[Thrombotic thrombocytopenic purpura successfully treated with plasma exchange]. / Zakrzepowa plamica maloplytkowa skutecznie leczona wymiana osocza.

This study is a presentation of a case of a 43 year old woman suffering from thrombotic thrombocytopenic purpura, the clinical course of which was complicated and in which no improvement was observed after fresh frozen plasma transfusions and treatment with steroids. The complete clinical and haematological remission was obtained only after intensive plasma exchange by therapeutical plasmapheresis.

Vasopressin secretion during hyperglycemia in insulin-dependent diabetics.

Plasma levels of vasopressin (AVP) were measured in ten insulin-dependent diabetic patients before and during intravenous administration of hypertonic glucose. Plasma glucose and plasma osmolality increased from 12.4 +/- 1.2 to 47.0 +/- 2.3 mmol/l and from 293 +/- 2.0 to 307 +/- 2.8 mosm/kg respectively. Plasma vasopressin increased in parallel from 5.6 +/- 0.6 to 7.7 +/- 0.6 pg/ml. The present results demonstrate that hyperglycemia may be an effective stimulus for AVP secretion in insulin-deficient diabetics.

Changes in plasma renin, insulin, aldosterone and arginine vasopressin during plasmapheresis.

1. Nineteen patients with a spectrum of immunologically related disorders were studied before and immediately after plasmapheresis for changes in plasma aldosterone, insulin and arginine vasopressin (AVP). Renin was also measured in 11 of these patients by direct radioimmunoassay. 125% of the initial plasma volume was replaced, which corresponded to a predicted removal of 72% for any plasma constituent. 2. The initial, final (experimental) and final (predicted) concentrations (means +/- SEM) were 337 +/- 50, 185 +/- 23 and 100 +/- 16 pg/ml respectively for renin, 465 +/- 86, 146 +/- 38 and 124 +/- 22 pmol/l respectively for aldosterone, 218 +/- 35, 69 +/- 11 and 63 +/- 11 pmol/l respectively for insulin, 7.2 +/- 1.9, 6.1 +/- 0.5 and 1.8 +/- 0.2 pmol/l respectively for AVP. The predicted final concentration was calculated from the initial concentration and the fraction of plasma volume exchanged. The experimental final concentration was lower than the initial concentration for renin, aldosterone and insulin (P less than 0.001) but not for AVP. The predicted final concentration was lower than the experimental final concentration for AVP and renin (P less than 0.001) but not for aldosterone and insulin. Plasma volume, osmolality, glucose, sodium and potassium concentrations did not change significantly. 3. The concentrations of renin, aldosterone, insulin and AVP in the removed plasma were 84 +/- 17 pg/ml, 179 +/- 36, 98 +/- 15 and 4.8 +/- 0.7 pmol/l respectively. The amount subtracted expressed as percentage of the total amount present in plasma was markedly greater for AVP than for the three other plasma constituents.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal response to volume expansion in heart-transplant and kidney-transplant recipients.

The renal excretion of an intravenous sodium load by ten heart-transplant recipients with (five patients) or without (five patients) moderate renal failure was compared with the results obtained in two matched control groups of ten kidney-transplant recipients with similar renal function. All patients were treated with prednisone and cyclosporine except, for the latter treatment, the kidney-transplant recipients without renal failure. A supplementary control group of five healthy subjects who did not receive any treatment was also included in the study. Fractional sodium and osmolal clearances were greater in heart-transplant than in kidney-transplant recipients for both the patients with and the patients without renal failure. These two parameters were also greater in heart-transplant recipients without renal failure than in healthy subjects. Free water clearance was smaller in the heart-transplant recipients than in the corresponding control patients. Fractional potassium clearance was not different from group to group. These results demonstrate that heart-transplant recipients excrete a greater fraction of the filtered sodium load than their controls. This increased fractional excretion of sodium cannot be attributed to the cyclosporine treatment or the moderate chronic renal failure which both have been taken into account in the comparisons. The unchanged blood pressure during the saline load and the high or normal plasma renin activity levels in the heart-transplant recipients make it also unlikely that the exaggerated natriuresis was the consequence of the higher blood pressure observed in these patients. The chronic cardiac denervation which is the consequence of surgery in these patients could play a role in the mechanism of the saline diuresis.

Massive plasma arginine vasopressin (AVP) removal during hemofiltration stimulates AVP secretion in humans.

Arginine vasopressin (AVP) was measured in the plasma and its ultrafiltrate in 11 patients with end-stage renal failure treated by hemofiltration. Nineteen liters of ultrafiltrate were produced in 170 min and continuously replaced by an isoosmotic substitution fluid to maintain constant body weight. Plasma and ultrafiltrate AVP concentrations were not significantly different and did not change with time. The AVP clearance rate due to hemofiltration was 114 +/- 2.6 (+/- SE) ml/min, which represented more than two thirds of the predicted MCR in these patients. Corrected plasma osmolality, body weight, mean blood pressure, hematocrit, and PRA did not change during the hemofiltration session. These results indicate that there is a compensatory increase in AVP production which maintains plasma AVP unchanged in response to the increased MCR resulting from hemofiltration. The responsible stimulus could be a direct effect of the decrease in plasma AVP on the AVP-secreting neurones. Alternatively, ultrafiltration itself, via the hemodynamic changes it produces or the loss of an unrecognized inhibitory substance, may be the stimulus to AVP secretion.

