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Biomedical subjects

F Mallamaci

Publications and source records attributed to F Mallamaci.

At least 19 recordsLinked to original sources
PubMed1998

Plasma adrenomedullin during acute changes in intravascular volume in hemodialysis patients.

BACKGROUND: Adrenomedullin, is a potent vasorelaxant that is highly expressed in the adrenal medulla, kidney, heart and lung. Since there is indirect evidence that hypervolemia enhances the release of this peptide, we measured plasma adrenomedullin in 9 uremic patients on chronic dialysis treatment and in 10 healthy subjects matched for age and gender. METHODS: Measurements were performed in baseline conditions, after isotonic fluid subtraction (by isolated ultrafiltration) and during a 70 degrees tilt. Tilt was performed in volume-depleted state, that is, after isolated ultrafiltration (UF). In the control experiment patients underwent sham UF (UF = 0) followed by a period of supine resting identical to the one they had spent in tilted position in the active experiment. Adrenomedullin was measured on pre-extracted plasma samples (Sep-Pak C-18 cartridges) by a specific RIA for human adrenomedullin 1-52. RESULTS: The average plasma adrenomedullin was 2.6 times higher (P < 0.01) in uremic patients (103 +/- 8 pg/ml) than in healthy subjects (39 +/- 7 pg/ml). After fluid subtraction (-2.6 +/- 0.2 liter) adrenomedullin fell to 79. +/- 8 pg/ml (P = 0.02) but remained well above the upper limit of the 95% CI in normal subjects (52 pg/ml). There was no relationship between adrenomedullin and ANF changes. In the control experiment sham UF did not modify plasma adrenomedullin. Tilt did not significantly change plasma adrenomedullin either in dialysis patients or healthy subjects. CONCLUSIONS: Plasma adrenomedullin is markedly raised in uremic patients on dialysis, which confirms that the kidney has a major role in the clearance of this peptide. However, the fall in plasma adrenomedullin after isolated UF indicates that the plasma concentration of this peptide is influenced by the body fluid volume status. Whether or not adrenomedullin participates in the counter-regulatory response to fluid subtraction in uremic patients remains to be explored by specific antagonists of this substance.

Adrenomedullin↗
PubMed1998

Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients.

It is well established that nocturnal hypoxemia in sleep apnea causes an inversion of the circadian arterial pressure rhythm and triggers nocturnal hypertension. Since sleep apnea is very frequent in dialysis patients, we hypothesized that nocturnal hypoxemia may be a factor that contributes to alter the 24-hour arterial pressure profile in these patients. To test the hypothesis 32 dialysis patients underwent 24-hour blood pressure (BP) monitoring and continuous monitoring of arterial O2 saturation during the night-time. Hemodialysis patients were studied during the non-dialysis day. All patients underwent an echocardiographic study. Thirteen patients had no episode of nocturnal hypoxemia (group I), 7 had at least one episode overnight but less than 2 episodes/hr (group II) and 12 had > or = 2 episodes/hr (group III). The average daytime systolic pressure was similar in the three groups. However, the average nocturnal systolic pressure fell in the first group (-2.5 +/- 4.2%) and rose in the second (+2.0 +/- 3.6%) and in the third (+3.9 +/- 2.2%) group (one way ANOVA, P < 0.005). The relative wall thickness of the left ventricle (RWT) was significantly (P < 0.05) higher in group III than in group I, and in the aggregate (N = 32) there was an inverse relationship between average nocturnal SaO2 and RWT (r = -0.43, P = 0.015). The proportion of patients with concentric remodeling or concentric hypertrophy was higher (P = 0.05) in the group with a more severe degree of nocturnal hypoxemia (group III, 8 of 12) than in the other two groups (group I, 3 of 13; group II, 2 of 7). Nocturnal hypoxemia is associated with the "non-dipping" arterial pressure profile in dialysis patients. Disturbed respiratory control during the night may represent an important cardiovascular risk factor in dialysis patients.

Adolescent↗
PubMed1997

The heart rate response pattern to dialysis hypotension in haemodialysis patients.

