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PubMed2004

The role of diuretic renography in the evaluation of obstructed hydronephrosis after pediatric pyeloplasty.

BACKGROUND: The purpose of this study was to clarify the value of renal drainage half-time in the evaluation of pediatric hydronephrosis after dismembered pyeloplasty. METHODS: We reviewed the records of 30 children who underwent dismembered pyeloplasty for unilateral ureteropelvic junction obstruction with no other associated urological abnormality. The follow-up duration was more than 5 years for all patients. Pre- and postoperative evaluation included technetium-99m dimercaptosuccinic acid (99mTc-DMSA) renal scan, technetium-99m diethylenetriaminepentaacetic acid (99mTc-DTPA) diuretic renography, and ultrasonographic examination. According to postoperative renal drainage half-time on diuretic renography, patients were divided into 2 groups: group A with normal renal drainage and group B with prolonged renal drainage for evaluation of their renal functional status. RESULTS: Postoperative diuretic renography revealed normal drainage (group A) in 54% of patients and prolonged drainage (group B) in 46%. The anteroposterior diameter (APD) of the renal pelvis of all patients showed improvement after pyeloplasty. There was no significant difference in improvement of the renal pelvic APD between the 2 groups. Furthermore, 92% of group A and 91% of group B maintained stable or had improved differential renal function (DRF) postoperatively. CONCLUSIONS: Drainage half-time is not a reliable parameter for diagnosing obstructed hydronephrosis after pediatric pyeloplasty. We suggest that the renal pelvic APD and DRF should be considered when postoperative obstructed hydronephrosis is diagnosed using the criterion of prolonged renal drainage half-time on diuretic renography.

Female↗
PubMed1992

Renal functional response to captopril during diuretic therapy.

Antihypertensive agents may modify the renal effects of angiotensin converting enzyme inhibition (ACEI). This potential interaction, which is important in the diagnosis of renovascular hypertension was studied in two rat models with and without diuretic treatment prior to ACEI. Acute intravenous administration of furosemide or hydrochlorothiazide in one-kidney, one-clamp animals (1K1C) did not change glomerular filtration rate (GFR) or effective renal plasma flow (ERPF). ACEI administration after furosemide and hydrochlorothiazide decreased GFR (p less than 0.001, p less than 0.01) but not ERPF. Chlorothiazide administered to 1K1C prior to ACEI, decreased GFR (p less than 0.02) but not ERPF captopril administration to 1K1C which received hydrochlorothiazide intraperitoneally for 7-10 days decreased GFR (p less than 0.007) and ERPF (p less than 0.02), while two-kidney, one-clamp animals (2K1C) decreased GFR only in the clamped kidney (p less than 0.005). ERPF in 2K1C increased only in the contralateral kidney (p less than 0.01). Without diuretic 1K1C animals decreased GFR and ERPF after ACEI (p less than 0.005, P less than 0.001). In the clamped kidney of 2K1C rats, GFR and ERPF decreased significantly (p less than 0.0005, p less than 0.004) and contralateral kidney ERPF increased (p less than 0.001), but GFR did not. The consequences of ACEI on GFR are similar with or without diuretic. These data suggest that diuretic therapy may not significantly interfere with ACEI evaluation of renovascular hypertension.

Animals↗
PubMed1990

Efficacy and tolerance of sustained-release diltiazem 300 mg and a diuretic in the elderly.

A randomized, double-blind, parallel study has been performed to compare the antihypertensive action and clinical and biological tolerance of monotherapy with two different substances: sustained-release diltiazem 300 mg and a diuretic combining 25 mg of hydrochlorothiazide and 50 mg of triamterene (HCT-T). Antihypertensive treatment was suspended at least 15 days before initiation of a placebo period that lasted 14 days and allowed confirmation of persisting hypertension. Eighty-five patients who were at least 65 years old were included in the study: 42 in the group treated with sustained-release diltiazem 300 mg and 43 in the group treated with a diuretic. All of them presented with mild to moderate arterial hypertension, characterized by supine diastolic blood pressures (supine DBP) of 95-115 mm Hg. Duration of treatment was 3 months. After 1 and 3 months, efficacy and tolerance of the antihypertensive treatment were evaluated. On day 30, a significant decrease (p less than 0.0001) in the main parameter, i.e., supine DBP, as well as other parameters such as standing diastolic blood pressure (standing DBP), supine systolic blood pressure (supine SBP), and standing systolic blood pressure (standing SBP) was observed. Blood pressure was reduced by 18, 16, 28, and 26 mm Hg, respectively, in the sustained-release diltiazem 300 mg group and by 13, 12, 21, and 18 mm Hg, respectively, in the diuretic group. Moreover, on day 90, blood pressure values were maintained in the diuretic-treated group, whereas an additional significant reduction in supine DBP (p less than 0.002) was noted in the sustained-release diltiazem 300 mg-treated group (-4.8 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Diuretic renography in children: a non-invasive method for the assessment of upper urinary tract pathologies.

