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Aldactone (Spironolactone)

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Generic Aldactone is an effective medication which helps to fight with hyperaldosteronism, hypokalemia, edema, ascites, hirsutism, alopecia (baldness), acne. It can be also used together with other medicines to treat myasthenia gravis, precocious puberty, high blood pressure. Generic Aldactone acts by controlling the level of water and salt and by decreasing the potassium loss from your body.

Other names for this medication:
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Also known as:  Spironolactone.


Generic Aldactone is a perfect remedy, which helps to fight with hyperaldosteronism, hypokalemia, edema, ascites, hirsutism, alopecia (baldness), acne. It can also be used together with other medicines to treat myasthenia gravis, precocious puberty, high blood pressure.

Generic Aldactone acts by controlling the level of water and salt and by decreasing the potassium loss from your body.

Aldactone is also known as Spironolactone, Spirotone, Spiractin, Osyrol, Spiroctan, Spirolon, Verospiron.

It is aldosterone receptor antagonists.

Generic name of Generic Aldactone is Spironolactone.

Brand names of Generic Aldactone are Aldactone, Spiractin, Spirotone, Spironol, Berlactone, Novo-Spiroton.


You can feel the effects of Generic Aldactone after 2 weeks of treatment. It depends on the health state and other factors of the patient.

Take Generic Aldactone tablets orally with water, at the same time every day.

Do not crush or chew it.

Take Generic Aldactone once (in the morning) or twice a day.

If you want to achieve most effective results do not stop taking Generic Aldactone suddenly.


If you overdose Generic Aldactone and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Aldactone overdosage: diarrhea, vomiting, nausea, red skin rash, loss of energy, slow heartbeat, weakness in legs, feeling drowsy, confusion.


Store below 25 degrees C (77 degrees F). Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Aldactone are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Aldactone if you are allergic to Generic Aldactone components.

Do not take Generic Aldactone if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Aldactone can harm your baby.

Do not take Generic Aldactone if you are taking potassium-sparing diuretics (such as Aldactazide, amiloride (Moduretic, Midamor)), triamterene (such as Maxzide, Dyazide, Dyrenium)).

Be careful using Generic Aldactone if you take inhibitors (enalapril (such as Vasotec), fosinopril (such as Monopril), captopril (such as Capoten), benazepril (such as Lotensin), lisinopril (such as Zestril, Prinivil), quinapril (such as Accupril), moexipril (such as Univasc), ramipril (such as Altace), trandolapril (such as Mavik)); oral steroids (dexamethasone (such as Decadron, Dexone), prednisone (such as Deltasone), methylprednisolone (such as Medrol)); aspirin and other nonsteroidal anti-inflammatory medicines (naproxen (such as Aleve, Naprosyn), ibuprofen (such as Advil, Motrin), indomethacin (such as Indocin)); diuretics; barbiturates, phenobarbital; digoxin (such as Digitek, Lanoxicaps, Lanoxin)); high blood pressure medicines, lithium (such as Lithobid, Eskalith); perindopril (such as Aceon).It can be dangerous to use Aldactone if you suffer from or have a history of liver disease, kidney disease, potassium high levels in your blood, problems with urination.

Be careful with this drug if you are going to have a surgery.

Avoid food with high level of salt.

Avoid dehydration.

Avoid medicines which cause lightheadedness.

You should be careful when you are driving or operating machinery.

Do not stop taking Generic Aldactone suddenly.

aldactone renal dosing

We investigated the relationship between spironolactone use and all-cause mortality in acute decompensated heart failure (ADHF) patients with severe renal dysfunction. The clinical benefit of spironolactone in the treatment of heart failure (HF) has been described in several large randomized clinical trials. However, its clinical benefits have not been studied in hospitalized ADHF patients with severe renal dysfunction (estimated glomerular filtration rate [eGFR] <45 mL/min per 1.73 m(2)).

