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- Melin, Jan, et al.
(författare)
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Bedside BNP as a marker of overhydration in hemodialysis patients
- 2017
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Ingår i: Journal of the American Society of Nephrology. - 1046-6673 .- 1533-3450. ; 28:Suppl., s. 878-878
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundManagement of hydration status in dialysis patients is a great challenge to nephrologists, and new tools to understand the hydration status (HS) are needed. The aim of this study was to investigate the usefulness of brain natriuretic peptide (BNP), analyzed bedside, as a marker of overhydration (OH) in hemodialysis (HD) patients.MethodsWe investigated the distribution of BNP, measured by Alere Triage® BNP Test, and analyzed the correlation between BNP and HS, defined by bioimpedance spectroscopy (BIS) in 64 HD patients. We assumed there would be a difference in HS between patients with high levels of BNP (h-BNP) and low levels of BNP (l-BNP) and choose an arbitrary cut off of 500 ng/ml, and then differences between the groups were tested for significance. HS, blood pressure (BP) and heart rate was measured, and BNP analyzed, before one mid-week dialysis session. Blood samples were also drawn for analysis of NT-proBNP and inflammatory markers. Demographic data, comorbidities, lab values and nutritional status were collected from medical records.ResultsA positive correlation was found between BNP and OH (r = 0.4), although many severely overhydrated patients had normal or just slightly elevated BNP. BNP levels were above 500 in 38 % (n=24) of the participants. The level of OH before dialysis was higher in the h-BNP group than in the l-BNP group. There was no difference in BP before or after dialysis, but patients in the h-BNP group were older, had lower muscle strength and lower Hemoglobin and Albumin levels compared to the l-BNP group.ConclusionA normal BNP does not rule out OH as defined by BIS in HD patients, on the other hand euvolemia was rare in patients with elevated BNP. This suggests that BNP might serve as a marker of OH in a subgroup of old and frail patients. In a further study we aim to investigate if the relationship between BNP, when elevated, and OH is reproducible at an individual level.
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| 2. |
- Abedini, Sadollah, et al.
(författare)
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Inflammation in renal transplantation
- 2009
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Ingår i: Journal of the American Society of Nephrology. - 1046-6673 .- 1533-3450. ; 4:7, s. 1246-1254
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND OBJECTIVES: Renal transplant recipients experience premature cardiovascular disease and death. The association of inflammation, all-cause mortality, and cardiovascular events in renal transplant recipients has not been examined in a large prospective controlled trial. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: ALERT was a randomized, double-blind, placebo-controlled study of the effect of fluvastatin on cardiovascular and renal outcomes in 2102 renal transplant recipients. Patients initially randomized to fluvastatin or placebo in the 5- to 6-yr trial were offered open-label fluvastatin in a 2-yr extension to the original study. The association between inflammation markers, high-sensitivity C-reactive protein (hsCRP), and IL-6 on cardiovascular events and all-cause mortality was investigated. RESULTS: The baseline IL-6 value was 2.9 +/- 1.9 pg/ml (n = 1751) and that of hsCRP was 3.8 +/- 6.7 mg/L (n = 1910). After adjustment for baseline values for established risk factors, the hazard ratios for a major cardiac event and all-cause mortality for IL-6 were 1.08 [95% confidence interval (CI), 1.01 to 1.15, P = 0.018] and 1.11 (95% CI, 1.05 to 1.18, P < 0.001), respectively. The adjusted hazard ratio for hsCRP for a cardiovascular event was 1.10 (95% CI, 1.01 to 1.20, P = 0.027) and for all-cause mortality was 1.15 (95% CI, 1.06 to 1.1.25, P = 0.049). CONCLUSIONS: The inflammation markers IL-6 and hsCRP are independently associated with major cardiovascular events and all-cause mortality in renal transplant recipients.
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| 4. |
- Al-Rabadi, Laith Farah, et al.
