Vincenzo Barbera

Sudden cardiac death and chronic kidney disease: From pathophysiology to treatment strategies

Chronic kidney disease (CKD) patients demonstrate higher rates of cardiovascular mortality and morbidity; and increased incidence of sudden cardiac death (SCD) with declining kidney failure. Coronary artery disease (CAD) associated risk factors are the major determinants of SCD in the general population. However, current evidence suggests that in CKD patients, traditional cardiovascular risk factors may play a lesser role. Complex relationships between CKD-specific risk factors, structural heart disease, and ventricular arrhythmias (VA) contribute to the high risk of SCD. In dialysis patients, the occurrence of VA and SCD could be exacerbated by electrolyte shifts, divalent ion abnormalities, sympathetic overactivity, inflammation and iron toxicity. As outcomes in CKD patients after cardiac arrest are poor, primary and secondary prevention of SCD and cardiac arrest could reduce cardiovascular mortality in patients with CKD.

Pulmonary Hypertension and Right Heart Failure in Chronic Kidney Disease: New Challenge for 21st-Century Cardionephrologists.

Pulmonary hypertension is defined as an increased systolic pulmonary pressure of >30 mm Hg, and it shows a 40% prevalence in hemodialysis patients due to vascular access (both central venous catheter and arteriovenous fistula). Secondary pulmonary hypertension in chronic kidney disease patients is strictly related to pulmonary circulation impairment together with chronic volume overload and increased levels of cytokines and growth factors, such as FGF, PDGF, and TGF-β, leading to fibrosis. Endothelial dysfunction, together with lower activation of NOS, increased levels of serum endothelin and fibrin storages, involves an extensive growth of endothelial cells leading to complete obliteration of pulmonary vessels. Pulmonary hypertension has no pathognomonic and distinctive symptoms and signs; standard transthoracic echocardiography allows easy assessment of compliance of the right heart chambers. The therapeutic approach is based on traditional drugs such as digitalis-derived drugs, vasodilatory agents (calcium channel blockers), and oral anticoagulants. New pharmacological agents are under investigation, such as prostaglandin analogues, endothelin receptor blockers, and phosphodiesterase-5 inhibitors.

Nonvitamin K-dependent oral anticoagulants (NOACs) in chronic kidney disease patients with atrial fibrillation

Atrial fibrillation (AF) represents the most common arrhythmia in patients with chronic kidney disease (CKD). As in the general population, in CKD patients AF is associated with an increased risk of thromboembolism and stroke. However, CKD patients, especially those on renal replacement therapy (RRT), also exhibit an increased risk of bleeding, especially from the gastrointestinal tract. Oral anticoagulation is the most effective form of thromboprophylaxis in patients with AF presenting increased risk of stroke. Limited evidence on efficacy, the increased risk of bleeding as well as some concern regarding the use of warfarin in CKD, has often resulted in the underuse of anticoagulation CKD patients. A large body of evidence suggests that non-vitamin K-dependent oral anticoagulant agents (NOACs) significantly reduce the risk of stroke, intracranial hemorrhage, and mortality, with lower to similar major bleeding rates compared with vitamin K antagonist such as warfarin in normal renal function subjects. Hence, they are currently recommended for patients with atrial fibrillation at risk for stroke. However, NOACs metabolism is largely dependent on the kidneys for elimination and little is known in patients with creatinine clearance <25ml/min who were excluded from all pivotal phase 3 NOACs trials. This review focuses on the current pharmacokinetic, observational, and prospective data on NOACs in patients with moderate to advanced chronic kidney disease (creatinine clearance 15-49ml/min) and those on dialysis.

Nutritional therapy in autosomal dominant polycystic kidney disease

CKD-related nutritional therapy (NT) is a crucial cornerstone of CKD patients’ treatment, but the role of NT has not been clearly investigated in autosomal dominant polycystic kidney disease (ADPKD). Several clinical studies have focused on new pharmacological approaches to delay cystic disease progression, but there are no data on dietary interventions in ADPKD patients. The aim of this paper is to analyze the evidence from the literature on the impact of five nutritional aspects (water, sodium, phosphorus, protein intake, and net acid load) in CKD-related ADPKD extrapolating—where information is unavailable—from what occurs in CKD non-ADPKD patients Sodium intake restriction could be useful in decreasing the growth rate of cysts. Although further evidence is needed, restriction of phosphorus and protein intake restriction represent cornerstones of the dietary support of renal non-ADPKD patients and common sense can guide their use. It could be also helpful to limit animal protein, increasing fruit and vegetables intake together with a full correction of metabolic acidosis. Finally, fluid intake may be recommended in the early stages of the disease, although it is not to be prescribed in the presence of moderate to severe reduction of renal function.

