1,721,014 research outputs found
Chelanti del fosforo a base di ferro : quali nuovi vantaggi? = Iron-based Phosphate Binders for ESRD Patients
No full textL'iperfosforemia osservata in pazienti in stadio terminale di malattia renale (CKD) si associa ad un aumento di morbilità e mortalità cardiovascolare. I chelanti del fosforo, somministrati per via orale, sono prescritti a questi pazienti per prevenire l'assorbimento intestinale del fosforo assunto con la dieta e di conseguenza per ridurne i livelli sierici. Ai chelanti del fosforo attualmente disponibili si associano diversi problemi come il bilancio positivo di calcio per i chelanti del fosforo a base di calcio, o i costi troppo elevati per quanto riguarda i chelanti del fosforo non a base di calcio. I chelanti del fosforo a base di ferro rappresentano una nuova classe di chelanti del fosforo. Molti chelanti del fosforo a base di ferro sono stati testati tramite studi clinici. Il citrato ferrico (JTT-751) e l'ossi-idrossido sucroferrico (PA21) sono i due chelanti a base di ferro che sono stati approvati in campo clinico dopo essere risultati sicuri ed efficaci nel ridurre i livelli di fosfato sierico. Il ferro presente nel citrato ferrico viene parzialmente assorbito, diversamente da quello dell'ossi-idrossido sucroferrico. L'utilizzo del citrato ferrico può avere come risultato un'importante riduzione dell’utilizzo di agenti stimolanti l'eritropoiesi (ESA) e ferro endovena, con conseguente riduzione di costi. L'ossi-idrossido sucroferrico si dimostrò efficace nell'abbassare i livelli di fosforo sierico nei pazienti in dialisi con un'efficacia simile a quella del sevelamer carbonato, ma con ridotto carico di pillole e migliore aderenza terapeutica. Il citrato ferrico potrebbe essere più adatto nel trattamento dell'iperfosforemia cronica nei pazienti con insufficienza renale cronica che necessitano di supplementazione marziale; tuttavia il suo utilizzo potrebbe essere ostacolato da un potenziale sovraccarico di alluminio, in quanto il citrato ne facilita l'assorbimento. L'ossi-idrossido sucroferrico, il solo approvato in Europa al momento, potrebbe essere più adatto ai pazienti con insufficienza renale cronica e iperfosforemia che non richiedano supplementazione di ferro, con minore carico di pillole.Several factors influence the choice of phosphate binder for patients, including older age, male gender, post-menopause, diabetes, low bone turnover, vascular/valvular calcification and inflammation. Unlike calcium-based phosphate binders, non-calcium-based phosphate binders, such as sevelamer and lanthanum carbonate, have been able to reduce the progression of bone disease to adynamic bone among patients with CKD. New iron-based phosphate binders are now available. With multiple options available for the reduction of phosphate, the focus has been on agents that do not contain calcium. This is because it is thought that calcium itself functions as a substrate for calcification
Cardiorenal acute kidney injury: Epidemiology, presentation, causes, pathophysiology and treatment
No full textPathophysiology of the Cardiorenal Syndromes Types 1–5: Updates from the Eleventh Consensus Conference of the Acute Dialysis Quality Initiative (ADQI)
No full textAccording to the recent definition proposed by the Consensus conference on Acute Dialysis Quality Initiative Group (Ronco in Cardiorenal Med 1:3–4, 2011), the term cardiorenal syndrome (CRS) has been used to define different clinical conditions in which heart and kidney dysfunction overlap. Type 1 CRS (acute cardiorenal syndrome) is characterized by acute worsening of cardiac function leading to AKI (Ronco in Contrib Nephrol 164:33–38, 2010; Eren et al. in Cardiorenal Med 2:168–176, 2012) in the setting of active cardiac disease such as ADHF, while type 2 CRS occurs in a setting of chronic cardiac decompensation. Type 3 CRS is closely linked to acute kidney injury (AKI), while type 4 represents cardiovascular involvement in patients with chronic kidney disease. Type 5 CRS represents cardiac and renal involvement in several diseases such as sepsis, hepatorenal syndrome, and immune-mediated diseases. Understanding the clinical phenotype of CRS is critical in initiating appropriate therapy and applying the underlying pathophysiologic principles in each subtype to achieve optimal outcomes