Thirty-eight kidneys from 20 children were studied with diuretic renography and the findings in 32 kidneys were compared with the results obtained using IVP. The diuretic renography findings were consistent with those of the IVP in 72 percent of the patients. The main disparity was the dilated nonobstructed pattern observed in the kidneys with normal IVP's, which is pointed out as being an asset of diuretic renography in revealing the functional status of kidneys. The sensitivity in detecting true obstruction was found to be 67 percent (4/6), and the specificity 95 percent (20/21). The accuracy of the technique was 85 percent with a false (+) rate of 5 percent (1/21) and false (-) rate of 33 percent (2/6). Diuretic renography is a simple, safe, non-invasive technique, easily applied to children with high specificity in excluding obstruction in a dilated renal pelvis.

Child↗
PubMed1991

Renal dopamine not renal nerve mediates diuretic and natriuretic effect of ANF in rats.

Our previous study demonstrated that acutely or chronically unilateral renal denervation did not blunt intravenous ANF--induced hypotensive and ipsilateral renal effects. The present study was further to examine the permissive role of renal nerve and dopamine in the renal action of ANF. Experiments were conducted on anesthetized rats with either acute unilateral ureter ligation (n = 8), reserpine pretreatment (10 mg/kg, n = 7), mechanically controlled renal arterial pressure (n = 8) or blockade of dopamine D1 receptors by SCH23390 (n = 8, 0.8 micrograms/kg.min). The arterial blood pressure and renal clearance responses to intravenous (0.30-0.45 micrograms/kg.min) or intrarenal (0.10-0.15 micrograms/kg.min) infusion of ANF were measured. The results showed that unilateral ligation of the ureter to physiologically inhibit the contralateral renal efferent nerve activity did not alter the depressor, diuretic and natriuretic effects of ANF. Reserpine pretreatment blunted the diuretic and natriuretic response to intravenous administration of ANF. However, ANF-induced diuresis and natriuresis was persistently observed in both kidneys of rats with the left renal arterial pressure being controlled at a level comparable to that seen in the reserpine-pretreated group. Blockade of intrarenal dopamine D1 receptors by SCH23390 completely abolished the diuretic and natriuretic response to intrarenal infusion of ANF. These results support the notion that the diuretic and natriuretic effect of ANF is not resulted from a decrease in renal sympathetic efferent nerve activity, and further indicate that a mechanism associated with activation of the renal dopamine D1 receptors mediates the renal effect of ANF in rats.

Animals↗
PubMed1991

Cellular mechanism of stimulation of renin secretion by the mercurial diuretic mersalyl.

The aim of the present study was to elucidate the cellular mechanism by which the mercurial diuretic mersalyl stimulates renin secretion in rabbit renal cortical slices in vitro. The stimulatory effect of mersalyl on renin secretion was rapid, reversible and concentration dependent. The stimulation was not dependent on the presence of ions such as Na+, Cl- and Ca++, and it was unaffected by inhibitors of Na+/K+/2Cl- cotransport, such as bumetanide and furosemide. However, the stimulation was blocked and reversed by thiols, such as L-cysteine and dithiothreitol. Furthermore, the maximal stimulatory effect of mersalyl on renin secretion was not additive to that produced by the non-diuretic mercurial sulfhydryl reagent P-chloromercuriphenylsulfonate nor to that produced by the non-mercurial diuretic sulfhydryl reagent, ethacrynic acid. These results support the hypothesis that mersalyl stimulates renin secretion by forming a reversible mercaptide bond with sulfhydryl groups, located perhaps on the plasma membrane of juxtaglomerular cells. These particular sulfhydryl groups appear to have no functional role in the diuretic action of mersalyl.

4-Chloromercuribenzenesulfonate↗
PubMed1991

Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver.

