[The role of psychological interventions in dialysis: an exploratory study]. / Intérêt des interventions psychologiques en dialyse : étude exploratoire.

Patients suffering from end-stage renal disease (ESRD) have a very reduced quality of life accompanied by a severe emotional distress (high worries-anxiety-depression). However, in Belgium, no regular psychological intervention is proposed to dialyzed patients. Our objective is to show that psychological intervention can significantly decrease the emotional distress of patients with ESRD. Eleven sessions of structured interventions are proposed to ESRD patients. Eligibility criteria are to be major, to not present confusion or/and dementia, to have been on dialysis treatment for at least 3months, to have obtained 14 or more on HAD-scale. Interventions carry on the management of anxious and depressive symptoms and of the disease itself. This constitutes three independent modules. Questionnaires are filled in by the patients at various stages to evaluate the anxiety and the depression (HADS), the worries (Penn State) and the quality of life (KDQoL-SF). Results for the 47 ESRD patients show a significant reduction of the scores of anxiety, depression and worries and a significant growth of quality of life. In parallel, a decrease in the serum calcium-phosphorus product analyzed before dialysis has been noted.

[How to manage chronic kidney disease before dialysis]. / La prise en charge de l'insuffisance rénale chronique avant la dialyse.

Chronic renal failure is usually a silent disease until its late stage, especially in elderly people. Screening for such disease is particularly useful in hypertensive diabetic patients above 50 years. The causes are indeed often vascular or metabolic (directly or not directly linked to diabetes mellitus). Other less frequent causes are yet possible. The search for the right diagnosis of renal insufficiency is always requested to apply the appropriate treatment, combined with medical measures for secondary and tertiary prevention. This review will give general advices to avoid the development of renal disease (stages 3 and 4) or its progression, and also insist on the potential nephrotoxic effects of some drugs.

[A non frequent cause of kidney disease]. / Le cas clinique du mois. Une cause peu fréquente d'insuffisance rénale chronique.

The EDTA (European Dialysis and Transplantation Association) statistic data on kidney diseases in ageing population point out vascular and/or metabolic origins. We report here a case of a rare cause of renal insufficiency, a Gougerot-Sjögren primary syndrome, diagnosed in an old patient. Renal and salivary gland biopsies were performed. The invasive investigation allowed an accurate diagnosis and an etiologic treatment.

[Concentration of free intracellular magnesium in the myocardium of spontaneously hypertensive rats treated chronically with calcium antagonist or angiotensin converting enzyme inhibitor]. / Concentrations de magnésium intracellulaire libre dans le myocarde de rats spontanément hypertendus traités chroniquement par antagoniste calcique ou inhibiteur de l'enzyme de conversion.

In this study, we determined a) whether chronic antihypertensive treatment could alter myocardial free intracellular magnesium concentrations, b) whether changes in magnesium concentration would correlate with resistance to anoxia of hypertensive rat hearts. Six-month old male spontaneously hypertensive (HT) rats (n = 11) were compared to rats from the same strain treated with a calcium channel antagonist, nitrendipine (60 mg/kg/j; n = 11) or with a converting-enzyme inhibitor, perindopril (2 mg/kg/j; n = 9) during three months. The hearts were perfused in retrograde isovolumic mode and submitted to a standardized anoxia-recovery protocol. Aortic perfusion pressure and left ventricular pressure were constantly monitored. P-31 NMR spectra were simultaneously recorded and allowed to quantify the changes in myocardial inorganic phosphate, phosphocreatine and ATP. The pH was derived from the chemical shifts of inorganic phosphate and phosphocreatine, and the free intracellular magnesium concentration from the alpha-beta chemical shifts of ATP. Both treatments lowered systolic blood pressure and reversed left ventricular hypertrophy, perindopril being slightly more efficient at the dose administered. Intracellular magnesium concentration, calculated from the P-31 NMR spectra, was 277 +/- 17 microM in the untreated hypertensive group, 311 +/- 15 microM in the nitrendipine group and 401 +/- 17 microM in the perindopril group (p < 0.001 versus untreated and nitrendipine). There was a significant correlation between intracellular magnesium concentration and left ventricular developed pressure at the early stage of post-anoxic recovery (r = 0.61; p < 0.01). P-31 NMR spectroscopy demonstrates an increase in myocardial free intracellular magnesium concentration following chronic administration of an angiotensin-converting enzyme inhibitor, perindopril, spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympatholytic drugs and cardiac remodelling in human and experimental arterial hypertension.

