Biomedical subjects
Publications and source records attributed to J L Rodicio.
A case of angioimmunoblastic lymphadenopathy (AIL) is presented in which the transient presence of a Fanconi syndrome was detected. Both the AIL and the Fanconi syndrome were ameliorated after steroid therapy.
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The effect of a 3-day oral course of ranitidine on plasma aldosterone level has been studied in 6 normotensive volunteers maintained in a state of sodium depletion. A significant fall in plasma aldosterone (p less than 0.05-0.02), in both the overnight recumbency levels and in the levels obtained during a two hour period of ambulation was observed. The change took place in the absence of variation in plasma renin activity and potassium. Plasma cortisol and prolactin levels were lower after ranitidine at the beginning of the test but their values were not significantly different after ambulation during ranitidine therapy. Ranitidine appears to interfere with aldosterone secretion in vivo.
We report the first case of congenital renal arteriovenous fistula in which renin-mediated arterial hypertension was the only clinical manifestation.
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The influence of an increased endogenous production of angiotensin II and of sodium homeostasis upon the response of plasma aldosterone to metoclopramide administration has been investigated in 5 normal volunteers. Our results show that the increase of plasma aldosterone after metoclopramide administration is independent of angiotensin II, ACTH and potassium, and that it increases even further due to the endogenous production of angiotensin II induced by postural changes. The state of sodium balance seems to influence the response of plasma aldosterone to metoclopramide administration as it occurs with other stimuli of aldosterone secretion.
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In a retrospective study we have examined 20 liver specimens from haemodialysis patients with a mean time on treatment of 27 months. Thirteen specimens were biopsies, the remaining came from autopsies. The presence of refractile particles was found in 55 per cent of biopsies and 100 per cent of autopsies. Its presence was not constantly associated with morphological lesions of the liver. We believe that the deposition of this material could be a fortuitous finding with uncertain clinical implications.
The participation of renal prostaglandins in the nephrotic syndrome has been investigated by the measurement of the urinary excretion of prostaglandin E2 (PGE2), renal function and the renin-angiotensin-aldosterone system before, during and after the administration of indomethacin in a group of patients diagnosed as having chronic idiopathic glomerulonephritis with and without nephrotic syndrome. Our results indicate increased renal production of PGE2 in nephrotic patients. This contributes to the maintenance of renal function, probably by counteracting an activated renin-angiotensin system and could be accompanied by a simultaneous and deleterious enhancement of the degree of proteinuria. Nevertheless, the participation of angiotensin II in this last even cannot be excluded.
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The role played by renal prostaglandin E2 in the maintenance of hypertension in chronic renal disease has been investigated through studying the response of body weight, blood pressure, glomerular filtration rate (GFR), 24-hour natriuresis, plasma renin activity (PRA), plasma aldosterone and urinary PGE2 excretion to the administration of indomethacin (2mg/kg daily, during 3 days). A group of 37 patients diagnosed as having chronic renal parenchymatous disease with creatinine clearance above 25 ml/min was included in the study. 21 of them were hypertensive (BP greater than 160/95). 27 normotensive volunteers were also studied and considered as the control group. The initial study disclosed similar levels of PGE2, PRA and plasma aldosterone in volunteers, normotensive patients and hypertensive patients, although the sodium intake was lower in the last two groups. A positive correlation between PRA and urinary PGE2 was found both in normotensive (r = 0.507, p less than 0.01) and in hypertensive patients (r = 0.609, p less than 0.01). The administration of indomethacin induced a diminution of PRA, plasma aldosterone and urinary PGE2 levels together with an increase in diastolic blood pressure (p less than 0.05-0.01) in both volunteers and patients. The remaining parameters measured did not change in volunteers or in normotensive patients. On the contrary, in hypertensive patients, during indomethacin administration, lower values of creatinine clearance (p less than 0.005) and 24-hour natriuresis (p less than 0.05) together with an increase in body weight (p less than 0.01) were observed. These results point to the existence of a protective role of renal prostaglandin E2 upon renal function when hypertension appears in the course of chronic renal parenchymatous disease.
