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Biomedical subjects

A Botey

Publications and source records attributed to A Botey.

At least 73 records · Page 4Linked to original sources
PubMed1981

[Early diagnosis of renal ischemia in arterial hypertension by means of urine N-acetyl-beta-D-glucosaminidase (author's transl)].

Essential arterial hypertension, malignant hypertension and renovascular hypertension were studied in 64 patients, divided into 5 groups according to creatinine clearance (Ccreat) and ophthalmic fundus. Urine N-Acetyl-b-d-glucosaminidase (NAG) was expressed in units/mg creatinine in urine. Results were; Group A: Ccreat greater than 60, ophthalmic fundus less than II (n=33), NAG 13.5 + 4.5; Group B: CCreat. greater than 60, ophthalmic fundus III-IV (n=4) NAG 42.4 +/- 12.5; Group C: Ccreat. less than 60, ophthalmic fundus less than II (n = 14) NAG 31.2 +/- 10,5; Group D: (clinically malignant arterial hypertension) Ccreat. less than 60, ophthalmic fundus III--IV (n = 8), NAG 91.1 +/- 55.7 and Group E: (renovascular hypertension) Ccreat. greater than 60, ophthalmic fundus less than II (n = 5), NAG 35.5 +/- 12.9. Only the patients in Group A had NAG within normal limits. Differences were found between groups: A-B (p less than 0.001), A-D (p less than 0.001), A-E (p less than 0.001) and C-D (p less than 0.001). Urine NAG is considered to be an early sign of renal involvement in arterial hypertension, an indication of the severity and a sign of ischemia even when the involvement is unilateral only, and helpful in the management of renovascular hypertension.

Acetylglucosaminidase↗
PubMed1981

[Prolonged hypotension after the first dose of atenolol (author's transl)].

A 30 year-old male patient with accelerated arterial hypertension relatively resistent to diazoxide received a single oral dose of 100 mg of atenolol, following which hypotension of more than 24 hours duration and acute renal failure ensued. These alterations were reversible and did not recur with subsequent doses of atenolol. Prior therapy with diazoxide might have potentiated the hypotensive action of atenolol. The abnormality could be due to a phenomenon of hyperreactivity to the first dose of atenolol, similar to what has been described following first doses of prazosin or labetalol. This observation suggests that atenolol therapy must be started with caution, especially in patients previously treated with diazoxide.

Acute Kidney Injury↗
PubMed1981

[Essential hypertension and diabetes].

Exchangeable sodium (E-Na), plasma volume (PV), and plasma renin activity (PRA) have been studied in 19 patients with essential hypertension and diabetes, and the results compared to those of non-diabetic patients with benign essential hypertension. None of the cases had renal disease or hypertension with systolic predominance. E-Na was 114 +/- 9.74 (SD), significantly superior to that of normal subjects (p less than 0.001). An elevated E-Na was observed in 52.6% of the diabetic group, while PV was normal. PRA levels were normal in most patients, mean 1.28 +/- 1.97 ng ml-1 h-1, only two patients disclosing an elevated PRA (10.5%). No relationship was found between PRA and age, blood pressure, and E-Na. From the comparison of results between diabetic and non-diabetic hypertension patients it appears that: 1) no differences between mean PRA and E-NA exist, although a greater percentage of diabetics have an elevated E-Na, and 2) in the non-diabetic group there is a positive correlation between E-NA and PV, while in the diabetic group such a correlation is negative (p less than 0.05). The finding of an elevated body sodium in patients with essential hypertension and diabetes probably represents a true abnormality in the body composition of these patients, although there is no explanation for the fact that it is unassociated to an increase of the plasma volume, as opposed to essential hypertension in non-diabetics.

Adult↗
PubMed1981

Postsynaptic adrenergic unresponsiveness in hypotensive haemodialysis patients.

In order to ascertain the significance of autonomic dysfunction in hypotensive maintenance haemodialysis patients, plasma norepinephrine (NE) was measured by radioenzymatic assay in 15 nondiabetic uraemic subjects of similar age and time on dialysis, five of them chronically hypotensive and 10 normotensive. Hypotensive patients had: 1) Significantly higher NE levels than their normotensive counterparts, both in basal conditions and after orthostatism and 2) significantly lesser increments in mean arterial blood pressure during a NE infusion than the normotensive group. Rather than implicating a mechanism based on autonomic neuropathy, our results suggest that in haemodialysis patients with chronic hypotension, there is a defect located at the adrenergic postsynaptic level.

