Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIURETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1999

Urinary flow rate recording: the impact of a single dose of a diuretic on clinic logistics and flow rate parameters.

PURPOSE: We determine the impact of a single dose of a diuretic given to patients scheduled for flow rate recording on clinic waiting time and flow rate parameters, and whether such practice induces artifacts in recording independent of those inherent in repeat recordings. MATERIALS AND METHODS: A total of 99 volunteers with a mean age plus or minus standard deviation of 54 +/- 10.9 years with no known urological condition participated in an open label, crossover study. On 2 separate occasions they came to the clinic for a flow rate recording, and were randomized to receive 20 mg. furosemide upon arrival at the first or second visit. Clinic waiting time, pre-void bladder volume, voided volume, maximum flow rate and other parameters were captured in a database and analyzed. RESULTS: Independent of diuretic use an increase in voided volume and maximum flow rate (19.8 to 21.2 ml. per second) was noted from the first to second visit. Diuretic use independent of sequence induced an increase in voided volume and significant reduction in waiting time (155 versus 81 minutes, p <0.001) without affecting maximum flow rate (19.9 versus 21.1 ml. per second, p = 0.058). Diuretic use on the second visit enhanced the learning effect on maximum flow rate, while first visit use negated the learning effect on the second visit. Waiting time reduction was significant independent of sequence. The positive correlation between voided volume and maximum flow rate remained unchanged with or without the diuretic. CONCLUSIONS: Repeat flow rate recordings are associated with a measurable learning effect leading to an increase in maximum flow rate. The use of 20 mg. furosemide reduces waiting time without inducing additional artifacts or significant changes in flow rate parameters. This practice is recommended for busy offices or clinical research centers to enhance urine flow, patient satisfaction and ultimately compliance with care.

Adult↗
PubMed1999

Use of diuretic renogram in evaluation of patients before and after endopyelotomy.

OBJECTIVES: Endopyelotomy is a widely accepted alternative in the treatment of ureteropelvic junction (UPJ) obstruction, with success rates between 63% and 88%. However, various methods have been used to evaluate patients with UPJ obstruction, making it difficult to compare results. Diuretic renography has the potential to unify the evaluation if performed in standard ways. In this report, we present a standardized protocol for diuretic renography. METHODS: Nineteen endopyelotomies were performed by one surgeon (E.B.K.) at our institution. The 16 patients were evaluated with technetium 99m MAG-3 diuretic renography. The presence or absence of obstruction was classified according to the differential renal function, time activity curves, and Tmax to T 1/2max time. Three patients had a postoperative Whitaker's test. RESULTS: Eight patients had pre- and postoperative diuretic renograms at our institution. This group was stratified by their differential renal function. Among 4 patients with differential renal function greater than 35%, 3 of 4 showed progressive improvement in renal function postoperatively, 4 of 4 had a Tmax to T 1/2max time less than 10 minutes, and 3 of 4 ha d unobstructed time activity curves. Five patients had postoperative renograms only. Of these 5 patients, 4 had differential renal function greater than 35% and 3 of 5 had normal-appearing curves and normal Tmax to T 1/2max time. Three patients required a second endopyelotomy and 2 of these underwent a dismembered pyeloplasty. CONCLUSIONS: Standardized diuretic renography should be used as an objective test for the evaluation of patients with UPJ obstruction. The successful outcome of an endopyelotomy depends on the preoperative renal function of the involved kidney. Whitaker's test may be used for equivocal cases.

Adult↗
PubMed1975

Diuretic-induced oedema.

Diuretics are now commonly prescribed for women with so-called idiopathic oedema. Two patients with idiopathic oedema, one of whom was oedematous on diuretics, had the diuretics stopped. In one the oedema became much worse, and in the other oedema developed. However, this oedema disappeared spontaneously in both patients and they have remained free of oedema on no treatment. It is suggested that in some patients treated with diuretics compensatory mechanisms to retain sodium and water may be stronger than the diuretic-effect itself and may lead to perpetuation of unnecessary treatment.

Adult↗
PubMed2003

[Value of the diuretic isotopic renogram in the follow-up of the upper urinary tract after cystectomy and urinary diversion using intestine].

