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PubMed1985

Changes in blood pressure and thermographic values resulting from use of a beta-blocker plus diuretic and of an alpha-beta-blocker plus diuretic.

Changes in arterial blood pressure and in thermographic values were evaluated in two groups of 15 hypertensive patients, each of which was treated, on a random basis, with a combination of atenolol plus chlorthalidone or a combination of labetalol plus chlorthalidone. Both combinations produced a statistically significant reduction in blood pressure values (p less than 0.01) with no changes in heart rate. Telethermographic investigations revealed the presence of hypothermia of the hands before treatment in all the hypertensive patients examined, but not in the control group (10 normal subjects with no vascular and/or hyperthermic disease). After one month of treatment, no changes in peripheral vascularization were observed in the group treated with atenolol plus chlorthalidone, except for 4 cases showing mild improvement, probably due to a reduction in peripheral resistance as a result of the treatment and to a consequent increase in blood flow in the area investigated. In the group treated with labetalol plus chlorthalidone, on the other hand, a substantial recovery of vascular flow was observed in 12 patients as a result of the treatment, while the remaining 3 patients showed a fair degree of improvement (2 degrees C). Both preparations lent themselves to simplified administration regimens with good patient compliance and no adverse reactions.

Adult↗
PubMed1999

Diuretic resistance: physiology and therapeutics.

Diuretic drugs are usually effective treatment for edema when used judiciously. However, some patients become resistant to their effects. Adaptation to diuretic drugs and diuretic resistance may be caused by similar mechanisms. Diuretic adaptations can be classified as those that occur during diuretic action, those that cause sodium retention in the short term (causing 'post-diuretic NaCl retention'), and those that increase sodium retention chronically (the 'braking phenomenon'). Recent experimental work has indicated ways in which kidneys adapt to chronic diuretic treatment. First, nephron segments downstream from the site of diuretic action increase NaCl reabsorption during diuretic administration because delivered NaCl load is increased. Second, when diuretic concentrations in the tubule decline, the kidney tubules act to retain Na until the next dose of diuretic is administered. Third, the ability of the diuretic to increase renal NaCl excretion declines over time, an effect that results both from depletion of the extracellular fluid volume and from structural and functional changes of kidney tubules themselves. These adaptations all increase the rate of NaCl reabsorption and blunt the effectiveness of diuretic therapy. Many times, a second diuretic drug is effective treatment for diuretic resistance. Recent experimental results suggest that a second drug may act synergistically because it blocks the adaptive processes limiting the effectiveness of the first diuretic. Based on an understanding of the mechanisms of diuretic adaptation and resistance, treatment regimens can be designed to block specific adaptive mechanisms and improve diuretic effectiveness.

Adaptation, Physiological↗
PubMed2002

[Value of aldosterone receptor blockade in diuretic therapy of patients with chronic heart failure].

PATHOGENESIS: All forms of chronic heart failure (high-output and low-output failure) are accompanied by an "arterial underfilling" inducing the activation of various neurohumoral systems (renin-angiotensin-aldosterone system, sympathic nervous system, non-osmotic stimulation of vasopressin). Elevated levels of those neurohormones detrimentally modulate renal function. Subsequently, renal salt and volume retention occurs leading to the main symptoms of heart failure, edema formation and dyspnea. DIURETIC THERAPY: Diuretics, which have been discovered more than 40 years ago, beneficially influence renal salt- and volume retention by their effects on tubular sodium reabsorption. While thiazides are recommended in mild forms, loop diuretics are used in severe stages of congestive heart failure. The clinician has to consider the changed pharmacokinetic and -dynamic properties during the application of diuretics in patients with chronic heart failure. In addition, increased sodium reabsorption occurs immediately after cessation of diuretic action often nullifying the preceding diuresis. Thus, salt- and volume restriction should be guaranteed, and a regular application of loop diuretics during the day should be preferred due to the short-acting nature of currently available loop diuretics. Sometimes, diuresis does not longer occur during the treatment with one substance (diuretic resistance), although the therapeutic goals of water excretion have not been achieved. After ruling out factors reducing the actions of diuretics (non-compliance, hyponatremia, etc.), a sequential nephron blockade should be initiated (combination of loop diuretics and a thiazide or an aldosterone-receptor antagonist) to increase diuresis and to elevate symptoms of volume overload. SIDE EFFECTS: Loop diuretics and thiazides often induce mild hypokalemia, which has been demonstrated to be not as benign as thought before. Chronic treatment with oral potassium supplements has several drawbacks, as urine excretion of potassium is subsequently increased and supplementation is not as effective as believed. Diuretic-induced hypokalemia seems to be aldosterone dependent. As aldosterone levels increase during diuretic therapy even during chronic treatment with an angiotensin-converting enzyme (aldosterone-escape) a combined treatment including an aldosterone-receptor antagonist has been suggested. Beneficial effects of aldosterone-receptor blockade on mortality (RALES trial) appear to be mediated be extrarenal and renal mechanisms. The suggested beneficial renal mechanisms of aldosterone receptor blockade are discussed in detail in the review. CONCLUSION: In conclusion, diuretic therapy of patients with congestive heart failure is effective to relieve symptoms and, presumably, to prolong life. As renal function and pharmacokinetics and -dynamics of diuretics are changed in heart failure, diuretic treatment has to be adapted to provide optimal treatment. Increased levels of aldosterone appear to play an important role in diuretic-induced hypokalemia, and in the progression of heart and renal failure. Thus, aldosterone receptor antagonists should be used in the treatment of heart failure more frequently.