BACKGROUND: Hypotension during haemodialysis may be caused by the activation of a cardiovascular reflex causing abrupt sympathetic withdrawal, vasodilatation and bradycardia (bradycardic hypotension). However, the frequency of this type of hypotension is undefined and it is unclear whether or not it underlies a peculiar predisposition to vasodepressor syncope. OBJECTIVE: To assess the prevalence of bradycardic hypotension and to test the hypothesis that dialysis patients are predisposed to vasodepressor syncope. RESULTS: Sixty hypotensive episodes were recorded in 20 patients (> or = 2 episodes in 15 patients). Heart rate increased in 35 episodes, did not change in 19 episodes and decreased in six episodes. The HR response pattern to hypotension was reproducible in 10 patients (always tachycardia, 6; always unchanged heart rate 4). Patients developing bradycardic hypotension (n = 5) all had an erratic HR response to hypotension (i.e. bradycardia preceded or followed by tachycardia or by no HR change) and were characterized either by the typical haemodynamic pattern of hypovolaemia (predialysis hypotension, tachycardia and low TBW) or by being treated with a very high UF rate (> 0.3 ml/kg/min). Post-dialysis echocardiography showed that the LVEDD was less (one-tailed P = 0.055) in patients with bradycardic hypotension than in those with tachycardic responses or with unchanged HR. On tilt testing (after dialysis) three of 11 (27%) dialysis hypotensive patients developed bradycardic hypotension. This proportion was identical to that expected in healthy subjects and in control patients without syncope. CONCLUSIONS: Tachycardia is the more frequent heart rate response to dialysis hypotension in uraemic patients. Bradycardic hypotension in dialysis patients is associated with a haemodynamic profile indicating a more severe degree of cardiovascular underfilling. Bradycardic hypotension probably represents a physiological response to hypovolaemia rather than the expression of a peculiar predisposition to vasodepressor syncope.

Adult↗
PubMed1997

The influence of volume depletion and central hypovolemia on the plasma concentration of parathyroid hormone in dialysis patients.

Because changes in extracellular volume during dialysis cause reflex neurohonnonal changes that may influence parathyroid hormone (PTH) release independently of calcium, the influence of isotonic volume depletion (by isolated ultrafiltration) and central hypovolemia (70 degrees tilt) on serum PTH1-84 was studied in 16 hemodialysis patients. Tilting was performed in volume depleted state, i.e., immediately after hemodialysis. In the control study, patients underwent sham ultrafiltration (UF = 0) and after dialysis maintained the supine position for the same length of time they remained in the tilt position in the active experiment. Isolated ultrafiltration (-2.3 +/- SEM 0.3 L) caused a 21% fall in mean arterial pressure (from 101 +/- 6 to 80 +/- 6 mmHg, P < 0.01), a fall that was accompanied by a marked increase in plasma catecholamine levels (norepinephrine P < 0.001, epinephrine P < 0.025), in plasma renin activity (P < 0.001) and in plasma arginine vasopressin (P < O.001). Atrial natriuretic factor showed a slight reduction, whereas the plasma endothelin-1 level did not change. Serum Ca showed the expected, hemoconcentration-dependent rise (from 4.1 +/- 0.1 to 4.4 +/- 0.1 meq/L, P < 0.01). Interestingly, UF caused a marked rise in plasma PTH1-84 concentration (from 252 +/- 62 to 335 +/- 72 pg/ml, P < 0.01). UF-induced changes in serum PTH1-84 were related to norepinephrine changes (r = 0.57) as well as to plasma renin activity (r = 0.50). After hemodialysis, tilting induced a pronounced rise in serum PTH1-84 (from 102 +/- 29 to 200 +/- 55 pg/ml), and these changes were slightly related to plasma epinephrine (r = 0.49) but independent of other parameters. In the control experiment, neither sham UF nor recumbency modified serum PTH. In hemodialysis patients, serum PTH is sensitive to changes in extracellular and central blood volume of magnitude sufficient to decrease arterial pressure. Avoiding marked volume stimuli might help to refine the interpretation of the Ca/PTH curves during hemodialysis in these patients.

Adult↗
PubMed1996

Reproducibility of the response to short-term low salt intake in essential hypertension.