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Comprehensive management of premenstrual syndrome (PMS) is reviewed, including assessment, counseling, diet, relaxation techniques, exercise, social adaptation, hormonal and medical treatment. Studies of PMS are remarkable for high (40-95%) placebo response, and good results with any treatment, especially in the 1st cycle in uncontrolled studies, but poor performance of therapies in random, double-blind, placebo-controlled studies. Heterogeneous groups of subjects, small numbers and too few cycles may contribute to these findings. The 1st step in treating PMS is thorough assessment and counseling, with at least a hour of listening to the patient. A healthy, varied diet should be suggested, limiting refined sugars, salt, red meat, diary products, chocolate, caffeine products, tobacco, alcohol, and increasing complex carbohydrates and PUFAs, in several small meals. PMS patients rarely have abnormal glucose tolerance tests, but they often exhibit related symptoms. Relaxation and exercise should be prescribed so as to raise endorphins, lower stress, increase control and provide enjoyment. Starting with non-hormonal medications, 100 mg vitamin B6 daily and 1.5 g evening primrose oil bid are suggested to regulate dopamine, serotonin and prostaglandin metabolism. Depending on symptoms, spironolactone diuretics, non-steroidal antiinflammatory drugs or anxiolytics may be prescribed. Hormone treatment ranges from progesterone per rectum or vagina, or oral progestins (usually didrogesterone), estradiol sc, implants, orally or transdermally, oral contraceptives, to hormonal antagonists such as bromocriptine, danazol or LH-RH analogues. The theoretical case for hormone treatments is not established, although some women obtain relief from certain treatments.

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A 47-year-old woman presented with hypokalemia (2.4 mmol/L). She also had hypomagnesemia, hypocalciuria, and hyperreninemic hyperaldosteronism. Sequence analysis revealed a compound heterozygous mutation, R655C and R955Q, in the SLC12A3 gene. These findings were compatible with Gitelman's syndrome (GS). Eplerenone, a selective aldosterone blocker, in combination with oral potassium chloride improved serum potassium level (3.6 mmol/L) with no apparent adverse effect. Although eplerenone has an advantage over spironolactone for its selective affinity for the aldosterone receptor, the efficacy and safety of eplerenone for GS is little understood. Our observation suggests that eplerenone is a useful treatment option for GS.

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Aldosterone-induced hypertension is associated with renal damage that may be mediated by endothelin-1 (ET-1). We evaluated whether inflammatory cell infiltration and DNA-binding activity of the transcription factors nuclear factor kappa B (NF-kappa B) and activator protein-1 (AP-1) were increased in kidneys from aldosterone-infused rats. The role of ET-1 in these processes was evaluated by treating rats with the ET(A)-receptor blocker, BMS 182874. Rats were infused with aldosterone (0.75 microg/h) via a mini-osmotic pump and were given 1% NaCl in the drinking water in the absence and presence of BMS 182874 or of the aldosterone receptor blocker, spironolactone. Renal sections were used to assess inflammatory cell infiltration, which was identified immunocytochemically using monoclonal antibodies against macrophages (ED1+). Electrophoretic mobility shift assays evaluated the DNA-binding activity of NF-kappa B and AP-1 in renal tissue. Systolic blood pressure (BP) was increased in the aldosterone-infused group compared with controls (123+/-6 versus 110+/-10 mmHg, P<0.05). BMS 182874 and spironolactone significantly decreased BP (P<0.05). Macrophage infiltration was increased in the kidneys of aldosterone-infused rats compared with controls. Renal binding activity (arbitrary units) of AP-1, in contrast with that of NF-kappa B, increased in aldosterone-infused rats compared with control rats (AP-1, 4.2+/-0.3 versus 1.0+/-0.1, P<0.05; NF-kappa B, 1.6+/-0.5 versus 1.2+/-0.5). BMS 182874 and spironolactone decreased macrophage infiltration (by 70% and 50% respectively) and AP-1 binding activity (1.0+/-0.3 and 0.8+/-0.3 respectively). In conclusion, kidneys from aldosterone-infused rats exhibited macrophage infiltration and increased AP-1 DNA-binding activity. These processes were attenuated by BMS 182874. Our findings suggest that renal damage in aldosterone-dependent hypertension is associated with inflammatory processes that are mediated in part via ET-1.

