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PubMed2006

Beyond diuretics: management of volume overload in acute heart failure syndromes.

Diuretics are an established foundation of therapy for patients with chronic heart failure (HF) as well as for those hospitalized for treatment of acute HF syndromes. Despite the accepted use of diuretics in acute HF syndromes, treatment patterns with diuretics vary widely, and there are no data from randomized studies on the benefit of diuretics on morbidity or mortality in patients hospitalized with acute HF syndromes. Additional pharmacologic therapies that complement or replace diuretics in this setting, especially in patients with diuretic resistance, include positive inotropes, nitrovasodilators, and natriuretic peptides, but data are likewise lacking on important clinical outcomes. Ultrafiltration has also been used as a nonpharmacologic strategy to treat patients with acute HF syndromes who exhibit resistance to diuretics. Effective monitoring of volume status with newer modalities may allow more selective use of diuretics and diuretic-like modalities, but additional randomized trial data are clearly needed to establish ideal strategies to promote volume removal in acute HF syndromes.

Acute Disease↗
PubMed1999

Does diuretic therapy increase the risk of renal cell carcinoma?

Several studies have suggested that systemic hypertension as a disease or its therapy could increase the risk for malignancies. Diuretics reduce cardiovascular morbidity and mortality and constitute a cornerstone in the antihypertensive arsenal. To analyze the relation between diuretic therapy and the risk of malignancies, we conducted a comprehensive review of pertinent previous publications by searching the MEDLINE database for related articles in all languages published between January 1966 and April 1998. Within the past decade, we found 9 case control studies and 3 cohort studies in which the relation between diuretic use and renal cell carcinoma was examined. In the case control studies, the odds ratio of renal cell carcinoma occurring in patients treated with diuretics averaged 1.55 with a 95% confidence interval of 1.42 to 1.71 (p <0.00001) compared with nonusers of diuretics. In the 3 cohort studies of 1,226,229 patients, diuretic therapy was associated with a more than twofold risk of renal cell carcinoma when compared with patients not on diuretics. In 1 cohort study, and in the 7 case control studies in which the effects of gender were reported, women had a higher odds ratio (2.01, confidence interval 1.56 to 2.67) than men (1.69 confidence interval 1.34 to 2.13). Thus, cumulative evidence, possibly stronger in women than in men, suggests that the long-term use of diuretics may be associated with renal cell carcinoma. Although diuretics remain the best documented drug class to reduce morbidity and mortality in systemic hypertension, our data suggest a need for continued vigilance to assess the risk-benefit ratio of all drugs used for long-term therapy of cardiovascular disorders.

Carcinoma, Renal Cell↗
PubMed2005

[Mechanism of action of xipamide and its classification as a "low ceiling diuretic". Pharmacodynamic-pharmacokinetic studies in healthy volunteers and in kidney and liver patients].

Xipamide (CAS 14293-44-8) shows structural features comparable with the thiazide- as well as the class of loop diuretics. According to earlier findings this diuretic, in contrast to the thiazides, should not decrease the glomerular filtration rate (GFR) and be effective even in patients with advanced renal failure. Therefore recently the question, which class of diuretics xipamide should be related to, has been increasingly discussed. In order to solve this issue, the diuretic effect of xipamide was assessed in healthy volunteers once without and once under strict water and salt restriction. Additionally, changes in GFR were monitored by means of measurement of the creatinine clearance. Kinetic parameters were determined in plasma and urine; further, in patients with liver cirrhosis, renal elimination kinetics of the diuretic were correlated with the concentration of direct plasma bilirubin, as a marker of cholestasis, at the beginning of a treatment with xipamide, 40 mg qd. The investigations proved that xipamide, like a typical thiazide diuretic, gives rise to a temporary decrease in GFR of about 30 %, provided the renin-angiotensin-aldosterone system of the volunteer is activated by previous salt and water restriction. Xipamide leads to an increase of K+ and Mg2+ excretion, but to a decrease of Ca2+ excretion in urine, a charactaristical feature of the thiazide-like diuretics. The correlation between Na+ excretion and drug excreted in urine over time showed a functional graph that is characteristic for a "low ceiling" thiazide diuretic. In patients with renal failure FE(Na) was increased when related to the GFR-adjusted drug excretion rate, whereas it was diminished in conditions with decreased effective circulating volume like in liver cirrhosis with ascites. It could be shown that the elimination kinetics of xipamide are determined by renal drug clearance, which proportionally decreases with GFR. In patients with liver failure, a decrease of non-renal drug clearance went along with an increase in urinary drug excretion. The amount of drug excreted in urine (Ae) proportionally increased with the concentration of the patients' direct plasma bilirubin. Thus, from a pharmacological as well as clinical point of view xipamide acts like a thiazide diuretic. As could be shown for other thiazides some time ago, xipamide is effective not only in patients with cardiovascular diseases, but also in those with advanced renal failure.