Thirty four patients with peritoneoscopy and/or biopsy proven uncomplicated cirrhosis of liver with ascites were studied for the effect of diuretic therapy on ascitic fluid protein and cell count. Renal function tests, liver function tests, ascitic fluid protein concentration and cell count were estimated prior to diuretic therapy and once every week till the end of therapy. There was no change in mean total serum protein (5.71 +/- 0.58 g/dl to 5.72 +/- 0.63 g/dl). The rise in mean ascitic fluid protein from 1.55 +/- 0.77 g/dl to 1.76 +/- 0.79 g/dl was not significant (P greater than 0.05). Twenty one patients (Group I) showed a rise in ascitic fluid protein concentration while 13 patients (Group II) did not show a rise or showed a fall in protein concentration during diuretic therapy. The rise in ascitic fluid protein concentration in Group I from 1.62 +/- 0.69 g/dl to 2.05 +/- 0.67 g/dl was statistically significant (P less than 0.05). Group I patients had a mean weight loss of 6.21 +/- 3.66 kg as compared to 3.15 +/- 2.00 kg in Group II patients (p less than 0.05). There was no other difference between Group I and Group II patients. Only 5 patients showed a rise in ascitic fluid cell count (more than 50 cell/mm3). It is concluded that diuretic therapy alters ascitic fluid protein concentration in a majority of patients but has no significant effect on cell count.

Adolescent↗
PubMed1990

[Metabolic and acid-base changes in intensive diuretic therapy in heart failure].

A group of 65 patients with advanced heart failure was examined with the aim to disclose changes in serum glucose, creatinine, potassium, chloride, and acid-base balance under the influence of intensive diuretic therapy. 50 patients were treated with ordinary furosemide and amiloride combination (average observation time 25 days), in 15 cases amiloride was replaced by captopril 75-150 mg/day (average observation 15.5 days). The results are as follows: 1. We found no rise of glycaemia in non-diabetics with either ordinary diuretic therapy or captopril. On the contrary: stress hyperglycaemia in the beginning of the therapy normalized in the course of it. 2. There was a significant rise of serum creatinine during the first two weeks of therapy with furosemide and amiloride. Reversal of this trend followed after captopril. 3. There was no fall in the average serum chloride concentration during ordinary diuretic therapy. Adding captopril to the regime brought about a rise in serum chloride. 4. Serum potassium had no tendency to fall either after furosemide and amiloride or furosemide and captopril. 5. The acid-base balance showed no shift towards metabolic alkalosis during an intensive but rational diuretic regime either with or without captopril. On the contrary: mild initial metabolic alkalosis had a tendency to normalize with proceeding cardiac compensation.

Acid-Base Equilibrium↗
PubMed1990

Intratubular albumin blunts the response to furosemide-A mechanism for diuretic resistance in the nephrotic syndrome.

An attenuated response to loop diuretics is a frequent observation in the nephrotic syndrome. To determine if the presence of albumin in renal tubular fluid attenuates diuretic response in normal rats, in vivo loop segment microperfusion was performed in normal rats at 20 nl/min with perfusates containing 6.0 microM furosemide in the presence and absence of 3.8 microM albumin. Compared to loop segments perfused without diuretic (control), furosemide reduced (P less than .001) fractional chloride uptake from 56 +/- 2 to 34 +/- 2%. After addition of albumin to furosemide perfusate, fractional loop chloride reabsorption was 45 +/- 1%; a value greater (P less than .01) than that observed in furosemide perfused loop segments, but less (P less than .05) than that observed in control loop segments. Albumin added to perfusate in the absence of furosemide had no effect on fractional loop segment chloride uptake. Addition of 1.7 microM immunoglobulin G to furosemide perfusate failed to attenuate furosemide response. Absolute loop segment chloride reabsorption demonstrated a similar pattern. Tubule fluid perfusion rates determined in vivo and loop segment fluid reabsorption were equivalent in all groups. Thus, albumin in renal tubule fluid attenuates the effect of furosemide on loop segment chloride reabsorption in the rat. This blunted response presumably occurs because of a reduction in the amount of pharmacologically active drug due to albumin-furosemide binding. Consequently, albumin-furosemide binding in the renal tubule may contribute to the diuretic resistance in nephrotic syndrome.

Absorption↗
PubMedDate not supplied

[Comparison of the efficacy of monotherapy with a beta-blocker, a diuretic, and ACE inhibitors in the control of blood pressure during stress].