Benzothiadiazines↗
PubMed1984

Site and mechanism of the action of diuretics.

The mechanism of action of diuretics can be established by studying the molecular mechanism of action, the site of action within the nephron, and the relationship between the pharmacokinetics of the diuretic and its effect. The molecular mechanism of action is known for diuretic agents such as acetazolamide (carbonic anhydrase), theophylline (phosphodiesterase), digitalis glucosides (Na-K-ATPase), spironolactone (aldosterone antagonism) and dopamine (specific receptors?). The "receptor" for the clinically most important diuretics, i.e. loop diuretics, thiazides, and other potassium-sparing diuretics is, however, unknown. It appears from recent studies of the ion transport in the diluting segment that there probably is a sodium-chloride co-transport in this segment and that loop diuretics specifically inhibit the active chloride transport. The main site of diuretic action is well established for the different groups of diuretics: carbonic anhydrase inhibitors act on the proximal tubulus, loop diuretics on the diluting segment, thiazides on the cortical diluting segment/distal tubulus, and potassium-sparing agents on distal tubulus/collecting ducts. Moreover, some diuretics have additional tubular sites of action. It is also important to realize that other effects of diuretics, e.g. inhibition of the tubuloglomerular feedback mechanism or renal and extra-renal hemodynamic effects, can modify the tubular diuretic effect. Finally, the renal handling of diuretics is of importance to the diuretic effect by determining the concentration of the drug at the "receptor" sit (s). It is emphasized that knowledge of the different aspects of the mechanisms of action of diuretics is a prerequisite for rational use of diuretics, clinically as well as experimentally.

Animals↗
PubMed1999

Diuretics in cardiovascular therapy: the new clinicopharmacological bases that matter.

Diuretics in current use include early distal tubular (i.e., thiazide-type), loop (i.e., furosemide-type), and potassium-and-hydrogen-retaining substances. Available oral formulations of diuretics differ in terms of their renal excretory potency in man, as formally assessed through the effect of a single dose on 24-hour natriuresis in healthy subjects. The 2.5 mg formulation of the loop diuretic torasemide does not increase mean 24-hour natriuresis, and it is therefore considered a very-low-dose formulation. Amiloride 5 mg and torasemide 5 mg and 10 mg, which increase mean 24-hour natriuresis by less than 40%, are considered low-dose or low-potency diuretic formulations of diuretic substances. Hydrochlorothiazide 25 and 50 mg, furosemide 40 and 80 mg, and torasemide 20 mg, which increase mean 24-hour natriuresis by more than 40%, are considered high-dose or high-potency formulations. A rebound in natriuresis follows the early-after-dosing increase in this variables caused by loop diuretics; hence many oral formulations of loop substances are less potent natriuretics than most oral formulations of thiazide-type diuretics. Hydrochlorothiazide 25 mg and furosemide 80 mg have similar natriuretic potencies. During once-daily administration of diuretic formulations of diuretics to subjects without edema and normal renal function, the increases in 24-hour natriuresis and diuresis that follow the first dose disappear or attenuate markedly. This is due to neuroendocrine reactions to diuretic-induced sodium loss and its attendant hemodynamic shifts. Some of these reactions, e.g. the increase in plasma aldosterone that takes place, account for an elevation in kaliuresis that occurs during once-daily treatment with a high-dose formulation of a thiazide-type diuretic. Common fixed-dose combinations of a thiazide-type or a loop diuretic and a potassium-and-hydrogen-retaining substance generally do not change kaliuresis, but they increase natriuresis strikingly. Thiazide-type and loop diuretics decrease and increase calciuresis respectively; none of these actions wanes during prolonged administration. Plasma renin activity and aldosterone do not rise in response to very-low-dose formulations of loop diuretics taken once daily. Glomerular filtration rate tends to fall in the course of once-daily administration of high-dose formulations of diuretics, but not during prolonged once-daily treatment with very-low-dose formulations of loop diuretics.

