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PubMed2005

ATRA therapy restores normal renal function and renal reserve and prevents renal failure.

This article presents clinical data which suggest that the current dosage of losartan 50 to 100 mg/day may not be the optimum in many cases, especially if used as monotherapy in the treatment of proteinuria and we may have to increase to 200 mg/day. However, about 30% of patients cannot take angiotensin-converting enzyme inhibitor (ACEI) because of the side effect of cough. To potentiate the anti-proteinuric effect of losartan, especially for patients who do not adhere to a low salt diet, a 12.5-mg dose of hydro-chlorothiazide may further decrease proteinuria. The main message of this article is that we would have to, in many instances, increase the dose of losartan to a minimum of 100 mg/day or 100 mg twice a day for some patients for optimal therapy. The second message is to monitor the creatinine clearance test (CCT) and to start therapy when CCT is reduced and not wait for serum creatinine to rise to abnormal levels (renal impairment) before starting therapy. The first group involves half a dozen patients with hypertension but no proteinuria. Therapy with losartan is shown to improve the renal function. This data suggest that losartan, apart from its use in reduction of proteinuria, can be used in patients with mild renal impairment without proteinuria to reverse the mild renal impairment and preserve renal function. The second group deals with 3 patients with low creatinine clearance. After a followup period of an average of 3 years, they all developed renal impairment. In another 6 patients, the data suggest that we should perhaps treat patients with low CCT as soon as possible and with dose ranging from 100 to 200 mg/day if necessary, to derive maximum beneficial effect. The third group highlights 5 patients with high CCT due to glomerular hyperfiltration. With time, the high CCT decreases and renal impairment sets in. The data suggest that patients with high CCT should be treated early to prevent renal impairment. The fourth group illustrates 6 patients where their proteinuria was markedly reduced with the increase of losartan from 100 mg/day to 200 mg/day, suggesting that losartan 200 mg/day is probably the optimum dose. In conclusion, apart from its traditional usage in reduction of proteinuria to retard progression to renal failure, the data suggest that losartan is also indicated in patients with renal impairment in the absence of proteinuria; patients with low CCT, patients with high CCT and patients who do not respond to a dosage of 100 mg/day should have the dosage increased to 100 mg twice daily to increase efficacy of losartan. It is hoped that with these new and earlier indications as well as increased dosage of losartan starting with 100 mg, whenever possible, and increasing to 200 mg/day, if there is no response, we can prevent more patients from developing renal failure. Based on these observations, further randomised controlled trials should be designed to address these issues.

Adult↗
PubMed1979

Cutaneous reaction to spironolactone resembling lupus erythematosus.

A cirrhotic male patient was admitted with a skin eruption. He had been taking spironolactone and hydrochlorothiazide for two months prior to admission. The morphology and distribution of skin lesions resembled that of systemic lupus erythematosus (SLE). Histologic changes in the skin biopsy specimen were consistent with SLE. Biopsy specimens of normal and affected skin were reported to show weak focal deposition of IgM and complement at the dermal-epidermal junction. However, there was a striking absence of serologic evidence of SLE. The rash disappeared when all medications were discontinued and reappeared when the patient was given spironolactone. The character and distribution of the rash after spironolactone administration was identical to the previous lesions. It disappeared again when spironolactone was withdrawn. This response to spironolactone is good evidence that it and not chlorothiazide was responsible for the rash. The latter drug has been reported to cause SLE-like skin changes.

Diagnosis, Differential↗
PubMed2005

Hydrochlorothiazide-induced acute non-cardiogenic pulmonary edema.

We report the case of a 64 year-old male with non cardiogenic pulmonary edema episodes after oral administration of 12.5 mg of hydrochlorothiazide. In vitro immunologic study with basophil activation test and late cellular activation study (CD69 and production of interferon gamma) with chlorothiazide were performed, and no activation was observed. As a consequence, like in previous cases published, the pathogenic mechanism remains unknown, and it probably is an idiosyncratic reaction.

Antihypertensive Agents↗
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↗
PubMed1991

Effects of different antihypertensive drug classes on survival in animal models.