Bilirubin↗
PubMed1987

Beta-blockers versus diuretics in hypertensive men: main results from the HAPPHY trial.

Men aged 40-64 years with mild to moderate hypertension [diastolic blood pressure (DBP) 100-130 mmHg] were randomized to treatment with a diuretic (n = 3272) or a beta-blocker (n = 3297), with additional drugs if necessary, to determine whether a beta-blocker based treatment differs from thiazide diuretic based treatment with regard to the prevention of coronary heart disease (CHD) events and death. Patients with previous CHD, stroke or other serious diseases, or with contraindications to diuretics or beta-blockers were excluded. If normotension (DBP less than 95 mmHg) was not achieved by monotherapy, other antihypertensive drugs were added, but the two basic drugs were not crossed over. Patients were assessed at 6-monthly intervals. The mean follow-up for end-points was 45.1 months. Blood pressure (BP) side effects and end-points were recorded in a standardized manner. Entry characteristics and the BP reduction achieved were very similar in both treatment groups. All analyses were made on an intention-to-treat basis. The incidence of CHD did not differ between the two treatment groups. The incidence of fatal stroke tended to be lower in the beta-blocker treated group than in the diuretic treated group. Total mortality and the total number of end-points were similar in both groups. The percentage of patients withdrawn due to side effects was similar, whereas the number of reported symptoms, according to a questionnaire, was higher for patients on beta-blockers. The incidence of diabetes did not differ between the two groups. Subgroup analyses did not detect a difference in the effect of beta-blockers compared with diuretics in smokers as opposed to non-smokers, and beta-blockers also had the same effects as diuretics in the quartile with the highest predicted risk for CHD. Beta-blockers and thiazide diuretics were approximately equally well tolerated. The two drugs had a similar BP reducing effect although additional drugs had to be given more often in the diuretic group. Antihypertensive treatment based on a beta-blocker or on a thiazide diuretic could not be shown to affect the prevention of hypertensive complications, including CHD, to a different extent.

Adrenergic beta-Antagonists↗
PubMed2004

Diuretics and mortality in acute renal failure.

OBJECTIVE: According to recent research, diuretics may increase mortality in acute renal failure patients. The administration of diuretics in such patients has been discouraged. Our objective was to determine the impact of diuretics on the mortality rate of critically ill patients with acute renal failure. DESIGN: Prospective, multiple-center, multinational epidemiologic study. SETTING: Intensive care units from 54 centers and 23 countries. PATIENTS: Patients were 1,743 consecutive patients who either were treated with renal replacement therapy or fulfilled predefined criteria for acute renal failure. INTERVENTIONS: Three distinct multivariate models were developed to assess the relationship between diuretic use and subsequent mortality: a) a propensity score adjusted multivariate model containing terms previously identified to be important predictors of outcome; b) a new propensity score adjusted multivariate model; and c) a multivariate model developed using standard methods, compensating for collinearity. MEASUREMENTS AND MAIN RESULTS: Approximately 70% of patients were treated with diuretics at study inclusion. Mean age was 68 and mean Simplified Acute Physiology Score II was 47. Severe sepsis/septic shock (43.8%), major surgery (39.1), low cardiac output (29.7), and hypovolemia (28.2%) were the most common conditions associated with the development of acute renal failure. Furosemide was the most common diuretic used (98.3%). Combination therapy was used in 98 patients only. In all three models, diuretic use was not associated with a significantly increased risk of mortality. CONCLUSIONS: Diuretics are commonly prescribed in critically ill patients with acute renal failure, and their use is not associated with higher mortality. There is full equipoise for a randomized controlled trial of diuretics in critically ill patients with renal dysfunction.