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Heart failure is a common indication for admission to the hospital among old adults. The hospital stay for uncomplicated heart failure is often too long. We hypothesized that a rapid optimization of care and a guideline-based approach would allow an early discharge of patients, still maintaining a greater quality and efficiency of care.

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Data of patients undergoing adrenalectomy for benign PA were compared to patients with APAC. Retrospective chart analysis was performed. All patients received spironolactone for 6-8 weeks preoperatively.

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The effect of aldosterone on connective tissue growth factor (CTGF) was examined in rat embryonic ventricular myocytes. Upon aldosterone treatment, CTGF expression was significantly increased in a dose and time-dependent manner. To explore the molecular mechanism for this upregulation, we examined the role of mineralocorticoid receptor. Pre-treatment of an antagonist (spironolactone) at 5-fold excess of aldosterone blocked the CTGF induction by aldosterone, suggesting that the upregulation was mediated by mineralocorticoid receptor. Aldosterone treatment resulted in activation of ERK1/2, p38 MAPK, and JNK pathways with a more transient pattern in p38 MAPK. Blocking studies using pretreatment of the inhibitor of each pathway revealed that p38 MAPK cascade may be important for aldosterone-mediated CTGF upregulation as evidenced by the blocking of CTGF induction by SB203580 (p38 MAPK inhibitor), but not by PD098059 (ERK1/2 inhibitor) and JNK inhibitor I. Interestingly, JNK inhibitor I and PD098059 decreased the basal level of CTGF expression. On the other hand, pretreatment of spironolactone abrogated the p38 MAPK activation, indicating that mineralocorticoid receptor mechanism is linked to p38 MAPK pathway. Taken together, our findings suggest that aldosterone induces CTGF expression via both p38 MAPK cascade and mineralocorticoid receptor and that cross-talk exists between the two pathways.

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Serum fibrosis markers were measured in 880 participants of the Cardiovascular Health Study (mean age 77+/-6 years, 48% women). Participants with systolic HF (n=131, left ventricular ejection fraction <55%) and those with diastolic HF (n=179, left ventricular ejection fraction > or =55%) were compared with controls (280 with cardiovascular risk factors, and 279 healthy individuals) using a nested case-control design. Fibrosis markers included carboxyl-terminal peptide of procollagen type I, carboxyl-terminal telopeptide of collagen type I, and amino-terminal peptide of procollagen type III. Echocardiography was used to document systolic and diastolic function parameters. Analysis of variance and logistic regression analysis (per tertile odds ratios [OR]), adjusted by age, gender, race, hypertension, atrial fibrillation, coronary heart disease, baseline serum glucose, serum cystatin C, serum creatinine, C-reactive protein, any angiotensin-converting enzyme inhibitor, spironolactone or any diuretic, NT-proBNP, and total bone mineral density were performed. Systolic HF was associated with significantly elevated carboxyl-terminal telopeptide of collagen type I (OR=2.6; 95% CI=1.2 to 5.7) and amino-terminal peptide of procollagen type III (OR=3.3; 95% CI=1.6 to 5.8), when adjusting for covariates. Associations of diastolic HF were significant for carboxyl-terminal telopeptide of collagen type I (OR=3.9; 95% CI=1.9 to 8.3) and amino-terminal peptide of procollagen type III (OR=2.7; 95% CI=1.4 to 5.4). HF was not associated with elevated carboxyl-terminal peptide of procollagen type I (P>0.10), and fibrosis markers did not significantly differ between HF with diastolic versus those with systolic dysfunction (P>0.10) whereas NT-proBNP mean values were higher in systolic heart failure than in diastolic heart failure (P<0.0001).

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This meta-analysis provides the evidence that add-on use of spironolactone in patients with resistant hypertension is effective in lowering SBP and DBP, suggesting an add-on use of spironolactone as fourth line therapy in patients with resistant hypertension.