Data on the influence of antihypertensive drug treatment on mortality of hypertensive rats are reviewed. Dihydropyridine calcium antagonists, verapamil, the angiotensin-converting enzyme (ACE) inhibitor captopril, and a triple combination of reserpine, hydralazine, and chlorothiazide normalized or markedly prolonged survival. Captopril was less effective in sodium chloride-induced, low-renin Dahl rat hypertension. Dihydralazine prolonged but did not nearly normalize survival. The K(+)-channel activator minoxidil was relatively ineffective. Data on diuretics or beta-blockers are insufficient or unavailable. Calcium antagonists nitrendipine and nimodipine and the ACE inhibitor captopril improved survival and prevented vascular lesions and calcinosis even at doses that failed to achieve normotension. All drugs that normalized survival also reduced heart weights. Minoxidil invariably increased heart weights and failed to improve survival. (Di)hydralazine assumed an intermediate position.

Animals↗
PubMed1991

Diuretics, hypochloremia, and outcome in bronchopulmonary dysplasia patients.

We evaluated retrospectively the outcome of patients with severe bronchopulmonary dysplasia who required hospitalization (greater than 90 days) to determine the role of diuretics aminophylline and chloride deficiency in the fatal outcome of these patients. Total cumulative amounts of furosemide, chlorothiazide, spironolactone accrued during hospitalization (dosage per patient per day), and a diuretic index (logarithm of the sum of the cumulative dosage of the three diuretics) were calculated for each patient. Other predetermined variables included in the analysis were birth weight, gestational age, duration of mechanical ventilation, duration of oxygen therapy, caloric intake, fluid and electrolyte intake, echocardiographic data, and duration and type of acid base balance disturbances. No differences were found between survivors and nonsurvivors in diuretic and aminophylline use. Hypochloremia did not discriminate between the groups. Duration of mechanical ventilation, the ratio between days with serum bicarbonate concentration greater than 30 mEq/l and total days of hospitalization, and the difference between head circumference at discharge or death and birth head circumferences were the most important factors which contribute to the difference between survivors and non survivors.

Acid-Base Imbalance↗
PubMed1986

Unexpected hearing loss in high-risk infants.

Eleven high-risk infants who had normal auditory brainstem responses at the time of discharge from the neonatal intensive care unit were found on follow-up between 13 and 48 months later to have significant sensorineural hearing loss. All 11 infants were the products of high-risk pregnancies and deliveries. Birth weights ranged from 890 to 3,700 g, but seven had birth weights of more than 1,500 g. Gestational ages ranged from 28 to 42 weeks. The length of hospitalization ranged from 45 to 167 days. All of the infants had respiratory distress, requiring prolonged mechanical ventilation with resultant chronic lung disease. All of the infants had received pancuronium, morphine, ampicillin, and gentamicin, and ten had also received furosemide and chlorothiazide. Other frequent clinical complications included abnormal CNS findings during the neonatal intensive care unit stay (ten infants), acidosis (pH less than 7.25) on the initial blood gas test (eight infants), and persistent fetal circulation in all seven infants with birth weights greater than 1,500 g. Developmentally, eight of nine children tested between 12 and 36 months of age were normal in all respects other than the hearing loss and the related language impairment. We conclude that infants who have been very ill in the newborn period, including term infants, may remain at risk for development of significant sensorineural hearing loss even though they have passed an initial auditory brainstem responses screening test in the newborn period.

Audiometry↗
PubMed1988

Initial observations of rabbit retinal pigment epithelium-choroid-sclera preparations.

Retinal pigment epithelium (RPE)-choroid-sclera preparations from black dutch-belted rabbits were sealed in an Ussing chamber maintained at 37-39 degrees C. Typical preparations produced a spontaneous voltage (Ve) of 12.5 mV (retina side positive) and possessed an electrical resistance (R) of 350 ohm-cm2. Both of these values can be attributed to the RPE. Ouabain and amiloride diminished the Ve without affecting R. Ouabain was effective when applied to the apical but not to the basolateral side of the preparation, suggesting the presence of a Na-K ATPase on rabbit RPE apical membrane similar to that found in bullfrogs, embryonic chickens, cats and dogs. Dinitrophenol also reduced Ve. Digoxin, furosemide, bumetanide, ethacrynic acid and chlorothiazide had no apparent effect upon Ve and R. The lack of response to furosemide, bumetanide and ethacrynic acid strongly suggests that, unlike RPE from other species, rabbit RPE does not possess Na-dependent Cl transport and/or does not possess furosemide receptors on its apical membrane.

Amiloride↗
PubMed1989

Furosemide directly stimulates prostaglandin E2 production in the thick ascending limb of Henle's loop.