Aldosterone↗
PubMed2006

Effects of clonidine on diuretic response in ascitic patients with cirrhosis and activation of sympathetic nervous system.

The effects of the addition of clonidine to diuretics on the mobilization of ascites in the short term (diuretic response and requirement of diuretics) and the long term (readmissions for tense ascites and requirement of diuretics) were examined in patients with cirrhosis and with increased sympathetic nervous system (SNS) activity. We also studied neurohormonal, hemodynamic effects and side effects of clonidine and diuretics. Patients were randomized to receive placebo (group 1, n = 32) or clonidine (0.075 mg) twice daily (group 2, n = 32) for 3 months. After 8 days and for 10 days duration, spironolactone (200 mg/day) was added in both groups. After this period, the dosages of diuretics were individually increased until diuretic response. Responding patients were discharged and followed at the outpatient clinic. During the first hospitalization, the time needed for diuretic response was shorter in group 2 than in group 1. The mean requirement for diuretics was significantly higher in group 1 than in group 2, and the diuretic complications (hyperkalemia and renal impairment) were significantly lower in group 2. Clonidine induced a permanent decrease in SNS activity and delayed decrease in renin/aldosterone levels. During the follow-up, the time to the first readmission for tense ascites was shorter in group 1 than in group 2. Readmissions related to tense ascites or diuretic complications were significantly lower in group 2. The mean requirement for diuretics was significantly higher in group 1 than in group 2. In conclusion, the additional administration of clonidine to diuretics induced an earlier diuretic response associated with fewer diuretic requirements and complications.

Angiotensins↗
PubMed1984

Site and mechanism of action of diuretics.

Diuretics have a central role in the treatment of edema and hypertension. This function is primarily an induction of a net negative balance of solute and water. Reviewed herein are the transport properties of each nephron segment that governs salt and water reabsorption with specific reference to the mechanisms by which the various diuretic agents affect those transport processes. Under normal circumstances, the proximal tubule reabsorbs about 50 to 66 percent of the filtered fluid by both active and passive mechanisms. However, diuretics that inhibit proximal reabsorption are "weak" diuretics since distal compensatory mechanisms can overcome their effect. The thin descending limb of Henle is highly permeable to water and relatively impermeable to solutes. Thus, its main physiologic function is to allow osmotic water abstraction. Although diuretics have no direct epithelial effect on this segment, many of the diuretics decrease fluid reabsorption from it by abolishing the papillary osmotic gradient. The decreased water absorption from the descending limb of Henle has a major role in over-all increased diuresis since nephron segments distal to the descending limb are impermeable to water in the absence of vasopressin. The thin ascending limb of Henle is impermeable to water while being highly permeable to sodium and chloride. Diuretics have no direct effect on the thin ascending limb of Henle. The medullary and cortical segments of the thick ascending limb of Henle absorb sodium chloride by active mechanisms as a result of a secondary active chloride transport mechanism that depends on the presence of sodium (co-transport mechanism). This transport mechanism is located on the luminal membrane. Most of the "loop" diuretics effect this process from the luminal side by having a direct inhibitory effect on this co-transport process. The diuretics that have a primary effect on the medullary segment (furosemide, bumetanide, ethacrynic acid) inhibit the concentrating mechanisms, whereas the diuretics that are effective primarily in the cortical segment (thiazides plus the diuretics affecting the medullary segment) inhibit the urinary diluting mechanism. The loop diuretics are physiologically the most potent family of diuretics. The cortical collecting duct segment reabsorbs sodium by active mechanisms. These processes are stimulated by aldosterone. The diuretics that affect these processes are considered weak diuretics, but they do have the metabolic effect of potassium sparing.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗
PubMed1976

The rational use of diuretics in the treatment of arterial hypertension.