Acute Kidney Injury↗
PubMed2005

Thiazide diuretics enhance nocturnal blood pressure fall and reduce proteinuria in immunoglobulin A nephropathy treated with angiotensin II modulators.

OBJECTIVE: We examined whether thiazide diuretics could restore nocturnal blood pressure (BP) decline and reduce urinary protein excretion in patients with glomerulopathy treated with angiotensin II modulators (angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers). METHODS: Twenty-five Japanese outpatients (11 men, 14 women; mean age 43 +/- 12 years) with biopsy-proven immunoglobulin (Ig)A nephropathy, preserved renal function (serum creatinine concentration </=1.2 mg/dl), stable non-nephrotic proteinuria (0.5-3 g daily), and treatment with angiotensin II modulators were studied. The patients received a diuretic, trichlormethiazide (2 mg daily) for 4 weeks after a baseline period lasting for 4 weeks. RESULTS: Diuretic therapy significantly reduced conventional, 24-h, daytime and night-time blood pressures. Nocturnal blood pressure fall was significantly enhanced by diuretic therapy and a significant interaction existed between diuretic therapy and nocturnal fall in mean arterial pressure, which indicated that the degree of nocturnal blood pressure fall was affected by diuretic therapy. The urinary protein excretion rate was significantly reduced from 1.10 +/- 0.62 to 0.63 +/- 0.39 g/day by diuretic therapy. Diuretic/baseline ratio of urinary protein excretion rate was not correlated with diuretic/baseline ratio of conventional, 24-h and daytime mean arterial pressures, but with diuretic/baseline ratio of night-time mean arterial pressure (r = 0.54, P = 0.006). CONCLUSIONS: Diuretics enhanced nocturnal BP decline and reduced urinary protein excretion in patients with IgA nephropathy treated with angiotensin II modulators. The combination of angiotensin II modulators and diuretics may have additional therapeutic advantages in relieving the renal and cardiovascular risks by reducing nocturnal high blood pressure.

Adult↗
PubMed1986

Thiazides and loop-diuretics therapeutic aspects.

Thiazides and compounds with similar models of action exert their most important renal effects on the cortical-diluting segment of the nephron, most likely from the peritubular side. In contrast, the most important site of action of loop-diuretics is the luminal side of the ascending part of the diluting segment. The different sites of action explain the clinically proven efficacious combination of thiazides and loop-diuretics in severe cardiac failure. Most thiazides and loop-diuretics are eliminated via renal tubular secretion, which leads to decreased renal clearance in patients with chronic heart failure (CHF) as their renal blood flow is decreased even if glomerular filtration rate (GFR) is maintained. A rational approach to enhance the effects of loop-diuretics is to combine them with drugs that increase renal blood flow, thereby increasing the rate of delivery of the drug to its site of action. Dilutional hyponatremia is an important complication of treatment with diuretics. An efficacious treatment of that condition seems to be a combination of loop-diuretics and ACE-inhibitors. Thiazides decrease the urinary excretion of calcium, while loop-diuretics have the opposite effect. The possibility of loop-diuretic induced osteopenia cannot be ruled out, which should be considered when choosing between thiazides and loop-diuretics for the treatment of mild to moderate CHF.

