either of candesartan or amlodipine.

Adult↗

PubMed2007

Efficacy of indapamide SR compared with enalapril in elderly hypertensive patients with type 2 diabetes.

BACKGROUND: Blood pressure control is the main influential variable in reducing microalbuminuria in patients with type 2 diabetes. In this subanalysis of the Natrilix SR versus Enalapril Study in hypertensive Type 2 diabetics with micrOalbuminuRia (NESTOR) study, we have compared the effectiveness of indapamide sustained release (SR) and enalapril in reducing blood pressure and microalbuminuria in patients > or =65 years of age. METHODS: Of the 570 hypertensive patients with type 2 diabetes and persistent microalbuminuria in the NESTOR study, 187 (33%) individuals > or =65 years of age were included in this analysis. Of these, 95 patients received indapamide SR 1.5 mg and 92 patients received enalapril 10 mg, taken once daily in both cases. Adjunctive amlodipine and/or atenolol was added if required. RESULTS: The urinary albumin-to-creatinine ratio decreased by 46% in the indapamide SR group and 47% in the enalapril group. Noninferiority of indapamide SR over enalapril was demonstrated (P = .0236; 35% limit of noninferiority) with a ratio of 0.95 (95% CI: 0.68, 1.34). Mean arterial pressure decreased by 18 mm Hg and 15 mm Hg in the indapamide SR and the enalapril groups, respectively (P = .1136). The effects of both treatments seen in these elderly patients were similar to those observed in the main population, although the extent of the reduction in microalbuminuria was slightly higher. Both treatments were well tolerated, and no difference between groups was observed regarding glucose or lipid profiles. CONCLUSION: Indapamide SR is not less effective than enalapril in reducing microalbuminuria and blood pressure in patients aged >65 years of age with type 2 diabetes and hypertension.

Aged↗