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Biomedical subjects

B Miranda

Publications and source records attributed to B Miranda.

At least 91 records · Page 5Linked to original sources
PubMed1988

Renal effects of fenoldopam in refractory hypertension.

Fenoldopam, a dopamine-1 (D1) agonist, was administered by a 6-h intravenous infusion to patients with refractory hypertension [diastolic blood pressure (DBP) greater than 115 mmHg while on triple therapy] in order to achieve a fall in DBP of 30 mmHg. The evolution of blood pressure, heart rate, glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, renal excretion of sodium, potassium, chloride, calcium, uric acid, phosphate, plasma renin activity (PRA), aldosterone and prolactin were evaluated. A significant fall in blood pressure (P less than 0.01) accompanied by an increase in heart rate (P less than 0.01) was attained after 30 min. GFR and RPF increased significantly (P less than 0.01) but the filtration fraction fell. Urine volume and urinary output of sodium, potassium, chloride, calcium, uric acid and phosphate increased markedly (P less than 0.01). Meanwhile, plasma potassium fell (P less than 0.01) and the hormonal parameters showed no significant change. We concluded that in refractory hypertension fenoldopam has potent renal and systemic vasodilatory properties through which blood pressure falls. The hypotensive effect of fenoldopam is also facilitated by its marked diuretic and natriuretic properties. The absence of variations of plasma prolactin confirm the D1 selectivity of fenoldopam and the lack of increase in PRA indicates that fenoldopam blocks the renin-angiotensin-aldosterone system.

Adult↗
PubMed1988

Control of hypertension with the angiotensin converting enzyme inhibitor captopril reduces glomerular proteinuria.

Recent experimental and clinical data have suggested that angiotension converting enzyme (ACE) inhibitors may decrease glomerular proteinuria by specific effects on the glomerulus. We studied a group of 15 adult patients with chronic renal failure and proteinuria due to various glomerulopathies. These patients had mild to moderate hypertension which was effectively controlled with conventional antihypertensive therapy. We then treated the patients with captopril, maintaining a similar dietary protein and salt intake. After 6 months of study, proteinuria was reduced significantly without reduction in inulin or para-aminohippurate clearance. This supports the concept that captopril may have salutary effects on the glomerulus, independently of its effect on systemic blood pressure.

Blood Pressure↗
PubMed1988

Persistence of the natriuretic effect of calcium entry blockers.

In order to elucidate whether or not the natriuretic properties of calcium entry blockers persist during the long-term administration of the drug, we have investigated the renal capacity to excrete an intravenous sodium load (2,000 ml of isotonic saline in 4 h) in a group of eight mild to moderate essential hypertensive patients, before and after 1, 8, and 24 weeks of treatment with nitrendipine. The following parameters were measured before and hourly during saline infusion: blood pressure, and plasma and urine sodium and potassium. For 5 days prior to the performance of the test, the patients received a diet containing 120 mEq of sodium daily. Nitrendipine induced a significant fall of both systolic and diastolic blood pressure (p less than 0.05-0.01) that was maintained throughout the study. A significant increase of the cumulative renal sodium output (microEq/min/h) was observed after 1, 8, and 24 weeks (p less than 0.05-0.001) of therapy with the calcium entry blocker. Meanwhile, plasma sodium and potassium and the kaliuresis did not change significantly. These results indicate that the natriuretic effect of calcium entry blockers is still present after long-term treatment.

Adult↗
PubMed1988

Renal effects of amino acid infusions in patients with panhypopituitarism.

Strong evidence indicates that a high protein diet accelerates end-stage renal disease by increasing glomerular capillary pressure subsequent to renal vasodilatation. The mechanisms underlying this vasodilatation remain undefined, but they have been suspected to be mediated by a pituitary factor. To test this possibility, we measured changes in renal plasma flow and glomerular filtration rate induced by an intravenous infusion of a solution of amino acids in two patients with panhypopituitarism. These patients exhibited changes in renal hemodynamics comparable to those recorded in nine healthy volunteers. The results do not support involvement of the pituitary gland in the acute renal response to amino acids.

Adenoma↗
PubMed1987

Influence of a low sodium diet on the renal response to amino acid infusions in humans.