INTRODUCTION: In our experience we often observe urinary upper tract dilatation after urinari diversion with bowel. To spare useful approaches and therapeutics we have used diuretic renogram. MATERIAL AND METHOD: 26 patients with urinary diversion (Mainz II or Paduana ileal neobladder). We performance ultrasound, urography and diuretic renogram. RESULTS: Follow-up is between 1 y 4 years. After urinary diversion, 54% of the upper tracts are dilated but only 39.3% of them are obstructed in the diuretic renogram. Normal urographic tracts are normal or have good response in the diuretic renogram. Results goes on in the time. CONCLUSIONS: Diuretic renogram is a useful tool in the diagnosis of upper urinary tract obstruction after urinary diversion.

Cystectomy↗
PubMed2000

[Diuretic therapy of hypertensives with Type 2 diabetes; rational therapy or malpractice?].

There is overwhelming evidence that effective antihypertensive therapy with diuretics reduces total mortality and cardiovascular morbidity. Therefore, diuretics have a well established place in the pharmacotherapy of hypertension. However, their role in the treatment of hypertensives with type-II-diabetes is a matter of controversy due to their potentially adverse effects on glucose-, lipid- and electrolyte metabolism which--in type-II-diabetics--may potentially offset the beneficial effects of blood pressure lowering. However, results of large-scale, prospective, randomised intervention trials demonstrate that in type-II-diabetics the beneficial effects of blood pressure reduction per se are more important than any potentially adverse effects on metabolic surrogate parameters. The reduction in total mortality and cardiovascular morbidity as a result of effective antihypertensive therapy is more pronounced in type-II-diabetics than in non-diabetics. This holds also true for a diuretic based antihypertensive therapy in type-II-diabetics. Clearly their effects on glucose-, lipid- and electrolyte metabolism are of minor, if any, clinical relevance. The hypertensive type-II-diabetic benefits from diuretics--they prolong life and improve its quality. Therefore, antihypertensive therapy with diuretics constitutes a rational pharmacotherapy founded on the principles of evidence based medicine and must not be considered as malpractice.

Antihypertensive Agents↗
PubMed2004

[Forgotten metabolic side effects of diuretics: lipids, glucose and vitamin B1 (thiamin) metabolism].

Diuretics could lead to an impairment of lipid and glucose metabolism. These potentially adverse effects of the diuretics could be compensated by non-pharmacological strategies such as weight loss or physical activity. Diuretics lead to an increased urinary loss of vitamin B1 (thiamine), a diuretic side effect which is often forgotten. In the setting of a high vitamin B1 intake the increased urinary excretion is of no pathophysiologic relevance. However, in the setting of low or suboptimal dietary intakes of thiamine the insufficient thiamine nutriture may be of importance. Vitamin B1 plays an important role in energy metabolism, especially also at the level of the heart muscle. Wet beri-beri is the characteristic vitamin B1 deficiency disease, which is besides others also characterized by heart failure. Evidence suggests that heart failure can be improved by the additional administration of Vitamin B1. Older individuals under a chronic diuretic therapy should obtain an oral vitamin B1 supplementation.

Diabetes Mellitus, Type 2↗
PubMed2002

Monitoring of transtubular potassium gradient in the diuretic management of patients with cirrhosis and ascites.

BACKGROUND/AIMS: Aldosterone antagonists are the diuretics of first choice in the treatment of cirrhotic ascites. However, there is still no reliable clinical parameter to evaluate their efficacy. Transtubular potassium gradient (TTKG), the accurate indicator of aldosterone bioactivity, may serve as a guide for the proper use of the aldosterone antagonists. METHODS: In 23 patients with cirrhotic ascites, the daily administered initial dosage of 100 mg of spironolactone was increased by 100 mg/day at intervals of 5 days until either diuresis commenced or TTKG fell below 3.0, the value indicating complete blockade of aldosterone bioactivity. For the non-responders with TTKG lower than 3.0, furosemide was given in addition to spironolactone. RESULTS: Basal TTKG correlated significantly with plasma aldosterone concentration (r = 0.60, P = 0.002). Spironolactone induced the decrease of TTKG in 20 patients, from 5.3 +/- 0.5 to 2.9 +/- 0.2 (mean +/- SE, P < 0.001). A TTKG value of 3.0 could classify seven patients, who did not respond to low dose spironolactone, into two distinct groups at that time, indicating different further diuretic regimen. All patients achieved diuretic responses without complication by this TTKG-guided modification of diuretics. CONCLUSIONS: TTKG may be a suitable guide for the diuretic management of cirrhotic ascites by accurately reflecting the effect of aldosterone antagonists.