Ivabradine, heart failure and chronic kidney disease
Get PDFThe incidence and prevalence of congestive heart failure are actually increasing worldwide, especially inWestern countries. In Europe and the United States, congestive heart failure represents a disabling clinical disease, accountable for increased hospitalization and health care costs. European guidelines have underlined the importance of pharmacological treatment to improve both patients’ outcomes and quality of life. The latest clinical trials to evaluate ivabradine’s efficacy have underlined its usefulness as a stand-alone medication and in combination with conventional congestive heart failure therapy, including in chronic kidney disease patients
Il trattamento del diabete mellito di tipo 2 nei pazienti affetti da malattia renale cronica: cosa aspettarsi dai nuovi ipoglicemizzanti orali
Get PDFWorldwide, an estimated 200 million people have chronic kidney disease (CKD), whose most common causes include hypertension, arteriosclerosis, and diabetes. About 40% of patients with diabetes develop CKD. Intensive blood glucose control through pharmacological intervention can delay CKD progression. Standard therapies for the treatment of type 2 diabetes include metformin, sulfonylureas, meglitinides, thiazolidinediones and insulin. While these drugs have an important role in the management of type 2 diabetes, only the thiazolidinedione pioglitazone can be used across the spectrum of CKD (stages 2–5) and without dose adjustment. Newer therapies, particularly dipeptidyl peptidase-IV inhibitors, glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors are increasingly being used in the treatment of type 2 diabetes. However, a major consideration is whether these newer therapies can also be used safely and effectively across the spectrum of renal impairment
Anticoagulanti orali non vitamina K dipendenti (NOACs) nei pazienti affetti da malattia renale cronica e fibrillazione atriale non valvolare
No full textLa fibrillazione atriale (FA) rappresenta l'aritmia più comune nei pazienti con malattia renale cronica (CKD) in cui si associa, come nella popolazione generale, ad un aumento del rischio tromboembolico e di stroke con il progressivo ridursi del filtrato glomerulare (GFR). In tali pa zienti,e soprattutto in quelli sottoposti a terapia dialitica (RRT),è presente inoltre un incremento delrischio emorragico, soprattutto a carico deltratto gastroenterico.
Glianticoagulanti orali costituiscono la forma ditromboprofilassipiCJ eflicace neipazienticon FA che presentino un rischio maggiore di stroke. Tuttavia, le limitate evidenze scientifiche riguar danti la loro eflicacia,nonché l'aumento delrischio emorragico ed alcuniaspettiriguardanti l'uso dalwarfarin in CKD hanno spesso portato ad un loro scarso utilizzo in tali pazienti.
Un crescente numero di studi sembra suggerire che nei soggetti con normale funzione renale ifarmacianticoagulanti oralinon vitamina K dipendenti (NOACs) riducono significativamente il rischio distroka, emorragia intracranica e mortalità, conriduzione deisanguinamentimaggioriin confronto agliantagonisti della vitamina K (come il warfarin).Pertanto, essi sono raccomandati nei pazienti con FA a rischio distroke.Tuttavia, dalmomento che loro escrezione è fortemente influenzata dallivello difunzione renale,attualmente disponiamo discarse informazioni sulloro utilizzo neipazienti con clearance della creatinina inferiore a 25 mllmin poiché essistatiesclusi da tutti i trialdi fase 3 riguardantil'impiego deiNOACs.
