Chronic cisplatin tubulopathy in humans and animals: clear-cut discrepant findings.
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Animals↗
Biomedical subjects
M G Bianchetti
Publications and source records attributed to M G Bianchetti.
[An avoidable cause of parental anxiety and unnecessary medical workup: diaper crystals (pannolithiasis)].
Five infants aged 6 to 23 months had a history of passing crystals in urine. They were not ill, but micturition was reported to be associated with pain in two of them. Physical examination was normal, and urinalysis and culture were negative. In one case we observed "jelly-like crystals" of about 2 mm diameter which dissolved spontaneously in tap water. When the parents were re-questioned it became evident that all used a new brand of highly absorbent diapers. "Jelly-like crystals" developed in our laboratory when the absorbent material of the new diapers was put in contact with urine or tap water. The new highly absorbent diapers help to keep the baby dry. However, "jelly-like crystals" may be observed and possibly alarm both parents and physicians. Information for parents and physicians may avoid unnecessary anxiety or medical workup.
Crystallization↗
[Simple coagulation prophylaxis using low-molecular heparin enoxaparin in pediatric hemodialysis].
The use of low molecular weight heparins for the prevention of clotting in extracorporeal circulation during hemodialysis has been reported in adults. In seven children (aged 7 to 18 years) with end stage renal failure an initial bolus of the low molecular weight heparin enoxaparin (dosage: 24 to 36 mg/m2) provided simple and proper anticoagulation with no hemorrhage during at least four hours. The tolerance was excellent.
Adolescent↗
Chronic renal magnesium loss, hypocalciuria and mild hypokalaemic metabolic alkalosis after cisplatin.
Renotubular handling of sodium, potassium (K) calcium (Ca), phosphate, hydrogen ions and glucose, and urinary concentrating ability were studied in three children (aged 8, 8.5, 11 years) with renal magnesium (Mg) loss, persisting for more than 2 years after discontinuation of cisplatin treatment for neuroblastoma. A group of healthy children served as controls. Besides renal Mg wasting, a clear-cut tendency towards reduced calciuria associated with normal or slightly elevated plasma Ca was observed. Plasma K tended to be low (3.4-3.7 mmol/l), and plasma chloride was normal. Plasma bicarbonate (HCO3) ranged from 24.9 to 27.8 mmol/l, and urinary pH was always less than 6.0, indicating a renal HCO3 threshold exceeding 24 mmol/l. Plasma creatinine levels, glucosuria and phosphaturia, and urinary concentrating capacity were adequate. Comparable features were found in three children (aged 4.5, 9, 13 years) with primary renotubular hypomagnesaemia-hypokalaemia and hypocalciuria. This study complements the picture of chronic cisplatin tubulopathy in childhood demonstrating that, apart from Mg wasting, a reduced Ca excretion, and a tendency to hypokalaemia and metabolic alkalosis exist. Thus cisplatin may induce renal functional damage identical to that found in primary renotubular hypomagnesaemia--hypokalaemia with hypocalciuria.
Alkalosis↗
Calciuria in Bartter's syndrome.
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Bartter Syndrome↗
[Growth in children with non-dialysis dependent chronic kidney insufficiency].
Chronic renal failure leads to growth retardation in every second patient with the congenital and in every third with the acquired form. The pathophysiologic events of chronic renal failure are discussed, together with their possible direct or indirect impact on growth. Documentation of such events has important therapeutic implications. In recent years dietary measures have assumed paramount importance in the treatment of growth retardation in chronic renal failure. Treatment of individually assessed pathophysiologic conditions constitutes essential support for the dietary measures.
Anemia↗
[Acute poisoning with a narcotic (Tramadol) in an infant of five weeks].
Accidental rectal administration of 27 mg/kg of the narcotic analgesic Tramadol to a five-week-old infant resulted in severe cerebral depression, which had to be treated with Naloxone during 48 hours. The severity and the duration of this intoxication are not explained solely by the high dosage of Tramadol. A decreased elimination kinetics and an increased permeability of the blood-cerebrospinal fluid barrier probably also account for the pattern of the present intoxication.