Diuretics↗
PubMed2002

Phototoxicity to diuretics and antidiabetics in the cultured keratinocyte cell line HaCaT: evaluation by clonogenic assay and single cell gel electrophoresis Comet assay).

BACKGROUND: Potential phototoxicity has been described for a number of drugs and chemical substances. Psoralens, chlorpromazines and fluoroquinolones have been described as inducing photomutagenicity and photocarcinogenicity in vitro and in vivo. We wanted to investigate oral antidiabetics and diuretics for potential phototoxicity and possible DNA damage in the HaCaT cell line. METHODS: : The oral antidiabetics tolbutamide, glibenclamide and glipizide, and the diuretics bendroflumethiazide, butizide, furosemide, hydrochlorothiazide and trichlormethiazide were dissolved in DMSO to final concentrations of 1 mM, 0.1 mM, and 0.01 mM, incubated together with the cells, and exposed to UVA1 (23 or 48 J/cm2). Cell survival was evaluated in a clonogenic assay and phototoxic DNA damage was investigated by single cell gel electrophoresis (comet assay). To investigate possible inhibiting effects of antioxidants, L-ascorbic acid and alpha-tocopherol were added at a final concentration of 1 mM 24 h before treatment with the drugs. RESULTS: Bendroflumethiazide, furosemide, hydrochlorothiazide, trichlormethiazide and tolbutamide induced dose-dependent phototoxicity in the clonogenic assay. Cells incubated with bendroflumethiazide, tolbutamide and glibenclamide and irradiated with UVA1 demonstrated increased oxidative DNA damage, revealed as alkali-labile sites in the comet assay. Pretreatment with L-ascorbic acid or alpha-tocopherol suppressed the UVA-induced DNA damage in cells incubated with 1 mM bendroflumethiazide, furosemide, glibenclamide, glipizide, tolbutamide or trichloromethiazide. CONCLUSION: Several oral antidiabetics and diuretics show phototoxic effects in the HaCaT cell line. Inhibiting effects of antioxidants point towards involvement of reactive oxygen species in phototoxic DNA damage, suggesting a link between the phototoxic and photocancerogenic potential of the sulfonamide-derived oral antidiabetic and diuretic drugs. Excessive exposure to UV light may be deleterious for patients treated with oral antidiabetic and diuretic drugs.

Cell Death↗
PubMed1985

Tubular action of diuretics: distal effects on electrolyte transport and acidification.

We used clearance and free-flow micropuncture techniques to evaluate the influence of several diuretic agents, given both individually and in various combinations, on transport of sodium, potassium, and fluid, and on acidification and ammonium transport, within the distal tubule of the rat kidney. The loop diuretics, furosemide and piretanide, sharply increased fractional delivery of fluid, sodium, and potassium into the distal tubule, and, as a result, sodium reabsorption and potassium secretion were enhanced in this nephron segment. These two drugs also stimulated urinary acidification and increased urinary phosphate, titratable acid, and ammonium excretion. These effects took place both within the loop of Henle and along the distal tubule. Amiloride and triamterene alone inhibited distal tubular sodium reabsorption and potassium secretion, and, when given with one of the loop diuretics, suppressed both the kaliuresis and the increased acid and ammonium excretion induced by the latter agents. Hydrochlorothiazide and tizolemide inhibited sodium reabsorption within the distal tubule, and were associated with a stimulation of potassium secretion within this segment. Addition of one of these two latter distally acting agents to either of the loop diuretics led to a further augmentation of sodium excretion, but to a reduction of potassium excretion, compared to the responses seen after the loop diuretics alone.

Ammonia↗
PubMed1992

Effect of loop diuretics on organic osmolytes and cell electrolytes in the renal outer medulla.

