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BACKGROUND@#The clinical importance of hypokalemia is likely underrecognized in Chinese dialysis patients, and whether its clinical effect was mediated by serum albumin is not fully elucidated. This study aimed to explore the association between serum potassium and mortality in dialysis patients of a Chinese nationwide multicenter cohort, taking albumin as a consideration.@*METHODS@#This was a prospective nation-wide multicenter cohort study. Restricted cubic splines were used to test the linearity of serum potassium and relationships with all-cause (AC) and cardiovascular (CV) mortality and a subsequent two-line piecewise linear model was fitted to approach the nadir. A mediation analysis was performed to examine relations of albumin to potassium and mortalities.@*RESULTS@#A total of 10,027 patients were included, of whom 6605 were peritoneal dialysis and 3422 were hemodialysis patients. In the overall population, the mean age was 51.7 ± 14.8 years, 55.3%(5546/10,027) were male, and the median dialysis vintage was 13.60 (4.70, 39.70) months. Baseline serum potassium was 4.30 ± 0.88 mmol/L. After a median follow-up period of 26.87 (14.77, 41.50) months, a U-shape was found between potassium and mortality, and a marked increase in risk at lower potassium but a moderate elevation in risk at higher potassium were observed. The nadir for AC mortality risk was estimated from piecewise linear models to be a potassium concentration of 4.0 mmol/L. Interestingly, the significance of the association between potassium and mortality was attenuated when albumin was introduced into the extended adjusted model. A subsequent significant mediation by albumin for potassium and AC and CV mortalities were found ( P < 0.001 for both), indicating that hypokalemia led to higher mortality mediated by low serum albumin, which was a surrogate of poor nutritional status and inflammation.@*CONCLUSIONS@#Associations between potassium and mortalities were U-shaped in the overall population. The nadir for AC mortality risk was at a potassium of 4.0 mmol/L. Serum albumin mediated the association between potassium and AC and CV mortalities.
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Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , População do Leste Asiático , Hipopotassemia/etiologia , Falência Renal Crônica/mortalidade , Potássio/sangue , Estudos Prospectivos , Diálise Renal , Albumina Sérica/análiseRESUMO
Objective:To investigate the etiology, clinicopathological changes and genetic variation characteristics of familial juvenile hyperuricemia nephropathy (FJHN) through pedigree investigation and gene test conducted on a patient with FJHN.Methods:Clinical data of the proband family members were collected, routine pathological examination of the proband kidney tissue was conducted, and the expression of the Uromodulin (UMOD) protein in the proband kidney tissue was detected by immunofluorescence staining. Peripheral blood specimens of proband and their relatives were collected, and gene sequencing analysis related to urinary system diseases including UMOD was performed by double-stranded DNA probe gene capture and high-throughput sequencing. Results:Seven family members in the family were involved and the inheritance method was consistent with autosomal dominant inheritance. Among the seven affected individuals only a 3-year-old child didn't show any clinical abnormalities. All of the remaining six patients had hyperuricemia accompanied with renal dysfunction and three of them were end-stage renal disease and two of them died of uremia. Proband renal pathological results showed chronic tubulointerstitial lesions and focal glomerular sclerosis with no obvious deposition of immune complexes. Immunofluorescent staining showed that strong positive signals of UMOD protein accumulated in the tubular epithelial cells, which was very specific and could be used to differentiate FJHN from other interstial nephritis. A total of four patients including the proband were tested and all had found heterozygous mutation c.377G>A of UMOD gene, a new missense mutation located on exon 3. Conclusion:Involved patients in this family present a typical autosomal dominant inheritance pattern, clinically manifested as hyperuricemia with early renal function impairment, renal pathology manifested as non-immune complex-mediated glomerular sclerosis and renal interstitial fibrosis, and there is abnormal accumulation of UMOD protein in renal tubular epithelial cells. Genetic testing shows a new gene locus mutation c.377G>A, confirming the diagnosis of FJHN. Patients with unexplained hyperuricemia and characteristic pathological changes should undergo renal tissue fluorescent staining of UMOD protein, which may be a simple and feasible method to detect the abnormality of UMOD protein.
