Diuretics are commonly used to control edema across various clinical fields. Diuretics inhibit sodium reabsorption in specific renal tubules, resulting in increased urinary sodium and water excretion. Loop diuretics are the most potent diuretics. In this article, we review five important aspects of loop diuretics, in particular furosemide, which must be considered when prescribing this medicine: (1) oral versus intravenous treatment, (2) dosage, (3) continuous versus bolus infusion, (4) application in chronic kidney disease patients, and (5) side effects. The bioavailability of furosemide differs between oral and intravenous therapy. Additionally, the threshold and ceiling doses of furosemide differ according to the particular clinical condition of the patient, for example in patients with severe edema or chronic kidney disease. To maximize the efficiency of furosemide, a clear understanding of how the mode of delivery will impact bioavailability and the required dosage is necessary.
Biological Availability ; Diuretics ; Edema ; Furosemide ; Humans ; Renal Insufficiency, Chronic ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors*

Diuretic therapy for the treatment of edema in patients with end-stage renal disease (ESRD) is unsatisfactory, and a combination of thiazide and loop diuretics may produce better clinical effects. To evaluate the influence of thiazide on loop diuretic therapy for ESRD, we performed a crossover study of furosemide versus hydrochlorothiazide plus furosemide treatment. The diuretic effects of furosemide (160 mg i.v.) alone versus a combination of hydrochlorothiazide (100 mg p.o.) and furosemide were studied in ten ESRD patients with proteinuria greater than 1 g/day. The diuretic effects were compared for 24 h urine volume and electrolyte excretion. To detect the influence of thiazide that may have been obscured in the widely dispersed data, pharmacodynamic analysis of urine furosemide excretion rate versus fractional excretion of sodium (FeNa) was also performed using mixed-effect modeling. Combination therapy was not significantly different from furosemide monotherapy in terms of 24 h urine volume, chloride, or sodium excretion. Hydrochlorothiazide was not a significant covariate in the furosemide effect for the pharmacodynamic model. In patients with ESRD and severe proteinuria (>1,000 mg/day), the combination of hydrochlorothiazide with furosemide therapy did not increase the diuretic effect of furosemide.
Cross-Over Studies ; Diuretics ; Edema ; Furosemide ; Humans ; Hydrochlorothiazide* ; Kidney Failure, Chronic* ; Proteinuria ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors

No abstract available.
Diuretics*

Acute decompensated heart failure syndrome is the most common cause of cardiovascular hospitalization with a high rate of in-hospital mortality. The clinical presentation is characterized by different clinical profiles due to various underlying causes, precipitating factors, volume status, and tissue perfusion status. Therefore, clinicians should carefully examine the hemodynamic status of acute decompensated heart failure patients in the initial management. Risk stratification might provide guidance to clinicians who care for patients with acute decompensated heart failure syndromes, and might improve decision-making in emergent care when decisions must be made quickly and accurately. Intravenous loop diuretics are the main treatment option for the relief of congestive symptoms. This article reviews how to assess hemodynamic status of acute decompensated heart failure patients and how to perform risk stratification of patients. Additionally, the initial treatment approach with a variety of pharmacological therapies including inotropic agents, diuretics, beta-blockers, angiotensinogen converting enzyme-inhibitors, angiotensin receptor blockers, digoxin, and other medications that are routinely prescribed in the management of acute decompensated heart failure patients are also discussed.
Angiotensin Receptor Antagonists ; Angiotensinogen ; Digoxin ; Diuretics ; Estrogens, Conjugated (USP) ; Heart Failure* ; Hemodynamics ; Hospital Mortality ; Hospitalization ; Humans ; Perfusion ; Precipitating Factors ; Sodium Potassium Chloride Symporter Inhibitors