The development of modern pharmacologic diuretic agents has revolutionized the therapy of arterial hypertension. The diuretics currently available are easily administered orally, are effective in the presence of alkalosis or acidosis, are non-toxic and have a low incidence of side effects which are readily circumvented or treated. Loop diuretics such as furosemide have the capacity to be effective in patients with diminished renal function or clinical situations that have a powerful stimulus to sodium retention. In clinical circumstances when renal potassium loss is to be prevented such as in patients receiving digitalis, the addition of a potassium-sparing diuretic to either a thiazide or furosemide will achieve the clinical goal of providing an effective diuresis while inhibiting potassium excretion. The mechanism of antihypertensive activity of the diuretic agents appears to be the reduction of extracellular fluid volumes and plasma volumes. Hence, the clinical dictum that to be effective as an antihypertensive agent, diuretics should be administered in diuretic doses. Besides being the cornerstone of initial antihypertensive therapy, diuretics also play an important role in antihypertensive therapy of patients with moderate to severe hypertension who are receiving potent antihypertensive drugs of the vasodilator or sympatholytic class of compounds. Indeed, one of the most important steps in the successful therapy of these patients receiving multiple drugs, is the re-assessment of the diuretic agent. The sodium retention and consequent fluid volume expansion associated with the administration of these potent antihypertensive agents may often cause these patients to develop apparent drug resistance since the thiazide diuretics are not potent enough to counteract the powerful stimulus to sodium retention caused by these antihypertensive agents. The re-evaluation of the diuretic agent at this point will usually necessitate the substitution of furosemide for thiazide or the doubling of the dose of the present loop diuretic. A working knowledge of the physiology of urine formation and the sites of action of currently available diuretic agents will enable the clinician to tailor the diuretic agent to the clinical circumstances of an individual patient and allow the clinician to rationally select a diuretic for the treatment of arterial hypertension.

Antihypertensive Agents↗
PubMed1994

Diuretic strategies in patients with renal failure.

A thorough understanding of the clinical pharmacology of diuretic agents, particularly loop diuretics, is crucial in patients with abnormal (and those with normal) renal function. Renal insufficiency represents a pathophysiological state characterised by diuretic resistance. Diuretic resistance is defined as a diminished pharmacological response, or diminished natriuresis, to a given dose of a diuretic. The phenomenon of diuretic resistance is demonstrated by a shift in the dose-response curve relating urinary diuretic excretion rates (dose) with sodium excretion (response). Pharmacokinetic factors underlie the diuretic resistance observed in patients with renal failure. Diminished renal blood flow and sodium filtration, accumulation of organic acids that inhibit tubular secretion of the diuretic, and inadequate cumulative sodium excretion to meet patients' needs contribute to the diuretic-resistant state. In contrast, the pharmacological response of remnant (i.e. remaining) nephrons to diuretic agents remains intact. The time course of delivery of diuretics to their intraluminal site of action is an independent determinant of natriuretic response. An administration regimen that continuously maintains effective rates of excretion of diuretics into the urine would be expected to cause a greater overall natriuretic effect than the same amount of diuretic administered in intermittent doses. Thus, diuretic administration strategies that take account of the altered pharmacological responses in patients with renal failure are necessary to provide effective and safe treatment. Additionally, such strategies warrant revision by the prescribing physician as renal function changes over time.

Diuretics↗
PubMed1991

Pharmacodynamic and kinetic considerations on diuretics as a basis for differential therapy.

