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PubMed1997

Molecular and clinical implications of loop diuretic ototoxicity.

Recent advances in molecular biology have been applied to inner ear research. Loop diuretic ototoxicity has been suggested, but not proven, to share a common mechanism with diuretic effects on renal tubules. The discovery of the molecular nature of the Na-K-2Cl cotransporter in the cochlea provided a better understanding of loop diuretic ototoxicity. In this review, we describe clinical reports of loop diuretic ototoxicity and other information obtained by physiological, biochemical and morphological investigations related to the mechanism sensitive to loop diuretics. Based on recent evidence for the molecular nature of the Na-K-2Cl cotransporter expressed in the mammalian cochlea, the underlying mechanisms of ototoxicity induced by loop diuretics are described.

Animals↗
PubMed2001

ACE inhibitors, beta-blockers, calcium blockers, and diuretics for the control of systolic hypertension.

The objective of this study was to determine which of the common groups of antihypertensive drugs is most effective at lowering systolic blood pressure (SBP) in elderly patients with previously untreated hypertension and the percentage of patients controlled with single or sequential monotherapy. Subjects were recruited from patients attending other outpatient clinics and entered into the study if their SBP was more than 150 mm Hg after three visits. Patients were given a low and high dose of each of the main classes of drugs or placebo for 1 month each. The study was a balanced, randomized crossover design with five periods: placebo; angiotensin converting enzyme inhibitors; beta-blocking drugs; calcium-blocking drugs; and thiazide diuretics. Blood pressure (BP) was measured 24 to 26 h after the previous dose. A questionnaire for side effects was administered at each visit. Seventy-four patients entered the study. beta-Blockers could not be used in 15 patients because of asthma or bronchospasm and these had two placebo periods. There were 9 of 66 patients on P, 9 of 46 on beta-blockers, 4 of 65 on calcium-blocking drugs, 4 of 65 on diuretic, and 1 of 62 patients on ACE inhibitors who did not progress to the higher dose because of side effects. Decreases in SBP compared to randomized placebo were calcium-blocking drugs 15 mm Hg = diuretic 13 mm Hg > ACE inhibitors 8 mm Hg = beta-blockers 5 mm Hg. Blood pressure decrease correlated with placebo BP (P < .0005, r = 0.53 to 0.70). When corrected for placebo, target SBP (<140 mm Hg) was reached in between 6% to 15% of patients on monotherapy. Sequential monotherapy achieved target in 29%. Angiotensin converting enzyme inhibitors, calcium-blocking drugs, and diuretics had no more side effects than placebo. Patients on beta-blockers had more side effects and the well-being score was reduced. Diuretics and calcium-blocking drugs are more effective in elderly patients at lowering SBP pressure. beta-Blockers were relatively ineffective, were frequently contraindicated, and had more side effects. Monotherapy achieved control in only a small number of patients. In elderly people with essential hypertension, therapy should be instituted with diuretics or calcium-blocking drugs, but combination therapy will usually be required to achieve goal.

Adrenergic beta-Antagonists↗
PubMed2003

Effects of diuretic treatment on cardiac and circulating RAS in chronic heart failure post-myocardial infarction in rats.

BACKGROUND: Cardiac angiotensin converting enzyme (ACE) is activated by an increase in wall stress and is involved in remodeling processes. Heart failure is often treated with ACE inhibitors and diuretics although diuretic treatment could activate the renin-angiotensin system (RAS). AIMS: To examine the effects of diuretic treatment on cardiac and circulating RAS in post-infarction chronic heart failure. METHODS: Myocardial infarction was produced by coronary artery ligation in spontaneously hypertensive rats. The rats were randomly assigned to receive either ramipril (1 mg/kg/day), furosemide (4 mg/kg/day), or combination therapy for 6 weeks, commencing 2 weeks after infarction. RESULTS: All three treatment protocols equivalently attenuated reactive hypertrophy of the right ventricle and ventricular septum and improved left ventricular systolic function. Both cardiac ACE mRNA and activity were significantly increased in untreated rats. This increase was attenuated by both ramipril and furosemide and further depressed by the combination. The increase in activity was completely inhibited by either agent alone. Plasma renin activity was upregulated by ramipril or ramipril plus furosemide but not influenced by infarction or furosemide alone. CONCLUSIONS: Furosemide and ramipril significantly reduced cardiac ACE and remodeling. Diuretics work favorably and do not interfere with the effects of ACE inhibitors. Possibly, a reduction in wall stress due to decreased volume overload accounts for the effects of diuretics on cardiac ACE in the treatment of post-infarction remodeling in hypertensive hearts. These data suggest a new mechanism for the frequently observed beneficial effect of diuretics in heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Synthesis and diuretic activity of alkyl- and arylguanidine analogs of N,N'-dicyclohexyl-4-morpholinecarboxamidine in rats and dogs.