Scopo della presente review è quello di puntualizzare i principali aspetti di farmacocinetica nonché le evidenze note,anche prospettiche,relativamente ai NOACs neipazienti con malattia renale cronica in fase conservativa (clearance della creatinina < 25 mllmin) ed in quelli sottopo stia trattamento dialitico
Treatment of secondary hyperparathyroidism : the clinical utility of etelcalcetide
Get PDFSecondary hyperparathyroidism (SHPT), a very frequent, severe, and worsening complication of chronic kidney disease, is characterized by high serum parathyroid hormone (PTH), parathyroid gland hyperplasia, and disturbances in mineral metabolism. Clinically, SHPT shows renal osteodystrophy, vascular calcification, cardiovascular damage, and fatal outcome. Calcium-sensing receptor (CaSR) is the main physiological regulator of PTH secretion; its activation by calcium rapidly inhibits PTH. Another important player in regulating mineral metabolism is vitamin D receptor (VDR), which is under the influence of vitamin D and influences the intestinal absorption of calcium and phosphate, PTH gene expression, and bone calcium mobilization. Serum phosphate levels influence fibroblast growth factor 23 (FGF-23) production, a phosphatonin that modulates serum phosphate reabsorption, PTH synthesis, and vitamin D production. Current therapeutic approaches consist of 1) phosphate intake control by diet or phosphate binders, 2) vitamin D by VDR activation, and 3) calcimimetic agents that activate CaSR. Recently, a new long-acting peptide (etelcalcetide) belonging to the calcimimetics class was approved for intravenous use in hemodialysis patients with SHPT. Etelcalcetide binds directly to CaSR, by a sulfide bond, inhibiting the production and secretion of PTH by parathyroid glands. After intravenous administration in rats, etelcalcetide is quickly distributed to the tissues and eliminated by kidneys, while in uremic animals the nonrenal excretion is only 1.2%. In hemodialysis patients, the treatment itself is the main route of elimination. Etelcalcetide in hemodialysis patients with SHPT was more effective than placebo and cinacalcet, with a PTH reduction of >30% in 76% of patients with etelcalcetide versus 10% with placebo. Particular attention was paid to the safety of the drug; the most common adverse event was asymptomatic blood calcium reduction, similar to cinacalcet, while gastrointestinal symptoms were less frequent. This promising new drug available for better control of SHPT will, together with drugs already in use, optimize the treatment to normalize the biochemical parameters
Type-5 Cardiorenal Syndrome (CRS-5): An up to Date
Get PDFCardiorenal syndromes (CRS) involve disorders of the heart or kidney whereby one organ dysfunction leads to the dysfunction of another. Five types of CRS are defined. While the first 4 types describe acute/chronic cardiorenal or renocardiac syndromes, type-5 CRS refers to secondary CRS or cardiorenal involvement in systemic conditions and describes the concomitant presence of renal and cardiovascular dysfunction. Type-5 CRS is a recently defined clinical syndrome and complete epidemiological data on this entity are still lacking. In the following review, epidemiological, pathophysiological, clinical, and therapeutic approaches to type-5 CRS will be discussed according to more recent findings.</jats:p
Chronic Hyperkalemia in Cardiorenal Patients : Risk Factors, Diagnosis, and New Treatment Options
No full textChronic hyperkalemia (HK) is a serious medical condition that often manifests in patients with chronic kidney disease (CKD) and heart failure (HF) leading to poor outcomes and necessitating careful management by cardionephrologists. CKD, HF, diabetes, and renin-angiotensin-aldosterone system inhibitors use is known to induce HK. Current therapeutic options are not optimal, as pointed out by a large number of CKD and HF patients with HK. The following review will focus on the main risk factors for developing HK and also aims to provide a guide for a correct diagnosis and present new approaches to therapy
Progression of cardiac valve calcification and decline of renal function in CKD patients
No full textBackground: No study has evaluated the efficacy of non-calcium-containing phosphate binders in slowing progression of cardiac valve calcification or deterioration of kidney function in patients with chronic kidney disease not on dialysis. This study addressed these issues. Methods: Outpatients (n = 170) with stage 3-4 chronic kidney disease and either mitral or aortic valve calcification were evaluated in this single-center, singlearm, prospective observational study. Patients received sevelamer hydrochloride (1,600 mg/day) for 1 year. Cardiac valve calcification progression was assessed by echocardiography, and decline of renal function by estimated glomerular filtration rate. Parathyroid hormone, FGF-23 and C-reactive protein (CRP) serum concentration and urinary phosphorus excretion were assayed. Results: At the end of treatment with sevelamer (12th month), mitral valve calcification had decreased by 79.3% from baseline. At baseline, 69 patients had grade 1, 97 patients grade 2 and 4 patients grade 3 calcification scores; at the end of the study, 60 patients showed grade 1, and no mitral valve calcification was registered in the remaining patients. An aortic valve score of 1 was found in 32%, score of 2 in 58%, score of 3 in 9% and score of 4 in 1% of patients at baseline; at the end of the study, a score of 1 was found in 95% and a score of 2 in 5% of patients. Significant slowing down of renal function decline (p<0.001), reduction of FGF-23 and CRP concentration (p<0.0001) and phosphorus excretion (p<0.0001) were observed. Conclusions: One-year treatment with a non-calciumcontaining phosphate binder may hamper the progression of cardiac valve calcification and slow the decline of renal function, as well as reduce serum concentration of FGF-23 and CRP and urinary phosphorus excretion
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