Diuretics are classified according to their site of action in the nephron: loop diuretics, thiazides, and antikaliuretics. During peak diuresis the pattern of electrolyte excretion is constant and characteristic for a class of diuretics. The ratio of diuretic-induced excretion of K+ to Na+ is 0.12 for loop diuretics, 0.20 for thiazides, and -0.21 for antikaliuretics. The ratio of Ca2+ to Na+ is 0.02 for loop diuretics and 0.003 for thiazides. Mg2+ excretion follows K+ excretion in a ratio of 0.15. The natriuretic effect of a diuretic directly depends on the renal clearance of the drug and is proportionate to the number of intact nephrons. Not only loop diuretics but also thiazides and antikaliuretics were demonstrated to be effective natriuretic drugs down to end-stage renal disease. In renal failure FENa is doubled with every halfening of GFR. Loop diuretics increase FENa to a maximum of 24%, thiazides to 10-15%, and FENa is doubled by antikaliuretics. Comedication of loop diuretics with thiazides in renal failure may therefore be more effective than increasing monotherapy. In liver disease, nonrenal drug clearance is reduced the more the patient's direct bilirubin rises thus causing an increase in AUC and urinary excretion of parent drug and metabolites. Despite increased Ae, the cirrhotic patient may become resistant to diuretics as many patients with congestive heart failure or nephrotic syndrome. This is considered to be due to reduced Na+ load available at the diuretic's site of action following avid proximal Na+ reabsorption. In reduced EABV a short-term comedication of loop diuretics with carboanhydratase inhibitors is considered a more effective diuretic strategy than vigorously increasing monotherapy.

Biotransformation↗
PubMed1997

Diuretic usage and withdrawal patterns in a Dutch geriatric patient population.

OBJECTIVES: To describe diuretic usage and withdrawal patterns in a population of very old geriatric patients and to evaluate the long-term probability of remaining free from diuretic therapy after withdrawal. DESIGN: Retrospective analysis of medical records and 1-year follow-up study. SETTING: University Hospital Nijmegen and Rijnstate Hospital Arnhem, a non-academic teaching hospital, The Netherlands. PARTICIPANTS: All 1547 patients, aged 75 years or older, visiting geriatric medicine departments in the two hospitals for the first time in the years 1990 through 1993. MEASUREMENTS: Data on medical history, physical examinations, and medication use were obtained from medical records. Diuretic withdrawal and motivation was recorded as reported. Record review indicating diuretic withdrawal prompted a 1-year follow-up investigation and collection of additional updated information from family care and/or nursing-home physicians. RESULTS: A total of 593 three patients (38.3%) were using diuretics. Use of diuretics increased with age from 33.6% in patients aged 75 to 79 years to 47.4% in patients aged 90 years or older (P < .05). Diuretics were withdrawn in 218 patients (36.8%), in 101 patients because of doubts about the initial or persistent indication for diuretic use and in 91 patients because of adverse effects. No reasons for withdrawal were reported in 26 patients. Withdrawal of diuretics was attempted more often in cases of diuretic prescriptions for unknown reasons (51.2%) or ankle edema without heart failure (45.0%) than when prescriptions were for heart failure (28.5%) or hypertension (35.4%). The overall probability of remaining free of diuretic therapy for 1 year was 0.41. Success of diuretic withdrawal was significantly less when congestive heart failure was the initial indication for prescription (probability 0.24). We did not find other clinical parameters related to the success of withdrawal. CONCLUSIONS: Our study demonstrates that diuretic therapy can be withdrawn for at least a 1-year period in a substantial number of very old geriatric patients receiving these medications, regardless of the initial indications for prescription. However, withdrawal is performed without application of uniform criteria. Future prospective studies should be directed at developing clear guidelines for diuretic withdrawal in order to facilitate identification of eligible patients and to further improve the success of withdrawal attempts.

Age Factors↗
PubMed2001

Diuretic therapy and resistance in congestive heart failure.