In experimental animals, a high protein diet has been shown to accelerate end-stage renal disease by inducing glomerular hyperperfusion. In this study, we found that intravenous administration of amino acid, used as one component of parenteral nutrition, to normal volunteers resulted in a significant increase in renal blood flow (from 517 +/- 29 to 754 +/- 60 ml/min) and glomerular filtration rate (from 106 +/- 6 to 165 +/- 12 ml/min) without altering systemic blood pressure, renal excretion of electrolytes, plasma renin activity, or plasma aldosterone concentration, and excretory rates of prostaglandins E2 were increased (from 665 +/- 61 to 1,034 +/- 153 pg/min). These amino acid-induced renal hemodynamic effects were abolished when the volunteers received a low sodium diet (20 mEq/day) for three days before the amino acid infusions. However, the hemodynamic effects were restored when the subjects receiving low sodium diets were pretreated with captopril. Under these conditions, amino acid infusions increased renal blood flow (from 388 +/- 11 to 597 +/- 27 ml/min) and glomerular filtration rate (from 80 +/- 4 to 118 +/- 9 ml/min). Reduction of prostaglandin synthesis with indomethacin in volunteers receiving a normal sodium intake was also capable of significantly decreasing the amino acid effects on renal hemodynamics. The results indicate that the renal hemodynamic effects of amino acid infusion are strongly influenced by angiotensin II and prostaglandin formation.

Adult↗
PubMed1987

Dopaminergic modulation of aldosterone secretion in the normal menstrual cycle.

A group of eight normotensive female volunteers with regular menstrual cycles were studied during two menstrual cycles: a control cycle and one in which they received lisuride, a D1-D2 dopamine agonist (0.025 mg/8 hr). The following tests were performed in both halves of both cycles: 1) the response of prolactin (PRL) to thyrotropin-releasing hormone (TRH) administration; 2) the response of plasma renin activity (PRA) and plasma aldosterone (PA) to furosemide for 2 hours in the upright posture; and 3) the response of PRL, PRA, PA, plasma potassium (K), and cortisol (F) to metoclopramide administration. An increased response of PRL to TRH and PA to furosemide in the upright position and to metoclopramide were found in the luteal phase of the control study (p less than 0.05). After lisuride administration, in the interphase, differences in the responses of PRL to TRH and PA to furosemide in the upright position disappeared, whereas that of PA to metoclopramide increased further. We conclude that the increase of aldosterone normally observed during the luteal phase of the menstrual cycle is at least partly conditioned by diminished dopaminergic tone and that the response of aldosterone secretion to furosemide-induced sodium depletion and its response to metoclopramide stimulation may be modulated by two different types of dopamine receptors.

Adult↗
PubMed1987

Acute renal failure in cirrhosis associated with macroscopic hematuria of glomerular origin.

Two patients with alcoholic cirrhosis developed an acute impairment of renal function during an episode of macroscopic hematuria, one of them requiring hemodialysis treatment. Later, when gross hematuria disappeared, renal function gradually improved. The histological findings in both patients showed a mild mesangial glomerulonephritis with IgA deposits on immunofluorescence, the presence of red blood cells casts obstructing the lumen in 40% to 50% of the renal tubules, and a marked tubular necrosis.

Acute Kidney Injury↗
PubMed1986

Dopamine control of aldosterone secretion in end-stage renal failure.

The role of the tonic inhibitory effect of dopamine on aldosterone secretion has been investigated in 10 patients with chronic renal failure (CRF) on hemodialysis, in 8 normotensive renal transplant recipients (Tx) with normal renal function and in 8 normotensive volunteers (NV). The following tests were performed: the response of plasma aldosterone (PA) to metoclopramide administration; the response of plasma prolactin (PRL) to TRH administration, and the changes induced by Lisuride (a dopaminergic agonist, on the values of PA and PRL). The basal values of PA and PRL were higher in CRF than in NV and Tx. The inverse was true for plasma renin activity (PRA) values. The response of PA and PRL to metoclopramide showed blunted increases in CRF when compared to NV, in the absence of changes of PRA, cortisol and potassium. After TRH administration, PRL increase in CRF was also inferior. Lisuride induced a decrease of both PA and PRL both in CRF and NV. In Tx, basal values of PA and PRL were similar to NV. Nevertheless, the response to metoclopramide and TRH were partially blunted when compared to that of NV. These results point to the existence of a deranged dopaminergic regulation of aldosterone secretion in end-stage renal failure patients. The alterations are partially corrected by a well-functioning kidney graft.