Benzothiadiazines↗
PubMed2001

Effect of diuretics on fetal growth: A drug effect or confounding by indication? Pooled Danish and Scottish cohort data.

AIMS: The diabetogenic effect of diuretics, as well as the indication for prescribing them, may impact on fetal growth. We analysed whether the purchase of prescription drugs for diuretics during pregnancy was associated with measures of fetal growth. METHODS: During 1991-98 all women who purchased prescription drugs for diuretics during pregnancy were identified in the Northern Jutland Prescription Database (NJDP), Denmark, and in the Medicines Monitoring Unit's Database (MEMO), Scotland. Information on birth weight and gestational age was obtained from the Danish Birth Registry, the Danish Hospital Discharge Registry and the Scottish Tayside Neonatal Database. Information on diabetes, hypertension and prepregnancy weight were obtained by hospital record review in a sample of women in the Danish cohort. Women who did not purchase prescription diuretics during pregnancy were used as a reference group in both cohorts. RESULTS: Danish women who purchased prescription loop diuretics during pregnancy gave birth to infants with higher birth weights than women who did not use diuretics; mean difference 104.7 g (95% CI; 2.6, 206.9). However, the high prevalence of diabetes (10.3%) among Danish women who purchased prescription loop diuretics during pregnancy might explain this result. Both the Danish and the Scottish women who purchased prescription diuretics during their pregnancy were at increased risk of preterm delivery (< 37 completed weeks); ORs: 1.8 (CI; 1.2, 2.7)NJDP, 1.9 (CI; 0.9, 4.3)MEMO. The proportion of hypertension among women who purchased prescription thiazides was 15.8%, and the risk of having an infant with a birth weight (BW) < 2500 g was increased; ORs: 2.6 (CI; 1.4, 5.0)NJDP, 2.4 (CI; 0.8, 7.8)MEMO. CONCLUSIONS: Prescribing diuretics during pregnancy was associated with differences in birth weight and incidence of preterm delivery. Confounding by indication may explain the findings.

Benzothiadiazines↗
PubMed1988

The use of diuretic medicines by elderly people in residential homes.

Data relating to the use of diuretics from a descriptive epidemiological study of drug use in residential homes for elderly people were analysed. Of the 1,888 residents included in the study, 797 (42%) received diuretics. Significantly more females than males received diuretics (ratio of 3.1:1) and recipients were significantly older than non-recipients. They received a total of 894 diuretics of which 413 (46.2%) were loop diuretics, 168 (18.6%) were thiazide diuretics and 278 (31.2%) were potassium-sparing diuretics. The single most frequently used diuretic was frusemide. Diuretics were involved in 209 potential drug-drug interactions which represented 41% of the total number of potential drug-drug interactions. Of these interactions 19 were considered to be potentially highly clinically significant.

Aged↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: drug absorption in the management of congestive heart failure: loop diuretics.

Congestive heart failure is a disease state distinguished by the regular presence of both renal and hepatic abnormalities in drug handling. One such abnormality involves flaws in the process of drug absorption. In most instances, congestive heart failure-related abnormalities in drug absorption are of inconsequential significance. However, this is not the case with loop diuretics. Loop diuretic action ordinarily tracks the rate and extent of absorption if a sufficient amount of diuretic has been given to exceed the threshold for diuretic effect. In congestive heart failure, both the rate and absolute amount of loop diuretic absorbed can be reduced as a function of the heart failure state itself. In this setting, drug dissolution characteristics can assume added significance. Furosemide is the loop diuretic with the widest intra- and interpatient variability of absorption. Alternatively, the loop diuretic torsemide is rapidly and fairly completely absorbed independent of the heart failure state. This pattern of absorption establishes it as the preferred loop diuretic in the otherwise diuretic-resistant heart failure patient. However, the exact role of torsemide in the outpatient management of congestive heart failure remains to be determined.