Random screening identified N,N'-dicyclohexyl-4-morpholinecarboxamidine (U-18177, 1) as an orally effective nonkaliuretic diuretic in rats. The diuretic profile of 1 and its 1-adamantyl analog (U-37883A, 4) was confirmed orally in dogs, when they were less potent than standard diuretics but showed furosemide-like natriuresis at > or = 100 mumol/kg. However, acute 1 at 61 and 90 mumol/kg iv resulted in lethal cardiac toxicity in dogs. Many analogs of 1 exhibited qualitatively similar diuretic profiles, but none was sufficiently safe to warrant development. Compound 1 also reversed minoxidil's vasodilation in dogs, which led to vascular interaction studies suggesting that analog 4 may block ATP-sensitive K channels. This K channel-blocking mechanism may contribute to the diuretic activity of the series. This is the first report broadly characterizing the diuretic activity of 1 and representative guanidine analogs in rats and dogs and its toxicity and minoxidil-blocking effects in dogs.

Adamantane↗
PubMed1977

Aminobenzoic acid diuretics. 9. 3,4-Disubstituted 5-acylaminobenzoic acids and related compounds.

A number of 3,4-disubstituted 5-acylamino-, 5-alkylamino-, and 5-ureidobenzoic acids corresponding to previously described 3,4-disubstituted 5-sulfamoylbenzoic acid diuretics were prepared and screened for their diuretic properties in dogs. The tabulated results reveal that several 3,4-disubstituted 5-formamido and 5-acetamidobenzoic acids possess considerable diuretic potency demonstrating that a 5-sulfamoyl or 5-methylsulfonyl substituent is not a necessity for potent diuretic activity of 3,4-disubstituted benzoic acids. 4-Benzoyl-3-benzyloxy-5-formamidobenzoic acid, one of the mo-t potent compounds of the present series, is approximately one-tenth as potent as bumetanide. The dose response and diuretic pattern indicate high-ceiling diuretic activity and suggest a mode of action similar to that of bumetanide.

Aminobenzoates↗
PubMed1990

Optimization of the therapeutic index by adjustment of the rate of drug administration or use of drug combinations: exploratory studies of diuretics.

The purpose of this investigation was to explore theoretically certain strategies for optimizing the therapeutic index of drugs and to assess these strategies experimentally with two diuretics. Diuretic agents allow dosing rate flexibilities because the temporal profile of diuretic action can vary considerably as long as the total diuretic effect per day is the same. They can also be used in combination. Experiments were designed to determine if the therapeutic index of furosemide and hydrochlorothiazide can be optimized by administering one or the other at a certain rate or by administering the two drugs together in a certain ratio and at a certain rate. Male Lewis rats received one or the other drug, or combinations of the two, by i.v. infusion at different rates. Several timed urine collections were made under steady-state conditions, with excreted urine replaced volume for volume by i.v. lactated Ringer's solution. The urine flow rates and the urinary excretion rates of the diuretics and of Na+ and K+ were determined. The relationship between the diuretic effect of either of the two drugs given alone and the respective drug excretion rate could be described by the Hill equation. The ratio of urine flow rate to K+ excretion rate exhibited a marked dependence on hydrochlorothiazide excretion rate (highest ratio at high excretion rates), whereas the K+/Na+ excretion rate ratio was constant over a wide range of hydrochlorothiazide excretion rates. There was no significant change of these ratios with changing excretion rate of furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

[Diuretic therapy in congestive heart failure--new views on spironolactone therapy].

