L'ecocardiografia e il Nefrologo: una "Pocket Guide" per Nefrologi Curiosi

Abstract non disponibile (Cardionephrology

L'ecocardiografia e il nefrologo: seconda e ultima puntata della "pocket guide"

Abstract non disponibile (Cardionephrology

La malattia renale cronica e il trattamento dello scompenso cardiaco congestizio: il ruolo del cardionefrologo

Il rene è coinvolto, in prima battuta, nel mantenimento dell'omeostasi dei fluidi e dell'equilibrio idro-elettrolitico ed acido-base, nonché nell'eliminazione delle scorie tossiche. La funzione renale sembra essere strettamente collegata a quella cardiovascolare e, negli ultimi anni, il termine di 'sindrome Cardio-Renale' è stato utilizzato per spiegare le correlazioni cliniche tra patologia renale e cardiaca. Lo scompenso cardiaco congestizio (SCC) rappresenta la prima causa di ospedalizzazione nei Paesi occidentali e i pazienti affetti presentano spesso, in associazione, un quadro di malattia renale cronica (MRC) di grado variabile. Sono stati considerati diversi modelli fisiologici e fisiopatologici per spiegare come una condizione di malattia renale cronica possa influenzare lo stato di insufficienza cardiaca. Sicuramente la via metabolica del guanosin monofosfato ciclico (cGMP) e quello dell'ossido nitrico (NO) giocano un ruolo fondamentale di concerto con l'azione dei peptidi natriuretici atrial natriuretic peptide (ANP) e brain natriuretic peptide (BNP) sotto il controllo del sistema delle fosfodiesterasi sieriche. I pazienti con sovraccarico di circolo necessitano di terapie farmacologiche specifiche. La terapia diuretica, spesso in associazione (vedi tiazidici + diuretici d'ansa), rappresenta ancora quella di prima scelta ma, nei pazienti, refrattari alla terapia diuretica a dosi massimali, l'impiego di metodiche extracorporee, quali l'ultrafiltrazione (nelle sue diverse modalità d'impiego), può essere di grande aiuto per il paziente scompensato dal punto di vista cardiologico. (Cardionephrology

Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha-2-adrenergic, but not I1-imidazoline, receptor activation in female rats

Aims—This study dealt with the effect of chronic ethanol administration on hemodynamic responses elicited by α2-adrenergic (α-methyldopa) or I1-imidazoline (rilmenidine) receptor activation in telemetered female rats. Main methods—The effects of α-methyldopa or rilmenidine on blood pressure (BP), heart rate (HR) and their variability were investigated in rats that received liquid diet without or with ethanol (5% w/v) for 12 weeks. To evaluate the effect of each drug on cardiovascular autonomic control (BP and HR variability) in the absence or presence of ethanol, three time-domain indices of hemodynamic variability were measured: (i) standard deviation of mean arterial pressure (SDMAP), (ii) standard deviation of beat-to-beat intervals, and (iii) root mean square of successive differences in R-R intervals. Key findings—In liquid diet-fed control rats, i.p. rilmenidine (600 μg/kg) or α-methyldopa (100 mg/kg) reduced BP along with decreases and increases, respectively, in HR. Both drugs had no effect on HR variability but reduced BP variability (SDMAP), suggesting a reduced vasomotor sympathetic tone. Ethanol feeding attenuated reductions in BP and SDMAP evoked by α-methyldopa but not by rilmenidine. Significance—We conclude that chronic ethanol preferentially compromises α2- but not I1- receptor-mediated hypotension in female rats probably via modulation of vasomotor sympathetic activity. These findings highlight the adequacy of rilmenidine use to lower BP in hypertensive alcoholic females

Main results of the Ouabain and Adducin for Specific Intervention on Sodium in Hypertension Trial (OASIS-HT): a randomized placebo-controlled phase-2 dose-finding study of rostafuroxin