Diuretics↗
PubMed1986

Chloride transport inhibition by various types of loop diuretics in fish opercular epithelium.

Isolated opercular epithelia of killifish (Fundulus heteroclitus), mounted in an Ussing chamber, were used to study the effects of various diuretics on chloride transport, measured as short-circuit current (SCC). The acidic 'loop' diuretics, ethacrynic acid and azosemide, and the basic 'loop' diuretics, muzolimine and MK 447, reduced SCC and exhibited similar dose-effect curves, with EC50s for SCC of 64, 17, greater than 500 and 224 microM, respectively. The alkaline diuretic tizolemide (HOE 740) and the p-COOH-analogue of sulphanilamide were inactive, suggesting that the chloruretic effects of these agents are of a thiazide type. The method can thus discriminate between the effects of loop and thiazide types of diuretics, but not between those of structurally highly different 'loop' diuretics of an acidic and basic nature. Monomethylation of the SO2NH2 group of bumetanide had no effect on the activity of this agent whereas dimethylation reduced it fourfold. The (-)enantiomers of the 'loop' diuretics indacrinone and ozolinone were four and greater than 100 times more active, respectively, than the (+)forms. These results are in accordance with those obtained for the same drugs in the mammalian kidney, and point to the presence of a highly specific binding site for these diuretics. Attempts were also made to explore the prerequisites for binding of the loop diuretic to the active site. Pretreatment of the opercular epithelium with an alpha-L-fucose-binding lectin did not prevent the inhibitory actions of furosemide and indacrinone. Probenecid and (+)ozolinone, both of which block organic anion transport, did not prevent the effects of bumetanide and (-)ozolinone.

Animals↗
PubMed2005

Gout, not induced by diuretics? A case-control study from primary care.

BACKGROUND: It is taken for granted that diuretics may induce gout, but there is a general lack of evidence on this topic. OBJECTIVES: To determine the incidence of gout in patients who use diuretics, taking into account concurrent hypertension and cardiovascular diseases. METHODS: A case-control study was designed. From a primary care population all patients with a first gout registration (59 men, 11 women; mean (SD) age 55.1 (13.5)) were identified as cases. To relate the occurrence of gout to diuretic use a matched reference series of three controls for each case was compiled. Conditional logistic regression analyses were applied to estimate incidence rate ratios (IRRs) of gout, and 95% confidence intervals (CIs), in subjects with and without diuretic treatment, hypertension, and cardiovascular diseases. Additional stratification analyses were made, particularly in the subjects not using diuretics. RESULTS: The IRRs of gout in subjects with v those without diuretic treatment, hypertension, heart failure, and myocardial infarction were 2.8 (95% CI 1.2 to 6.6), 2.6 (95% CI 1.2 to 5.6), 20.9 (95% CI 2.5 to 173.8), and 1.9 (95% CI 0.7 to 4.7), respectively. After adjustment, the IRR of gout for diuretic use dropped to 0.6 (95% CI 0.2 to 2.0), while the IRRs of gout for hypertension, heart failure, and myocardial infarction were still >1. This was also the case for subjects with hypertension or myocardial infarction, who had not used diuretics. CONCLUSION: The results suggest that diuretics do not actually increase the risk of gout. Cardiovascular indications for treatment may have confounded previous inferences.

Adult↗
PubMed1990

Diuretics and electrolyte disturbances in 1000 consecutive geriatric admissions.

