Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon

1992 ◽  
Vol 83 (1) ◽  
pp. 75-80 ◽  
Author(s):  
C. Henríquez-la Roche ◽  
B. Rodríguez-Iturbe ◽  
G. Parra
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E2 ◽  
Idiopathic Hypercalciuria ◽  
Water Restriction ◽  
Water Diuresis ◽  
Control Subjects ◽  
Calcium Diet ◽  
High Calcium ◽  
And Control ◽  
Primary Phenomenon

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P<0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean ± SEM) was 11.62 ± 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 ± 0.48 nmol/day in the control subjects (P= 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.

Identical Effects of Indomethacin on Renal Function in Healthy Uninephrectomized Subjects and in Healthy Control Subjects

1994 ◽  
Vol 86 (6) ◽  
pp. 715-721 ◽  
Author(s):  
C. B. Nielsen ◽  
S. S. Sørensen ◽  
E. B. Pedersen
Keyword(s):  
Renal Function ◽  
Urinary Excretion ◽  
Prostaglandin E2 ◽  
Excretion Rate ◽  
Control Group ◽  
Urinary Excretion Rate ◽  
Control Subjects ◽  
Time Control ◽  
Healthy Control ◽  
Remnant Kidney

1. Animal studies have shown that prostaglandins are important for renal function after unilateral nephrectomy. In order to investigate the importance of prostaglandins for renal function in the fully adapted remnant kidney in healthy uninephrectomized subjects, the acute effects of indomethacin on renal haemodynamics, lithium clearance, urinary excretion rates of prostaglandin E2, sodium and water, and plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide and arginine vasopressin were measured in 14 healthy uninephrectomized subjects (median time after nephrectomy 1.7 years) and in 14 matched healthy control subjects. In addition, nine healthy control subjects were studied without indomethacin and served as a time-control group. 2. Before indomethacin ingestion there was a significantly higher single-kidney urinary excretion rate of prostaglandin E2 in the uninephrectomized group (uninephrectomized group, 349.2 fmol/min; control group, 76.6 fmol/min; time-control group, 96.3 fmol/min). 3. Indomethacin ingestion resulted in equal changes in all parameters in both groups. These were significant decreases in glomerular filtration rate (−11.3% versus −14.6%), renal plasma flow (−6.5% versus −13.0%), urinary flow rate (−49.8% versus −49.4%), fractional sodium excretion (−44.5% versus −47.4%), lithium clearance (−33.2% versus −23.8%) and urinary excretion rate of prostaglandin E2 (−93.8% versus −86.7%) (uninephrectomized versus control subjects, values are medians). In the time-control group no changes were observed in these parameters. 4. It is concluded that healthy uninephrectomized subjects with a fully adapted remnant kidney have a normal renal response to acute indomethacin-induced inhibition of prostaglandin synthesis.

Calcium and magnesium in essential hypertension

1988 ◽  
Vol 75 (4) ◽  
pp. 395-402 ◽  
Author(s):  
D. M. Tillman ◽  
P. F. Semple
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Systolic Pressure ◽  
Ionized Calcium ◽  
Serum Concentrations ◽  
Total Calcium ◽  
Control Subjects ◽  
Calcium Magnesium ◽  
The Difference ◽  
And Control