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aldactone 25 tablet 2017-04-04

Isolated hearts were perfused for 30 min and then subjected to 30 min of global ischemia (I) followed by a period of 30 min of reperfusion (R). Drugs were administered for 30 min either before or after ischemia. Drug regimens tested were RU, Capt, Los, RU + Capt, RU + Micronase 5 Mg Los, Capt + Los, and RU + Capt + Los (Triple). Recovery of cardiac hemodynamics was evaluated.

aldactone dosage acne 2015-05-29

Evidence suggests that spironolactone, an aldosterone antagonist, has effects on many cell types independent of its binding to cytosolic mineralocorticoid receptors. We tested the effects of spironolactone on ex vivo-activated human blood leucocytes using gene expression analyses (GeneChip, 12,000 genes) and enzyme immunoassay for quantitating secreted pro- and anti-inflammatory cytokines. Furthermore, to evaluate the safety and efficacy of spironolactone as an anti-inflammatory drug 21 patients with rheumatoid arthritis (RA), juvenile idiopathic arthritis Diovan 5 Mg (JIA) or other arthritides were treated for up to 22 months with 1-3 mg/kg/day. Spironolactone, at in vivo attainable doses, markedly suppressed transcription of several proinflammatory cytokines and, accordingly, inhibited release of tumour necrosis factor, lymphotoxin, interferon-gamma, granulocyte-macrophage colony-stimulating factor and interleukin 6 (70-90% inhibition). Release of these cytokines was also suppressed when testing whole blood from RA patients receiving 50 mg spironolactone twice daily, indicating that pharmaceutical use of the drug may suppress the release of inflammatory cytokines. Spironolactone therapy was generally well tolerated, although treatment had to be stopped in two adults on concomitant methotrexate therapy. Sixteen patients (76%) responded favourably. American College of Rheumatology criteria (ACR)20 or better was achieved in six of nine RA patients; four reached ACR70. Eight of nine JIA patients improved. In conclusion, spironolactone inhibits production of several proinflammatory cytokines considered to be of pathogenic importance in many immunoinflammatory diseases and shows positive effect in patients with chronic arthritis. Its effect as an anti-inflammatory drug should be explored, because prolonged spironolactone therapy is reasonably safe and economically attractive compared with many modern anti-inflammatory therapies.

aldactone medicine uses 2016-02-10

Chronic inhibition of nitric oxide synthase by N(omega)-nitro- L-arginine methyl ester (L-NAME) causes progressive renal injury with systemic hypertension and interstitial macrophage infiltration. We have previously shown that there is Risperdal 8 Mg local activation of the renin-angiotensin-aldosterone system in the renal cortex as a major pathogenic feature of macrophage infiltration. In this study, we measured the effects of the aldosterone antagonist, spironolactone, on renal injury in L-NAME-treated male Wistar rats. After 12 weeks of L-NAME-treatment, rats had increased systolic blood pressure, urinary protein excretion, and serum creatinine and histological analysis showed glomerulosclerosis, interstitial fibrosis, and macrophage infiltration. Treatment with spironolactone significantly prevented these renal changes, whereas treatment with hydralazine had no effect. The cortical expression of osteopontin was significantly elevated in L-NAME-treated rats, and expression of its mRNA significantly correlated with the number of infiltrating macrophages and degree of interstitial fibrosis. Spironolactone treatment markedly suppressed osteopontin expression. Our results suggest that reduced nitric oxide bioavailability caused renal inflammation and fibrosis through an aldosterone receptor-dependent mechanism associated with osteopontin expression independent of its systemic hemodynamic effects.

aldactone 200 mg 2016-07-04

Hyperkalemia is a complications of the use of angiotensin converting enzyme inhibitors, angiotensin receptor antagonists and aldosterone Amoxil 750 Mg antagonists. These drugs are commonly used for the treatment of hypertension and cardiac failure. We report a 84 year-old female treated with losartan 50 mg/day and spironolactone 25 mg/day that presented with a hyperkalemia of 8.4 mEq/l and bradicardia, drowsiness and respiratory depression. She required hemodialysis and ventilatory assistance. She was discharged in good conditions five days after admission.

