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Basso F.,St Bortolo Hospital | Basso F.,IRRIV International Renal Research Institute Vicenza | Milan Manani S.,St Bortolo Hospital | Milan Manani S.,IRRIV International Renal Research Institute Vicenza | And 12 more authors.
CardioRenal Medicine | Year: 2013

Background: Several methods have been developed to assess the hydration status in chronic hemodialysis (HD) patients. The aim of this study was to compare body bioimpedance spectroscopy (BIS) with ultrasound (US) lung comet score (ULCs), B-type natriuretic peptide (BNP) and inferior vena cava diameter (IVCD) by US for the estimation of dry weight before and after HD and to analyze all methods in terms of fluid status variations induced by HD. An additional aim of this study was to establish the interoperator reproducibility of these methods. Methods: Two nephrologists evaluated BIS, ULCs, IVCD during inspiration (min) and expiration (max), the inferior vena cava collapsibility index (IVCCI) as well as BNP before and after HD in 30 patients. The same operators measured BIS, ULCs and IVCD in 28 HD patients in a blinded fashion. Results: There was a significant reduction in BIS, ULCs, IVCD and BNP after HD (p < 0.001), but a less significant reduction in IVCCI (p = 0.13). There was a significant correlation between BIS and ULCs, BNP and indexed IVCD (IVCDi)min (p < 0.05) before and after HD, and between BIS and IVCDimax only before HD. Conclusion: All methods were able to describe hyperhydration before and after HD, except for IVCCI after HD. All techniques correlated with BIS before HD. After HD, ULCs correlated better with BIS than IVCD in terms of evaluation of fluid status. It could be expected that the ULCs can give a real-time evaluation of interstitial water. The reproducibility of the measurement of BIS, IVCD and ULCs between the two operators was high. Copyright © 2013 S. Karger AG.


Pastori S.,San Bortolo Hospital | Pastori S.,IRRIV International Renal Research Institute Vicenza | Pastori S.,University of Padua | Virzi G.M.,San Bortolo Hospital | And 16 more authors.
CardioRenal Medicine | Year: 2015

Cardiorenal syndrome type 1 (CRS1) pathophysiology is complex, and immune-mediated damage, including alterations in the immune response with monocyte apoptosis and cytokine release, has been reported as a potential mechanism. In this study, we examined the putative role of renal tubular epithelial cell (RTC) apoptosis as a pathogenic mechanism in CRS1. In particular, we investigated the caspase pathways involved in induced apoptosis. We enrolled 29 patients with acute heart failure (AHF), 11 patients with CRS1, and 15 controls (CTR) without AHF or acute kidney injury (AKI). Patients who had AKI prior to the episode of AHF or who had any other potential causes of AKI were excluded. Plasma from different groups was incubated with RTCs for 24 h. Subsequently, cell apoptosis, DNA fragmentation, and caspase-3, -8, and -9 activities were investigated in RTCs incubated with AHF, CRS1, and CTR plasma. A p value <0.5 was considered statistically significant. A quantitative analysis of apoptosis showed significantly higher apoptosis rates in CRS1 patients compared to AHF patients and CTR (p < 0.01). This increase in apoptosis was strongly confirmed by caspase-3 levels (ρ = 0.73). Caspase-8 and -9 were significantly higher in CRS1 patients compared to AHF patients and CTR (p < 0.01). Furthermore, caspase-3 levels showed a significantly positive correlation with caspase-8 (ρ = 0.57) and -9 (ρ = 0.47; p < 0.001). This study demonstrated the significantly heightened presence of dual apoptotic disequilibrium in CRS1. Our findings indicated that apoptosis may have a central role in the mechanism of CRS1, and it could be a potential therapeutic target in this syndrome. © 2015 S. Karger AG, Basel.