Adult↗
PubMed1980

[Partial defect in the secretion of antidiuretic hormone and disproportionate polydipsia (author's transl)].

A 20-year-old patient was evaluated because of polydipsia and polyuria; by means of the dehydration test a partial defect in the secretion of antidiuretic hormone (ADH) was demonstrated, since the urinary osmolality after the administration of exogenous vasopressin was superior by 25 percent to the maximum spontaneous urinary osmolality reached after a period of fluid restriction. Nevertheless, there was also a component of psychogenic polydipsia because the daily basal fluid intake was superior to 15 liters, and in view of the fact that the urinary osmolality could reach 600 mOsm/kg, the endocrine defect cannot totally be responsible for the enormous volume of fluid intake. This is the first case in the world literature in which the association between potomania and deficiency in the secretion of ADH is reported. Since ADH is one of the factors which regulate the behaviour of various animal species it is possible that its deficiency may be directly responsible for the psychic disorder which led to the potomania. It is also possible that an anatomical hypothalamic lesion, too small to be demonstrated, might have a simultaneous effect on the centers regulating thirst and the neurons producing vasopressin.

Adult↗
PubMed1980

[Hemolytic-uremic syndrome in the adult (author's transl)].

This article presents six cases of hemolytic-uremic syndrome, defined as the combination of acute renal insufficiency, microangiopathic hemolytic anemia, and thrombocytopenia, in six adult patients, two men and four women, between 20 and 52 years old. Three of the cases were considered idiopathic, two secondary to the use of oral contraceptives, and one appeared after an abortion. All of the patients presented severe hypertension, frequently accompanied by increased renin levels; in no cases was there any important coagulation disorder. In all of the biopsies there were lesions denoting intravascular thrombosis in the arterioles and medium-sized arteries of the kidney, as well as thickening of the glomerular basal membrane. Immunofluorescence was positive for fibrinogen and C3 in the majority of biopsies examined. Two patients suffered acute pancreatitis, hypertension having perhaps been an important factor in this complication. One of the two patients died as a result of acute hemorrhagic pancreatitis and was the only death in the series. Of the five remaining subjects, three required periodic hemodyalisis and the other two presented a considerable degree of chronic renal failure, which confirms that the prognosis for the hemolytic-uremic syndrome is much worse for the adult than for the child.

Adult↗
PubMed1979

Renin-induced massive proteinuria in man.

A 30 year old man developed renovascular hypertension and extreme elevation of plasma renin activity. Daily proteinuria ranged from 13 to 31 g. There were no criteria for the diagnosis of malignant hypertension. A primary glomerulopathy was excluded by a basically normal renal biopsy from the unprotected kidney. On electron microscopy the epithelial cell foot processes were not fused, thus ruling out simultaneous lipoid nephrosis. The source of renin was removed by means of a left nephrectomy. Following the procedure the patient became normotensive, the renin values normalized and the proteinuria disappeared. The results suggest that renin can cause significant proteinuria in man.

Adult↗
PubMedDate not supplied

Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease?

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.

Addison Disease↗
PubMedDate not supplied

High prevalence of antithyroid antibodies in anti-glomerular basement membrane antibody-mediated disease.

Anti-glomerular basement membrane antibody (anti-GBM Ab)-mediated disease and autoimmune thyroiditis are characterized by the presence of organ-specific antibodies. The diagnosis of autoimmune thyroiditis is usually based on the presence of serum antithyroid antibodies. Few studies have addressed the relationship between anti GBM-Ab mediated disease and autoimmune thyroid pathology. Given that this disorder is often asymptomatic, associations of the two pathologies may be under-diagnosed. This study investigated the prevalence of serum antithyroid antibodies (antithyroglobulin (anti-TG) and anti-thyroid peroxidase (anti-TPO)) in patients with anti-GBM Ab-mediated disease. Antithyroid antibodies presence was investigated in sera from 35 patients in whom anti-GBM Ab-mediated disease had been diagnosed. Anti-glomerular basement membrane antibodies and anti-thyroid antibodies (anti-TG and anti-TPO) were assayed using an enzyme-linked immunosorbent assay. Forty-five percent of patients with anti-GBM Ab-mediated disease (16/35) had positive antithyroid antibody titers. Eighteen percent (3/16) suffered from subclinical hypothyroidism. In conclusion, the high prevalence of antithyroid antibodies in these patients suggests a possible pathogenic link between autoimmune thyroiditis and anti GBM Ab-mediated disease.

Adult↗