aldactone generic name 2016-12-01

Despite cure of primary aldosteronism by surgical resection, hypertension persists postoperatively in 30% to 50% of patients. The aim of this study was to determine factors influencing long-term outcome of Mobic Renal Dosing blood pressure after unilateral adrenalectomy for primary aldosteronism.

aldactone 60 mg 2017-02-20

A 55 year old man with hypertensive cardiovascular disease and uremia was studied. Atrial standstill was Omnicef Dosing Peds confirmed by intracardiac electrocardiography and by inability to stimulate the atria using intraatrial cardiac electrical pacing. Atrial standstill was observed to persist for at least three months in duration. This rare cardiac mechanism disorder of atrial standstill, its characteristics and possible mechanisms are reviewed.

aldactone tab 25mg 2015-07-24

The role of aldosterone-antagonists in the treatment of congestive heart failure. Despite the advances of the treatment of Imodium 5 Mg congestive heart failure, nearly half of the patients diagnosed with this disease five years ago are alive today. Experimental and human studies have demonstrated, that under special pathologic condition, the heart extracts aldosterone, and aldosterone extraction in the heart stimulates increased collagen turnover culminating in ventricular remodeling. Aldosterone blockade has been shown to be effective in reducing total mortality and hospitalization for heart failure in patients with systolic left ventricular dysfunction due to chronic heart failure (RALES study with spironolactone) and in patients with systolic left ventricular dysfunction post acute myocardial infarction (EPHESUS study with eplerenone). These clinical studies have shown that mineralocorticoid receptor activation remains important despite the use of angiotensin converting enzyme inhibitor or angiotensin receptor blocking agent and a beta blocker. In the ACC/AHA (and in the European and Hungarian) guidelines for the evolution and management of chronic heart failure, the indication of spironolactone was defined of Class Ila, Level of Evidence: B in CHF of stage C. The eplerenone (in US: INSPRA) was approved for the management of CHF patients after myocardial infarction with ejection fraction < 40%. Eplerenone, compared with spironolactone, is associated with a lower incidence of gynecomastia and other sex hormone-related adverse effect (breast pain, menstrual abnormalities). The spironolactone should not be used in patients with a creatinine above 220 mikromol/l. Despite the guidelines recommendation, spironolactone has been widely used in patients without consideration of their functional class or ejection fraction, without optimization of background treatment with ACE inhibitors and beta-blockers.

aldactone generic 2016-12-11

Agranulocytosis associated with spironolactone administration is described in a Protonix Iv Dose 57-year-old man. Four days after initiation of spironolactone, leukocyte counts decreased from 8.2 to 2.3 X 10(9)/L with 6% neutrophils. Spironolactone, domperidone, and prochlorperazine were discontinued. Domperidone and prochlorperazine were reintroduced and there was concomitant improvement of the leukocyte and neutrophil counts. Substitution of triamterene for spironolactone was not associated with recurrent leukopenia. The potential association of spironolactone with granulocytopenia warrants increased awareness of this rare but serious adverse drug reaction.

aldactone and alcohol 2015-06-08

To evaluate Shatavari Churna Dose the blood pressure (BP) and cardiomyocyte nuclei hypertrophy of spontaneously hypertensive rats (SHR) treated with spironolactone and with spironolactone and an angiotensin-converting enzyme inhibitor and calcium channel blocker.

aldactone 500 mg 2015-04-27

On average, the women in the study were older Zocor 80mg Tab than the men (75 versus 68 years) and less often suffered from a coronary heart disease (56 versus 66%). Women were more likely to have hypertension (59 versus 49%), diabetes mellitus (29 versus 26%), or valvular heart disease (42 versus 36%). Fewer women had an ultrasonographic evaluation of ventricular function (59 versus 74%) and, among those investigated, fewer had left ventricular systolic dysfunction (44 versus 72%). These observed results remained stable after adjustment for age and other possible confounding variables. Medication with a documented positive impact on survival, i.e. angiotensin converting enzyme (ACE) inhibitors, beta-blocking drugs and the diuretic spironolactone, was prescribed less often to women than men. Women, however, received symptomatic medication such as other diuretics and digoxin more often than men.