Accidents↗
Metabolic studies in primary tubular hypomagnesaemia-hypokalaemia.
13 1/2 year old boy with short stature and pubertal delay had infrequent episodes of tetany. Biochemical determinations demonstrated low plasma and high urinary magnesium and potassium levels, hypocalciuria, slightly increased plasma bicarbonate, slightly reduced fractional distal reabsorption of chloride and sodium, high plasma renin activity and high urinary excretion of prostaglandins (E2, F2 alpha). The other parameters of renal functions were normal. Endocrine evaluation of short stature and pubertal delay was normal. Intracellular magnesium and potassium levels in lymphocytes and erythrocytes were within normal limits. Cyclooxygenase blockade with Indomethacin 2.5 mg/kg daily during 4 weeks normalized urinary excretion of prostaglandins and corrected in part low plasma and high urinary potassium levels, but had no effect on magnesium, calcium, sodium and chloride handling. These data raise the possibility that tubular hypomagnesaemia-hypokalaemia could be solely explained by a low renal threshold for magnesium.
Adolescent↗
Potassium and norepinephrine- or angiotensin-mediated pressor control in pre-hypertension.
Blood pressure (BP), plasma electrolytes, renin, aldosterone, angiotensin II (AII) or catecholamines, the chronotropic effects of intravenous isoproterenol, norepinephrine (NE) or AII, the pressor responses to NE or AII, and the relationship between plasma AII and aldosterone concentrations were studied before and after 10 days of dietary supplementation with potassium 100 mmol/day, in normotensive members of normotensive (N = 12) or hypertensive (N = 12) families, and 11 patients with borderline essential hypertension. Under control conditions, the pressor responsiveness to NE was significantly enhanced in normotensive with positive family history for hypertension and hypertensive subjects; the other variables were comparable in the groups. After potassium supplementation, plasma potassium, renin, aldosterone or AII, and the relationship between AII and aldosterone levels increased significantly, while body weight, plasma catecholamines, the chronotropic effects of isoproterenol, AII or NE, the pressor effects of AII and plasma clearance of AII or NE were unchanged in all groups. In normotensive members of hypertensive families and patients with hypertension, BP was decreased and the exaggerated pressor responsiveness to NE was normalized; these variables were not modified in normotensive members of normotensive families. These observations are consistent with a potassium-remediable disturbance in NE- but not AII-dependent regulation of BP in the pathogenesis of essential hypertension.
Adult↗
Twenty four hour intermittent, ambulatory blood pressure monitoring.
Blood pressure and heart rate were measured every 30 minutes during the day and every hour during the night in 43 children (20 girls and 23 boys, aged 10 to 16) with a portable automated monitor. The apparatus was better accepted in girls than in boys, and the failure rate was lower during the day. The overall failure rate was 22%, which corresponds with comparable studies in adults. During the night blood pressure and heart rate fell by 10% and 14% of the daytime values, respectively. Mean (SD) blood pressure was significantly higher in boys than in girls (126/72 (17/8) v 109/64 (9/5) mm Hg) and measurements correlated positively with age, body weight, and height of the subjects. Heart rate was not significantly influenced by gender or age. A positive correlation between heart rate and blood pressure was found when expressed as standard normal deviations or hourly variations. In children intermittent monitoring of ambulatory blood pressure and heart rate is a suitable method for measuring individual diurnal patterns.
Adolescent↗
Cardiovascular hypersensitivity to norepinephrine in normotensive members of hypertensive families: influence of dietary sodium and potassium intake.
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Adult↗
Blood pressure control in normotensive members of hypertensive families.