Cardiac pump failure leads to a reduction of the effective arterial volume. This is sensed by the kidney via afferent sympathetic fibres. The renal response to the perceived lack of volume is the retention of sodium and water. Although initially homeostatic, this renal counterregulation is maladaptive later on and may contribute to further cardiac compromise by increasing preload (volume retention) and afterload (hyperreninism). The renal sodium retention in congestive heart failure is a consequence of the activation of the sympathetic nervous system and of the renin-angiotensin-aldosterone system. The retention of osmotically free water is partly caused by the nonosmotic secretion of antidiuretic hormone from the posterior pituitary and partly by a diminished osmoregulatory capacity of the kidney due to diuretic therapy and/or (pre-)renal insufficiency. In the near future specific blocking drugs of vasopressin receptors should become available which could make a significant contribution to the management of hyponatremia in this setting. For the management of extracellular volume overload a negative sodium balance is the central objective. A moderate reduction of sodium intake is helpful to achieve this goal and has the additional benefit of reducing thirst and renal potassium loss. However, the majority of patients require (loop) diuretics in addition. Patients who are refractory to high and repeated doses of loop diuretics may respond to a combination of diuretics which act on different nephron segments. Diuretics increase the risk of hypokalemia which can trigger life-threatening tachyarrhythmia, particularly in patients with cardiac dysfunction. Hypokalemia is therefore an indicator of an adverse outcome. Secondary hyperaldosteronism--which can persist despite effective therapy with ACE-inhibitors--is the major cause of hypokalemia in this setting. The randomized aldactone evaluation study (RALES) has shown that spironolactone (25 mg/day) reduced the risk of hypokalemia and decreased morbidity, mortality and clinical symptoms in patients with heart failure. The recent encouraging results with vasopressin receptor antagonists and spironolactone point to the fact that the therapeutic modification of maladaptive homeostatic renal mechanisms plays an increasingly important role in the modern diuretic management of heart failure beyond symptomatic relief from volume overload.

Antidiuretic Hormone Receptor Antagonists↗
PubMed2000

[Which hypertensive patient requires diuretic therapy?].

Over the last decade the role of diuretics as first-line agents for the treatment of hypertension has diminished substantially. The present review encourages the reader to reconsider the current trend for a decline in the use of these inexpensive antihypertensive drugs whose efficacy is well documented. Diuretics have been used in 16 placebo controlled studies with over 13,000 patients as first-line drugs to lower blood pressure. These drugs were shown to reduce total mortality by 11%, cerebrovascular events by 34% and coronary morbidity by 29%. The magnitude of blood pressure reduction with low-dose thiazide diuretics is comparable to that of a therapy with high-dose thiazides, without the serious metabolic side effects observed with the higher dosage. In combination with other antihypertensive agents, diuretics counteract the compensatory regulatory responses, such as volume expansion and edema formation. Moreover, it has been shown that a combination with low-dose thiazides may not only further decrease blood pressure but also reduce cerebrovascular and coronary mortality. Advantages of diuretics in the treatment of hypertension can be appreciated in special clinical conditions, for instance in patients with edema, heart failure, renal failure, nephrotic syndrome and portal hypertension. Low-dose diuretics still have a place as first-line drugs for the treatment of mild, uncomplicated essential hypertension. Moreover, as opposed to other blood pressure lowering agents, there is sufficient scientific evidence for the primary preventive effect of low-dose thiazide.

Antihypertensive Agents↗
PubMed1994

Coadministration of thiazides increases the efficacy of loop diuretics even in patients with advanced renal failure.

It is commonly assumed that thiazide diuretics are ineffective in patients with advanced renal failure (GFR < 30 ml/min/1.73 m2). Thiazides act on the nephron segment distal to the ascending thick loop of Henle, that is, the site of action of loop diuretics. Blockade of sodium reabsorption in the thiazide-sensitive segment should therefore obliterate the compensatory increase in sodium reabsorption seen after administration of loop diuretics and thus potentiate the natriuretic efficacy of loop diuretics even in advanced renal failure. In a single-blind, randomized, placebo controlled crossover study we compared the natriuretic and chloruretic effect of the loop diuretic, torasemide, given alone or in combination with the thiazide diuretic, butizid, in 10 patients with advanced renal failure (mean CIn 13.1 +/- 5.9 ml/min/1.73 m2). For two weeks patients adhered to a diet containing a standardized amount of Na+ and K+. On the 6th and 13th study days, two sham infusions were given to patients in order to assess basal 24-hour urinary electrolyte excretion. On the 7th and 14th days they were randomly allocated to receive either 50 mg i.v. torasemide in combination with a sham infusion or torasemide in combination with 20 mg i.v. butizid. Administration of torasemide alone significantly (P < 0.01) increased mean cumulative 24-hour excretion of sodium (from 154 +/- 30 to 232 +/- 59 mmol/24 hr) and chloride (from 128 +/- 21 to 233 +/- 84 mmol/24 hr) as compared with baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

The place of diuretics in preventing cardiovascular events.