Diuretics are among the most commonly used drugs. They primarily block active reabsorption of sodium at different sites in the nephron, thereby increasing urinary losses of NaCl and H2O. This ability to induce a negative fluid balance has made these drugs particularly useful in the treatment of a variety of conditions, edematous: congestive heart failure, nephrotic syndrome, liver cirrhosis, chronic renal failure, idiopathic edema, and nonedematous states: hypertension, hypercalcemia, nephrolithiasis, and syndrome of inappropriate antidiuretic hormone secretion. The diuretics are generally divided into three major classes, which are distinguished by the sites at which they impair the sodium reabsorption: loop diuretics at the thick ascending limb of the loop of Henle, thiazide-type diuretics at the distal tubule, and potassium-sparing diuretics at the cortical collecting tubule. The loop diuretics that are generally the most potent are furosemide, torasemide, and ethacrynic acid. The thiazide-type diuretics include chlorothiazide and metolazone. Spironolactone and amiloride are potassium-sparing diuretics. Diuretics should be started at an effective single dose and given intermittently with a subsequent increase in dose or frequency of administration. As a general rule, the rate of diuresis in an edematous patient should not exceed 1 to 2kg weight loss per day. In renal failure patients, loop diuretics at a higher than normal dose are required to get the desired diuretic effect because the diuretic excretion is often limited, in part due to the retention of organic anions. The patients with liver cirrhosis are responsive to spironolactone. After the administration of diuretics, even if a net diuresis is induced, the response is short-lived as a new steady state is rapidly established because the diuretic-induced sodium losses are counterbalanced by neuro-humorally mediated increases in tubular reabsorption at nondiuretic sensitive sites. This process is called compensatory antidiuresis or diuretic tolerance. Therefore sodium restriction is important when a patient is taking loop diuretics, and the concurrent use of a thiazide diuretic can inhibit downstream NaCl reabsorption, resulting in an exaggeration of diuresis. The most common side-effects are those encountered in virtually all the effective drugs: hypovolemia, hypokalemia and potassium depletion, hyperuricemia, and metabolic alkalosis. Other side-effects include hyperglycemia, hyperlipidemia, hyperuricemia, ototoxicity and sexual dysfunction. In addition, diuretics have the potential to increase the toxicity of several other agents. Nonsteroidal antiinflammatory drugs may antagonize the natriuretic effects of diuretics. The combination of potassium-sparing diuretics and angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers may result in severe hyperkalemia.
Alkalosis ; Amiloride ; Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Anions ; Chlorothiazide ; Diuresis ; Diuretics* ; Edema ; Ethacrynic Acid ; Extremities ; Furosemide ; Heart Failure ; Humans ; Hypercalcemia ; Hyperglycemia ; Hyperkalemia ; Hyperlipidemias ; Hypertension ; Hyperuricemia ; Hypokalemia ; Hypovolemia ; Kidney Failure, Chronic ; Liver Cirrhosis ; Loop of Henle ; Metolazone ; Natriuretic Agents ; Nephrolithiasis ; Nephrons ; Nephrotic Syndrome ; Potassium ; Renal Insufficiency ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors ; Spironolactone ; Water-Electrolyte Balance ; Weight Loss

The premenstrual syndrome is a common sense one: the cyclic appearance of one or more of a large constellation of symptoms just prior to menses, occuring to such a degree that lifestyle or work is affected, followed by a period of time entirely free of symptoms. Symptoms are believed to the result from interaction between central neurotransmitters and normal menstrual hormonal changes. Pharmacologic management to support efficacy includes selective serotonin reuptake inhibitors administered daily or premenstrually and serotonergic tricyclic antidepressants. Anxiolytics and potassium sparing diuretics have demonstrated mixed results in the literature. Hormonal therapy is available towards producing anovulation. There is a good clinical evidence for GnRH agonist with addback hormonal therapy. Oral contraceptive pills prevent ovulation and should be effective for the treatment of PMS. Treatment usually begins with lifestyle changes, over-thecounter medications. Physicians should be aware of the risks from many alternative therapies commonly touted in the popular press.
Anovulation ; Anti-Anxiety Agents ; Antidepressive Agents, Tricyclic ; Complementary Therapies ; Diuretics, Potassium Sparing ; Female ; Gonadotropin-Releasing Hormone ; Life Style ; Neurotransmitter Agents ; Ovulation ; Premenstrual Syndrome* ; Serotonin Uptake Inhibitors