BACKGROUND: The reproducibility of the arterial pressure response to change in salt intake in essential hypertensives has been little investigated. OBJECTIVE: To study the reproducibility of the response to salt in 14 untreated patients with mild essential hypertension. METHODS: After a run-in phase (1 month), each patient ingested, in random order and with cross-over, 1 week of high salt intake (170 mmol/day) and 1 week of low salt intake (40 mmol/day). The identical experimental protocol was then repeated after an average interval of 3.4 months. Arterial pressure was measured (clinic arterial pressure and 24 h ambulatory monitoring) on the seventh day of each diet period. The reproducibility of the arterial pressure response was assessed in terms the intraclass correlation coefficient and the K statistics. RESULTS: There was a good compliance with the dietary prescription because the urinary Na excretion was on average very close to the prescribed intake both during the first and during the second salt intake period. Both clinic and 24 h arterial pressure fell significantly (P < 0.01) and to the same extent in the low-salt phases of the study. Clinic arterial pressure was consistently higher than 24 h ambulatory arterial pressure but the average changes induced by salt depletion were similar. The variability of 24 h ambulatory arterial pressure at constant salt intake was lower than that of clinic arterial pressure. However, the arterial pressure response to salt showed the same variability with the two methods. The reproducibility of the dichotomous classification of patients into salt-sensitive and -resistant was low both in terms of 24 h ambulatory and in terms of clinic blood pressure. CONCLUSION: Although on rechallenging the average arterial pressure response to salt remains unchanged in essential hypertensives, the individual responses are variable and the reproducibility of the dichotomous classification is unsatisfactory. The problem of dichotomizing patients into salt-sensitive and -resistant ones is only in very little part resolved by more precise arterial pressure estimates.

Adult↗
PubMed1996

Does high salt intake cause hyperfiltration in patients with essential hypertension?

In animal models of salt-dependent hypertension, hyperfiltration is associated with a faster decline in renal function and there is evidence that in hypertensive man, increased creatinine clearance is a marker of early hypertensive nephropathy. We have studied the influence of salt intake on the glomerular filtration rate (GFR) (Creatinine Clearance) in 14 patients with mild hypertension. Each patient was studied in random order and according to a crossover design, at habitual salt intake, at high salt intake (ie habitual +50/100 mmol/day) and at low salt intake (habitual -50/100 mmol/day). Protein, calcium and potassium intake was fixed across the three study periods. The control group was formed by seven healthy subjects. High salt intake, caused a significant (P < 0.01) increase in 24 h mean arterial pressure (MAP) and the expected suppression in plasma renin activity (PRA) and in plasma aldosterone. Seven patients were classified as salt-sensitive. The GFR was significantly higher (P < 0.01) at high salt intake (125 +/- 10 ml/min) than at habitual (113 +/- 7 ml/min) and at low salt intake (97 +/- 6 ml/min). On aggregate urinary salt excretion was significantly related with the GFR (P < 0.01 by correlation analysis for repeated observations) and the slope of this relationship predicted that a 100 mmol/day increase in salt intake is associated with the 14.6 ml/min rise in the GFR. The relationship between GFR and 24 h urinary salt in salt sensitive patients did not differ from that in salt resistant patients. The GFR response to salt loading was largely independent of the renin-aldosterone system. No change in arterial pressure nor in GFR was observed in healthy subjects. At fixed protein intake, changes in salt intake in the physiological range are associated with important GFR variations in mild hypertensives. As long as hyperfiltration in mild hypertension is a predictor of renal function deterioration, high salt intake, independent of the effect of arterial pressure, could be a factor that contributes to nephronic obsolescence in patients with essential hypertension.

Adult↗
PubMed1995

Urinary and plasma endothelin 1 in essential hypertension and in hypertension secondary to renoparenchymal disease.

An alteration in renal metabolism of endothelin may contribute to hypertension in the SHR and it has been shown that the excretion rate of endothelin is reduced in patients with essential hypertension. We measured plasma and urinary endothelin 1 (ET-1) in 20 untreated essential hypertensives with normal renal function, in eight normotensive healthy subjects, and in 13 hypertensive patients with primary renoparenchymal disease. Plasma ET-1 was higher (P < 0.01) in essential hypertensives (median 1.69, interquartile range 1.2-3.3 pg/ml) than in normal subjects (0.84, 0.37-1.10 pg/ml) but significantly less (P < 0.01) than in hypertensives with renoparenchymal disease (3.57, 1.45-9.52 pg/ml). ET-1 levels slightly correlated with diastolic pressure in essential hypertensives (r = 0.43, P < 0.05) and tended to be correlated with systolic pressure in hypertensives with renal disease (r = 0.47, P = 0.08). ET-1 excretion in essential hypertensives (137, 99-154 ng/24 h) and in normal subjects (120, 62-150 ng/24 h) was significantly lower than in renal hypertensives (191, 123-241 ng/24 h). The ET clearance/GFR ratio (ClET/GFR) was markedly reduced (30%, 21-67%) in essential hypertensives and substantially raised in renal hypertensives (164%, 86-314%) in comparison with normal subjects (83%, 35-94%). Since the ClET/GFR ratio should be 100% if all filtered ET-1 is excreted, the data indicate that ET-1 is synthesized at a reduced rate and/or broken down at an enhanced rate by the kidney in essential hypertension and confirm that there is a high ET-1 generation rate in remnant nephrons in hypertension secondary to renal disease.