Background. The Ouabain and Adducin for Specific Intervention on Sodium in Hypertension (OASIS-HT) Trial was a phase 2 dose-finding study of rostafuroxin, a digitoxygenin deivative, which selectively antagonizes the effects of endogenous ouabain (EO) on Na+,K+-ATPase and mutated adducin. Rostafuroxin lowered blood pressure (BP) in some animal models and in humans. Methods. OASIS-HT consisted of 5 concurrently running double-blind cross-over studies. After 4 weeks without treatment, 435 patients with uncomplicated systolic hypertension (140-169 mm Hg) were randomized to rostafuroxin (0.05, 0.15, 0.5, 1.5 or 5.0 mg/d) or matching placebo, each treatment period lasting 5 weeks. The primary endpoint was the reduction in systolic office BP. Among the secondary endpoints were diastolic office BP, 24 h ambulatory BP, plasma EO concentration and renin activity, 24-h urinary sodium and aldosterone excretion, and safety. ANOVA considered treatment sequence (fixed effect), subjects nested within sequence (random), period (fixed), and treatment (fixed). Results. Among 410 analyzable patients (40.5% women; mean age, 48.4 years), the differences in the primary endpoint (rostafuroxin minus placebo) ranged from -0.18 mm Hg (P=0.90) on 0.15 mg/d rostafuroxin to 2.72 mm Hg (P=0.04) on 0.05 mg/d. In the 5 dosage arms combined, the treatment effects averaged 1.30 mm Hg (P=0.03) for systolic office BP; 0.70 mm Hg (P=0.08) for diastolic office BP; 0.36 mm Hg (P=0.49) for 24-h systolic BP; and 0.05 mm Hg (P=0.88) for 24-h diastolic BP. In the 2 treatment groups combined, systolic (-1.36 mm Hg) and diastolic (-0.97 mm Hg) office BPs decreased from week 5 to 10 (P for period effect ≤=0.028), but carry-over effects were not significant (P≥=0.11). All other endpoints were not different on rostafuroxin and placebo. Minor side-effects occurred with similarly low frequency on rostafuroxin and placebo. Conclusions. In 5 concurrently running double-blind cross-over studies rostafuroxin did not reduce BP at any dose. Trial Registration: NCT00415038 http://www.clinicaltrials.gov)

Therapeutic strategies to slow chronic kidney disease progression

Childhood chronic kidney disease commonly progresses toward end-stage renal failure, largely independent of the underlying disorder, once a critical impairment of renal function has occurred. Hypertension and proteinuria are the most important independent risk factors for renal disease progression. Therefore, current therapeutic strategies to prevent progression aim at controlling blood pressure and reducing urinary protein excretion. Renin-angiotensin-system (RAS) antagonists preserve kidney function not only by lowering blood pressure but also by their antiproteinuric, antifibrotic, and anti-inflammatory properties. Intensified blood pressure control, probably aiming for a target blood pressure below the 75th percentile, may exert additional renoprotective effects. Other factors contributing in a multifactorial manner to renal disease progression include dyslipidemia, anemia, and disorders of mineral metabolism. Measures to preserve renal function should therefore also comprise the maintenance of hemoglobin, serum lipid, and calcium-phosphorus ion product levels in the normal range

Free adrenaline and noradrenaline excretion related to occupational stress.

Urinary levels of free adrenaline and noradrenaline were measured in two groups of healthy male industrial workers exposed to alternate four-day periods of working conditions with and without time stress, to test the hypothesis that the sympathetic nervous system is overactivated by occupational stress. Thirty confectionary workers alternated piece-work (payment by results) and work with a fixed daily wage while 30 metal workers alternated work on an assembly line with work off it. Under time stress urinary free adrenaline was 450 per cent and noradrenaline 230 per cent of the levels for similar work without time stress but involving equal oxygen consumption. These differences were statistically highly significant and they persisted on retesting after six months of alternating work regimens. They support the concept that occupational stress in industrial workers influences the adrenosympathetic system and they indicate a possible method for assessing the effects of high levels of sympathetic activity on the aetiology of ischaemic heart disease