Low-dose diuretics are recommended for the initial choice of antihypertensive therapy in the 7th US Joint National Committee report and are accepted as an appropriate choice among other classes of drugs in the 2003 European Society of Hypertension guidelines. The rationales for the use of low-dose diuretics include the following: Renal dysfunction interfering with normal natriuresis is likely a fundamental defect in the pathogenesis of hypertension. Subtle renal insufficiency that interferes with sodium excretion is a common consequence of uncontrolled hypertension. Diuretic-based therapy has been clearly documented in placebo-controlled, randomized trials to reduce cardiovascular morbidity and mortality, particularly in the treatment of elderly hypertensives.In multiple comparative trials, diuretic-based therapy has been shown to provide equal cardiovascular protection to that provided by newer agents. Diuretics enhance the antihypertensive efficacy of all other classes of agents. As lower blood pressure goals of therapy have been found to be needed, diuretic enhancement of other agents' efficacy has become even more essential. With such low doses, side effects are minimal in degree and infrequent in appearance.

Antihypertensive Agents↗
PubMed2001

Inhibition of COX-2 counteracts the effects of diuretics in rats.

BACKGROUND: It is well established that the diuretic- and renin-stimulated effects of loop diuretics can be attenuated by nonselective cyclooxygenase inhibitors. Since it is yet unclear which of the isoforms of cyclooxygenases, COX-1 and COX-2, is relevant in this context, our study aimed to determine the effects of selective COX-2 inhibition on the renal effects of the loop diuretic furosemide, as well as the diuretic hydrochlorothiazide, which acts on the distal tubule. METHOD: Male Sprague-Dawley rats were treated with furosemide (12 mg/day subcutaneously by osmotic pump) or hydrochlorothiazide (30 mg/kg body weight/day orally by gavage). In addition, parallel groups received rofecoxib (1 to 10 mg/kg body weight/day) for selective inhibition of COX-2. Controls were treated with vehicle. RESULTS: Induction of COX-2 mRNA expression due to furosemide was paralleled by increased renal excretion of prostanoids. Also, hydrochlorothiazide led to a rise in prostanoid excretion. Rofecoxib blunted the diuretic-induced increase in prostanoid excretion, thus confirming an effective blockade of COX-2. Moreover, the COX-2 inhibitor rofecoxib dose-dependently attenuated diuresis and saluresis, as well as the stimulation of the renin system induced by furosemide. Furthermore, rofecoxib completely reversed diuresis and saluresis and prevented the increase of plasma renin activity induced by hydrochlorothiazide. CONCLUSIONS: These findings suggest that COX-2-derived prostanoids are of major relevance in modulating the renal effects of diuretics. COX-2 inhibitors might be valuable drugs to treat salt and water wasting during Bartter and Gitelman diseases.

Animals↗
PubMed2001

Role of diuretics in the preservation of residual renal function in patients on continuous ambulatory peritoneal dialysis.

BACKGROUND: Patients on continuous ambulatory peritoneal dialysis (CAPD) are dependent on residual renal function for solute and water clearances, and this declines with time on dialysis. Loop diuretics have been postulated to slow this decline. METHODS: Sixty-one patients new to dialysis were randomly assigned to either furosemide 250 mg every day or no furosemide at the time of CAPD training and were followed prospectively. Urine volume (UV), urea clearance (C(Urea)), and creatinine clearance on cimetidine (C(Cr)) were measured at randomization at six months and at one year. Patients underwent a standard four-hour peritoneum equilibrium test, and total body water was measured by bioelectrical impedance. Results were expressed on an intention-to-treat basis. RESULTS: UV, C(Cr), and C(Urea) were similar at randomization (1020 +/- 104 vs. 1040 +/- 130 mL/24 hours, 4.95 +/- 0.51 vs. 4.07 +/- 0.40 mL/min/1.73 m2, 0.91 +/- 0.09 vs. 0.84 +/- 0.08, diuretic vs. control). UV in the diuretic-treated group increased, whereas in the control group, it declined (+176 vs. -200 mL/24 hours at 6 months and +48.8 vs. -305 mL/24 hours at 1 year, P < 0.05). C(Cr) and C(Urea) declined at a constant rate and were unaffected by diuretic administration (0.12 +/- 0.05 vs. 0.071 +/- 0.04 mL/min/1.73 m2/month, 0.020 +/- 0.01 vs. 0.019 +/- 0.01 per month). Urinary sodium excretion increased in the diuretic group and declined in the control group (+0.72 +/- 0.85 vs. -2.56 +/- 1.31 mmol/24 hours/month, P = 0.04). Body weight rose in both groups (4.3 vs. 3.0 kg), but the percentage of total body weight rose in the control group and remained constant in the diuretic group (52 +/- 2.4 vs. 64 +/- 6.6%, P = 0.10). CONCLUSIONS: Long-term furosemide produces a significant increase in UV over 12 months when on CAPD and may result in clinically significant improvement in fluid balance. However, furosemide has no effect on preserving residual renal function.