Adolescent↗
PubMed1994

Assessment of the salt-arterial pressure relationship in mild hypertensive subjects by 24-hour ambulatory monitoring.

1. We have assessed the relationship between salt intake and 24 h ambulatory arterial pressure in middle aged men with essential hypertension. 2. During the run-in phase (1 month) we estimated the habitual sodium intake (the average Na excretion of two 24 h urine collections) of each participant (n = 14). In the randomized and crossover part of the study we contemplated a 'habitual' sodium intake phase, in which each individual received a fixed diet (about 30 mmol of Na+ and 65 mmol of K+) with additional salt so as to equalize the average intake of the run-in phase, as well as high sodium phases (habitual intake +50 and +100 mmol/day) and low sodium phases (habitual intake -50 and -100 mmol/day). After the trial, 10 patients underwent an additional week of fixed salt intake to assess the reproducibility of 24 h ambulatory monitoring. 3. Average 24 h arterial pressure at habitual sodium intake was significantly lower than that at high intake and significantly higher than at low sodium intake. Clinic arterial pressure showed similar trends but only systolic pressure changes at low sodium intake achieved statistical significance. 4. Analysis of the data on an individual basis showed a linear increase in 24 h mean arterial pressure with increasing levels of sodium intake in all but two cases (flat response in one case and a non-linear rise in the other case). The response pattern of clinic measurements was much less homogeneous. In the aggregate, there was a highly significant linear trend for ambulatory arterial pressure to rise with increasing levels of salt intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Influence of extracellular volume expansion on circulating PTH1-84 in subjects with mild essential hypertension.

The effect of acute volume expansion by saline (1 L/40 min) on serum parathyroid hormone (PTH) concentration was studied in 28 subjects with mild essential hypertension. At the zenith volume expansion there was a significant increase in systolic pressure (7 +/- 2 mm Hg, P < .01) while diastolic pressure and heart rate showed minor (NS) variations. The rise in systolic pressure was accompanied by a significant (P = .02) decrease in plasma ionized calcium (from 1.12 +/- 0.03 to 1.08 +/- 0.03 mmol/L) and by a marked PTH increase (from 36 +/- 3 to 60 +/- 4 pg/mL, P < .01). The arterial pressure variations were independent of changes in serum PTH. In a second experiment (n = 11), aimed at preventing the changes in calcium concentration brought about by hemodilution, we infused the same volume of saline with the addition of 1.25 mmol of elemental calcium. In this study PTH showed a small, nonsignificant, decrease while systolic pressure changes were similar to those of the first study (ie, an isolated 9 +/- 4 mm Hg increase in systolic pressure). In a third experiment (n = 7), aimed at studying the effect of raised plasma PTH concentration in isocalcemic conditions, PTH1-38 was continuously infused (1 ng/kg/min) during the volume expansion phase performed with the same solution as used in the second experiment. The hemodynamic changes were again identical to those of the other studies (an isolated 9 +/- 3 mm Hg increase in systolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1994

Influence of ANF on the cardiovascular response to volume expansion in haemodialysis patients.