Perfusion of isoprenaline in the dog may induce left ventricular hypertrophy (LVH), and this effect is suppressed by propranolol. Cultured foetal cardiomyocytes exposed to catecholamines show an increase in protein synthesis and RNA turnover. In spontaneously hypertensive rats (SHR), and perhaps in man, sympatholytic agents appear to be more effective in preventing or reversing LVH than some other antihypertensive drugs. These data suggest that, if increased load remains the main trigger mechanism for cardiac remodelling in arterial hypertension, the sympathetic nerve activity may modulate the response of the cardiac cells.

[Effect of long-term administration of vasodilators and "antitrophic" agents on the structure and function of the heart in hypertensive rats]. / Effets de l'administration chronique d'un vasodilatateur et d'un agent "antitrophique" sur la structure et la fonction du coeur de rat hypertendu.

In this study, we determined whether the persistency of cardiac hypertrophy after chronic vasodilation therapy with minoxidil (minox) was associated with functional or metabolic alterations in hypertensive rat hearts before, during and after an ischemic insult. In addition, we investigated the effects of the simultaneous administration of difluoromethylornithine (dfmo), a substance that could block hypertrophy by a direct inhibition of protein synthesis. Four groups of male Wistar rats were prepared: 1) normotensive controls (n = 8), 2) untreated renovascular hypertensive rats (HT, n = 15), 3) hypertensives treated with minox (8 mg/kg, n = 19), 4) hypertensives treated with minox and dfmo (1.7 g/kg, n = 20). After 21 days of treatment, the animals were sacrificed. In a small number of hearts, ornithine decarboxylase (ODC) activity was assayed in order to verify that dfmo, which is a suicide inhibitor of ODC, had effectively interrupted the polyamines pathway. The other hearts were prepared for retrograde perfusion at 35 degrees C and at constant flow (10 ml/min x g). Cardiac function was monitored via the balloon inserted in the left ventricle (LV) and the following protocol was applied: a) baseline period (24 min), b) ischemia (24 min), c) recovery (36 min). Finally, the hearts were weighed and LV wall thickness and inner radius were measured. Blood pressure was maintained near normotension in the two treated groups. Mean systolic pressure (in mmHg) was 145 +/- 4 with minox and 144 +/- 3 with minox + dfmo versus 181 +/- 4 in the HT group (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

The induction of cardiac hypertrophy by catecholamines can be dissociated from their inotropic effect.

In this study, ornithine decarboxylase, the first and rate-limiting enzyme of the polyamine pathway, was used as a marker of the very early stages of cardiac hypertrophy. Our data show that ornithine decarboxylase is independently regulated by ventricular wall stress and adrenergic receptors, and support the theory that catecholamines have a pressure-independent trophic effect. The infusion of beta 2-adrenergic agonist, terbutaline, at 10(-7) mol/l, did not affect the cardiac performance of isovolumic perfused rat hearts. Despite the lack of functional changes, ornithine decarboxylase activity, as assayed in vitro by 14C-ornithine decarboxylation, was markedly increased in both left and right ventricles. Further investigation showed that ornithine decarboxylase stimulation by catecholamines, unlike ornithine decarboxylase basal activity, was dependent on the extracellular calcium level. Furthermore, passive increases in ventricular wall stress in non-beating hearts also increased left ventricular ornithine decarboxylase activity.