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Biomedical subjects

B Truniger

Publications and source records attributed to B Truniger.

At least 55 records · Page 3Linked to original sources

[Bufuralol: do beta blockers reduce blood circulation in the kidneys?].

In 8 ambulatory patients with stable essential hypertension (WHO grade I and II) the effects of a new beta-blocker with marked sympathomimetic activity on arterial blood pressure, creatinin clearance and renal plasma flow, as measured by total PAH clearance (constant infusion technique), were studied. In contrast to previous findings no significant reduction in creatinin clearance or renal blood flow was observed during a 3-5 weeks' observation period. The small reduction in calculated renal vascular resistance was not statistically significant. In addition to its postulated peripheral vasodilatory effect, bufuralol appears to interfere less than propranolol with renal hemodynamics and renal excretory function.

Adrenergic beta-Antagonists↗

[Uremic arteriopathy and ischemic skin changes].

The syndrome of uremic arteriopathy with ischemic skin manifestations--livedo reticularis, skin infarction and ulcerative necrosis--is described in a series of 6 patients. In all patients (3 female and 3 male, age 53-73 years) the syndrome occurred after slowly progressive renal failure and in 5 cases during temporary exacerbation of chronic renal failure and after alkalinizing treatment for marked metabolic acidosis. All patients had evidence of secondary hyperparathyroidism. In 4 the Ca X P product was in excess of 4.90, but only once above the critical product of 5.60 (greater than 70 when conventional units are used). Diagnosis was based on the clinical appearance of the skin involvement and the finding of vascular calcifications (x-ray and skin biopsy). The secondary hyperparathyroidism appears to play an important role in the pathogenesis of the syndrome. An increase in plasma phosphate or Ca X P product, calciphylaxis and/or alkalinizing therapy may release the precipitation of calcium salts in the interstitium or in the vessel walls. Therapy is confined to decreasing plasma phosphate and therewith the Ca X P product by means of phosphate binders or a diet low in phosphate. The unpredictable, often rapid success of parathyroidectomy awaits further clarification.

Aged↗

Redistribution of intrarenal blood flow after carotid artery occlusion in the rat.

As indicated by changes in microsphere distribution in the rat, acute bilateral carotid artery occlusion (CAO) was found to cause a small but significant increase in outer cortical flow fraction. When renal perfusion pressure was kept constant, no redistribution occurred upon CAO. In denervated kidneys the redistribution induced by CAO did not differ from that observed in contralateral control kidneys. Animals pretreated with prostaglandin inhibitors showed a significant redistribution in the 'unprotected' right kidney and a minor increase in outer cortical flow fraction in the normotensive kidney. It is concluded that: (1) the increase in outer cortical flow fraction induced by CAO in the rat is due to an increase in perfusion pressure, and (2) that this redistribution is independent of sympathetic vasoconstrictor stimuli, catecholamines and prostaglandins.

Animals↗

[Central pontine myelinolysis and Schwartz-Bartter syndrome].

Central pontine myelinolysis (CPM) occurred in a typical patient with severe alcoholism presenting with severe initial hyponatremia and a rapidly progressive pontomesencephalic syndrome. A review on 141 cases of CPM is presented and the ties between CPM, hyponatremia/hypoosmolality and the syndrome of inadequate secretion of ADH are discussed. Correct interpretation of the patient's history (alcoholism, severe wasting disease) and the clinical picture (initial hypoosmolality with acute or subacute pontomesencephalic syndrome, possibly locked-in syndrome) should permit correct in-vivo diagnosis more frequently than hitherto.

Alcoholism↗

[Megalocytic interstitial nephritis. A contribution to the differential diagnosis of the large insufficient kidney].