1. Because disturbances of calcium metabolism have been described in hypertension, measurements of plasma and serum concentrations of ionized calcium, total calcium, magnesium and renin were made in 38 patients with essential hypertension and age- and sex-matched control subjects. Urinary excretion of calcium, magnesium and sodium was also determined. 2. The mean serum concentration of ionized calcium was 1.23 ± 0.04 (sd) mmol/l in the hypertensive group and 1.21 ±0.03 mmol/l in controls, and results were similar after correction for pH. There was a weak positive correlation between serum ionized calcium (pH 7.4) and systolic pressure (r = 0.26, P < 0.02), but no correlation with plasma renin concentration. 3. Although the difference between serum total calcium concentration in the hypertensive (2.29 ±0.09 mmol/l) and control (2.26 ±0.07 mmol/l) subjects was not significant, there was a significant correlation between total calcium and systolic pressure (r = 0.23, P < 0.05) which was maintained after correction for other variables. 4. There were no differences in plasma concentrations of parathyroid hormone or 1,25-dihydroxycholecalciferol between hypertensive and control subjects. 5. The hypertensive group showed higher urinary excretion of calcium (5.9 ±3.0 mmol/24h) than controls (4.6 ± 1.7 mmol/24 h), but the difference was not maintained after correction for sodium excretion. 6. Serum concentrations of magnesium were similar in the two groups, but urinary excretion of magnesium was significantly lower in hypertensive (3.7 ± 1.3 mmol/24 h) than control (4.5 ±1.6 mmol/24 h) subjects and there was an inverse correlation between magnesium excretion and blood pressure (r = 0.3–0.35, P < 0.01).

Total and non-dialyzable urinary hydroxyproline in acromegalics and control subjects

1981 ◽  
Vol 96 (4) ◽  
pp. 451-457 ◽  
Author(s):  
Johan Halse ◽  
Jan O. Gordeladze
Keyword(s):  
Urinary Excretion ◽  
Formation Rate ◽  
Bone Matrix ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Control Subjects ◽  
Urinary Parameters ◽  
Turn Over ◽  
And Control ◽  
Calcium Phosphate Metabolism

Abstract. The urinary excretion of total and non-dialyzable hydroxyproline (HYP) containing peptides has been studied in 25 patients with active acromegaly and 44 control subjects — all kept on a collagen free diet. Acromegalics had a greater excretion of both total and non-dialyzable HYP than controls, indicating an increased turn-over of collagen/bone matrix. The amounts of total and non-dialyzable HYP excreted in acromegalics were significantly correlated to mean fasting growth hormone levels. Both acromegalics and controls exhibited a significant coupling between the excretion of total and non-dialyzable HYP. Female control subjects demonstrated an age-dependent decrease in the excretion of both total and non-dialyzable HYP, whereas no such age-dependence could be observed in males. Age seemed to have a greater effect on the non-dialyzable fraction than on the total HYP excretion. These results may imply that collagen/bone matrix turn-over declines with age and that bone formation declines at a more rapid rate than resorption. In acromegalics the ratio of non-dialyzable to dialyzable HYP was not significantly different from control values, indicating that although turn-over is increased the actual matrix formation rate is normal in acromegaly. No correlation was found between serum or urinary parameters of calcium/phosphate metabolism or the urinary excretion of 3',5'-cyclic adenosine monophosphate and total or non-dialyzable HYP in acromegalics or controls.

Increased urinary excretion of prostaglandin E in patients with idiopathic hypercalciuria

1988 ◽  
Vol 75 (6) ◽  
pp. 581-587 ◽  
Author(s):  
Carlos Henríquez-La Roche ◽  
Bernardo Rodríguez-Iturbe ◽  
José Herrera ◽  
Gustavo Parra
Keyword(s):  
Water Deprivation ◽  
Sodium Intake ◽  
Urine Flow ◽  
Idiopathic Hypercalciuria ◽  
Prostaglandin E ◽  
Dietary Composition ◽  
Water Diuresis ◽  
Stone Formers ◽  
Male Patients ◽  
And Control

1. Because urinary prostaglandin excretion could play a role in idiopathic hypercalciuria (IH), we studied the excretion of prostaglandin E (PGE), calcium and sodium at various urine flows in 21 patients (14 males) with urolithiasis and IH, seven stone formers (five males) with normal calciuria and 20 controls (11 males). Dietary composition was comparable and sodium intake was restricted to 100–120 mmol/day. 2. Analyses were performed on 30 min urine collections obtained after overnight water deprivation and during water diuresis. Male IH patients had increased levels of urinary PGE at all ranges of urine flow. PGE excretion correlated directly with urine flow in patients and controls, but the slope of this relationship in individual IH male patients was steeper than in controls (P < 0.01). Calciuria correlated directly with urine output in patients with IH but not in controls. Calcium and sodium excretion were directly correlated (P < 0.0001) in patients and controls. There were no significant differences between absorptive IH (seven patients) and renal IH (eight patients). There were no significant differences between stone formers with normocalciuria and control subjects. 3. The findings suggest that increased urinary PGE could play a role in the hypercalciuria syndrome, possibly by promoting natriuresis.