The cardiovascular pressor responses to a stepwise increase in plasma norepinephrine or angiotensin II concentrations, induced by infusions, were studied in 23 normotensive subjects with a negative and 25 with a positive family history of essential hypertension. The two study groups had a similar mean age (24 +/- 2 (SD) yr), body weight, blood pressure (112/64 +/- 10/7 mmHg), heart rate, plasma and urinary sodium and potassium, and plasma norepinephrine, epinephrine, angiotensin II, renin and aldosterone levels. However, subjects with positive history differed from those with negative history of hypertension by a decreased pressor dose of infused norepinephrine (89 +/- 29 vs. 135 +/- 66 ng/kg/min; P less than 0.005), and a significant (P less than 0.01) shift to the left of the relationship between norepinephrine-induced changes in mean arterial pressure and concomitant changes in plasma norepinephrine. In contrast, the relation between stepwise increasing plasma angiotensin II levels and induced changes in diastolic blood pressure or plasma aldosterone did not differ significantly between the two study groups. These findings delineate a distinct abnormality which may often occur in normotensive offspring of hypertensive families. It is characterized by a selectively disturbed noradrenergic blood pressure control in the presence of a normal angiotensin-mediated blood pressure and aldosterone regulation.
Adult↗
Body sodium-blood volume state, aldosterone, and cardiovascular responsiveness after calcium entry blockade with nifedipine.
Exchangeable sodium, blood volume, plasma norepinephrine (NE), epinephrine, renin and aldosterone levels, and pressor responses to infused NE or angiotensin II (AII) were assessed in ten patients with essential hypertension on placebo, following 6 to 8 weeks of calcium-antagonist nifedipine (NIF), 3 X 10 to 20 mg/day, and after 6 to 8 weeks on NIF combined with the diuretic chlorthalidone (CHLOR), 25 to 50 mg/day. Pressor effects of infused calcium also were evaluated on placebo and NIF. Supine blood pressure was decreased from 151/97 +/- 5/2 (SEM) to 132/88 +/- 6/2 mm Hg after NIF alone (P less than 0.05) and to 124/83 +/- 7/3 mm Hg after NIF + CHLOR (P less than 0.01). Body wt was increased from 72.7 to 73.9 kg on NIF alone (P less than 0.05), but decreased to 72.1 (P less than 0.05 compared with placebo) after adding CHLOR. Exchangeable sodium also rose from 2642 +/- 237 to 3360 +/- 266 mmoles on NIF (+ 27%; P less than 0.01) and returned to control values (2638 +/- 248 mmoles) after addition of CHLOR. Plasma volume was only slightly modified on NIF (from 2621 +/- 193 to 2751 +/- 160 ml; + 5%), but was reduced to 2232 +/- 231 ml on NIF + CHLOR (P less than 0.05). Responses of circulating aldosterone to AII were similarly diminished (P less than 0.01) during both conditions. Heart rate, supine and upright plasma renin, aldosterone and catecholamine levels, and pressor responses to NE, AII, or calcium were not consistently changed.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Disturbed noradrenergic blood pressure control in normotensive members of hypertensive families.
The possible influence of a family history of hypertension on some variables of adrenergic blood pressure regulation was assessed. Blood pressure, heart rate, plasma renin activity, adrenaline and noradrenaline concentrations, and plasma or urinary electrolyte estimations did not differ significantly between two groups of normotensive subjects matched for age and sex with and without a family history of hypertension. Compared with subjects without a family history, however, an appreciably decreased pressor dose of infused noradrenaline, a distinct shift to the left in the relation between noradrenaline induced changes in mean arterial pressure and concomitant plasma noradrenaline concentrations, and an enhanced pressor response to given increases in plasma noradrenaline concentrations occurred in the group with a family history. These findings suggest that an imbalance between cardiovascular noradrenaline responsiveness and circulating noradrenaline is a common familial disturbance which could possibly predispose to the development of essential hypertension.
Adult↗
Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.
The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg X min was assessed in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P less than 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angiotensin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.
Adult↗
Correction of cardiovascular hypersensitivity to norepinephrine by potassium supplementation in normotensive members of hypertensive families and patients with essential hypertension.