Treatment of congestive heart failure has changed dramatically during the past 20 years, but diuretic drugs remain an essential component. Diuretics are essential despite the fact that these drugs stimulate the renin-angiotensin-aldosterone (RAA) axis and lead to adaptive responses that may be counterproductive. In this paper, new diuretic drugs and new uses of older drugs are discussed. These approaches emphasize low-dose combination therapy and may prove superior to traditional approaches that rely exclusively on loop diuretics. Such approaches aim to prevent adverse compensatory processes that appear to result from chronic diuretic treatment. These include acute and chronic increases in plasma renin activity and stimulation of the sympathetic nervous system, both of which increase afterload and may tend to increase mortality. They also include adaptive changes in nephron structure and function resulting from diuretic-induced increases in distal sodium load and diuretic-induced neurohormonal stimulation. These adaptations blunt the effectiveness of diuretic therapy. Diuretic strategies that rely on combinations of diuretics are emphasized as a method to prevent resistance. If diuretic resistance does develop, higher-dose combination regimens, continuous diuretic infusions and mechanical ultrafiltration can be used to overcome diuretic adaptations and restore diuretic efficacy. The goal of reducing the extracellular fluid volume with the least stimulation of the RAA axis and minimal changes in nephron architecture can be achieved in many patients.

Benzothiadiazines↗
PubMed1991

Effects of diuretics on outputs and flows of urine and urinary solutes in healthy subjects.

The effects of single oral doses of common formulations of diuretics (i.e. formulations on the market or designed to be marketed) on 24-hour diuresis and natriuresis in healthy subjects are considered as a measure of the renal excretory potency of diuretics. Common formulations of distal tubular diuretics (e.g. hydrochlorothiazide 25mg, xipamide 10mg and 20mg) are more potent diuretics and natriuretics than common formulations of loop diuretics [e.g. furosemide (frusemide) 40mg, torasemide 2.5, 5 and 10mg]. Indeed, some common formulations of loop diuretics, such as torasemide 2.5, do not increase 24-hour diuresis or natriuresis in healthy subjects. 24-hour kaliuresis and magnesiuresis are elevated by common formulations of distal tubular diuretics, but they are only slightly increased or (more usually) not affected by common formulations of loop diuretics, when single doses are administered to healthy individuals. Common formulations of loop diuretics have lower diuretic and natriuretic potency and lower kaliuretic and magnesiuretic effects than common formulations of distal tubular diuretics, because the pronounced elevations in urinary excretions caused by loop diuretics during the first 6 hours after dosing are followed by rebounds, with respect to post-placebo excretions, between 6 and 24 hours after dosing. These rebounds, which affect the urinary flows of fluid, chloride, sodium, potassium and magnesium, do not occur after administration of common formulations of distal tubular diuretics, at least during the first 24 hours after administration of single doses to healthy subjects. The time courses of urinary excretions after loop diuretics are dose dependent. Higher doses produce more rapid changes in the urinary flows of fluid, chloride, sodium, potassium and magnesium than lower doses, to the extent that single administration of torasemide 2.5 or 5mg to healthy subjects is followed by urinary fluid and solute flows whose time courses resemble those after administration of hydrochlorothiazide 25mg.

Administration, Oral↗
PubMed2000

Diuretic complications.

BACKGROUND: Diuretics are widely used and generally safe, but like any therapeutic agents, they may cause side effects. METHODS: A review of recent literature pertaining to diuretic usage was performed, with emphasis on specific reports of side effects. Reports of large-scale hypertension trials employing diuretics were also examined for descriptions of diuretic-related complications. RESULTS: All diuretics promote excretion of sodium. Depending upon the site and mode of action, some diuretics increase excretion of potassium, chloride, calcium, bicarbonate, or magnesium. Some can reduce renal excretion of electrolyte-free water, calcium, potassium, or protons. Consequently, electrolyte and acid-base disorders commonly accompany diuretic use. Except for the mildly natriuretic collecting duct agents, which are used mainly to limit potassium excretion, all diuretics can cause volume depletion with prerenal azotemia. Loop agents and distal convoluted tubule agents, such as the thiazides, produce hypokalemic, hypochloremic, metabolic alkalosis that responds to potassium chloride replacement. Carbonic anhydrase inhibitors produce less hypokalemia and volume depletion but commonly induce metabolic acidosis that is often symptomatic. The potassium-sparing agents also limit proton excretion, and spironolactone may produce metabolic acidosis. Hyperkalemia is a leading complication of the potassium-sparing agents, especially in patients with an underlying tendency for hyperkalemia. Thiazide diuretics, in particular, have been linked to glucose intolerance, which may be an effect of hypokalemia rather than the diuretic itself. Whether diuretic-induced hypokalemia increases cardiovascular risk is controversial. Loop agents and thiazides may lead to hyponatremia, which, in the case of thiazides, may cause permanent neurologic damage. Dose-related reversible or irreversible ototoxicity may complicate treatment with loop agents. Nephrocalcinosis, nephrolithiasis, hypomagnesemia, and hyperuricemia can potentially complicate treatment with some diuretic agents. Reported idiosyncratic reactions to diuretics include interstitial nephritis, noncardiogenic pulmonary edema, pancreatitis, and myalgias. CONCLUSIONS: Potential side effects of a diuretic can often be anticipated from its mode of action on the kidney. These complications may be mitigated with careful monitoring, dosage adjustment, and replacement of electrolyte losses. Other side effects are idiosyncratic and cannot be prevented.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Pharmacologic bases of cardiovascular therapy with diuretics].