Pathophysiology of the cardio-renal syndromes types 1–5: An uptodate

According to the recent definition proposed by the Consensus conference on Acute Dialysis Quality Initiative Group, the term cardio-renal syndrome (CRS) has been used to define different clinical conditions in which heart and kidney dysfunction overlap. Type 1 CRS (acute cardio- renal syndrome) is characterized by acute worsening of cardiac function leading to AKI (5, 6) in the setting of active cardiac disease such as ADHF, while type – 2 CRS occurs in a setting of chronic heart disease. Type 3 CRS is closely link to acute kidney injury (AKI), while type 4 represent cardiovascular involvement in chronic kidney disese (CKD) patients. Type 5 CRS represent cardiac and renal involvement in several diseases such as sepsis, hepato – renal syndrome and immune – mediated diseases.

The treatment of type 2 diabetes mellitus in patients with chronic kidney disease: What to expect from new oral hypoglycemic agents

Worldwide, 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 and intensive blood glucose control through pharmacological intervention can delay CKD progression. Standard therapies for the treatment of type 2 diabetes mellitus 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.

Penile Calciphylaxis in End Stage Renal Disease

Calciphylaxis, better described as “Calcific uremic arteriolopathy” (CUA), involves about 1–4% of hemodialysis patients all around the world with high mortality rates. We describe a rare clinical case of CUA in peritoneal dialysis patient associated with urological disease. Penile calciphylaxis represents rare clinical complication, and an early diagnosis and multidisciplinary approach are requested. Pathogenesis is still unclear, and therapeutic approaches need more long-term clinical trials to test their efficacy and safety.

Current and future perspectives of contrast-enhanced ultrasonography (CEUS) in nephrology

Contrast-enhanced ultrasonography (CEUS) is becoming an ultrasound device with many diagnostic applications. Employment of microbubbles as contrast media agents has allowed dynamic evaluation of micro- and macrovessels strengthening the characterization of ultrasonographic lesions not valuable with Power and Color Doppler analysis. CEUS does not involve ionizing radiations, then its not harmful for kidney function. CEUS seems to be particularly helpful in distinguishing between benign cysts and malignancies according to Bosniaks classification. CEUS can also be applied to diagnose ischemic or traumatic issues, renal artery stenosis, autosomal dominant polycystic kidney disease and urinary infections or traumatic injuries and for kidney graft evaluation. Further perspectives for CEUS lie in oncology for post-ablation kidney surveillance and in nanobubbles devices.

Left ventricul ar hypertrophy in patients with chronic kidney disease

Cardiovascular diseases such as coronary artery disease, congestive heart failure, arrhythmias, and sudden cardiac death represent main causes of morbidity and mortality in patients with chronic kidney disease (CKD). Their pathogenesis relates to the close linkage between heart and kidneys and involves both traditional and non-traditional risk factors. According to the well-established classification of cardio-renal syndrome, the cardiovascular involvement in chronic kidney disease is known as “type 4 cardiorenal syndrome” (chronic renocardiac syndrome). Uremic cardiopathy is mainly characterized by both left ventricular systolic and diastolic impairment, often associated to right heart dysfunction due to the presence of a vascular access for hemodialysis. The typical clinical picture is represented by left ventricular hypertrophy (LVH), the pathogenesis of which is multifactorial and closely linked to elevated blood pressure, vascular stiffness and atherosclerosis. The diagnosis is mainly made by ultrasound (2D and 3D echocardiography) and cardiac magnetic resonance imaging (CMRI), although echocardiography is most widely employed since it is non-invasive and cheaper than CMRI. The following chapter provides an overview of the epidemiology, pathophysiology, diagnosis, and treatment of left ventricular hypertrophy in CKD patients.

Chronic Hyperkalemia in Cardiorenal Patients: Risk Factors, Diagnosis, and New Treatment Options

Chronic 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.