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Biomedical subjects

A Dal Canton

Publications and source records attributed to A Dal Canton.

At least 73 records · Page 4Linked to original sources
PubMed1985

Mechanism of impaired urinary concentration in chronic primary glomerulonephritis.

To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40 ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm. These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.

Adolescent↗
PubMed1985

Mechanism of increased plasma urea after diuretic therapy in uraemic patients.

To clarify why diuretic therapy raises plasma urea in patients with chronic renal failure, three groups of uraemic subjects were treated with frusemide for 6 days. In group 1 (n = 9), frusemide significantly decreased body weight and increased average plasma urea from 18.7 mmol/l to 28.8 mmol/l (P less than 0.001). this rise in plasma urea was secondary to reduced urea excretion, which occurred in spite of an increase in urea filtration. In group 2 (n = 7), frusemide was associated with salt replacement, in order to prevent salt depletion; in these patients neither reduction in urea excretion nor increase in plasma urea occurred. In group 3 (n = 10), the marked diuretic-induced fall in urea clearance was found to be independent of enhanced proximal tubular reabsorption (measured in water diuresis). These results show that the rise in plasma urea is due to increased tubular reabsorption of urea, presumably in the distal part of the nephron, secondary to extracellular fluid (ECF) volume depletion.

Body Weight↗
PubMed1985

Role of prostaglandins in captopril-induced natriuresis.

To determine whether prostaglandins (PG) contribute to captopril-induced natriuresis, 20 hypertensive subjects were assigned to one of the following three groups: group a, captopril (C) administration; group b, C + indomethacin (I); group c, I alone. Captopril was given in a dose of 100, 200, 400 mg/day and indomethacin in a dose of 100mg/day for one week. In group a (n = 10), natriuresis was clearly increased in the seven day periods with captopril in a dose of 200 and 400mg/day but not at 100mg/day. After captopril 200 or 400mg/day, but not 100mg/day, urinary PGE2 and PGI2 excretion significantly increased while filtration fraction fell due to a rise in renal plasma flow. Plasma aldosterone (PA) significantly decreased after C(p less than 0.05). In group b (n = 7), natriuresis disappeared during captopril 200 or 400mg/day and indomethacin administration even when PA decreased as in group a. In group c (n = 3), natriuresis was unchanged. In conclusion, natriuresis by C is critically dependent upon increased secretion of PG.

Adult↗
PubMed1985

Is the antihypertensive effect of muzolimine due to volume depletion?

Long-term treatment with muzolimine in patients with essential hypertension has provided very interesting results. The administration of the drug caused an immediate significant decrease in blood pressure which was then maintained for as long as 30 months. The fall in blood pressure was initially associated with a significant decrease in body weight, a clear rise in plasma renin activity (PRA) and a significant increase in plasma aldosterone concentration; all these changes are consistent with a depletion of extracellular volume and blood volume. With time, however, the mentioned changes were reversed. Body weight, PRA and plasma aldosterone were normalized after three weeks of treatment and remained normal thereafter. This late observation suggests a normalization in extracellular fluid volume and blood volume, and an antihypertensive effect of the drug independent from volume depletion. How can this effect occur? One possible explanation is a direct vasodilatory effect of muzolimine which has been shown in experimental animals. Against such a possibility is the unsuccessful treatment of hypertension in oliguric patients on regular dialysis treatment. A second possibility is a decrease in sodium content of the arteriolar wall with the consequent decrease in vascular response to pressor agents (angiotensin II, catecholamines). A third possibility is a hemodynamic adjustment to the initial volume depletion which would normalize cardiac output and peripheral resistances (autoregulation) so that normal blood pressure is maintained as in normal subjects.

Adult↗
PubMed1984

Mechanism of impaired urinary concentrating ability in normokalemic primary aldosteronism.