After a female patient had presented with advanced renal failure, bilateral enormous increase in kidney size radiologically, urinary tract infection (E. coli) and septicemia, autopsy disclosed megalocytic interstitial nephritis (MIN). Clinical and pathological differentiation from renal parenchymal malakoplakia (RPM) is discussed. A literature survey of 15 cases of MIN and 35 observations of RPM points to certain differences between the two entities, i.e. an increased incidence of bilateral pathology in MIN, mor frequent extrarenal localizations in RPM, absent Michaelis-Gutmann bodies and a predominantly cortical distribution in MIN. The similarities, however, suggest that the two conditions might represent different stages of one and the same disease process.

Diagnosis, Differential↗

[Drug induced fluorosis in myeloma].

Osteolytic lesions of bone in multiple myeloma may be treated by florides. A patient is reported who had IgA-Myeloma, was treated with high doses of sodium floride for 16 months and developed the clinical and radiological picture of advanced fluorosis. Within one year after discontinuing sodium fluoride therapy the soft tissue calcifications disappeared almost completely. High bone turnover may account for the accelerated deveopment and disappearance of fluorosis in myeloma. Progressive renal failure due to myeloma and, perhaps, increased susceptibility of destructed bone to fluorides advocate restricted use of fluorides in the treatment of osteolytic bone lesions in myeloma.

Aged↗

Immunothrombocytopenia and IgA nephritis.

A 32 year old female patient demonstrates the rare combination of a typical IgA nephritis and familial immunothrombocytopenia. Although this association may be purely fortuitous, our observation adds a new facet to a spectrum of reports on (familial) "thromborenal syndromes". The pathogenesis of the IgA nephritis has not yet been clarified. However, since IgA deposits are found relatively frequently in the mesangium in a number of diverse underlying diseases, there might be common etiological factors. In view of this possibility more attention should be directed to the investigation of IgA associated diseases.

Adult↗

[Myasthenia gravis and visceral lupus erythematosus].

The patient described in this clinical demonstration suffered from severe myasthenia gravis shortly before the detection and for 3 years after surgical removal of a cystic thymoma. At the end of this period, when the myasthenia subsided, she developed systemic lupus erythematosus simultaneously with pleural implantation metastases of the thymoma. After local radiation therapy and under systemic immunosuppression she has remained asymptomatic since the spring of 1978. The pathogenetic and immunogenetic basis of myasthenia gravis and autoimmune diseases associated with thymoma and thymus hyperplasia is reviewed, and a plea is entered for more comprehensive and integrative internal medicine.

Acetylcholine↗

[Atenelol and bendrofluazide in the treatment of medium and severe hypertension (preliminary report)].

In 15 patients with moderate to severe hypertension (WHO II--III) atenolol was evaluated against a thiazide diuretic (bendrofluazide) in a single blind crossover study. Systolic blood pressure values were lowered more efficiently by the diuretic, while diastolic pressure values were significantly better controlled by atenolol. Atenolol and bendrofluazide, by mere addition of the pressure effects of the single components, clearly afforded the best pressure control. Side effects of atenolol were frequent but mild, never causing major concern with the patients or a dropout from the study. Although the pressure response to atenolol was significantly better in the normal and high renin group of patients, there was no statistically significant correlation between the reduction in plasma renin and blood pressure induced by atenolol. In turn, the pressure response to the diuretic was significantly better in low renin than in normal and high renin patients.

Atenolol↗

[Partial lipodystrophy and intramembraneous glomerulonephritis].

The case is presented of a young woman with partial lipodystrophy and intramembranous glomerulonephritis. Light and electron microscopic changes in the kidney biopsy are described and discussed. With immunosuppressive therapy very slow progression of the renal insufficiency was observed. Finally, regular dialysis treatment was required to sustain life. The follow-up after detection of intramembranous glomerulonephritis lasted 8 years.

Adult↗

Renal function and intrarenal hemodynamics in acutely hypoxic and hypercapnic rats.

