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AIM Acute kidney injury (AKI) shows an increasing incidence, accounting for a remarkable proportion of nephrology team in-hospital activity. The aim was to describe main features and outcomes of AKI observed in patients admitted to a tertiary care hospital. METHODS We conducted a retrospective analysis in all consecutive AKI patients referred for nephrology consultation (November 2018-February 2020) focusing on the factors associated with in-hospital mortality within 90 days and kidney function recovery (KFR) upon discharge. Demographic, clinical and laboratory data, as well as main features of AKI episodes, were collected from medical records of the entire hospital stay. AKI was defined according to KDIGO Clinical Practice Guideline. RESULTS Among 1145 patients referred for nephrology consultation, 559 were evaluated for AKI (598 episodes). Pre-existing CKD was present in 54.7% of patients. In 69.2% of cases AKI was evaluated within 48 h from its onset. Most of the episodes (66.6%) were classified as KDIGO Stage 3. In-hospital mortality within 90 days since admission was 43.3%. Multivariate Cox regression analysis showed a higher mortality risk for advancing age (HR 1.02/unit, 95% CI 1.01-1.03) and oliguria (HR 1.91, 95% CI 1.45-2.52), while a higher eGFR (HR 0.72/unit, 95% CI 0.54-0.95) and KFR within 7 days (HR 0.62, 95% CI 0.41-0.94) were associated to a lower mortality. KFR was observed in 96.4% of survivors. In patients with partial KFR, the loss of eGFR was -29.2 ± 17.9 ml/min. KFR incidence rate was 6.79 per 100-person days (95% CI 6.72-6.87) in survivors and 2.30 (95% CI 2.25-2.35) in non-survivors. CONCLUSION AKI-related nephrology activity accounts for most of the nephrologist workload as consultant. Referred AKI episodes are frequently severe and superimposed on CKD, carrying a relatively high mortality in a patient population developing AKI outside ICU. Early KFR appears strongly associated with a favourable impact upon in-hospital survival.

Galectin-3 is a 32- to 35-kDa member of the galectin family of b-galactoside-binding lectins, which is characterized by a carbohydrate recognition domain. Through its carbohydrate-binding function, it regulates cell growth, differentiation, and inflammation. It also plays a complex, context-dependent role in the kidneys. During the development, it promotes nephrogenesis and is strongly expressed in the ureteric bud and its derivatives. An increase in the concentration of galectin-3 has been reported to be associated with fibrosis of the kidneys. Elevated levels of plasma galectin-3 are also associated with increased risks of rapid renal function decline, incident chronic kidney disease, and progressive renal impairment, and also with cardiovascular endpoints, infection, and all-cause mortality in patients with renal function impairment. This review discusses a general survey on galectin-3 expressions in nephrogenesis, kidney injury in animal models, clinical renal diseases, and renal transplantation and t...

Traditionally computed tomography (CT) and more recently magnetic resonance (MR) are the imaging modalities of choice for the evaluation of peritoneum and peritoneal cavity in primary and secondary...

Vitamin D represents the precursor of calcitriol, crucial for bone and mineral metabolism. The high prevalence of vitamin D deficiency and the detection of vitamin D receptor (VDR) both in the heart and vessels have focused the interest on potential cardiovascular effects of vitamin D.Although several experimental data showed the protective role of vitamin D, on the other hand vitamin D “overdose” can contribute to heart and vascular calcification.Meta-analyses of randomized-controlled trials (RCTs) underlined the association of vitamin D deficiency and increased cardiovascular morbidity and mortality but no significant improvements on cardiovascular outcomes are provided by the supplementation of vitamin D.The following review provides an update on pathophysiology of vitamin D and vitamin D receptor (VDR) discussing on the association with cardiovascular risk factors and disease and on the role of vitamin D supplementation in preventing cardiovascular disease in chronic kidney disease (CKD) patients.

There is a great deal of data demonstrating a close association between chronic kidney disease (CKD) and cardiovascular disease, particularly coronary artery disease (CAD). About one half of deaths in patients with end-stage renal disease (ESRD) are of cardiovascular causes. The association between CKD and ischemic heart disease can be explained in part because both conditions are related to the traditional risk factors for atherosclerotic vascular disease. However, CKD might also have a casual role in the development and progression of CAD, with several mechanisms potentially involved. Among CAD patients, those with CKD have systematically a worse prognosis than those without CKD irrespective of the clinical presentation or the treatments applied. Current therapy is based on small trials and observational data and on the extrapolation of the strategies that have been proved useful in the general population, although many treatments that have been shown to improve the prognosis of CAD patients are underused in those with renal impairment. (Cardionephrology)