Electron microprobe analysis on freeze-dried cryosections was used to determine the effect of the loop diuretics torasemide and furosemide on intracellular electrolyte concentrations in individual cells of the outer and inner stripe of the outer medulla and on cell rubidium uptake, the latter a measure of basolateral Na-K-ATPase activity. In addition, the organic osmolytes glycerophosphorylcholine (GPC), betaine, inositol and sorbitol in cortex, outer medulla and inner medulla were measured using HPLC. Both loop diuretics significantly reduced sodium and chloride concentrations and rubidium uptake in thick ascending limb cells, but did not affect sodium concentration or rubidium uptake in the proximal straight tubule (PST) cells or in the light or dark cells of the outer medullary collecting duct (OMCD). Chloride concentrations in these cells (that is, PST cells, OMCD light and dark cells) were lowered by loop diuretics, albeit less than in thick ascending limb cells. Administration of both loop diuretics for only 20 minutes was sufficient to significantly depress tissue concentrations of GPC, betaine, and myo-inositol in the outer medulla and of GPC, betaine and sorbitol at the papillary tip. These results indicate that loop diuretics, presumably by blocking apical sodium entry, decrease thick ascending limb cellular sodium concentration and, as a consequence, reduce Na-K-ATPase activity as assessed by cell rubidium uptake. Although this has been shown previously in in vitro preparations, the present study confirms this for the first time in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Negative modulation of nitric oxide production by neurotensin as a putative mechanism of the diuretic action of SR 48692 in rats.

1. We investigated the effect of the non-peptide neurotensin (NT) antagonist SR 48692 on renal function in rats and the involvement of nitric oxide (NO) in the diuretic action of this compound. 2. In fed animals, SR 48692 dose-dependently (0.5 to 12.5 mg kg-1, p.o., 0.03 to 1 mg kg-1, i.p. and 0.1 to 1 microgram/rat, i.c.v.) increased urine output and urinary excretion of Na+, K+ and Cl- and reduced urine osmolality. The diuretic activity was also evident in water-deprived, fasted animals and in fasted, water-loaded rats. 3. NT (0.1 microgram/rat, i.c.v.) had no effect on urine output in fed rats, but reduced the diuretic action of SR 48692 (1 microgram/rat, i.c.v.). The opposite result was obtained in fasted, water-loaded animals: NT dose-dependently (0.01 and 0.1 microgram/rat, i.c.v.) inhibited diuresis and this effect was significantly inhibited by i.c.v. SR 48692. In this experimental condition, SR 48692 did not further increase the on-going diuresis. 4. The NO synthesis inhibitor N(1)-nitro-L-arginine methyl ester (L-NAME; 30 mg kg-1, i.p.) alone had no effect on urine output in fed rats but prevented the diuretic action of i.c.v. or i.p. SR 48692; L-arginine (1 g kg-1, i.p.) but not D-arginine (1 g kg-1, i.p.) restored the SR 48692-dependent increase in diuresis, L-NAME had no effect on furosemide-stimulated diuresis. 5. Systemically administered L-NAME or i.c.v. NT in fasted, water-loaded rats significantly reduced water diuresis but this effect was no longer seen in animals given i.p. L-arginine. Rats receiving i.c.v. NT, whose diuresis was significantly reduced, also excreted less nitrates and nitrites in urine. 6. Increased diuresis after central or systemic administration of SR 48692 to fed rats was paralleled by increased urinary excretion of nitrates and nitrites, this being consistent with peripheral enhancement of NO production after NT-receptor blockade by SR 48692. The increase in diuresis after furosemide also involved an increase of nitrates and nitrites in urine, but this effect was about half that attained with an equipotent diuretic dose of SR 48692. 7. In fed rats, the NO donor isosorbide-dinitrate, reduced systolic blood pressure (unlike SR 48692 which did not affect blood pressure) but also dose-dependently (1 and 5 mg kg-1, i.p.) stimulated urine output. 8. The overall effects of SR 48692 strongly support a link between the actions of endogenous NT, AVP and peripheral NO production in the modulation of renal excretion of water, Na+, K+ and Cl-.

Animals↗
PubMed1978

The use of the human erythrocyte as a model for studying the action of diuretics on sodium and chloride transport.