Studies were conducted to investigate direct effects of loop diuretics on prostaglandin E2 (PGE2) production using microdissected nephron segments. At first, the effect of indomethacin on the diuretic response to furosemide was re-evaluated in anesthetized rats. Indomethacin significantly attenuated the diuretic, natriuretic and chloruretic effects of furosemide without significantly affecting inulin and p-aminohippurate clearance or filtration fraction. But, in nondiuretic states, indomethacin had no significant effects on these parameters. Furosemide, ethacrynic acid and bumetanide significantly increased PGE2 production in cortical and medullary thick ascending limbs of Henle's loop (P less than .001), but not PGE2 production in the cortical and outer medullary collecting tubules. The effect of furosemide on PGE2 production in CTAL was dose-dependent, and higher concentrations of of furosemide than 10(-6) M significantly increased PGE2 production. On the other hand, chlorothiazide showed no PGE2 productive stimulation in these four nephron segments. This study demonstrates that the enhanced PGE2 production in the thick ascending limb of Henle's loop by furosemide and other loop diuretics is one possible mechanism of these drugs.

Animals↗
PubMed1988

[Natural history of arterial hypertension due to primary hyperreninism].

This case report deals with an eight-year duration severe high renin hypertension and its consequences. In 1975, a 13 years old girl was found to have blood pressure (BP) levels of 240/150 mmHg with bilateral papilloedema. Hypokalemic alkalosis, a 45 mm Sokolow index (SI) and very high peripheral renin activity (PRA) were also noticed. Renal vein renin sampling (RVRS) suggested secretion from the left kidney but intravenous pyelography and renal arteriography were normal. BP levels were first controlled by triple treatment but rose one year later, despite adjunction of beta-blockers. High PRA was again found, but without hormonal gradient on a second RVRS. From 1977 to 1982, BP never fell to normal levels despite quadruple treatment. In 1982, a stage II optic fundus, a 58 mm SI and 2 g/day proteinuria are noticed, so that a new complete etiologic work up is undertaken in 1983: PRA is still high, with a dramatic acute BP fall after captopril and no gradient on a third RVRS, but intravenous pyelography, tomodensitometry and selective arteriography disclose a 4 cm diameter poorly vascularized tumour on the surface of the lower pole of the right kidney. BP levels are controlled for three months by captopril + chlorothiazide. The tumour is removed in january 1984. RVRS by direct peroperative punction indicates (a posteriori) hormonal secretion from the right kidney lower pole. Histologic examination and immunofluorescence with antirenin serum corroborate the juxtaglomerular origin of the tumour. Eighteen months later, BP is permanently normal, SI is 30 mm, and there is no proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Diuretic-induced CNS magnesium alteration and digoxin intoxication.

Male Wistar rats were injected intraperitoneally for 3 consecutive days with hydrochlorothiazide (HCTZ; 15 mg/kg), chlorothiazide (CTZ; 100 mg/kg), bendroflumethiazide (BFTZ; 1.5 mg/kg), chlorthalidone (CHLOR; 15 mg/kg), methyclothiazide (METH; 1.0 mg/kg) or metolazone (MET; 1.5 mg/kg). Magnesium content was measured in the hypothalamus, medulla oblongata, cerebral cortex, heart, skeletal muscle and serum. Although there was no consistent alteration of Mg in the serum, skeletal muscle and heart, there was a significant effect on hypothalamic and medullary Mg. Compared to a control value of 17.20 +/- 1.24 mEg/kg in the hypothamus there was a decrease by HCTZ (26%; p less than 0.01), CTZ (24%; p less than 0.01) and BFTZ (30%; p less than 0.01). Similarly, there was a decrease by HCTZ (22%; p less than 0.01), CTZ (30%; p less than 0.01) and BFTZ (25%; p less than 0.01) on Mg in medulla. In contrast MET increases Mg in hypothalamus (31%; p less than 0.01) and medulla (26%; p less than 0.01). Furthermore, digoxin infusion (0.051 ml/min) in animals pretreated with HCTZ induced arrhythmias earlier than in animals receiving digoxin alone (30 vs. 60 min; p less than 0.01). The effects of digoxin toxicity in HCTZ-pretreated animals were partially reversed by CNS administration of 50 micrograms of Mg. These findings strongly suggest that thiazide-induced depletion of Mg in the CNS predisposes to digoxin intoxication.

