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

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.

1992 ◽  
Vol 83 (1) ◽  
pp. 75-80 ◽  
Author(s):  
C. Henríquez-la Roche ◽  
B. Rodríguez-Iturbe ◽  
G. Parra

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.


1998 ◽  
Vol 274 (6) ◽  
pp. R1619-R1625 ◽  
Author(s):  
Elzbieta Kompanowska-Jezierska ◽  
Claus Emmeluth ◽  
Lisbeth Grove ◽  
Poul Christensen ◽  
Janusz Sadowski ◽  
...  

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg ⋅ min−1 ⋅ kg body wt−1), plasma vasopressin concentration increased to 2.30 ± 0.20 pg/ml compared with 0.12 ± 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 ± 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 ± 15.8 μmol/min) than without vasopressin (4.6 ± 0.4 ml/min and 14.4 ± 4.1 μmol/min, respectively). Deamino-[Cys1,d-Arg8]vasopressin, a V2 receptor agonist (4 pg ⋅ min−1 ⋅ kg−1), mimicked the antidiuretic response (0.20 ± 0.03 ml/min) without changing UNaV (9.7 ± 4.4 μmol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 ± 0.02 ml/min), and abolished the natriuresis (13.4 ± 3.7 μmol/min). During AVP infusion, UNaV was highly correlated ( r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.


1983 ◽  
Vol 245 (1) ◽  
pp. F48-F57
Author(s):  
H. T. Campbell ◽  
P. A. Craven ◽  
F. R. DeRubertis

The effects of fluid intake on basal and vasopressin-responsive urinary PGE excretion (UPGEV) were examined in conscious rats under conditions of 1) ad libitum water intake, 2) water deprivation, and 3) water diuresis induced by ad libitum intake of 5% dextrose in water. UPGEV fell progressively during 40 h of water deprivation. Water diuresis after water deprivation increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5 U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats on ad libitum water intake but did not alter UPGEV during water deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin in rats on ad libitum water intake. Indomethacin accelerated by 8 h the onset of maximal antidiuresis in water-deprived rats but did not significantly alter water balance. During water diuresis, UPGEV declined in the first 8 h after Pitressin. Thereafter, UPGEV increased markedly, concurrent with early vasopressin escape. Indomethacin or meclofenamate inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V of the escape phase. Indomethacin or meclofenamate also impaired the excretion of an acute water load (5% body wt) given during escape. The spontaneous decline in UPGEV during hydropenia may serve to maximize physiologic antidiuresis. Conversely, the marked increase in UPGEV induced by administration of vasopressin during water diuresis may serve to suppress the antidiuretic response and thus play a role in the mediation of escape from physiologically inappropriate antidiuresis.


2006 ◽  
Vol 290 (3) ◽  
pp. F641-F649 ◽  
Author(s):  
Michael L. Pucci ◽  
Shinichi Endo ◽  
Teruhisa Nomura ◽  
Run Lu ◽  
Cho Khine ◽  
...  

During water deprivation, prostaglandin E2 (PGE2), formed by renal medullary interstitial cells (RMICs), feedback inhibits the actions of antidiuretic hormone. Interstitial PGE2 concentrations represent the net of both PGE2 synthesis by cyclooxygenase (COX) and PGE2 uptake by carriers such as PGT. We used cultured RMICs to examine the effects of hyperosmolarity on both PG synthesis and PG uptake in the same RMIC. RMICs expressed endogenous PGT as assessed by mRNA and immunoblotting. RMICs rapidly took up [3H]PGE2 to a level 5- to 10-fold above background and with a characteristic time-dependent “overshoot.” Inhibitory constants ( Ki) for various PGs and PGT inhibitors were similar between RMICs and the cloned rat PGT. Increasing extracellular hyperosmolarity to the range of 335–485 mosM increased the net release of PGE2 by RMICs, an effect that was concentration dependent, maximal by 24 h, reversible, and associated with increased expression of COX-2. Over the same time period, there was decreased cell-surface activity of PGT due to internalization of the transporter. With continued exposure to hyperosmolarity over 7–10 days, PGE2 release remained elevated, COX-2 returned to baseline, and PGT-mediated uptake became markedly reduced. Our findings suggest that hyperosmolarity induces coordinated changes in COX-2-mediated PGE2 synthesis and PGT-mediated PGE2 uptake in RMICs.


1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Koichi Mizumaki ◽  
Akira Fujiki ◽  
Masao Sakabe ◽  
Tamotsu Sakamoto ◽  
Yosuke Nakatani ◽  
...  