1. The Na+ and Cl- transport systems of human erythrocytes have been compared for their sensitivities to diuretics known to act in the ascending limb of Henle's loop. In addition, chemical analogues of 'loop' compounds and also diuretics which act in other areas of the nephron have been examined. 2. The Na+ transport system lacks specificity with respect to inhibition by 'loop' diuretics and also a related chemical analogue studied at equivalent concentrations. 3. The Cl- transport system is inhibited, at low concentrations, by diuretics known to act in the ascending limb of Henle's loop. 4. Erythrocyte Cl- transport offers a useful model with which to study the biochemical action of diuretics.

Biological Transport↗
PubMed1978

Effects of indomethacin alone and during diuretic or beta-adrenoreceptor-blockade therapy on blood pressure and the renin system in essential hypertension.

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or beta-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased alpha-adrenergic tone, which may limit the blood pressure-lowering effect of beta-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or beta-adrenoreceptor blockers.

Adult↗
PubMed1983

Interaction of diuretics and non-steroidal anti-inflammatory drugs in man.

1. The influence of four diuretics on renal prostaglandins was investigated in a study designed in two parts (A and B): A, 24 normal subjects on a constant sodium intake received frusemide (80 mg daily), or hydrochlorothiazide (100 mg), or triamterene (200 mg) or spironolactone (300 mg); B, the same subjects were pretreated for 3 days with indomethacin (150 mg daily), which was continued during the 3 day administration of the respective diuretics and during a 2 day post-diuretic period. 2. In study A, only triamterene provoked a rise in urinary prostaglandins E2 and F2 alpha (+ 474 +/- SEM 92%, P less than 0.01, and + 192 +/- 7%, P less than 0.01). In study B, prostaglandins were significantly inhibited in all subjects. After indomethacin, the natriuretic effect of frusemide and spironolactone was reduced by 80 +/- 12% (P less than 0.01) and 54 +/- 11% (P less than 0.001), whereas the natriuresis induced by hydrochlorothiazide and triamterene was unchanged. No correlation was found between urinary PGE2 and F2 alpha and natriuresis. 3. When triamterene was associated with indomethacin, two subjects developed reversible acute renal failure. 4. Plasma renin activity and urinary aldosterone were stimulated by the four diuretics in study A, but their response was blunted in study B. Urinary antidiuretic hormone was not modified by diuretics but was suppressed by indomethacin. 5. Diflunisal, a structurally unrelated nonsteroidal anti-inflammatory drug, given to 12 of the subjects provoked similar interactions with frusemide, hydrochlorothiazide and spironolactone. 6. The results suggest that prostaglandins contribute to the natriuretic effects of frusemide and spironolactone, but not to those of hydrochlorothiazide and triamterene.

Adult↗
PubMed1987

Loop-acting diuretics do not bind to Tamm-Horsfall urinary glycoprotein.

1. Binding between the radiolabelled loop-acting diuretics ([14C]frusemide, [14C]ethacrynic acid and [3H]bumetanide) and human Tamm-Horsfall glycoprotein or human serum albumin in vitro was evaluated by equilibrium dialysis. 2. The diuretic action and binding to urinary Tamm-Horsfall glycoprotein of the radiolabelled diuretics in vivo, after intravenous administration, were examined in rabbits. 3. In vitro, all three radiolabelled diuretics bound strongly to human serum albumin, but not to Tamm-Horsfall glycoprotein. 4. Radiolabelled frusemide and bumetanide, but not ethacrynic acid, caused a diuresis in rabbits, but no binding between the drugs and Tamm-Horsfall glycoprotein was seen in vivo. 5. Binding to Tamm-Horsfall glycoprotein does not appear to be an important mechanism in the action of loop diuretics.

Animals↗
PubMed2006

Effects of angiotensin-converting-enzyme inhibitors in combination with diuretics on blood pressure and renal injury in nitric oxide-deficiency-induced hypertension in rats.