Adult↗
PubMed2003

A double-blind randomized crossover trial of two loop diuretics in chronic kidney disease.

BACKGROUND: Torsemide has predictable absorption compared to furosemide. Thereby, torsemide results in more constant exposure to active drug. Our hypothesis was that this pharmacokinetic difference between these commonly used loop diuretics may translate into disparate antihypertensive responses in patients with chronic kidney disease (CKD). METHODS: We conducted a randomized, double-blind, two-period, crossover trial to compare the pharmacodynamics of torsemide and furosemide, in 14 subjects with stage 2 or 3 CKD. We first performed an inpatient study, where after the subjects were brought into sodium balance on a 200 mEq per day diet, a single bioequivalent dose of oral loop diuretic was administered with an intervening washout period. Measurements of urinary electrolytes were made. Subjects then participated in an outpatient study, wherein they received daily therapy for 3 weeks with the loop diuretics in random order. Twenty four-hour ambulatory blood pressure monitoring was performed before and after each drug to assess the antihypertensive response. RESULTS: In the inpatient phase, furosemide increased urinary sodium excretion from average (+/-SD) 199 +/- 49 mEq/day to 357 +/- 96 mEq/day and torsemide increased urinary sodium excretion from 213 +/- 79 mEq/day to 398 +/- 142 mEq/day. These differences between the diuretics were not significant, confirming bioequivalence. In the outpatient phase, furosemide reduced 24-hour ambulatory blood pressure from 147 +/- 17/78 +/- 11 mm Hg to 138 +/- 21/74 +/- 12 mm Hg (P = 0.021) and torsemide reduced it from 143 +/- 18/75 +/- 10 mm Hg to 133 +/- 19/71 +/- 10 mm Hg (P = 0.007). Although each diuretic was effective in reducing ambulatory blood pressure, the differences between diuretics were not statistically significant. CONCLUSION: Bioequivalent doses of torsemide and furosemide given in a randomized, double-blind design fail to demonstrate superiority of torsemide with respect to natriuresis or 24-hour ambulatory blood pressure control in subjects with stages 2 and 3 CKD.

Aged↗
PubMed1990

[Diuretic-induced edema].

The diagnosis of "diuretic-induced oedema" was made in 17 women (mean age 42.4 [23-60] years) who had developed generalized oedema after stopping their (chronic) intake of diuretics. Five patients were between 11 and 32% overweight, five of them were unusually old. A further four patients had severe concomitant diseases, such as primary lymphoedema, mitral valve defect and lupus erythematosus. In 10 of the 17 discontinuation was successful: the initial weight gain averaged 3.9 (1.5-7.5) kg. The maximal weight-gain, in a woman in the course of weaning her of the diuretic, was reversed within 20 days. Diuretic withdrawal after more than 20 years in a woman with mitral valve disease caused heart failure. Diuretic abuse caused prerenal failure in one women, but renal function became normal again after stopping of the diuretic and rehydration.

Adult↗
PubMed1981

[Potassium metabolism during antihypertensive treatment with beta-receptor blocker and diuretic treatment].