Although J-wave elevation (JWE) in the inferior or lateral leads is characteristic of subtype of idiopathic ventricular fibrillation (IVF), difference between malignant and benign JWE remains to be elucidated. So, we assessed the hypothesis that the rate dependent changes in JWE could be different between patients with IVF and control subjects. Six male patients with IVF and 18 age matched male controls with JWE (>2 mm) in the lateral leads were studied. CM-5 lead digital Holter ECG was recorded and J wave amplitude was automatically measured. J/RR relationships were evaluated by means of J/RR linear regression lines for 24 hours, and according to four 6-hour periods. From J-RR linear regression lines, J-RR slope (mm/sec), J wave amplitude (mm) at RR intervals of both 0.6 sec and 1.2 sec (J (0.6) and J (1.2) ) were determined. In all 6 patients with IVF, the time of spontaneous episodes of VF were investigated from the implantable cardioverter defibrillator (ICD) stored data. For 24 hours, J-RR slope was greater in IVF patients than in controls (3.5±0.7 vs 2.4±0.8, p<0.01). (J (0.6) ) wasn’t different between 2 groups; however, J (1.2) was greater in IVF patients than in controls (2.8±0.9 vs 2.0±0.6, p<0.05). In IVF patients, ST/RR slope was highest during 18:00–24:00; however, these circadian changes were blunted in controls. J(1.2) was greater during 18:00 – 6:00 in IVF patients than in controls. Seven (59%) of total 9 episodes of spontaneous VF of IVF patients occurred during 18:00 – 6:00. In patients with subtype of IVF, JWE augmented during bradycardia especially at night. This could relate to nighttime occurrence of IVF.


2011 ◽  
Vol 44 (5) ◽  
pp. 561-566 ◽  
Author(s):  
Patrícia Fernandes do Prado ◽  
Marília Fonseca Rocha ◽  
Joel Fontes de Sousa ◽  
Dênio Iuri Caldeira ◽  
Gustavo Fontes Paz ◽  
...  

INTRODUCTION: Visceral leishmaniasis (VL) is an expanding zoonosis in Brazil and is becoming urbanized in several Brazilian regions. This study aims to describe the epidemiological features of human and canine VL in the municipality of Montes Claros, State of Minas Gerais, by focusing on their spatial distribution. METHODS: Data concerning human cases and reactive dogs for VL from 2007 to 2009 were obtained from the Information System for Disease Notification (SINAN) and from reports of the local Centro de Controle de Zoonoses (CCZ), respectively. The addresses of human and canine cases have been georeferenced and localized in thematic maps, allowing their spatial visualization as well as the identification of areas at risk of VL transmission. RESULTS: Ninety-five cases of human VL were reported in the period. The 0-9-year-old age group (48.4%) was the most affected, within which the majority consisted of male patients (64%). Of the samples collected for the canine serological survey, 2,919 (6.3%) were reactive to VL. The spatial localization of these cases shows that the disease was scattered in the urban area of the municipality. Areas showing a higher dissemination risk were concentrated in the central, northwestern, and southern regions of the city. CONCLUSIONS: Identifying the areas most at risk in urban Montes Claros may help guide actions toward local epidemiological vigilance and control.


2019 ◽  
Vol 32 (9) ◽  
pp. 600
Author(s):  
Pedro Atilano Carvalho ◽  
Ana Monteiro ◽  
Bruno Almeida ◽  
Filomena Horta Correia ◽  
Vera Resende ◽  
...  

Introduction: Infections are a major problem and the presence of drug-resistant microorganisms has significant clinical and economic impact. The present study aims to evaluate the epidemiological profile of “problem” microorganisms isolated in a hospital in the north of Portugal.Material and Methods: All isolated microorganisms were analyzed, between January 2014 and June 2015. Data obtained was then processed using statistical software.Results: We analyzed 8146 microbiological isolations and found a prevalence of 23% of ‘problem’ microorganisms (in descending order of frequency: Enterococcus, Pseudomonas, Staphylococcus aureus e Streptococcus pneumonia), 57.55% of which isolated in male patients. The most frequent mechanism of drug resistance for the overall sample was the production of extended-spectrum beta-lactamase, and resistance to oxacillin for ‘problem’ microorganisms.Discussion: In this sample, we observed a much higher prevalence of ‘problem’ microorganisms than that reported in other countries, which shows the need of improvement of surveillance mechanisms and treatment of these cases. Microorganisms that showed higher resistance were Staphylococcus aureus (resistant to oxacillin) and Enterococcus (resistant to vancomycin). Those were isolated in patients with a higher mean age compared to non-resistant microorganisms. Most of these microorganisms were isolated in hospitalized patients or intermediate and intensive care units, what relates them with healthcare associated infections.Conclusion: The prevalence of infection by ‘problem’ microorganisms during the studied period was 23%. The detection and control of the spread of these microorganisms are paramount due to its impact on health costs, morbidity and survival of patients.


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