Considerazioni Bioetiche Sul Carico Psicosociale Dei Caregiver Dei Dializzati

Nel vasto campo della nefrologia solo recentemente è emerso il problema dei caregiver, volontari e non pagati, dei pazienti in dialisi. È un problema dalle numerose implicazioni, compresa la bioetica. Il crescente numero di dializzati e il parallelo incremento dei loro caregiver creano da una parte problemi ai sistemi assistenziali e, dall'altra, modificazioni psicosociali e della qualità della vita, associate a depressione, che, nel loro insieme, richiedono attenzione a chi si dedica agli altri, senza trovare chi si occupa di loro. Il tutto in una spirale di atteggiamenti di regressione psicologica e di incapacità ad affrontare situazioni cliniche e comportamentali alle quali i caregiver non sono preparati. In uno studio prospettico multicentrico sono state esaminate le risposte psicosociali dei caregiver di emodializzati, con il risultato che il 24% accusava la tipica sindrome da burn-out, il 47% riferiva difficoltà ad affrontare il quotidiano carico psicosociale e fisico e solo il 6% accettava con tranquillità e serenità di essere d'aiuto a un proprio familiare, malgrado le numerose difficoltà a cui andava incontro. Si è, inoltre, rilevato che le moderne strategie depurative domiciliari come la dialisi continua diurna e notturna comportano un grave carico psicosociale aggiuntivo per i caregiver, al punto da mettere in discussione la scelta di tali strategie quando comportano patologie depressive e consistenti abbassamenti della qualità della vita. Allora, ogni scelta va valutata sempre all'insegna dei vantaggi economici e logistici, che non possono, però, prescindere da oculati principi di bioetica clinica. (Bioethics

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

The role of salt abuse on risk for hypercalciuria

<p>Abstract</p> <p>Background</p> <p>Elevated sodium excretion in urine resulting from excessive sodium intake can lead to hypercalciuria and contribute to the formation of urinary stones. The aim of this study was to evaluate salt intake in patients with urinary lithiasis and idiopathic hypercalciuria (IH).</p> <p>Methods</p> <p>Between August 2007 and June 2008, 105 lithiasic patients were distributed into 2 groups: Group 1 (n = 55): patients with IH (urinary calcium excretion > 250 mg in women and 300 mg in men with normal serum calcium); Group 2 (n = 50): normocalciuric patients (NC). Inclusion criteria were: age over 18 years, normal renal function (creatinine clearance ≥ 60 ml/min), absent proteinuria and negative urinary culture. Pregnant women, patients with intestinal pathologies, chronic diarrhea or using corticoids were excluded. The protocol of metabolic investigation was based on non-consecutive collection of two 24-hour samples for dosages of: calcium, sodium, uric acid, citrate, oxalate, magnesium and urinary volume. Food intake was evaluated by the three-day dietary record quantitative method, and the Body Mass Index (BMI) was calculated and classified according to the World Health Organization (WHO). Sodium intake was evaluated based on 24-hour urinary sodium excretion.</p> <p>Results</p> <p>The distribution in both groups as regards mean age (42.11 ± 10.61 vs. 46.14 ± 11.52), weight (77.14 ± 16.03 vs. 75.99 ± 15.80), height (1.64 ± 0.10 vs. 1.64 <b>± plusorminus </b>0.08) and BMI (28.78 ± 5.81 vs. 28.07 ± 5.27) was homogeneous. Urinary excretion of calcium (433.33 ± 141.92 vs. 188.93 ± 53.09), sodium (280.08 ± 100.94 vs. 200.44.93 ± 65.81), uric acid (880.63 ± 281.50 vs. 646.74 ± 182.76) and magnesium (88.78 ± 37.53 vs. 64.34 ± 31.84) was significantly higher in the IH group (p < 0.05). There was no statistical difference in calcium intake between the groups, and there was significantly higher salt intake in patients with IH than in NC.</p> <p>Conclusions</p> <p>This study showed that salt intake was higher in patients with IH as compared to NC.</p

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

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

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