Renal clearance studies were performed during anti-diuresis (before and after hypertonic saline infusion) and during water diuresis in three hypertensive patients with normokalemic primary aldosteronism (NPA) and in matched patients with normoreninemic essential hypertension (EH). The NPA patients showed an impaired ability to concentrate urine. By progressively increasing Cosm with saline loading, TcH2O plateaued both in NPA and in EH patients; in the former, however, the plateau occurred earlier and was lower than in the latter. In water diuresis, absolute values of CH2O were higher in NPA due to increased distal delivery secondary to impairment in proximal tubular reabsorption. Fractional CH2O (i.e. the ratio between CH2O and distal sodium delivery), however, was lower in NPA than in EH patients. Both in antidiuresis (after saline loading) and in water diuresis the NPA patients exhibited an enhanced fractional excretion of sodium. In one of NPA patients, clearance studies were repeated after adrenalectomy. In this patient, normalization of BP and reduction of body weight were associated with a rise in Uosm and a reduction in Cosm in antidiuresis; Uosm and Cosm were restored to pre-surgical values by expanding extracellular fluid volume (ECV) with saline loading. In summary our results suggest that ECV expansion is the mechanism by which urine concentration is impaired in patients with NPA.

Adult↗
PubMed1984

Scleroembolization for treatment of hypertension caused by intrarenal arterial fibrodysplasia.

This paper reports a 13-year-old girl with severe hypertension due to fibrodysplasia of intrarenal arterial branches in the upper pole of the left kidney. Scleroembolization of the abnormal vascular region was carried out by injecting, via a transcutaneous catheter, an 80% solution of sodium iothalamate in ethanol, followed by a suspension of Gore-Tex particles in the same solution, which resulted in complete and persistent normalization of blood pressure.

Adolescent↗
PubMed1983

Percutaneous angioplasty for treatment of renovascular hypertension.

In this study, 10 patients with renovascular hypertension were treated with percutaneous transluminal angioplasty (PTA). The obstructive lesion was atherosclerotic in four cases, fibrodysplastic in five, and mixed in one. Stenosis was bilateral in two patients. Before PTA, all patients had sustained hypertension, in nine despite medication. Immediately after PTA, hypertension was cured (BP less than or equal to 140/90 mmHg without medication) in six patients, and improved (either a BP less than or equal to 140/90 or a decrease in diastolic BP greater than 15 mmHg, with equal or less medication) in three patients. The one failure occurred in the only patient in which PTA did not achieve a complete dilatation of the stenosed artery. The overall success rate was 90 per cent after a mean follow-up of 17.5 months.

Adult↗
PubMed1983

Epidemiology of hypertension in children.

In 1979-80, a cross-sectional study was carried out in 7118 Neapolitan school children aged 10-15 years. In 1980-81 and 1981-82 a longitudinal study was performed in a group of children with blood pressure above the mean + 1SD (in age and sex related peers) and in a group with blood pressure less than mean + 1SD. In the whole population blood pressure increased with age from 10 to 14 years. The major determinant of blood pressure was body weight, followed by heart rate. Three hundred and ninety-eight children (5.6%) were hypertensive having blood pressure greater than mean + 2SD. In children followed longitudinally, blood pressure was very labile; only 13 per cent of those originally having blood pressure mean + 1SD, in fact, remained in the same category. All of these, however, had blood pressure greater than mean + 2SD throughout the study.

Adolescent↗
PubMed1983

Renal function in pregnant rats with two-kidney goldblatt hypertension.

This study was carried out in female Wistar-Münich rats with two-kidney, one-clip hypertension, using clipped normotensive rats as controls. Metabolic studies were performed in the first two weeks of pregnancy, consisting of daily measurement of systolic blood pressure (BP) (tail-cuff), body weight (BW), and salt and water balance. At the end of metabolic studies, glomerular dynamics were studied in the unclipped kidney by micropuncture. During pregnancy, urinary output of Na+ and water was greater in hypertensive than normotensive rats. The greater natriuresis accounted for a reduced Na+ retention and a lower increase in maternal BW. Micropuncture studies showed an impaired renal auto-regulation. These results show that hypertension in pregnancy causes a salt-losing tendency, that may be secondary to incomplete renal autoregulation.

Animals↗
PubMed1982

Effects of pregnancy on glomerular dynamics: micropuncture study in the rat.