In a group of 26 patients diagnosed as essential hypertensive (EH) and in a control group (CG) of 27 normotensive volunteers the urinary excretion of PGE2, plasma renin activity (PRA) and plasma aldosterone were measured. EH patients were classified into normoreninemic (NREH) (n = 21) and hyporeninemic (LREH) (n = 5) by the response of PRA to the combined stimuli of ambulation and furosemide. Urinary PGE2 excretion was higher in NREH than in CG (p less than 0.05) while LREH showed values lower than in CG (p less than 0.001). Plasma aldosterone levels were similar in the three groups. In CG and EH patients PRA and urinary PGE2 were closely related (CG r = 0.516, p less than 0.05, EH patients r = 0.674, p less than 0.001). Indomethacin administration induced a decrease of PGE2 in both CG (n = 8) and NREH (n = 8) (p less than 0.01). In contrast, indomethacin induced no changes in PGE2 excretion of LREH (n = 5). Furthermore in the group of patients with NREH indomethacin induced a significant increase in blood pressure (p less than 0.01) and body weight (p less than 0.01) while glomerular filtration rate, 24 hour natriuresis PRA and plasma aldosterone decreased (p less than 0.01). On the contrary, in LREH indomethacin did not alter any of the parameters measured. These results indicate that LREH and NREH may be regarded as two different populations distinguishable not only by different secretion of PRA but also by different excretion of PGE2 in urine and by their characteristic response to indomethacin.
In order to control the progression of chronic renal failure through the maintenance of low-normal levels of serum phosphate, 10 patients (group I) were followed over a period of 10 months. They were maintained on a low phosphate diet and 12 g/day of aluminum hydroxide. Under this treatment, the serum phosphate decreased significantly compared to the phosphate levels determined prior to initiation of treatment, and compared to the serum phosphate levels of 10 controls with the same degree of renal failure (group II) but receiving conventional treatment. Despite the maintenance of normal levels of serum phosphate in group I, serum creatinine increased in the same proportion as in group II. A paired t test did not show any difference between the progression of the renal failure before or after the control of serum phosphate.
The clinical aspects and response to therapy of 130 hypertensive emergencies are reviewed in this report. According to the main features of the clinical picture, the patients were divided into neurologic, cardiac or mixed emergencies. The patients were evaluated with clinical examination, fundoscopy, routine biochemistry, ECG, and chest radiograms. According to the response of the blood pressure to the administration of hypotensive drugs, the patients were divided into two groups: group I, with good response to a single drug associated to frusemide, and group II, with good response to two or more drugs associated to frusemide. Neurologic emergencies appeared in 55 patients (42% of total), and cardiac emergencies in 45 (34%), the initial blood pressure beeing higher in the first group (p less than 0.005). The fundus showed hypertensive retinopathy degrees III-IV in 55% of the patients. Patients in group I had less elevation of the initial blood pressure, showed a better response to therapy, and had only mild side effects from the administered drugs. Group II had a mortality of 11% and, as expected, showed more complications due to side effects. The frequency of appearance of toxic side effects from the drugs given is reviewed, and a therapeutic schedule is proposed.
Idiopathic mesangial glomerulonephritis with IgA deposits was observed in two relatives, father and son, in a family of 5 members. In the father the disease started at age 43 with relapsing macroscopic hematuria, proteinuria, renal failure and hypertension, with a progressive course in the ensuing four years. The affected son, the oldest of three brothers, developed relapsing macroscopic hematuria at age 16; two years later renal function was normal and there was no hypertension, but microhematuria persisted without proteinuria. The mother and the other two brothers had no clinical or biological signs of renal disease. Serum immunoglobulins (IgG, IgA, and IgM) and complement (C3, C4, C3 proactivator) were normal in the patients and their relatives. Histocompatibility typing demonstrated the presence of HLA-Bw35 in the father and the two unaffected sons, being negative in the mother and the affected son. The analysis of HLA-Bw35 in 23 patients with IgA mesangial glomerulonephritis gave positive results in 30% of them, while the control group had a positivity of 15% (p non significant with the X2 test). The present observations suggest that IgA mesangial glomerulonephritis is a potentially familial and hereditary renal disease. HLA-Bw35 antigen appears not to be a genetic marker of the disease in our geographical area.