Cadaver kidney transplantation in hyperimmunized patients.
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Biomedical subjects
Publications and source records attributed to L M Ruilope.
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Besides the classical modulators of aldosterone secretion, new factors influencing positively or negatively aldosterone secretion have been described. These new factors and the effect of related drugs constitutes the aim of this review. The effect of dopamine agonists and H2-receptor antagonists on aldosterone secretion in normal volunteers as well as in different clinical situations characterized by an increased production of aldosterone opens a new field of investigation for the therapy of aldosterone secretion alterations.
In experimental animals, a high protein diet has been shown to accelerate end-stage renal disease by inducing glomerular hyperperfusion. In this study, we found that intravenous administration of amino acid, used as one component of parenteral nutrition, to normal volunteers resulted in a significant increase in renal blood flow (from 517 +/- 29 to 754 +/- 60 ml/min) and glomerular filtration rate (from 106 +/- 6 to 165 +/- 12 ml/min) without altering systemic blood pressure, renal excretion of electrolytes, plasma renin activity, or plasma aldosterone concentration, and excretory rates of prostaglandins E2 were increased (from 665 +/- 61 to 1,034 +/- 153 pg/min). These amino acid-induced renal hemodynamic effects were abolished when the volunteers received a low sodium diet (20 mEq/day) for three days before the amino acid infusions. However, the hemodynamic effects were restored when the subjects receiving low sodium diets were pretreated with captopril. Under these conditions, amino acid infusions increased renal blood flow (from 388 +/- 11 to 597 +/- 27 ml/min) and glomerular filtration rate (from 80 +/- 4 to 118 +/- 9 ml/min). Reduction of prostaglandin synthesis with indomethacin in volunteers receiving a normal sodium intake was also capable of significantly decreasing the amino acid effects on renal hemodynamics. The results indicate that the renal hemodynamic effects of amino acid infusion are strongly influenced by angiotensin II and prostaglandin formation.
Serum levels of vitamin A (VA) were measured in 71 hemodialysis (HD) patients and in 30 normal controls. 65 of the 71 patients were taking multivitamin preparations (MP) containing VA. The HD patients had significantly greater values: 7.81 +/- 2.86 mumol/l (224 +/- 82 micrograms/dl) versus 3.97 +/- 0.97 mumol/l (114 +/- 28 micrograms/dl; p less than 0.0005); those taking MP with large doses of VA showed the highest levels. Patients were divided as having normal (group I, n = 21) or elevated (group II, n = 50) serum levels of VA. Patients of group II had higher levels of serum calcium (Ca) and lower of serum phosphate (P) and PTH than those of group I. Four months after the withdrawal of oral VA, the serum levels of VA and Ca fell significantly in group II, while the serum P increased. On the contrary, in group I serum levels of VA, Ca and P remained unchanged. Serum triglycerides (TG) were significantly higher in group II but did not change after the withdrawal of VA. No differences between both groups of patients were observed for age, time on HD, residual diuresis, residual renal function, serum levels of cholesterol (CL) or anemia. A retrospective study of 18 hepatic biopsies of HD patients disclosed hyperplasia of Ito cells (VA-storaging cells) in 7 of them. These 7 biopsies belonged to patients who had taken large amounts of oral VA. Our data indicate that prolonged VA intake in HD patients is followed by an increase of serum CA, a decrease of serum P and PTH and a hepatic accumulation of VA.(ABSTRACT TRUNCATED AT 250 WORDS)
A 12-year-old boy presented with acute renal failure (ARF) accompanied by a disproportionate increase of serum uric acid level and massive uric acid crystalluria. After alkalinization and allopurinol therapy, serum uric acid and renal function returned to normal values. A further enzymatic study showed the existence of a partial hypoxanthine-guanine phosphoribosyl transferase (HPRT) deficit (less than 1% of HPRT normal activity). Although ARF is an exceptional form of presentation of HPRT deficiency, this possibility should be considered whenever an ARF is accompanied by disproportionate high levels of serum uric acid.
Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca2+ cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during long-term administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure.
We have prospectively investigated the effect of desferrioxamine (DFO) administration (2 gi.v. after every haemodialysis session for 6 months) on the normocytic and normochromic anaemia of seven haemodialysis patients. None had either clinical or analytical data characteristic of chronic aluminium intoxication. At the end of DFO therapy, the haematocrit had increased from 20.5 +/- 2.7% to 30.4 +/- 7.7% (P less than 0.005), and the transfusional requirements decreased from 3.5 +/- 2.2 units (range 1-8 units) in the 6 months prior to DFO, to 0.7 +/- 0.9 units (range 0-2 units) during DFO administration (P less than 0.01). No transfusion was required during the second half of the DFO therapy period. Serum ferritin decreased from 105g +/- 532 nmol/l (2649 +/- 1331 ng/ml) to 507 +/- 403 nmol/l (1268 +/- 1008 ng/ml) (P less than 0.025). Two months after DFO withdrawal the haematocrit value fell significantly to 22.2 +/- 1.6% (P less than 0.01). DFO therapy was restarted in one patient at a lower dose (1 gi.v. after every haemodialysis session) and an increase of haematocrit from 23.8% to 40.2% was again observed after 3 months of treatment. The tolerance to DFO was excellent. We conclude that DFO therapy should be considered in haemodialysis patients with severe anaemia and increased blood transfusion requirements.