(författare)
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Serine Protease HTRA1 as a Novel Target Antigen in Primary Membranous Nephropathy
- 2021
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Ingår i: Journal of the American Society of Nephrology. - : American Society of Nephrology (ASN). - 1046-6673 .- 1533-3450. ; 32:7, s. 1666-1681
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Tidskriftsartikel (refereegranskat)abstract
- Background Identification of target antigens PLA2R, THSD7A, NELL1, or Semaphorin-3B can explain the majority of cases of primary membranous nephropathy (MN). However, target antigens remain unidentified in 15%-20% of patients. Methods A multipronged approach, using traditional and modern technologies, converged on a novel target antigen, and capitalized on the temporal variation in autoantibody titer for biomarker discovery. Immunoblotting of human glomerular proteins followed by differential immunoprecipitation and mass spectrometric analysis was complemented by laser-capture microdissection followed by mass spectrometry, elution of immune complexes from renal biopsy specimen tissue, and autoimmune profiling on a protein fragment microarray. Results These approaches identified serine protease HTRA1 as a novel podocyte antigen in a subset of patients with primary MN. Sera from two patients reacted by immunoblotting with a 51-kD protein within glomerular extract and with recombinant human HTRA1, under reducing and nonreducing conditions. Longitudinal serum samples from these patients seemed to correlate with clinical disease activity. As in PLA2R- and THSD7A- associated MN, anti-HTRA1 antibodies were predominantly IgG4, suggesting a primary etiology. Analysis of sera collected during active disease versus remission on protein fragment microarrays detected significantly higher titers of anti-HTRA1 antibody in active disease. HTRA1 was specifically detected within immune deposits of HTRA1-associated MN in 14 patients identified among three cohorts. Screening of 118 "quadruple-negative" (PLA2R-, THSD7A-, NELL1-, EXT2-negative) patients in a large repository of MN biopsy specimens revealed a prevalence of 4.2%. Conclusions Conventional and more modern techniques converged to identify serine protease HTRA1 as a target antigen in MN.
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- Annuk, Margus, et al.
(författare)
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Oxidative stress and endothelial function in chronic renal failure
- 2001
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Ingår i: Journal of the American Society of Nephrology. - 1046-6673 .- 1533-3450. ; 12:12, s. 2747-2752
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- This study aimed to investigate the relationship between oxidative stress and endothelium-dependent vasodilation in patients with chronic renal failure (CRF). Thirty-seven patients with CRF underwent evaluation of endothelium-dependent vasodilation and endothelium-independent vasodilation by means of forearm blood flow measurements with venous occlusion plethysmography during local intra-arterial infusions of methacholine (evaluating endothelium-dependent vasodilation) and sodium nitroprusside (evaluating endothelium-independent vasodilation). Lag phase of lipoprotein fraction to oxidation, total antioxidative activity, diene conjugates, thiobarbituric acid reactive substances, lipid hydroperoxide, reduced glutathione (GSH), oxidized GSH (GSSG), and the GSH redox ratio (GSSG/GSH) were all measured as markers of oxidative stress. Two groups of healthy subjects (61 and 37 subjects, respectively) were used as controls. In one group, oxidative stress markers were measured, whereas endothelium-dependent vasodilation and endothelium-independent vasodilation were assessed in the other group. Compared with controls, the patients with renal insufficiency had an impaired endothelium-dependent vasodilation, a shorter lag phase of lipoprotein fraction, and higher levels of diene conjugates, lipid hydroperoxide, and GSSG levels. The GSSG/GSH ratio was lower in patients with CRF. Endothelium-dependent vasodilation was positively correlated with total antioxidative activity (r = 0.41, P = 0.016), GSH (r = 0.44, P < 0.0098), and lag phase of LDL (r = 0.35, P = 0.036) and negatively correlated with GSSG (r = -0.40, P < 0.018), GSSG/GSH (r = -0.47, P = 0.0057), and diene conjugates (r = -0.53 P < 0.0015) in patients with CRF. These results show that an impaired endothelium vasodilation function and oxidative stress are related to each other in patients with CRF.
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