In chronic kidney disease (CKD) and end-stage renal disease patients cardiovascular disease is the main cause of morbidity and mortality, with incidence of cardiac related mortality increasing as renal function declines. Even after controlling for traditional cardiovascular risk factors such as smoking, age, gender, dyslipidaemia, and arterial hypertension, patients with CKD have a higher incidence of major cardiovascular events. CKD is characterised by the presence of many other non-traditional cardiovascular risk factors, such as chronic inflammation and accelerated atherosclerosis, oxidative stress, and especially, secondary hyperparathyroidism. This review will summarise the current evidence on vascular calcifications and valvular heart disease in CKD patients, from pathophysiology to therapeutic strategies.

Hepatic and kidney failure are often closely linked (Hepato-Renal Sindrome - HRS). Acute kidney injury (AKI) represents a well-known complication of liver or biliary tract disease. Pathophysiology of HRS is still not completely clear. At this stage we know the biological pathways of several kidney abnormalities in end stage liver disease patients. At the same time patient's prognosis is poor with bad outcomes despite the reversible nature of the kidneys' involvement. Liver transplantation represents the ultimate treatment for HRS patients.

Atrial fibrillation (AF) represents the most common arrhythmia in patients with chronic kidney disease (CKD). As in the general population, AF is associated with an increased risk of thromboembolism and stroke, according to progressive decline of glomerular filtration rate (GFR). 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 clearance25 ml/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 advanced chronic kidney disease (creatinine clearance25 ml/) and those on dialysis.

Atrial fibrillation (AF) represents the most common arrhythmia in patients with chronic kidney disease (CKD). As in the general population, AF is associated with an increased risk of thromboembolism and stroke, according to progressive decline of glomerular filtration rate (GFR). 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 clearance25 ml/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 advanced chronic kidney disease (creatinine clearance25 ml/min) and those on dialysis.

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. 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 25) 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.

Galectin-3 is a 32- to 35-kDa member of the galectin family of b-galactoside-binding lectins, which is characterized by a carbohydrate recognition domain. Through its carbohydrate-binding function, it regulates cell growth, differentiation, and inflammation. It also plays a complex, context-dependent role in the kidneys. During the development, it promotes nephrogenesis and is strongly expressed in the ureteric bud and its derivatives. An increase in the concentration of galectin-3 has been reported to be associated with fibrosis of the kidneys. Elevated levels of plasma galectin-3 are also associated with increased risks of rapid renal function decline, incident chronic kidney disease, and progressive renal impairment, and also with cardiovascular endpoints, infection, and all-cause mortality in patients with renal function impairment. This review discusses a general survey on galectin-3 expressions in nephrogenesis, kidney injury in animal models, clinical renal diseases, and renal transplantation and the potential role of galectin-3 for treatment in kidney disease. (Cardionephrology)

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

Cardiovascular disease and major cardiovascular events represent main cause of death in both acute and chronic kidney disease patients. Kidney and heart failure are common and frequently co-exist This organ-organ interaction, also called organ cross-talk, leads to well-known definition of cardiorenal syndrome (CRS). Here we will describe cardiovascular involvement in patients with acute kidney injury (AKI). Also known as Type-3 CRS or acute reno-cardiac CRS, it occurs when AKI contributes and/or precipitates development of acute cardiac injury. AKI may directly or indirectly produces an acute cardiac event and it can be associated with volume overload, metabolic acidosis and electrolytes disorders such as hyperkalemia and hypocalcemia, coronary artery disease, left ventricular dysfunction and fibrosis which has been also described in patients with AKI with the consequence of direct negative effects on cardiac performance.

Vitamin D represents the precursor of calcitriol, crucial for bone and mineral metabolism. The high prevalence of vitamin D deficiency and the detection of vitamin D receptor (VDR) both in the heart and vessels have focused the interest on potential cardiovascular effects of vitamin D. Although several experimental data showed the protective role of vitamin D, on the other hand vitamin D “overdose” can contribute to heart and vascular calcification. Meta-analyses of randomized-controlled trials (RCTs) underlined the association of vitamin D deficiency and increased cardiovascular morbidity and mortality but no significant improvements on cardiovascular outcomes are provided by the supplementation of vitamin D. The following review provides an update on pathophysiology of vitamin D and vitamin D receptor (VDR) discussing on the association with cardiovascular risk factors and disease and on the role of vitamin D supplementation in preventing cardiovascular disease in chronic kidney disease (CKD) patients. (Cardionephrology)

Cardiorenal 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.