The Effects of a Neutral Stimulus (Buzzer) on Motor Responses and Disfluencies in Normal Speakers

1969 ◽  
Vol 12 (1) ◽  
pp. 179-184 ◽  
Author(s):  
Richard R. Martin ◽  
Gerald M. Siegel
Keyword(s):  
College Students ◽  
Neutral Stimulus ◽  
Motor Responses ◽  
Control Subjects ◽  
And Control ◽  
Speaking Task

Seventy-two college students were divided into three groups: Button Push-Speech (BP-S), Speech-Button Push (S-BP), and Control. BP-S subjects pushed one of two buttons on signal for 8 min. During the last 4 min, depression of the criterion button caused a buzzer to sound. After the button-push task, subjects spoke spontaneously for 30 min. During the last 20 min, the buzzer was presented contingent upon each disfluency. S-BP subjects were run under the same procedures, but the order of button-push and speech tasks was reversed. Control subjects followed the same procedures as S-BP subjects, but no buzzer signal was presented at any time. Both S-BP and BP-S subjects emitted significantly fewer disfluencies during the last 20 min (Conditioning) than during the first 10 min (Baserate) of the speaking task. The frequency of disfluencies for Control subjects did not change significantly from Baserate to Conditioning. In none of the three groups did the frequency of pushes on the criterion button change significantly from minute to minute throughout the 8-min button-push session.

Tests for Platelet Changes, Acute Phase Reactants and Serum Lipids in Diabetes mellitus and Peripheral Vascular Disease

1982 ◽  
Vol 48 (03) ◽  
pp. 289-293 ◽  
Author(s):  
B A van Oost ◽  
B F E Veldhuyzen ◽  
H C van Houwelingen ◽  
A P M Timmermans ◽  
J J Sixma
Keyword(s):  
Diabetes Mellitus ◽  
Vascular Disease ◽  
Peripheral Vascular Disease ◽  
Acute Phase ◽  
Serum Lipids ◽  
Diabetic Patients ◽  
Peripheral Vascular ◽  
Acute Phase Reactants ◽  
Control Subjects ◽  
And Control

SummaryPlatelets tests, acute phase reactants and serum lipids were measured in patients with diabetes mellitus and patients with peripheral vascular disease. Patients frequently had abnormal platelet tests and significantly increased acute phase reactants and serum lipids, compared to young healthy control subjects. These differences were compared with multidiscriminant analysis. Patients could be separated in part from the control subjects with variables derived from the measurement of acute phase proteins and serum lipids. Platelet test results improved the separation between diabetics and control subjects, but not between patients with peripheral vascular disease and control subjects. Diabetic patients with severe retinopathy frequently had evidence of platelet activation. They also had increased acute phase reactants and serum lipids compared to diabetics with absent or nonproliferative retinopathy. In patients with peripheral vascular disease, only the fibrinogen concentration was related to the degree of vessel damage by arteriography.

scholarly journals The fate of orally administered sialic acid: First insights from patients with N-acetylneuraminic acid synthase deficiency and control subjects

2021 ◽  
Vol 28 ◽  
pp. 100777
Author(s):  
Christel Tran ◽  
Licia Turolla ◽  
Diana Ballhausen ◽  
Sandrine Cornaz Buros ◽  
Tony Teav ◽  
...  
Keyword(s):  
Sialic Acid ◽  
Acetylneuraminic Acid ◽  
Control Subjects ◽  
And Control

Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

1980 ◽  
Vol 58 (5) ◽  
pp. 365-371 ◽  
Author(s):  
A. Berthelot ◽  
A. Gairard
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Sprague Dawley ◽  
Physiological Concentration ◽  
Deoxycorticosterone Acetate ◽  
Calcium Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
High Calcium ◽  
High Calcium Diet

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

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