The importance of thiazide-induced hyponatremia (TIH) is reemerging because thiazide diuretic prescription seems to be increasing after the guidelines recommending thiazides as first-line treatment of essential hypertension have been introduced. Thiazide diuretics act by inhibiting reabsorption of Na+ and Cl- from the distal convoluted tubule by blocking the thiazide-sensitive Na+/Cl- cotransporter. Thus, they inhibit electrolyte transport in the diluting segment and may impair urinary dilution in some vulnerable groups. Risk factors predisposing to TIH are old age, women, reduced body masses, and concurrent use of other medications that impair water excretion. While taking thiazides, the elderly may have a greater defect in water excretion after a water load compared with young subjects. Hyponatremia is usually induced within 2 weeks of starting the thiazide diuretic, but it can occur any time during thiazide therapy when subsequent contributory factors are complicated, such as reduction of renal function with aging, ingestion of other drugs that affect free water clearance, or changes in water or sodium intake. While some patients are volume depleted on presentation, most appear euvolemic. Notably serum levels of uric acid, creatinine and urea nitrogen are usually normal or low, suggestive of syndrome of inappropriate secretion of antidiuretic hormone. Despite numerous studies, the pathophysiological mechanisms underlying TIH are unclear. Although the traditional view is that diuretic-induced sodium or volume loss results in vasopressin-induced water retention, the following 3 main factors are implicated in TIH: stimulation of vasopressin secretion, reduced free-water clearance, and increased water intake. These factors will be discussed in this review.
Aged ; Aging ; Creatinine ; Diuretics ; Drinking ; Eating ; Female ; Humans ; Hypertension ; Hyponatremia ; Nitrogen ; Prescriptions ; Retention (Psychology) ; Risk Factors ; Sodium ; Sodium Chloride Symporter Inhibitors ; Thiazides ; Urea ; Uric Acid ; Vasopressins ; Water

PURPOSE: In this study, the etiology and the change of clinical characteristics of hyponatremia, in relation to the increased used of thiazide diuretics, have been assessed. METHODS: To perform a retrospective cohort study, a total sum of 322 patients who have been admitted in a single tertiary referral hospital between 2004 and 2009, were included. RESULTS: The most common cause of hyponatremia was due to thiazide diuretics (37.6%). Among the 121 patients who suffered from thiazide induced hyponatremia, 60 (48.0%) patients took combination thiazide. The incidence of hyponatremia has shown a tendency to increase from 2004 to 2009 (trend test, p<0.001). The incidence of hyponatremia due to the use of combination types has also increased (trend test, p<0.001). Thiazide induced hyponatremia showed no difference when compared to hyponatremia due the other causes, except the fact that the portion of female patients was higher (73.6% vs 64.6%, p<0.001), mean age was older (74.7 vs 69.9 years-old, p<0.001), and incidence of cerebrovascular accident was also higher (19.8% vs 6.5%, p<0.001). CONCLUSION: The use of thiazide is increasing and hence thiazide-induced hyponatremia is also increasing. This is thought to be particularly related to the increase of thiazide-combined drugs. Thiazideinduced hyponatremia shows a higher incidence in old age, female sex and those who have a history of a cerebrovascular event. Hence more caution is needed when using thiazide diuretics as antihypertensives, and plasma sodium levels should be monitored carefully.
Antihypertensive Agents ; Cohort Studies ; Diuretics ; Female ; Humans ; Hyponatremia ; Incidence ; Plasma ; Retrospective Studies ; Sodium ; Sodium Chloride Symporter Inhibitors ; Stroke ; Tertiary Care Centers

No abstract available.
Diagnosis* ; Diuretics ; Edema*

Diuretic effect of Bach hac fluid extract was investigated on white rat. Results showed that Bach hac (Acaramthus nasutin – Acanthaceae) in the dose of 4g/kg – 6g/kg body weight has increased the elimination of Na+, K+, Cl- and Ca++ ions through kidney, the effect was most obvious in the 2nd and 4th hours after administration under any doses.
Animal Experimentation ; diuretics ; Acanthaceae