Glomerular dynamics were investigated by micropuncture in 15-day pregnant Munich-Wistar rats. Female non-pregnant rats were used as control. In hydropenia, single nephron glomerular filtration rate (SNGFR) averaged 37.2 nl/min/g kidney weight in pregnant rats, and 26.2 nl/min/g kidney weight in controls (P less than 0.0005). During pregnancy, mean glomerular plasma flow (GPF) rose from 63.0 to 104.5 nl/min (P less than 0.0005), and glomerular capillary hydrostatic pressure (PG) from 44.8 to 50.6 mm Hg (P less than 0.0005). This rise in PG accounted for an increase in effective filtration pressure (EFP). Mean EFP at the efferent end of the glomerulus rose from near zero to 9.7 mm Hg, indicating filtration pressure disequilibrium. After extracellular fluid volume expansion with saline, GPF and EFP were still greater during pregnancy. A filtration pressure disequilibrium occurred also in non-pregnant rats, allowing calculation of definite values of the ultrafiltration coefficient (Kf). During pregnancy, mean Kf was reduced from 0.0332 to 0.0285 nl/(sec X mm Hg) (P less than 0.005). SNGFR was moderately, but not significantly, increased. These results show that during pregnancy glomerular dynamics is characterized by a rise in GPF and EFP, and by a reduction in Kf. Following these changes, a plasma-flow dependent rise in SNGFR occurs in hydropenia. After expansion, instead, SNGFR is unmodified because the dependence of ultrafiltration on plasma-flow declines while the influence of Kf increases at high values of GPF.

Animals↗
PubMed1981

Muzolimine: a new high-ceiling diuretic suitable for patients with advanced renal disease.

Muzolimine was administered by mouth to 24 patients with creatinine clearances ranging from 4 to 28 ml/min to treat oedema or hypertension, or both. In four of these 24 patients muzolimine was given after intravenous high-dose frusemide had been unsuccessful. Muzolimine significantly increased urine volume and excretions of sodium, chloride, and potassium ions. Its diuretic efficacy was further shown by a mean reduction in body-weight of 8% and by the disappearance of oedema in all affected patients, even those refractory to intravenous frusemide. No rebound phenomenon was observed after the drug was stopped. Mean blood pressure was reduced in all hypertensive patients. Blood pressure was restored to normal in five out of seven patients treated with muzolimine alone and 10 out of 11 in whom muzolimine had been added to previously unsatisfactory antihypertensive treatment. Muzolimine was well tolerated by all patients. Muzolimine appears to be the diuretic of choice when treating patients with advanced renal disease.

Adolescent↗
PubMed1981

Exaggerated natriuresis in the hypertensive man: clinical evidence for intrarenal hemodynamic heterogeneity.

7 hypertensive patients (H) and 8 normotensive volunteers (N) were loaded with NaCl (4.5 mEq Na +/kg body weight i.v.) during water diuresis (A) and antidiuresis (B). In 6 antidiuretic subjects (3H and 3N) urine volume (V) was progressively raised up to over 30 ml/min, by intravenous infusion (12 ml/min) of hypertonic (3%) saline (C). It is assumed that in (A) CH2O is an index of Na+ reabsorption in short Henle's loops. In (B) and (C) TcH2O is proportional to Na+ reabsorption in long Henle's loops. In (A) CcH2O was significantly lower in H. In (B) TcH2O was similar in H and N. In (C), TcH2O reached an earlier plateau in H than in N. These results demonstrate that exaggerated natriuresis depends on defective Na+ reabsorption in Henle's loops, suggesting that the defect depends upon the transmission of hypertension to medullary circulation. The increase in hemodynamic pressure in vasa recta opposes Na+ reabsorption both in short and in long Henle's loops. However, the effects on TcH2O of the decrease in Na+ reabsorption in long loops is blunted by the greater Na+ delivery, secondary to the increase in GFR, that follows the rise in filtration pressure.

Adult↗
PubMed1981

Echocardiographic detection of cardiac effects of arterio-venous dialysis fistula.

The effects of the dialysis fistula were evaluated by echocardiography in 10 patients with terminal renal failure. Echocardiography was performed the day before creation of the fistula (E0) and was then repeated 24 hours after surgery (E1), the day before the first dialysis (E2), the day following the fourth dialysis (E3) and, finally, after 6 months of RDT (E4). Left ventricular internal diameter was measured both in diastole (LVIDd) and in systole (LVIDs), allowing calculation of ventricular diameter percent shortening (LVID%), of ventricular diastolic (EDV) and systolic volume (ESV). In E1 the fistula caused a significant increase in LVIDd, accounting for a rise also in EDV. This ventricular dilation persisted in E2, but was abolished in E3 and in E4. LVIDs, ESV, and LVID% were unmodified throughout the study. these results show that the dialysis fistula causes an immediate rise in cardiac pre-load, which is rapidly reversed by RDT.

Adolescent↗