Animals↗
PubMed1987

Drug inhibition of penicillin tubular secretion: concordance between in vitro and clinical findings.

Using the rabbit kidney slice model of active tubular secretion, I studied the active accumulation of penicillin (PEN) in the absence and presence of competing drugs to evaluate the feasibility of using in vitro uptake to predict in vivo secretion. Active accumulation of PEN by these slices was saturable at high PEN concentrations and was inhibited by incubation conditions which decreased ATP production. PEN uptake in the presence of 1 mM concentrations of mannitol, tolazoline and tetraethylammonium was unchanged. However, PEN uptake in the presence of eight weak organic acid drugs (probenecid, phenylbutazone, sulfinpyrazone, salicylate, sulfamethizole, chlorothiazide, sulfamethoxypyridazine and indomethacin) was inhibited significantly. This inhibition appeared to be competitive in nature and the inhibitor-transport carrier protein dissociation constant (Ki) for each inhibitory drug was calculated (range, 0.38-74.8 X 10(-5) M). When these values for Ki obtained with PEN were compared to values obtained with methotrexate and p- aminohippurate, the values of Ki were similar, implying the presence of a similar transport carrier protein for PEN, methotrexate and p-aminohippurate. The effects of these eight drugs upon PEN clearance in vivo were extrapolated from the medical literature. The relative inhibitory strengths of these drugs based upon in vitro findings (drug plasma concentration/Ki ratios) and clinical findings (inhibition of PEN clearance) were concordant. This in vitro model for assessing inhibition of renal tubular secretion may be of general utility in predicting clinically important drug interactions between weak organic acid drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

2,4-Dinitrophenol↗
PubMed1985

Single-dose pharmacokinetics of fenquizone in healthy volunteers.

A pharmacokinetic study of fenquizone (Idrolone), a thiazide-like diuretic, was conducted with single oral doses in 6 healthy volunteers. The substance thus administered was readily absorbed from the gut, with peak plasma levels being detected on average at 3 h after dosing; after that, plasma concentrations of fenquizone decreased biexponentially in a pattern fitting an open two-compartment model. Plasma half-life values were 1 h for phase alpha and 17 h for phase beta. The half-life calculated from urinary concentrations was 18 h. The apparent distribution volume for phase beta was 686 l; renal clearance was 220 ml/min, and the absorption constant (Ka) was 1055 h-1. Cumulative urinary excretion accounted for 53.1% of the administered dose in 72 h. Thus the pharmacokinetic profile of fenquizone was that of an "intermediate-acting" diuretic about half-way between the short-acting hydrochlorothiazide, chlorothiazide and furosemide and the long-acting chlorthalidone. In summation, fenquizone is described as a low-dosage diuretic apparently not conducive to accumulation; its pharmacokinetic profile qualifies the product particularly well for maintenance therapy, such as is needed for the management of essential hypertension, both as sole medication and in fixed-ratio combination with beta-blockers, and at any rate with once-a-day administration.

Adult↗
PubMed1982

Calcium-dependent stimulation of renal medullary prostaglandin synthesis by furosemide.

The present study examined the actions of furosemide and other "loop" diuretics on immunoreactive prostaglandin E (iPGE) and [14C]arachidonate (AA) release in vitro in incubates of slices from rat and dog outer or inner medulla. The loop diuretics furosemide, ethacrynic acid, bumetanide and 3-benzylamino-4-phenylthio-5-sulfamoylbenzoic acid all significantly increased [14C]AA and iPGE release (1.5- to 4-fold) into the media of rat outer and inner medulla and dog outer medullary slice incubates. By contrast, equimolar concentrations of chlorothiazide and hydrochlorothiazide were without effects on these parameters. Stimulation of [14C]AA or iPGE by furosemide was abolished by exclusion of Ca++ from the incubation media or by addition of verapamil to complete media, but was not altered by exclusion of Na+. Ca++-free media or verapamil also abolished the increases in [14C]AA and iPGE induced by ionophore A23187. By contrast, these incubation conditions did not influence the iPGE responses to hypertonic mannitol or exogenous AA. The presence of Ca++-responsive acyl hydrolase activity was demonstrated in the microsomal fraction from rat outer medulla. However, this activity was not altered by addition of furosemide to the subcellular fraction in the presence or absence of Ca++. Thus, furosemide and other loop diuretics stimulate renal medullary iPGE synthesis in vitro, and may do so through Ca++-mediated or dependent enhancement of the release of AA.