Adult↗
PubMed1986

Effect of exogenous angiotensin II infusion after one year of captopril therapy in essential hypertension.

The effect of exogenous angiotensin II on plasma renin activity (PRA), plasma renin concentration (PRC) and plasma aldosterone (PA) was investigated in a group of 8 patients with essential hypertension after one year of captopril therapy. The results were compared with those obtained in a group of 18 normotensive volunteers not on captopril. Angiotensin II was infused at increasing doses until a pressor response (increase of diastolic blood pressure by 20 mm Hg) was evoked. The normotensive volunteers exhibited the expected decline of PRA during angiotensin II infusion. However, no significant change was observed in PRA nor in PRC levels in the group of hypertensive patients. The PA values increased significantly both in volunteers and patients (P less than 0.02). The dose of angiotensin II necessary to evoke a pressor response was higher in the hypertensive patients than in the normotensive volunteers (6.0 +/- 2.6 s.d. ng/kg/min vs 2.5 +/- 0.9; P less than 0.01). We conclude that patients with essential hypertension, after chronic treatment with captopril, show no inhibition of renin secretion in contrast with the controls. They also require more angiotensin II to evoke a pressor response during infusion of this peptide.

Adult↗
PubMed1985

Ureolytic Citrobacter freundii infection of the urine as a cause of dissolution of cystine renal calculi.

We report a case of cystinuria with staghorn renal lithiasis in a solitary right kidney and chronic renal failure. Right nephropyelolithotomy was performed and although 29 renal calculi were extracted many stones remained in situ. A permanent nephrostomy was left in the kidney. Several months later the urine was infected chronically with a ureolytic Citrobacter freundii bacteria and urinary pH oscillated between 8.0 and 9.2. Spontaneous dissolution of the cystine calculi was observed and many tiny fragments of cystine were expulsed through the nephrostomy, following which renal function improved. Despite the conditions favoring struvite calculi, formation did not occur.

Citrobacter↗
PubMed1985

Influence of lisuride, a dopaminergic agonist, on the sexual function of male patients with chronic renal failure.

The effects of Lisuride, a dopaminergic agonist, on the levels of plasma prolactin (PRL), testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and on the variations of libido and coital frequency of patients with chronic renal failure (CRF) have been investigated in a group of 20 male patients (ten normoprolactinemic and ten hyperprolactinemic). Ten patients were included in a hemodialysis program and another ten received conservation therapy (all had creatinine clearance rates below 15 mL/min). The response of PRL to TRH administration and that of LH and FSH to LH-RH administration have also been studied. Low levels of plasma testosterone found initially in all the patients, increased in both normoprolactinemic (P less than 0.05) and hyperprolactinemic patients (P less than 0.01) during Lisuride administration. PRL decreased (P less than 0.01) in both groups during therapy. The increase of plasma testosterone was greater in hyperprolactinemic patients (86% v 15% in normoprolactinemic) and was accompanied by a clear improvement in the studied parameters of sexual behaviors. The response of PRL to TRH was modified in hyperprolactinemic patients while that of LH and FSH to LH-RH was not modified, although Lisuride induced an increase of the basal value of LH (P less than 0.01) in the hyperprolactinemic group. The drug was fairly well tolerated, did not induce hypotension, and the overall incidence of side effects decreased along the study. These results stress the need for further studies with this agent in patients with chronic renal failure and sexual dysfunction.

Adult↗
PubMedDate not supplied

The potential organ donor pool: international figures.

By understanding the size and characteristics of the potential donor pool, the concentration and location of the potential donors and factors influencing low rates of donation, it is possible to identify opportunities to improve the organ donation system. The exact donor gap needs to be established for each hospital/area, as published figures do not necessary reflect local potential. Nevertheless, marked differences with respect to the minimum standards in the number, location, and characteristics of organ donors should be considered as suggestive of low performance. The first stage where potential donors are lost is the detection of people who can be diagnosed as brain dead and, hence, could be considered a potential organ donor. Improving the donor identification implies the development of donor detection programmes. That and other initiatives to improve the donation rate need to be started in hospitals after the assessment of the local potential and local factors specifically implicated in the local performance.

Cause of Death↗