The present study investigates the effects of chronic administration of ACEIs (angiotensin-converting-enzyme inhibitors; either zofenopril or enalapril) in combination with a diruetic (hydrochlorothiazide) on BP (blood pressure) increase and renal injury induced by L-NAME (NG-nitro-L-arginine methyl ester), an inhibitor of NO (nitric oxide) synthesis. Rats were untreated or received L-NAME alone, L-NAME+zofenopril+hydrochlorothiazide or L-NAME+enalapril+hydrochlorothiazide for 8 weeks. L-NAME treatment resulted in marked elevation in BP and mortality. Treatment with either ACEI and diuretic prevented the increase in BP induced by L-NAME, reduced the death rate and improved excretory parameters. Renal injury in the L-NAME group was severe, but, in the groups treated with either ACEI and diuretic, glomerular and tubulointerstitial lesions were not observed and the intensity, number and size of vessels affected was reduced. However, the efficacy of zofenopril+diuretic was superior to that of enalapril+diuretic in reducing vascular alterations. Oxidative stress indices and the expression of NO synthase and nitrotyrosine were normalized by the treatments. In conclusion, the combined treatment of zofenopril or enalapril with hydrochlorothiazide completely prevented the development of arterial hypertension induced by L-NAME. Renal morphological and functional alterations in the hypertensive animals were also almost completely normalized, but the treatment with zofenopril+diuretic produced a more complete organ protection. The protective effect is related to an activation of endothelial NO synthase expression and to a normalization of the oxidative stress parameters due to the inhibition of angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Effects of thiazide- and loop-diuretics, alone or in combination, on calcitropic hormones and biochemical bone markers: a randomized controlled study.

OBJECTIVE: Diuretics are commonly used drugs that in addition to their effect on the cardiovascular system also affect calcium homeostasis and bone metabolism. We evaluated the effects of loop diuretics (LD) and thiazide diuretics (TD) on calcitropic hormones and biochemical bone markers. DESIGN: A total of 50 postmenopausal women were randomized to 7 days of treatment with either the TD bendroflumethiazide, the LD bumetanide, bendroflumethiazide plus bumetanide, or placebo. Blood and urine (24 h) were sampled on each day. Statistical inferences were made versus the concomitant changes in the placebo group. RESULTS: Bendroflumethiazide increased the tubular reabsorption of calcium (TRCa) (+0.46 +/- 0.11%, P=0.009), plasma levels of parathyroid hormones (PTH) (+24 +/- 10%, P=0.06), and 1,25(OH)2D (+12 +/- 6%, P=0.03). Bumetanide decreased the TRCa (-0.5 +/- 0.1%, P=0.01) and increased plasma PTH and 1,25(OH)2D levels (+27 +/- 9%, P=0.02 and +36 +/- 12%, P=0.006, respectively). Treatment with either of the drugs did not alter plasma calcium, osteocalcin, bone alkaline phosphatase (bone-ALP) or urinary NTx/creatinine ratio. However, treatment with both drugs caused an increased plasma calcium level (+2.7 +/- 1.0%, P=0.007) and decreased plasma levels of bone-ALP (-21 +/- 3%, P=0.001), osteocalcin (-6 +/- 3%, P=0.03), and urinary NTx/creatinine ratio (-39 +/- 6%, P=0.001). CONCLUSION: Calcium homeostasis and bone metabolism are to a major degree influenced by diuretic treatment. Surprisingly, LD and TD exerted a similar effect on calcitropic hormones despite their opposite effects on the renal calcium excretion. In clinical practice, treatment with diuretics has to be considered as a cause of parathyroid stimulation.

Aged↗
PubMed2000

Interaction of cyclosporine and FK506 with diuretics in transplant patients.

BACKGROUND: The calcineurin inhibitors cyclosporine and FK506 are widely used for immunosuppression in solid organ transplantation. One of the side effects of these agents is renal magnesium wasting. The site of action and molecular mechanism of this effect are not known. We hypothesized that agents such as diuretics that cause renal magnesium wasting through a similar action would not have an additive effect on magnesium deficiency with calcineurin inhibitors. METHODS: The records of 50 heart transplant patients on calcineurin inhibitors were reviewed to determine levels of serum magnesium and required replacement dose of magnesium, diuretic usage, and other laboratory values. RESULTS: Loop diuretics did not change either the magnesium level or magnesium replacement requirements in patients on calcineurin inhibitors. In contrast, the thiazide diuretic resulted in an increase in serum magnesium and a decrease in magnesium replacement. Results were similar when the cyclosporine or FK506 groups were evaluated alone. Patients taking FK506 had lower serum magnesium values and higher requirements for magnesium replacement compared with patients taking cyclosporine. CONCLUSION: We conclude that calcineurin inhibitors and loop diuretics have a similar site of action.

Analysis of Variance↗