Amidohydrolases↗
PubMed1983

Effect of antihypertensive therapy on the vascular changes of spontaneously hypertensive rats.

The effect of antihypertensive therapy on vascular morphologic characteristics was studied in spontaneously hypertensive rats (SHRs). Starting at either 7 or 22 weeks of age, SHRs were given a combination of hydralazine, chlorothiazide, and reserpine, which reduced the blood pressure significantly below the level of untreated animals. Rats were sacrificed at either the 22nd or the 42nd week of age along with age-matched untreated SHRs and normotensive Wistar-Kyoto controls. The following treatment groups were thus obtained: a) treated from the 7th to the 22nd or 42nd week, b) treated from the 22nd to the 42nd week, and c) treated from the 7th to the 22nd and left untreated until the 42nd week. Ultrastructural and morphometric studies were carried out on the aorta and intrarenal vessels. The expansion of the subendothelial space and medial thickening in the aorta as well as the increase in external to luminal diameter ratios and wall thickness of intrarenal vessels were prevented in SHRs treated continuously from the 7th week on. The severity of vascular lesions was markedly reduced in animals treated from the 22nd to 42nd week. Discontinuation of therapy resulted in rapid reestablishment and progression of both aortic and renal vascular disease to a degree identical to that of untreated SHRs. The results indicate that hypertensive vascular changes are preventable by early treatment and, depending on their nature, can be arrested or reversed by delayed treatment.

Animals↗
PubMed1982

Renal calcifications: a complication of long-term furosemide therapy in preterm infants.

During the last four years ten premature infants developed renal calcifications while receiving long-term furosemide therapy. The drug was used in infants with present ductus arteriosus and later in the same infants with chronic lung disease. They had received furosemide in a dose of at least 2 mg/kg/day for at least 12 days before calcifications were noted on abdominal roentgenograms. Calcifications included small flecks, isolated stones, staghorn calculi, and nephrocalcinosis. Analysis of stones received from our infants showed calcium oxalate and calcium phosphate. Infants who were not receiving furosemide had no calcifications. The infants with renal calcifications had rates of calcium excretion ten to 20 times that of normal, age-matched premature infants in our nursery. When chlorothiazide was given to the infants, in addition to furosemide, a four- to 15-fold decrease in calcium excretion and a radiologic dissolution of the renal calcifications were documented. It is concluded that furosemide, in doses of at least 2 mg/kg/day for at least 12 days can be associated with renal calcifications. The probable mechanism of the stone formation is hypercalciuria, primarily caused by furosemide.

Ductus Arteriosus, Patent↗
PubMed1982

Diuretics and zinc.

Distal tubule diuretics (DTDs), including chlorothiazide, hydrochlorothiazide, bendroflumethiazide, chlorthalidone and xipamide, have been found to increase urinary zinc output through a poorly understood mechanism which could involve both direct and hormone-mediated processes. Significant zinc depletion may occur during long-term administration of DTDs, principally in conditions associated with diminished total body zinc levels such as hepatic cirrhosis, diabetes mellitus, gastro-intestinal disorders and several renal diseases. Attention to the early symptoms of zinc deficiency such as hypogeusia, hyposmia, abnormal dark adaptation and impotence and the monitoring of serum zinc levels are advisable during long-term treatment with common DTDs.

Adult↗
PubMed1982

Effects of different diuretics on tetracycline-induced hyperuraemia and hypercreatininaemia in the rat.

Tetracycline injection (45 mg/kg, i.v.) produced increases in plasma urea and creatinine levels in rats. The greatest increases occurred after 24 hr for urea and after 6 hr for creatinine, the latter effect persisted for at least 30 hr. The actions of six diuretics (acetazolamide, bumetanide, chlorothiazide, chlorthalidone, triamterene and indapamide) given orally either as pretreatment (1 hr before tetracycline injection) or post-treatment (4 hr after tetracycline injection) were examined. When given as pretreatments, all six diuretics reduced the hyperuraemia, and generally the hypercreatininaemia, that existed 24 hr after tetracycline injection. In contrast, when given as post-treatments, only bumetanide reduced the increase in urea and creatinine levels. It is postulated that this protective action of diuretics could occur by their displacement of tetracycline molecules from protein binding sites or by a-direct action on renal function.

Animals↗