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A group of eight normotensive female volunteers with regular menstrual cycles were studied during two menstrual cycles: a control cycle and one in which they received lisuride, a D1-D2 dopamine agonist (0.025 mg/8 hr). The following tests were performed in both halves of both cycles: 1) the response of prolactin (PRL) to thyrotropin-releasing hormone (TRH) administration; 2) the response of plasma renin activity (PRA) and plasma aldosterone (PA) to furosemide for 2 hours in the upright posture; and 3) the response of PRL, PRA, PA, plasma potassium (K), and cortisol (F) to metoclopramide administration. An increased response of PRL to TRH and PA to furosemide in the upright position and to metoclopramide were found in the luteal phase of the control study (p less than 0.05). After lisuride administration, in the interphase, differences in the responses of PRL to TRH and PA to furosemide in the upright position disappeared, whereas that of PA to metoclopramide increased further. We conclude that the increase of aldosterone normally observed during the luteal phase of the menstrual cycle is at least partly conditioned by diminished dopaminergic tone and that the response of aldosterone secretion to furosemide-induced sodium depletion and its response to metoclopramide stimulation may be modulated by two different types of dopamine receptors.
In our series of RT three cases of diffuse NRH of the liver were found. This rare entity is characterized by nodules of regenerative hepatocytes distributed throughout the liver without fibrosis. The incidence was 12.5% and probably is underestimated. Clinically, hepatomegaly, moderate thrombopenia and an elevation of GGT were present, but no case was previously suspected. NRH can lead to PH, and we should think of this entity in the differential diagnosis of PH following RT.
We reviewed the evolution of FENa in the EPP (first 4 weeks) in a group of CyA-treated patients as well as Aza-treated patients who did not present with acute rejection during this period of time. The CyA-treated patients showed lower values of FENa than did Aza-treated patients. Values of FENa below 1% were found in 51% of CyA- and 0% Aza-treated patients (P less than .01) before RFR. The finding of low FENa values was accompanied by more prolonged oliguric and RFR phases. Furthermore, the lower the level of FENa, the higher the prolongation of renal failure. We concluded that FENa values could probably be an index of CyA nephrotoxicity in the EPP.
The prolonged effects (42 days) of indomethacin treatment on the renin-angiotensin-aldosterone axis, renal hemodynamics, and renal excretory function in humans were studied. Indomethacin produced a 41% sustained depression in the 24-hour excretion of prostaglandin E2 and a mild (7%) decrease in inulin clearance but did not affect the clearance of p-aminohippurate, the 24-hour excretion of sodium and potassium, or the basal values of plasma aldosterone; however, it decreased the basal values of renin and prevented the stimulated (3 hours of walking) responses of plasma renin activity and plasma aldosterone. Indomethacin also produced a decrease in both the diuretic and saluretic response to furosemide and in the renal ability to concentrate urine. The indomethacin-induced hyporeninism and hypoaldosteronism were more pronounced when the subjects were receiving a sodium-restricted diet. This finding indicates that prolonged administration of anti-inflammatory drugs induces chronic hyporeninism and hypoaldosteronism. Prolonged treatment with indomethacin also produced some of the symptoms of a syndrome of hypoprostaglandinism, such as decreased plasma renin activity, plasma aldosterone, and urinary prostaglandin E2 in association with increases in plasma potassium levels and diastolic pressure.
The effect of exogenous angiotensin II on plasma renin activity (PRA), plasma renin concentration (PRC) and plasma aldosterone (PA) was investigated in a group of 8 patients with essential hypertension after one year of captopril therapy. The results were compared with those obtained in a group of 18 normotensive volunteers not on captopril. Angiotensin II was infused at increasing doses until a pressor response (increase of diastolic blood pressure by 20 mm Hg) was evoked. The normotensive volunteers exhibited the expected decline of PRA during angiotensin II infusion. However, no significant change was observed in PRA nor in PRC levels in the group of hypertensive patients. The PA values increased significantly both in volunteers and patients (P less than 0.02). The dose of angiotensin II necessary to evoke a pressor response was higher in the hypertensive patients than in the normotensive volunteers (6.0 +/- 2.6 s.d. ng/kg/min vs 2.5 +/- 0.9; P less than 0.01). We conclude that patients with essential hypertension, after chronic treatment with captopril, show no inhibition of renin secretion in contrast with the controls. They also require more angiotensin II to evoke a pressor response during infusion of this peptide.
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