In order to compare the efficacy of beta-blocking, diuretics and ACE-inhibiting monotherapy in controlling the blood pressure increase to stress, a study was conducted on 30 subjects (10 treated with atenolol, 10 with hydrochlorothiazide/amiloride combination, 10 with enalapril) with mild or moderate essential hypertension whose resting blood pressures were normalised by therapy. In the 3 groups of subjects blood pressure values at rest, during mental stress, static and dynamic exercise did not significantly differ before antihypertensive therapy. Atenolol and enalapril significantly reduced systolic and diastolic pressure below pretreatment values throughout and immediately after each test, differing from diuretic therapy which did not show any significant reduction in diastolic rises at the peak of hand-grip or in both systolic and diastolic pressures at the highest work-loads during dynamic exercise. In the recovery period of the exercise cycle test diuretics also produced a later normalisation of diastolic pressure. In conclusion, beta-blockers and ACE-inhibitors seem to be more effective than diuretics in the control of the blood pressure response to stress in hypertensive patients, suggesting that these drugs are the first choice treatment of mild to moderate hypertension.

Adult↗
PubMed1989

[Idiopathic and diuretic-induced edema].

In female patients with intermitting or permanent inclination to oedemas and intake of diuretics after exclusion of cardiac, renal, venous and lymphogenic causes should be thought of the clinical picture of the idiopathic and diuretic-induced oedema, respectively. Pathophysiologically, the two forms underlie an activation of the renin-angiotensin-aldosterone system with subsequent retention of water and common salt. In these cases the intake of diuretics is not indicated and may lead to the chronification of the oedemas. Therefore the physician is confronted with the responsible task to finish the permanent intake of diuretics by adequate explanation of the pathophysiological and pharmacological connections and to care for the frequently neurotic female patients in this difficult time. For a short time a treatment with aldosterone antagonists can be recommended and first therapeutic experiments with the application of ACE-inhibitors were successful. A special diet poor in common salt is not necessary and in the individual case a psychotherapeutic treatment of the female patients should be carried out.

Adult↗
PubMed1987

Kalemia during combined therapy with an angiotensin converting enzyme inhibitor and a potassium-sparing diuretic.

Both angiotensin converting enzyme (ACE) inhibitors and potassium-sparing diuretics tend to increase serum potassium levels. This retrospective study was undertaken to assess whether these two types of agents can nevertheless be combined safely. Twelve hypertensive patients were treated for 1-70 months (mean = 17) with an ACE inhibitor together with a potassium-sparing diuretic (spironolactone, n = 10; amiloride, n = 2). In addition, eight patients also took a thiazide or a loop diuretic. Nine patients had a normal and three a slightly impaired renal function. No clinically relevant hyperkalemia was observed during the course of the study. These data suggest that it is not impossible to combine an ACE inhibitor with a potassium-sparing diuretic, as long as renal function is normal and serum potassium concentration is monitored closely.

Adult↗
PubMed1986

Effect of nifedipine in hypertension not controlled by converting enzyme inhibitor and diuretic.

Nifedipine, in a slow release preparation, was given at a mean daily dosage of 47 +/- 4 mg to 12 patients with severe hypertension in whom arterial pressure was not satisfactorily controlled (mean blood pressure, 172 +/- 6/111 +/- 4 mmHg) by the association of a converting enzyme inhibitor and a diuretic. Nifedipine administration induced a marked decrease in blood pressure (to 133 +/- 3/85 +/- 3 mmHg), serum potassium and plasma aldosterone. Following adequate control of hypertension and because of severe hypokalaemia in some patients, the diuretic was discontinued in 10 subjects. After 1.7 +/- 0.5 months of treatment by the converting enzyme inhibitor and nifedipine, no change in arterial pressure occurred whilst serum potassium returned to normal in most patients. These results demonstrate that nifedipine may be useful in patients with residual elevation of arterial pressure when treated by converting enzyme inhibitor and diuretic. However, in such patients serum potassium level should be carefully monitored. In addition, our observations suggest that calcium blockers may be an effective alternative to diuretics in patients receiving a converting enzyme inhibitor.

Adult↗
PubMed1987

Diuretic-induced growth failure in rats and its reversal by sodium repletion.