Plasma ANF concentration in uraemic patients is very sensitive to changes in extracellular volume. It is unknown, however, if the release of this vasoactive hormone has a compensatory role in the haemodynamic response to extracellular volume expansion in these patients. We investigated the effect of isolated ultrafiltration followed by isovolumic re-expansion by saline in seven haemodialysis patients. The experiment was repeated on two occasions and the UF rate as well as the rate of volume re-expansion in the two studies were accurately matched. During the phase of volume re-expansion, we infused either ANF (0.83 microgram/min) or a placebo, in random order and cross-over. Central venous pressure, arterial pressure, haematocrit, and plasma ANF concentration were measured in baseline conditions, after ultrafiltration, and 0, 15, and 30 min after isovolumic re-expansion. In the control experiment (placebo), isolated ultrafiltration caused a marked reduction in central venous pressure and in arterial pressure and a pronounced haematocrit increase. These changes were reversed by volume re-expansion. In the active experiment, during the phase of volume re-expansion ANF infusion doubled plasma ANF concentration as compared to control experiment but it did not affect the ongoing haemodynamic response nor the haematocrit changes. Doubling of plasma ANF concentration has no influence on the haemodynamic and microcirculatory adaptations to acute volume expansion in haemodialysis patients. The data indicate that it is unlikely that raised plasma ANF concentration has a major role in the cardiovascular response to acute extracellular volume expansion in these patients.

Adult↗
PubMed1994

The influence of salt intake on plasma calcitonin gene-related peptide in subjects with mild essential hypertension.

BACKGROUND: Calcitonin gene-related peptide is a pleiotropic neuropeptide with potent vasodilatory properties, which interferes with renin release and might participate in cardiovascular homeostasis. DESIGN AND METHODS: We studied the influence of salt intake on the plasma concentration of calcitonin gene-related peptide, parathyroid hormone and on the renin-aldosterone system in 15 patients with mild hypertension. Each participant was studied after 1 week of high salt intake (200 mmol/day) and after 1 week of low salt intake (50 mmol/day). The order of the two diet periods was randomized and crossover. Plasma calcitonin gene-related peptide concentration was measured by radioimmunoassay after pre-extraction by reverse chromatography. Seven patients were classified as salt-sensitive and eight as salt-resistant. RESULTS: In the whole group the low salt intake caused a significant decrease in arterial pressure and the expected increase in plasma renin activity and in plasma aldosterone concentration. Such changes were accompanied by a significant increase in plasma calcitonin gene-related peptide. In salt-resistant patients in the sodium-replete state calcitonin gene-related peptide levels tended to be reduced in comparison with salt-sensitive patients. Sodium depletion, however, caused a more pronounced rise in plasma calcitonin gene-related peptide in salt-resistant hypertensives, who attained levels close to those in salt-sensitive hypertensives. Interestingly, in salt-resistant hypertensives changes in plasma calcitonin gene-related peptide were closely related to plasma renin activity (r = 0.71, P = 0.003), whereas no such correlation was found in salt-sensitive patients. Parathyroid hormone was not influenced by changes in salt intake. CONCLUSIONS: In subjects with mild hypertension calcitonin gene-related peptide is sensitive to changes in salt intake in the physiological range. Such a response seems to be linked to the individual arterial pressure response to salt, because salt-resistant patients showed reduced calcitonin gene-related peptide levels in the sodium-replete state and a more pronounced calcitonin gene-related peptide increase, closely related to plasma renin activity, during sodium deprivation.

Adult↗
PubMed1993

Influence of cardiovascular damage and residual renal function on plasma endothelin in chronic renal failure.

To study the influence of cardiovascular damage on plasma endothelin in chronic renal failure, we have measured the plasma concentration of this peptide in 32 uremic patients (7 undialyzed uremics, 8 CAPD patients and 16 hemodialysis patients) and in 9 healthy subjects. Sixteen patients had severe cardiovascular damage while the other 16 had no cardiovascular involvement. Endothelin was markedly raised (p < 0.01) in the uremic group as a whole (13.9 +/- 2.6 pmol/l) in comparison with the group of healthy subjects (8.6 +/- 1.6 pmol/l). Hemodialysis patients displayed endothelin levels much higher (p < 0.01) than CAPD patients and undialyzed uremics. Endothelin was directely related with BUN (r = 0.37) and with serum creatinine (r = 0.52) in dialysis patients. Similar correlations were also found in undialyzed uremics. Plasma endothelin was almost identical in patients with severe cardiovascular damage (15.5 +/- 1.6 pmol/l) and in those without cardiovascular involvement (15.9 +/- 2.6 pmol/l). There was no relationship between arterial pressure and plasma endothelin. Residual renal function is an important determinant of circulating endothelin even at very advanced stages of renal insufficiency. It appears unlikely that atherosclerosis plays a major role in the pathogenesis of high plasma concentration of this peptide in uremic patients.

Adult↗