Blood pressure (BP), plasma levels of norepinephrine (NE) and epinephrine, the chronotropic effect of isoproterenol, and the relationship between variations in BP and concomitant plasma NE levels obtained during NE infusion were studied under control conditions and after 10 days of dietary potassium supplementation (100 mmol/day) in 12 normotensive subjects with negative family history (FH) of hypertension (mean BP 111/70 +/- 9/7 mmHg), 11 normotensive subjects with positive FH (112/73 +/- 8/6 mmHg), and 10 subjects with untreated borderline to mild essential hypertension (131/89 +/- 15/9 mmHg). Under control conditions, the increase in circulating NE required to elevate mean BP by 20 mmHg was significantly lower in hypertensive subjects (6.1 +/- 4.0 nmol/l) or normotensive subjects with positive FH (5.0 +/- 2.4 nmol/l) than in normal subjects with negative FH (9.9 +/- 6.4 nmol/l); the other study parameters were similar. After potassium supplementation, plasma and urinary potassium increased and body weight decreased slightly in all groups; basal plasma NE and epinephrine levels and cardiovascular effects of isoproterenol were unchanged. However, in normotensive subjects with positive FH and hypertensive subjects, the increase in plasma NE required to elevate mean BP by 20 mmHg was normalized (to 8.9 +/- 5.9 and 9.9 +/- 6.9 nmol/l, respectively), while BP tended to decrease slightly. These findings indicate that dietary potassium supplementation may favorably modify noradrenergic BP-regulation in hypertension prone individuals.
Adult↗
Pressor factors and cardiovascular pressor responsiveness after short-term antihypertensive therapy with the calcium antagonist nifedipine alone or combined with a diuretic.
Exchangeable sodium, blood volume, plasma norepinephrine, epinephrine, renin levels, and pressor responses to infused norepinephrine or angiotensin II were assessed in 10 patients with essential hypertension on placebo, following six to eight weeks of monotherapy with nifedipine, 3 X 10-20 mg/day, and after six to eight weeks on nifedipine combined with the diuretic chlorthalidone, 25 to 50 mg/day. Supine blood pressure was decreased after nifedipine alone (P less than 0.05) and even further after nifedipine + chlorthalidone (P less than 0.01). Body weight and exchangeable sodium increased after nifedipine (P less than 0.05), but were decreased after adding chlorthalidone. Blood volume was unchanged after nifedipine, but was reduced on nifedipine + chlorthalidone (P less than 0.05). Heart rate, supine plasma renin, catecholamine levels, and pressor responses to norepinephrine or angiotensin II were not consistently changed on nifedipine alone or combined with chlorthalidone. These findings indicate that in the established phase of treatment, nifedipine may exert its antihypertensive effect without necessarily altering cardiovascular responsiveness to norepinephrine and angiotensin II. Moreover, mild sodium retention may develop on nifedipine at least in some hypertensive patients.
Adult↗
Acute effects of combined vasodilation and beta-adrenoceptor blockade with prizidilol on renal function.
1 The effects of a single oral dose of 600 mg of prizidilol on renal function were studied 5 to 6 h after dosing in six normal subjects and eight patients with essential hypertension. 2 Mean arterial blood pressure was reduced to 92% of the control value in normal subjects and to 75% in hypertensive patients. Heart rate increased slightly. 3 In normal subjects, effective renal plasma flow was increased to 107% of control values while glomerular filtration rate (83%), filtration fraction (79%), sodium (84%) and potassium (50%) clearances were significantly decreased. 4 In hypertensive subjects, effective renal plasma flow was increased to 120% of control values, while glomerular filtration rate (67%), filtration fraction (57%), sodium (27%) and potassium (72%) clearances were significantly decreased. 5 Plasma noradrenaline increased significantly in normal subjects (150%) and in patients (173%). Plasma renin activity, aldosterone and epinephrine levels did not change consistently. 6 The results indicate that the acute effects of prizidilol on blood pressure and renal function are more marked in hypertensive than in normotensive subjects. Prizidilol increases renal plasma flow like hydralazine and depresses glomerular filtration rate and fractional sodium excretion like endralazine. In addition to the fall in arterial pressure, efferent vasodilation and/or a specific effect on the glomerular ultrafiltration coefficient Kf may account for the striking decrease in filtration fraction.
Adrenergic beta-Antagonists↗