Old people are commonly receiving diuretics on admission to hospital. Diuretics are recognized as a risk factor for electrolyte disturbances; controversy exists about the relative risks of different combinations (in particular, co-amilozide [Moduretic]). We recorded the drug history and serum electrolytes in 1000 consecutive admissions to a geriatric hospital, and examined the relative prescribing rates of various diuretics in the community. Full results were obtained in 929 patients. A history of diuretic prescription was present in 353 (38%) of the patients; the mean serum sodium in this group (95% CI 136.0-137.1 mmol/l) was lower than in the 586 not prescribed diuretics (137.1-137.9 mmol/l). The difference was small but statistically significant (95% CI difference = 0.3-1.6 mmol/l; P less than 0.01). Hyponatraemia (serum sodium less than 130 mmol/l) was not significantly commoner in the 41 patients prescribed co-amilozide than in patients prescribed other diuretics. In general patients prescribed potassium-retaining diuretics had a lower serum sodium than the others. There was a significant positive correlation between the serum potassium and the log [serum urea] (r = 0.26, P less than 0.001) and a weak negative correlation existed between sodium and potassium (r = -0.14; P less than 0.001). There was an association between the prescription of potassium-retaining diuretics and a higher serum potassium; also an association between the prescription of a loop or thiazide diuretic and a lower serum potassium. These interactions were shown by multiple regression analysis to be independent and additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed2004

Food: an unrecognized source of loop diuretic resistance.

Food significantly affects the pharmacokinetics of oral loop diuretics in healthy individuals, but studies have not been performed in patients with edema. Because of this omission, food's effect on pharmacokinetics has been overlooked and may decrease the pharmacodynamic response in patients who rely on diuretics. Despite this potential interaction, reference manuals do not provide warnings about the effects of food on loop diuretic absorption. We reviewed the published human studies investigating the effects of food on loop diuretics. Peak plasma concentrations and urinary recovery were significantly decreased when taken with food, but only one study showed a corresponding decrease in total urine output, which is likely related to the diuretic threshold effect. These healthy subjects probably were always above the diuretic threshold under both fed and fasting conditions and thus could not augment their urine output. Based on these data in healthy subjects, the special implications for patients who routinely take diuretics are discussed. Therefore, food is more likely to have a clinical effect on the diuretic threshold given its effect in healthy subjects and the special considerations for patients with edema. Additional studies are needed to help answer these questions. Until such data are available, the most conservative, effective clinical approach is to administer oral loop diuretics without food.

Administration, Oral↗
PubMed1986

The diuretic dilemma and the management of mild hypertension.

Diuretics are used in first-step antihypertensive monotherapy or in combination with adrenergic-inhibiting agents in the majority of hypertensive patients in the United States. A 30-year experience has demonstrated that blood pressure is lowered to as great or greater a degree with diuretics than when many of the presently available antihypertensive drugs, including converting enzyme inhibitors, calcium entry blockers, beta- or alpha-adrenergic inhibitors, or centrally acting sympatholytic agents, are used. Diuretics appear to be especially effective in the elderly and in black patients. All of the major hypertension clinical trials upon which we base our decisions for treatment have employed diuretics as step-1 therapy--with a reduction in morbidity and mortality. In addition, data suggest that more effective treatment of hypertension has contributed to the decrease of over 45% in deaths from cerebrovascular disease and the overall reduction of cardiovascular deaths over the past 15 to 20 years in the United States. The debate concerning the long term safety of diuretic therapy has focused on the USA Multiple Risk Factor Intervention Trial (MRFIT) results and several papers, suggesting that the lipid-raising or potassium-lowering properties of diuretics may produce adverse effects. Suggestions have been made that the use of other drugs without metabolic side effects may result in greater benefit with less risk, especially in the management of mild hypertension where the risk of the disease is not immediate or great. A review of the MRFIT and lipid data from long term studies has failed to establish the 'toxicity' of diuretic agents. In addition, recent studies have not confirmed previous observations that diuretic-induced hypokalaemia increases ventricular ectopy or contributes to sudden death. Although hypokalaemia should be avoided and corrected if it occurs, especially in patients with ischaemic heart disease, in the elderly, in patients with pretreatment ectopy or in patients on low potassium diets, the fear of this metabolic side effect of diuretics should not deter the physician from continuing the use of these agents both as monotherapy in most patients and as second-step therapy with an adrenergic-inhibiting drug.