Role of cardiac parasympathetic dysfunction in atrial natriuretic peptide response to volume changes in patients with chronic renal failure.

Plasma atrial natriuretic peptide (ANP) was measured by radioimmunoassay in 10 patients with end-stage renal failure during two successive 150-min periods of ultrafiltration and perfusion of an identical fluid volume (1,800-2,400 ml). The patients were divided into two groups of 'denervated' and 'intact' patients based on three different tests for cardiac parasympathetic dysfunction. Plasma ANP was higher in the denervated group than in the intact group throughout all the study, but decreased with the volume ultrafiltered and increased with the volume perfused in both groups. The sensitivity of ANP response to perfusion was greater in denervated than in intact patients. These results demonstrate the close relationship between plasma ANP and stepwise decremental or incremental changes in extracellular fluid volume. They also suggest that cardiac parasympathetic innervation plays a role in modulation of ANP secretion in humans.

Antidiuretic hormone response to volume depletion in diabetic patients with cardiac autonomic dysfunction.

Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact' patients) and 16 as with ('denervated' patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in 'denervated' and 'intact' patients respectively) and heart rate response (+ 1.06 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the 'intact' patients whereas it fell in the 'denervated' patients (-13.5%). PRA (+ 161.5 and + 231.2% in 'denervated' and 'intact' patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in 'intact' patients (+ 55.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men.

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal excretion of antidiuretic hormone in healthy subjects and patients with renal failure.

Urinary clearance of antidiuretic hormone (ADH) has been measured under basal conditions and during intravenous administration of arginine vasopressin in ten healthy subjects, and only under basal conditions in 18 patients with chronic renal failure and seven patients with acute renal failure at the polyuric phase of the disease. In healthy subjects studied under conditions of mild water diuresis plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 3.3 +/- 0.36 pg/ml, 25.2 +/- 5.5 pg/min, 7.5 +/- 1.2 ml/min and 6.4 +/- 1.0% (means +/- SEM) respectively. When plasma ADH was raised to levels between 7 and 26 pg/ml during intravenous administration of the hormone, urinary excretion rate and urinary clearance of ADH increased. Tubular reabsorption of ADH did not reach a plateau but progressively increased in the range of plasma ADH studied. In patients with chronic renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 2.8 +/- 0.19 pg/ml, 9.4 +/- 2.0 pg/min, 3.4 +/- 0.6 ml/min and 10.0 +/- 2.9% (means +/- SEM) respectively. Urinary excretion rate and urinary clearance were significantly lower than in healthy subjects. In patients with acute renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 4.6 +/- 0.47 pg/ml, 52.8 +/- 15.8 pg/min, 9.5 +/- 2.7 ml/min and 24.9 +/- 4.4% (means +/- SEM) respectively. Urinary excretion rate and fractional clearance were higher than in healthy subjects and patients with chronic renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of antidiuretic hormone in impaired water excretion of patients with congestive heart failure.

Plasma antidiuretic hormone (ADH), PRA, plasma osmolality, and the parameters of renal water excretion were measured after overnight dehydration and for 5 h after an oral load in 14 patients with congestive heart failure (CHF) treated with diuretics (group 1), 8 hypertensive patients without CHF also treated with diuretics (group 2), and 11 patients with coronary artery disease but without CHF who were not treated with diuretics (group 3). Under basal conditions, mean plasma osmolality was lower in group 1 than in group 3, but was not different in groups 1 and 2. Mean plasma ADH was higher in group 1 than in group 2 or 3. In response to the water load, plasma osmolality and plasma ADH levels decreased in the 3 groups. ADH levels remained significantly greater in group 1 than in groups 2 and 3 from 2-4 h after the water load despite more marked hypoosmolality in group 1 compared with that in either of the 2 control groups. Plasma ADH was significantly correlated with plasma osmolality only in the 2 control groups. Mean PRA was greater in patients with CHF and patients without CHF treated with diuretics than in untreated patients. Cumulative water excretion was lower in patients with CHF than in patients in the 2 control groups from 2-5 h after the water load. At 5 h, the mean percentage excretion of the ingested loads was 56.8%, 90.7%, and 91.2% in the patients of groups 1, 2, and 3 respectively. Free water clearance was lower and minimal urinary osmolality was greater in the patients with CHF than in those in the 2 control groups. Two patients with CHF, who excreted more than 75% of the water load, also had low plasma basal ADH levels. These data show that patients with CHF have an inappropriate response of plasma ADH to a marked fall in plasma osmolality. This disorder is not due to the diuretic therapy, since hypertensive patients treated with diuretics behaved similarly to untreated patients without CHF. The reasons for this inappropriate response of plasma ADH during a water load in patients with CHF are probably multifactorial.