On the basis of microsphere distribution, inert gas washout, and standard clearance data, the effects of acute hypoxia and hypercapnia on the kidney were studied in anesthetized, mechanically ventilated rats. Moderate hypoxia (mean PO2, 48 mm Hg) did not significantly change diuresis, GFR, and tubular sodium rejection. Due to a decrease in renal vascular resistance (R) from 40.1 to 31.8 mm Hg ml-1 min, mean renal blood flow stayed constant in spite of a significant drop in mean arterial blood pressure. Hypoxic changes in R were not accompanied by significant changes in intrarenal distribution of blood flow (IDBF). In severe hypoxia (PO2 less than 45 mm Hg) with oliguria and marked arterial hypotension, R was the lowest of all groups (28.8 mm Hg ml-1 min). Hypercapnia did not significantly change the renal excretory parameters, although an increase in R (without change in IDBF), together with a decrease in MAP caused a marked drop in mean renal blood flow. From these studies we conclude: 1) in the anestheized rat, acute hypoxia caused significant changes in intrarenal hemodynamics without changes in excretory function, 2) hypoxic renal vasodilation persists even in severe hypotension with oliguria and anuria, 3) in acute hypoxia and hypercapnia, changes in renal blood flow and renal vascular resistance are not accompanied by significant changes in IDBF.

Animals↗

Effects of angiotensin II and noradrenaline on intrarenal haemodynamics in the rat.

The haemodynamic effects of angiotensin II and noradrenaline were studied in the rat kidney. These pressors were given by intravenous infusion in stepwise increasing doses. Intrarenal haemodynamics were analyzed by the 133xenon washout technique, 85krypton autoradiography and silastic casting of the renal vascular tree. Angiotensin II induced significant changes in intrarenal haemodynamics before any changes in systemic blood pressure were detected. The decrease in mean renal blood flow (2.91 ml.min-1.g-1 in controls, 1.76 ml.min-1.g-1 in rats given 50 mug of angiotensin II.kg-1.h-1) reflects a reduction in component I blood flow rate (from 3.9 to 2.9 ml.min-1.g-1) as well as a decrease in the fraction of total renal blood flow supplied to component I of the washout curve (from 84% to 62%). With noradrenaline an increase in total renal resistance occurred simultaneously with the elevation of mean arterial blood pressure. The resulting reduction in mean renal blood flow (from 2.76 ml.min-1.g-1 in controls to 1.55 ml.min-1.g-1 in rats given 1000 mug of noradrenaline kg-1.h-1) reflects a decrease in component I blood flow rate with lower infusion rates and a drop in component I flow fraction (from 82% to 52%) whith higher doses. In contrast to canine kidneys, no evidence for a patchy cortical vasoconstriction was found in the rat. Using autoradiography it was possible to attribute component I to the renal cortex and subcortical area of the kidney.

Angiotensin II↗

[Emergency stiuations connected with electrolyte disorders. Special aspects].

Electrolyte-induced situations which are dangerous to life usually result from disturbances of the extracellular volume (ECV), osmolarity, the potassium level or the acid-base equilibrium. In recent years (thanks to the wide spread use of hormone therapy for mammary carcinoma) severe hypercalcemia has increased in importance as a life-threatening complication, while hypocalcemia, at least in adults, should only very seldom lead to unexpected emergencies. As long as serious clinical symptoms do not suggest an emergency, assessment of the threat to the patient as a result of the existing electrolyte disturbance often causes some difficulty. Besides the extent of the deviation from normal, the rate of development of the disturbance determines the resulting danger: chronic hypo-osmolarity, and especially hyperosmolarity are occasionally tolerated without symptoms while acute disturbances of the same or a less extent lead to severe central nervous symptoms. A similar state of affairs is also true of the emergency situations arising from disturbances of the acid-base equilibrium, among which the respiratory disorders are particularly important clinically. In the case of threatening disorders of the potassium metabolism, the accompanying circumstances (digitalis, simultaneous disorders and treatment of the acid-base equilibrium) often determine the clinical significance and danger to the patient. Clinical symptoms, anticipation ("expecting the unexpected"), prevention and treatment of emergency situations of fluid volume, osmolarity, potassium and acid-base equilibrium are the subjects of this paper.

Adult↗