Diuretics may have high, medium or low diuretic potency and their main site of diuretic action at the ascending limb of Henle's loop or at different biochemical sites of the distal tubulus. Loop diuretics have high diuretic potency, act abruptly, are not antihypertensives when prescribed as a monotherapy and are potentially ototoxic. The diuretics acting at the distal tubulus have a gentle time-course of diuretic activity and variable potencies and other properties. The mose frequent side-effect of diuretics is hypokalemia, whose development may be partially prevented by the prescription of a sodium restricted diet. Arrhythmias provoked by diuretics-induced hypokalaemia should be treated with magnesium and potassium. The most frequent drug interaction of diuretics is with unspecific inhibitors of prostaglandin's synthesis (aspirin and indomethacin) which decrease diuretic effects. Diuretics are indicated in the treatment of acute heart failure because of their direct and indirect vasoactive properties, in the treatment of chronic cardiac insufficiency because of their diuretic and vasodilatatory properties and, those diuretics which show as antihypertensives, are first choice drugs in hypertension.

Bartter Syndrome↗
PubMed2006

Diuretics for heart failure.

BACKGROUND: Chronic heart failure is a major cause of morbidity and mortality world-wide. Diuretics are regarded as the first-line treatment for patients with congestive heart failure since they provide symptomatic relief. The effects of diuretics on disease progression and survival remain unclear. OBJECTIVES: To assess the harms and benefits of diuretics for chronic heart failure SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (Issue 2 2004), MEDLINE 1966-2004, EMBASE 1980-2004 and HERDIN database. We hand searched pertinent journals and reference lists of papers were inspected. We also contacted manufacturers and researchers in the field. SELECTION CRITERIA: Only double-blinded randomised controlled trials of diuretic therapy comparing one diuretic with placebo, or one diuretic with another active agent (e.g. ACE inhibitors, digoxin) in patients with chronic heart failure were eligible for inclusion. DATA COLLECTION AND ANALYSIS: Two reviewers independently abstracted the data and assessed the eligibility and methodological quality of each trial. Extracted data were entered into the Review Manager 4.2 computer software, and analysed by determining the odds ratio for dichotomous data, and difference in means for continuous data, of the treated group compared with controls. The likelihood of heterogeneity of the study population was assessed by the Chi-square test. If there was no evidence of statistical heterogeneity and pooling of results was clinically appropriate, a combined estimate was obtained using the fixed-effects model. MAIN RESULTS: We included 14 trials (525 participants), 7 were placebo-controlled, and 7 compared diuretics against other agents such as ACE inhibitors or digoxin. We analysed the data for mortality and for worsening heart failure. Mortality data were available in 3 of the placebo-controlled trials (202 participants). Mortality was lower for participants treated with diuretics than for placebo, odds ratio (OR) for death 0.24, 95% confidence interval (CI) 0.07 to 0.83; P = 0.02. Admission for worsening heart failure was reduced in those taking diuretics in two trials (169 participants), OR 0.07 (95% CI 0.01 to 0.52; P = 0.01). In four trials comparing diuretics to active control (91 participants), diuretics improved exercise capacity in participants with CHF, difference in means WMD 0.72 , 95% CI 0.40 to 1.04; P < 0.0001. AUTHORS' CONCLUSIONS: The available data from several small trials show that in patients with chronic heart failure, conventional diuretics appear to reduce the risk of death and worsening heart failure compared to placebo. Compared to active control, diuretics appear to improve exercise capacity.

Diuretics↗