Virzi G.M.,IRRIV International Renal Research Institute Vicenza | Virzi G.M.,San Bortolo Hospital | Milan Manani S.,IRRIV International Renal Research Institute Vicenza | Milan Manani S.,San Bortolo Hospital | And 16 more authors.
Journal of Nephrology | Year: 2016

Background: Cell-free DNA (cfDNA) is present in the peritoneal effluent of stable peritoneal dialysis (PD) patients, but there are no data on cfDNA in PD patients with peritonitis. We investigated the variation of peritoneal cfDNA levels subsequent to peritonitis in PD patients. Methods: We enrolled 53 PD patients: 30 without any history of systemic inflammation or peritonitis in the last 3 months (group A) and 23 with acute peritonitis (group B). CfDNA was quantified in the peritoneal effluent. Peritoneal samples on days 1, 3, 10, 30 and until day 120 from the start of peritonitis were collected for white blood cells (WBC) count and cfDNA evaluation in group B. Results: Quantitative analysis of cfDNA showed significantly higher levels in group B on day 1, 3, 10 and 30 compared with group A (p < 0.05). A significant positive correlation was observed between cfDNA concentration and WBC on day 1 (rho = 0.89) and day 3 (rho = 0.5) (both, p < 0.05). However, no significant correlation was observed between cfDNA and WBC on days 10 and 30. In group B, peritoneal cfDNA levels tended to progressively decline during follow-up of peritonitis. From this decreasing curve, we estimated that 49 days are necessary to reach the value of 51 genome equivalents (GE)/ml (75th percentile in controls) and 63 days to reach 31 GE/ml (median). Conclusion: Our results demonstrate that cfDNA increases in peritoneal effluent of PD patients with peritonitis and tends to progressively decline in step with peritonitis resolution and membrane repair process. Peritoneal cfDNA quantification could be an innovative method to determine acute damage and an inverse index of the repair process. © 2015, Italian Society of Nephrology.


PubMed | University of Turin, IRRIV International Renal Research Institute Vicenza and San Bortolo Hospital
Type: Journal Article | Journal: Journal of nephrology | Year: 2016

Cell-free DNA (cfDNA) is present in the peritoneal effluent of stable peritoneal dialysis (PD) patients, but there are no data on cfDNA in PD patients with peritonitis. We investigated the variation of peritoneal cfDNA levels subsequent to peritonitis in PD patients.We enrolled 53 PD patients: 30 without any history of systemic inflammation or peritonitis in the last 3months (group A) and 23 with acute peritonitis (group B). CfDNA was quantified in the peritoneal effluent. Peritoneal samples on days 1, 3, 10, 30 and until day 120 from the start of peritonitis were collected for white blood cells (WBC) count and cfDNA evaluation in group B.Quantitative analysis of cfDNA showed significantly higher levels in group B on day 1, 3, 10 and 30 compared with group A (p<0.05). A significant positive correlation was observed between cfDNA concentration and WBC on day 1 (rho=0.89) and day 3 (rho=0.5) (both, p<0.05). However, no significant correlation was observed between cfDNA and WBC on days 10 and 30. In group B, peritoneal cfDNA levels tended to progressively decline during follow-up of peritonitis. From this decreasing curve, we estimated that 49days are necessary to reach the value of 51 genome equivalents (GE)/ml (75th percentile in controls) and 63days to reach 31 GE/ml (median).Our results demonstrate that cfDNA increases in peritoneal effluent of PD patients with peritonitis and tends to progressively decline in step with peritonitis resolution and membrane repair process. Peritoneal cfDNA quantification could be an innovative method to determine acute damage and an inverse index of the repair process.


PubMed | IRRIV International Renal Research Institute Vicenza and San Bortolo Hospital
Type: Journal Article | Journal: Heart failure reviews | Year: 2016

Cardiomyocyte apoptosis plays a pivotal role in the pathogenesis of heart failure. It may be induced by different stimuli, and it seems to be perpetuated by oxidative stress and inflammation. In this scenario, heart failure may trigger various cell-mediated and humoral pathways affecting distant organs, such as kidneys, contributing to higher therapeutic costs, morbidity and mortality. The term Cardiorenal Syndromes describes this condition and represents an important model for exploring the pathophysiology of cardiac and renal dysfunction. In this review, we have analyzed the mechanisms of organ interaction and the role of apoptosis in heart-kidney crosstalk, in particular its role in the pathogenesis of the different types of Cardiorenal Syndromes.

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