In a controlled, prospective, cross-over study 15 patients with essential hypertension received for four weeks either a combination of beta-receptor blocker and diuretic (twice 10 mg pindolol and 5 mg clopamide daily) or of three drugs: beta-receptor blocker, diuretic and sodium-preserving diuretic (twice daily 10 mg timolol, 25 mg hydrochlorothiazide and 2.5 mg amiloride). Both drug combinations produced quantitatively comparable and definite blood pressure lowering from 162/102 mmHg to 128/82 and 130/82, or 130/84 and 127/82, respectively, after two and four weeks. A significant fall in serum potassium from 4.24 to 3.77 and 3.92 mmol/l occurred with the combined two drugs but not the combination of three. With the two-drug combination renal potassium excretion was significantly raised at one of two control points in time. Heart rate remained constant with the two-drug treatment but fell significantly on three-drug administration. There were more side effects with the two-drug preparation. Combinations of beta-receptor blockers and diuretics are thus by no means potassium neutral but can cause renal potassium loss, fall in serum potassium and hypokalaemia. For this reason combining potassium-sparing diuretic with beta-receptor blocker and diuretics is reasonable and justified.

Adrenergic beta-Antagonists↗
PubMed1992

Mechanisms of diuretic effects on carbohydrate tolerance, insulin sensitivity and lipid levels.

Diuretics have long been recognized to increase the concentration of some atherogenic plasma lipids and to reduce insulin sensitivity and adversely influence carbohydrate tolerance, but the mechanisms responsible have not been conclusively established. Early studies reporting diabetes in diuretic-treated patients implicated potassium loss as responsible. More recent observations have extended this suggestion by also demonstrating a role for the renin-angiotensin-aldosterone system. In addition, direct effects of antihypertensive agents on insulin sensitivity have been demonstrated; both hormonal and haemodynamic factors have been implicated. Diuretic-induced lipid changes have also been consistently observed, but the mechanisms for these findings are much less clear. A link between the carbohydrate and insulin alterations and those of lipids has been suggested. Plasma catecholamine concentration may also be increased by diuretics and it is possible that this may also influence lipid metabolism. While the mechanisms of these metabolic effects of diuretics are not yet clearly established, useful clues based on dose relationships and susceptible populations can be discerned. Observations from combination drug therapies also provide additional information regarding potential mechanisms. The availability of new drug therapies associated with few metabolic changes further suggest that effective diuretic therapy need not always be associated with significant adverse metabolic changes.

Carbohydrates↗
PubMed1993

Withdrawing long-term diuretic treatment among elderly patients in general practice.

The aim of this study was to elaborate, implement and evaluate a strategy for discontinuation of long-term diuretic treatment in elderly patients in general practice. Thirty-three patients were enrolled for a supervised step-down and withdrawal of diuretics. After withdrawal, the patients were followed up for 6 months or until diuretic treatment was re-established. Withdrawal was successful according to the protocol in 18 cases. Diuretic withdrawal failed and the treatment was re-established in 15 cases, four of which were sudden cardiovascular events. Most withdrawal failures were identified by routine examinations through the follow-up programmes, thus they had few consequences for the patients. This demonstrates that careful follow-up is essential after diuretic withdrawal. Our findings support the view that a large proportion of elderly patients on diuretics may not need such treatment.

Aged↗
PubMed2001

Intraplatelet calcium levels in patients with acute renal failure before and after the administration of loop diuretics.

BACKGROUND: Intracellular calcium [Ca](i) has been found to be elevated in hypoxic cells in vitro and in erythrocytes and lymphocytes from patients who are septic. Loop diuretics decrease [Ca](i) in platelets from patients with hypertension and in red blood cells from normal volunteers. We report the results of a study designed to measure [Ca](i) in platelets from patients with acute renal failure (ARF) before and after the administration of loop diuretics. METHODS: Sixteen healthy adults and seven patients with ARF were enrolled into the study. Intraplatelet calcium was measured using a fluorescent probe (quin2). Patients with ARF all received intravenous (i.v.) dopamine, 2 microg/kg body weight, and 20% mannitol, 100 ml every 6 h and, in double-blind manner, either torasemide, frusemide, or placebo, 3 mg/kg body weight i.v. every 6 h. Data from subjects given either frusemide or torasemide have been considered together and termed the diuretic group. RESULTS: Basal levels of [Ca](i) in platelets from patients with ARF were significantly higher than in controls (126.9 +/-3 5.7 nmol/l vs 85.7 +/- 22.2 nmol/l, P = 0.02), but were not affected by the administration of loop diuretic (126.9 +/- 35.7 nmol/l vs 165.9 +/- 49.7 nmol/l, P = 0.09, pre- vs post-diuretic). CONCLUSIONS: Intraplatelet calcium is raised in patients with ARF. Loop diuretics have no significant effect on intraplatelet calcium in these patients.

Acute Kidney Injury↗