[Reparative possibilities of alopecia secondary to loss of the scalp substance].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to G Gambaro.
Explore the source record for details and available documents.
Altered urinary excretion of glycosaminoglycans (GAG) has been reported in patients with nephrolithiasis, with chronic glomerulonephritis, and incipient diabetic nephropathy, but evaluation of urinary GAG has not been reported in infections and proliferating diseases of the urinary tract. Urinary excretion of GAG was measured in 50 patients with idiopathic calcium nephrolithiasis (ICN) of whom 20 had associated urinary tract infection, in 20 subjects with recurrent infection of the urinary tract (UTI), and in 18 patients with bladder papillomatosis. Mean values were significantly lower in ICN, increased in papillomatosis, and in the normal range in UTI.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Intravenous injection of atrial natriuretic peptides (ANP) induces a preferential vasodilatation of the renal resistance vessels. A similar effect is exerted by dopamine. Exogenous administration of this catecholamine induces, like the atrial peptides, diuresis and natriuresis, an effect prevented by dopamine receptor antagonists. In view of these parallels, the influence of dopamine antagonists on the diuretic response of anaesthetized rats to ANP was tested. The unselective dopamine antagonists haloperidol (50 micrograms, i.v.) and chlorpromazine (50 micrograms, i.v.) prevented the diuretic and natriuretic effect of a partially purified atrial extract, and significantly blunted that of alpha-hANP (1 microgram). Dopamine receptors are classified as DA-1 and DA-2. The DA-2 receptor antagonists metoclopramide (50 micrograms, i.v.) and sulpiride (50 micrograms, i.v.) did not affect ANP induced natriuresis. The DA-1 receptor antagonists SCH 23390 and SK&F 83566 dose-dependently counteracted the renal response to the intravenous administration of ANP. The administration of haloperidol (25, 50 and 100 micrograms, i.v.) to rats undergoing a putative ANP dependent natriuresis (isotonic saline loading) dose-dependently reduced both urine volume and sodium excretion. Atriopeptin II (10(-9)-10(-10) M) displaced tritiated spiperone, a dopamine antagonist, from specific binding sites in homogenates of renal medulla, papilla and cortex. These results suggest that dopamine receptors, most probably of the DA-1 subclass, are involved in the natriuretic response to ANP. The present experiments do not allow the conclusion as to whether ANP directly interacts with the dopamine receptors or whether it affects these receptors by releasing dopamine.
Explore the source record for details and available documents.
We measured the rate of oxalate flux across the red-cell membrane in the steady state in 114 patients with a history of calcium oxalate kidney stones and in 25 controls. Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria. Oxalate exchange was significantly higher in the 98 patients with idiopathic stone formation than in the controls (-1.10 +/- 0.95 [SD] X 10(-2) min-1 vs. -0.31 +/- 0.12 X 10(-2); P less than 0.001); it was above the upper limits of normal in 78 of these patients. All 8 patients with hyperparathyroidism and the patient with primary hyperoxaluria had values in the normal range; 2 of the patients with renal or urinary tract malformation had values at the upper normal limit. A study of five families indicated that the abnormality is an autosomal monogenic dominant trait with complete penetrance and variable expressivity. Oxalate-tolerance tests were carried out in five pairs of brothers. One brother in each pair had the abnormality in oxalate flux, and had a significantly higher percentage of oxalate excretion at two hours after oxalate loading (18.09 +/- 3.07 [SD] vs. 10.37 +/- 3.08 percent; t = 3.97; P less than 0.005) and four hours (14.87 +/- 2.91 vs. 9.89 +/- 2.93 percent; t = 2.70; P less than 0.05). Treatment with oral hydrochlorothiazide (50 mg per day) or amiloride (5 mg per day) or both restored normal or nearly normal red-cell oxalate exchange in all of 33 patients who initially had increased rates. We conclude that an inherited cellular defect in oxalate transport may be a factor in "primary" calcium oxalate stone formation and that this defect may be corrected with diuretics.
Urinary excretion of glycosaminoglycans (GAGS) and sialic acid (SA), as well as the activity of two renal enzymes related to glycoprotein metabolism, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and two others unrelated to glycosaminoglycans and glycoprotein metabolism, gamma-glutamyltranspeptidase (gamma-Gt) and angiotensin-I-converting enzyme (ACE), were evaluated in 40 insulin-dependent diabetic patients with normal range albuminuria, 21 patients with mesangial glomerulonephritis, and 30 control subjects. Diabetic and glomerulonephritic patients excreted a significantly higher amount of GAGS and SA, and showed greater NAG and GAL activities; gamma-Gt and ACE levels were within normal ranges. No correlation could be demonstrated between diabetes duration and GAGS, SA, NAG and GAL findings. Moreover, no correspondence between degree of metabolic control, as reflected by glycosylated hemoglobin (HbA1a-c) and GAGS, SA, NAG and GAL emerged.
Explore the source record for details and available documents.
In order to obtain new insights into the relevance of inhibitors in whole urine by focusing on their reciprocal interactions, a statistical approach was followed in 35 controls and 27 calcium oxalate (CaOx) recurrent idiopathic stone formers. The inhibiting activity of CaOx crystal growth and the most widely accepted inhibitors (glycosaminoglycans, citrate, magnesium, pyrophosphate), stone constituents (calcium, oxalate, phosphate, urate) and other normal urinary substances were evaluated. It was seen that the inhibitors played a very small role in total inhibiting activity. On the other hand, considering other normal urinary constituents, almost all the inhibiting power of urine on crystal growth could be explained.
This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.
Explore the source record for details and available documents.
Ten type I and 10 type II hypertensive diabetic patients were treated for 12 weeks with captopril (50 mg twice daily). Good control of blood pressure was achieved without any significant adverse effect on carbohydrate metabolism or renal haemodynamics and without evidence of glomerular or tubular damage.
Explore the source record for details and available documents.
Red-blood-cell transmembrane oxalate flux was measured in a group of patients with idiopathic calcium oxalate nephrolithiasis and in normal controls. The mean transmembrane oxalate flux rate was significantly higher in stone-forming patients than in controls (0.93 +/- SD 0.31/min vs 0.29 +/- 0.11/min). 80% of stone-forming patients showed raised (greater than 2SD above the mean in controls) transmembrane oxalate flux. Anomalous cellular oxalate transport may be an important pathogenetic factor in calcium oxalate nephrolithiasis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.