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Objective To evaluate the role of phosphatidylinositol 3?kinase(PI3K)∕serine?threo?nine kinase(Akt)signaling pathway in propofol?induced invasion of human liver cancer cell line HepG2. Methods HepG2 cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum in a 5% CO2incubator at 37℃. HepG2 cells at the logarithmic growth phase were divided into 6 groups(n=18 each)using a random number table: control group(group C), propofol group(group P), PI3K∕Akt signaling pathway agonist IGF?1 group(group IGF), PI3K∕Akt signaling pathway inhibitor LY294002 group(group LY), IGF?1 plus propofol group(group IGF+P)and LY294002 plus propofol group (group LY + P). Propofol 120 μg∕ml was added in group P. IGF?1 10 nmol∕L was added in group IGF. LY294002 10 μmol was added in group LY. In group IGF+P, 10 nmol∕L IGF?1 was added, cells were in?cubated for 24 h, and then 120 μg∕ml propofol was added. In group LY+P, 10 μmol LY294002 was add?ed, cells were incubated for 24 h, and then 120 μg∕ml propofol was added. The invasion of cells was measured by Transwell invasion assay at 24 h of incubation. The expression of PI3K and Akt mRNA in cells was determined by real?time polymerase chain reaction. The expression of Akt, PI3K and phosphorylated Akt(p?Akt)was detected by using Western blot. Results Compared with group C, the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the expression of Akt mRNA was down?regulated in P, P+IGF, LY and P+LY groups, and the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expression of Akt mRNA was up?regulated in group IGF(P<0.05). Compared with group P, the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expres?sion of Akt mRNA was up?regulated in group P+IGF, and the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the ex?pression of Akt mRNA was down?regulated in group P+LY(P<0.05). The invasive cell count was signifi?cantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was de?creased, and the expression of Akt mRNA was down?regulated in group P+IGF as compared with group IGF (P<0.05)and in group P+LY as compared with group LY(P<0.05). Conclusion The mechanism by which propofol inhibits invasion of HepG2 cells is related to inhibiting activation of PI3K∕Akt signaling path?ways.
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Objective To evaluate the effects of dexmedetomidine on the cellular immune function of the rats with scald.Methods Seventy-two healthy male Sprague-Dawley rats,weighing 200-220 g,aged 120-150 days,were randomly divided into 3 groups (n =24 each):normal control group (group C),scald group (group S) and dexmedetomidine group (group D).Thirty percent of the total body surface was shaved and then exposed to 94 ℃ water for 12 s in S and D groups.The rats were resuscitated according to Parkland formula after scald in S and D groups,and in addition,dexmedetomidine 30 μg/kg was also intraperitoneally injected immediately after scald in D group.Before the model was established (T1) and at 12 and 24 h after scald (T2,3),blood samples from the inferior vena cava were collected for determination of T lymphocyte subsets CD3 +,CD4 + and CD8 +,NK cell,C-reactive protein (CRP),interleukin-6 (IL-6),IL-10 and tumor necrosis factor-alpha (TNF-α) level.CD4+/CD8+ was calculated.Arterial blood samples were collected for blood gas analysis.Results Compared with C,the CD3+,CD4+ and NK cell levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly decreased,and CD8+ levels,IL-6,IL-10,TNF-α,CRP and BE negative value were increased at T2,3 in S and D groups.Compared with group S,the CD3+,CD4+,NK cell and IL-10 levels,CD4+/CD8+,pH value,PaCO2 and PaO2 were significantly increased,and CD8+ levels,IL-6,TNF-α,CRP and BE negative value were decreased at T2,3 in group D.Conclusion Dexmedetomidine can improve the cellular immune function of the rats with scald.
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[Objective] Observing the treatment effect of recurrent hordeolum with wind-dispel ing heat-clearing and qi-regulating spleen-strengthening herbs.[Methods] 26 cases of use of wind-dispel ing heat-clearing and qi-regulating spleen-strengthening herbs combined with heat treatment of recurrent hordeolum compared with 26 patients initial y treated with hot water bottle only, to compare the clinical efficacy and recurrence situation of two groups. [Results] 2 groups treated for 4 courses, the total effective rate of the treatment group was significantly high, the recurrence rate was significantly lower than the control group, the difference was statistical y significant, P<0.05. [Conclusion] The treatment effect of recurrent hordeolum with wind-dispel ing heat-clearing and qi-regulating spleen-strengthening herbs is good, the recurrence rate is low, it is safe and feasible.