Arrhythmias, Cardiac↗
PubMed1986

The elderly patient. A special case for diuretic therapy.

Diuretics are among the most widely prescribed drugs, especially for the elderly with cardiac failure or hypertension. Progressive structural and functional changes occur in the kidneys after the fourth decade, leading to impairment of the ability of the kidneys to handle sodium, water and solutes. The renal reserves of the elderly are about half those of the young. In addition, the renin-aldosterone system shows reduced activity in old age. The pharmacokinetics and pharmacodynamics of diuretics in the elderly are reviewed, and the influence of congestive cardiac failure is emphasised with regard to the kinetics of diuretics and the deleterious effect of diuretic-induced hypokalaemia and hypomagnesaemia on the pharmacology of digoxin. Guidelines are suggested for the use of diuretics in the elderly, including the avoidance of unnecessary use, the careful choice of diuretic used, the need for small initial doses, and the prevention of hypokalaemia. The place of potassium-sparing agents for the elderly and adverse effects of diuretics, either mechanical, metabolic or toxic are discussed. Mechanical problems are related to the rate and volume of urine produced, and the resulting effects on bladder function and on blood volume. Although toxic effects are relatively rare, metabolic effects include electrolyte changes, impairment of glucose tolerance, and increased serum uric acid and lipids. Most of these adverse effects are preventable by careful management; the consensus is that they are not of sufficient clinical significance to outweigh the long record of efficacy and safety of diuretic therapy in the elderly. Diuretics will, and should, continue to be used extensively in elderly patients with hypertension and/or cardiac failure.

Aged↗
PubMedDate not supplied

[Renal function, organic acid transport and protein binding: the three elements defining the response to diuretics in clinical practice: an update].

Organic anion transporters (OATs), which are expressed in proximal tubule cells, mediate diuretic secretion into tubular fluid. Increased plasma levels of organic anions and urate and metabolic acidosis, i.e. two characteristic features of chronic renal insufficiency, could be factors contributing to diuretic resistance. These limitations demand increasing doses of diuretics up to a maximum level, or the use of a loop diuretic with non-renal metabolism. Diuretic responsiveness in nephrotic syndrome is limited by strong Na+ reabsorption in the distal nephron. Strategies to improve loop diuretic responsiveness include diuretic dosage and the combination of a loop diuretic with a distal acting diuretic. Strategies to limit protein excretion include the use of angiotensin converting enzyme inhibitors or angiotensin receptor blockers and appropriate salt intake limitation.

Diuretics↗
PubMedDate not supplied

[Diuretic therapy in heart failure].

Diuretic therapy is a drug therapy that increases urine volume, but not glomerular filtration rate (GFR). The diuretics act predominantly on tubular sites; the drugs that increase GRF are the aminophyllines, the positive inotropy or vasoactive substances that increase afferent arteriolar flux or intraglomerular pressure. We can divide the diuretics into six categories: 1) carbonic anhydrase inhibitors: acetazolamide, dichlorphenamide, methazolamide; 2) osmotic diuretics: glycerol, mannitol, urea; 3) loop diuretics: furosemide, bumetanide, ethacrynic acid, piretanide, torsemide; 4) thiazide and thiazide-like diuretics: chlorothiazide, trichlormethiazide, indapamide, chlorthalidone, metolazone; 5) potassium-sparers: a) kidney epithelial sodium channel inhibitors: amiloride and triamterene; b) aldosterone receptor antagonists: spironolactone, canrenoate potassium, eplerenone; 6) ADH antagonists: lithium salts, demeclocycline and ethanol. Diuretic therapy is useful in treating acute and chronic renal insufficiency, congestive heart failure, cirrhosis, overhydration and hypertension. Diuretic therapy increases urine volume, ion loss (except Na+, K+), and modifies diffusion (dilute urine) and convection mechanisms (reduced tubular absorption). Therefore, diuretics are very useful non-dangerous drugs.

Diuretics↗