Publications by authors named "Gastaldon F"

Article Synopsis
  • - The Renal Biopsy for Kidney Transplantation Therapy (ReBIrth) meeting held on May 31, 2022, in Bologna, Italy, focused on advancements in kidney transplantation, bringing together key experts in nephrology, surgery, and pathology.
  • - The paper highlights experiences with kidney transplants and aims to report on the histopathological features of failed kidney allografts, analyzed through a digital pathology platform.
  • - Findings suggest that digital pathology effectively identifies critical morphological and immunohistochemical traits, potentially enhancing the use of immunosuppressive therapy to reduce graft failure and improve patient care.
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Objectives: The study aim was to assess predictors of negative antibody response (AbR) in solid organ transplant (SOT) recipients after the first booster of SARS-CoV-2 vaccination.

Methods: Solid organ transplant recipients receiving SARS-CoV-2 vaccination were prospectively enrolled (March 2021-January 2022) at six hospitals in Italy and Spain. AbR was assessed at first dose (t), second dose (t), 3 ± 1 month (t), and 1 month after third dose (t).

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Article Synopsis
  • * Antibody levels in SOT recipients increased significantly within the first 76 days but showed a non-significant decrease after 118 days, while HCWs experienced a notable decrease in antibody levels over the same periods.
  • * Factors such as liver transplant type, time since SOT, specific mRNA vaccine used, and certain medications were linked to a better antibody response; meanwhile, older age and
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Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease, responsible for 10% of patients on renal replacement therapy. The disease is well known to be associated with many extrarenal manifestations. Leukopenia may also be present, even if it is not commonly identified as a typical extrarenal manifestation.

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and accounts for∼10% of patients on renal replacement therapy. In the last decade, no specific treatment was available and only preventive measures could be put in place to delay the onset of ESRD. Following the results of the TEMPO 3:4 study, tolvaptan was approved in many countries, for the purpose of slowing the progression of renal insufficiency.

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Introduction: Intraperitoneal volume (IPV) should be individualized and aimed to maintain an intraperitoneal pressure (IPP) lower than 17 cm H2O. IPP is very variable, given its relation with body size. However, it is not yet fully understood which anthropometric variable mostly affects IPP and the relation between IPP and organomegaly in polycystic kidney disease (PKD) patients is not known.

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A series of selenylated-oxadiazoles were prepared and their interaction with DNA was investigated. The photophysical studies showed that all the selenylated compounds presented absorption between 270 and 329 nm, assigned to combined n→π* and π→π* transitions, and an intense blue emission (325-380 nm) with quantum yield in the range of  = 0.1-0.

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease, accounting for 10% of European patients on renal replacement therapy. In the previous years, many approaches to slow the progression of ADPKD were studied and many clinical trials published. In addition to having diagnostic role, the description of the genotype is even important to predict the progression of the disease and contributes, combined with several other factors, to a more precise patients classification.

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The hemolytic uremic syndrome (HUS) is one of the thrombotic microangiopathies and it consists of the triad of nonimmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The atypical form of HUS (aHUS) is related to causative mutations in complement genes. Some conditions act as a trigger for aHUS in individuals that have a genetic background predisposing to complement activation.

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Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases with a reported prevalence of 1:400 to 1:1000. Since the intact kidneys can compensate for the loss of glomerular filtration in ADPKD patients, renal insufficiency usually remains undetected until almost the fourth decade of life. Hereafter, reliable diagnostic and prognostic biomarkers to identify ADPKD progression are urgently needed.

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Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease. Studies have suggested a possible prognostic role of copeptin in determining the rate of progressive kidney function decline in ADPKD patients. However, it remains unresolved whether the changes in copeptin levels are specific for ADPKD or merely reflect a decline in glomerular filtration rate (GFR) regardless of the etiology of chronic kidney disease (CKD).

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Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disease with variable rate of progression. It is associated with inter- and intra-familial variability. Neutrophil gelatinase-associated lipocalin (NGAL) has been implicated in pathological conditions and it is proposed as a biomarker for CKD progression.

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Autosomal dominant polycystic kidney (ADPKD) is the most common inherited renal cystic disease and it occurs in all races, the reported prevalence is between 1:400 and 1:1000. It is characterized by development of cysts in both kidneys and progressive renal function loss. Among most Autosomal Dominant Polycystic Kidney patients, renal function remains intact until the fourth decade of life.

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Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic cause of chronic kidney disease (CKD) in adults. It is associated with both inter- and intra- familial variability, which can be explained by genetic heterogeneity, modifier genes and a genetic background. NGAL, a 25-kDa protein released from tubular cells after harmful stimuli, is a new biomarker.

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Background: Autosomal dominant polycystic kidney disease (ADPKD) is an inherited condition caused by PKD1 and PKD2 mutations. Complete analysis of both genes is typically required in each patient. In this study, we explored the utility of High-Resolution Melt (HRM) as a tool for mutation analysis of the PKD2 gene in ADPKD families.

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The cardiorenal syndrome type 4 (Chronic Renocardiac Syndrome) is characterized by a condition of primary chronic kidney disease (CKD) that leads to an impairment of the cardiac function, ventricular hypertrophy, diastolic dysfunction, and/or increased risk of adverse cardiovascular events. Clinically, it is very difficult to distinguish between CRS type 2 (Chronic Cardiorenal Syndrome) and CRS type 4 (Chronic Renocardiac Syndrome) because often it is not clear whether the primary cause of the syndrome depends on the heart or the kidney. Autosomal dominant polycystic kidney disease (ADPKD), a genetic disease that causes CKD, could be viewed as an ideal prototype of CRS type 4 because it is certain that the primary cause of cardiorenal syndrome is the kidney disease.

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder, with a prevalence of 1:400 to 1:1000. ADPKD is genetically and clinically heterogeneous. In addition, significant intrafamilial renal disease variability is evident.

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Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder, with a prevalence of 1 : 500 to 1 : 1,000. ADPKD is genetically heterogeneous: the genes involved are PKD1 and PKD2. ADPKD occurs worldwide and in all ethnic groups and is an important cause of CKD Stage 5.

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Uremia is associated with a state of immune dysfunction. Dysregulation of homeostasis may be directly related to abnormal apoptosis regulation in uremia, which is crucial for the maintenance of the biological system. We demonstrated that plasma from three groups of uremic subjects, i.

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Pro-apoptotic molecules are generated during sepsis which may be responsible for alteration of organ function in sepsis. Removal of systemic apoptotic activity may affect recovery from sepsis. Current high flux membranes might not be sufficiently permeable to eliminate pro-apoptotic factors.

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Background: The correction of anemia using erythropoeitin (EPO) is accorded high priority in the management of patients undergoing hemodialysis (HD). Target hemoglobin (Hb) levels have been established in many countries. Following an observation that the mean facility EPO dose in a chain of facilities in the United States varied by more than two-fold, an examination of the practice of anemia correction in other settings was carried out.

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The management of anemia in uremic patients undergoing hemodialysis requires the appropriate combination of erythropoietin treatment, iron supplementation, and on occasion androgen therapy. Identifying and correcting functional iron deficiency is crucial to optimizing erythropoietin efficiency. Recently, however, the trend to administer maintenance iron with resultant high serum ferritin and high transferrin saturation has led to an increase in reports of iron overload.

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The main target for low flux hemodialyzers is an efficient low molecular weight solutes clearance. Such efficiency is largely dependent on the optimization of diffusion between blood and dialysis solution. The diffusion process can be impaired if there is a mismatch between blood and dialysate flow distribution in the dialyzer.

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