The aim of diuretic therapy is the prevention of excessive sodium accumulation. However, sodium retention is necessary for growth. Inasmuch as many of the clinical conditions for which diuretics are used are associated with growth retardation, we investigated the influence of diuretic therapy on growth in an animal model. In Part I, 32 weanling Sprague-Dawley rats were fed a diet adequate for growth which contained 0.08% sodium and 0.17% potassium. Daily i.p. injections of saline (0.4 ml) containing furosemide in doses of 0, 50, 100 or 200 mg/M2 were given for 9 days. There was a dose-related reduction in weight gain which could not be explained by lower food intake. The highest dose group gained only 58% as much as the control group. Balance studies and muscle, bone and carcass analysis demonstrated that this was accounted for by decreases in protoplasmic, bone, fat and extracellular fluid volume accretion. In Part II, 32 weanling rats, all treated daily with furosemide (100 mg/M2 i.p.) received replacement of NaCl, KCl, both or neither in their drinking water. Sodium replacement resulted in increased growth rates whereas potassium replacement alone had no effect on growth. Sodium replacement also increased the balance of all measured minerals. We conclude that diuretic therapy causes growth retardation by preventing retention of sodium needed for growth.

Animals↗
PubMed1986

Does a diuretic cause a further fall in blood pressure in hypertensive patients already on nifedipine?

The effect of the addition of a diuretic, bendrofluazide, for 1 month was studied in 12 hypertensive patients who were already on treatment with nifedipine tablets (20 mg b.i.d.) When nifedipine was maximally effective, that is, at 2 hours after the last dose, the diuretic had no further blood-pressure-lowering effect. These results suggest that unlike most other blood-pressure-lowering agents, there is little point in giving a diuretic to patients who are already on nifedipine, and if blood pressure is not controlled on nifedipine alone, it may be more effective to add either a beta blocker or a converting enzyme inhibitor. This has the advantage of avoiding the metabolic problems of diuretics.

Adult↗
PubMed1975

[Mechanism of the natriuretic and diuretic action of neurohypophyseal hormones].

Administration to rats against the background of spontaneous urine excretion of pituitrine, vaso pressin and oxytocine caused a diuretic and natriuretic effect on account of the reduction of the tubular reabsorption. In rats with removed adrenal glands the preparations under study did not produce any diuretic influence, and natriuresis was observed only in administration of vas opressin. The diuretic effect of the preparations was absent against the background of hypophysectomy, whereas the natridiuretic effect was retained. It is supposed that the diuretic influence of the neurohypophyseal hormones was associated with the activation of the hypophysis-adrenal system, and some other additional mechanism took part in the natridiuretic effect.

Adrenal Glands↗
PubMed1984

The effects of two combinations of a beta-blocker and a diuretic on diuresis in normal subjects.

Combinations of a beta-blocker and a diuretic often produce a greater fall in blood pressure than does either drug alone. Furthermore, beta-blockers prevent an increase in plasma renin activity, thereby attenuating diuretic-induced potassium excretion and also the reduction in hypotensive response to the diuretic. This study was designed to compare the effects of the two fixed-dose combinations atenolol 100 mg plus chlorthalidone 25 mg (Tenoretic; ICI) and sotalol 320 mg plus hydrochlorothiazide 50 mg (Sotazide; B-M) on the pattern of diuresis and the biochemical composition of the urine in normal subjects. These preparations differ mainly in that the plasma half-lives of chlorthalidone and hydrochlorothiazide are 60 hours and 6 hours respectively; the former therefore accumulates when given once daily while the latter does not. These two preparations were found to have similar effects on the pattern of diuresis and the biochemical values. It is therefore concluded that the relationship between the serum chlorthalidone level and the fall in serum potassium level is in keeping with the flat dose-response curves for the thiazide and phthalimide diuretics.

Adult↗
PubMed1994

[The effect of diuretics on the magnitude of the effect of isosorbide dinitrate given as a single dose and after long-term administration. Ergometric study in patients with stable angina pectoris].

The authors assessed in 24 men with stable angina pectoris, using means of ergometry, the antiischaemic and antianginose effects of a combination of the nitrate Iso-Mack retard and the diuretic Moduretic. The effects were compared with the effects of Iso-Mack retard administered alone and with the effects of placebo. The examination was made after a single dose of the drugs and after three-week administration. The authors revealed that a single dose of the diuretic significantly enhanced the effects of nitrate. During long-term administration the diuretic did not prevent a significant diminution of the nitrate effects. Finally the authors discuss possible mechanisms of development of tolerance for nitrates and possibilities how to influence this tolerance by a diuretic.

Adult↗