Acute and acute-on-chronic kidney injury of patients with decompensated heart failure: impact on outcomes

BACKGROUND: Acute worsening of renal function, an independent risk factor for adverse outcomes in acute decompensated heart failure (ADHF), occurs as a consequence of new onset kidney injury (AKI) or acute deterioration of pre-existed chronic kidney disease (CKD) (acute-on-chronic kidney injury, ACKI). However, the possible difference in prognostic implication between AKI and ACKI has not been well established. METHODS: We studied all consecutive patients hospitalized with ADHF from 2003 through 2010 in Nanfang Hospital. We classified patients as with or without pre-existed CKD based on the mean estimated glomerular filtration rate (eGFR) over a six-month period before hospitalization. AKI and ACKI were defined by RIFLE criteria according to the increase of the index serum creatinine. RESULTS: A total of 1,005 patients were enrolled. The incidence of ACKI was higher than that of AKI. The proportion of patients with diuretic resistance was higher among patients with pre-existed CKD than among those without CKD (16.9% vs. 9.9%, P = 0.002). Compared with AKI, ACKI was associated with higher risk for in-hospital mortality, long hospital stay, and failure in renal function recovery. Pre-existed CKD and development of acute worsening of renal function during hospitalization were the independent risk factors for in-hospital death after adjustment by the other risk factors. The RIFLE classification predicted all-cause and cardiac mortality in both AKI and ACKI. CONCLUSIONS: Patients with ACKI were at greatest risk of adverse short-term outcomes in ADHF. Monitoring eGFR and identifying CKD should not be ignored in patients with cardiovascular disease

Primerjalna študija genetske raznovrstnosti talnih bakterij in gliv v različnih sukcesijah vegetacije na krasu v provinci Guizhou, Kitajska

To study the soil genetic diversity of bacteria and fungi in different vegetation successions (grassland, shrubbery, primary forest and secondary forest) from the karst area, the Polymerase Chain Reaction-Denaturing Gradient Gel Electrophoresis (PCR-DGGE) technology was applied. The results showed that: (1) the diversity of bacterial communities and the fungal communities in karst area were higher than non karst area in each vegetation succession. Compared with the survey from bacterial (the Shannon index was 2.97 in primary forest, 2.91 in secondary forest, 3.18 in shrubbery, 3.14 in grassland and 2.68 in non karst), fungal diversity between karst areas (the Shannon index was 3.56 in primary forest, 3.78 in secondary forest, 3.73 in shrubbery and 3.70 in grassland) and non karst areas (the Shannon index was 3.08) was more evident, which may be related to the alterations of the composition of plant community and the source of carbon in soil with the vegetation succession of karst ecosystem; (2) The comparation of bacterial diversity index and the richness comprehensively evaluated as follows: shrubbery > grassland > primary forest > nsecondary forest. The diversity index and the richness of fungal communities was as follows: secondary forest > shrubbery > grassland > primary forest. The results suggest that the fungal communities have been greatly changed via vegetation successions, but the diversity index and the richness of the bacterial communities have not been seriously affected. The results provide scientific basis for understanding karst surface ecosystem, which contributes to the future aim of protecting the karst from desertification.Za proučevanje genetske pestrosti talnih bakterij in gliv v različnih sukcesijah vegetacije (travišče, grmičevje, primarni gozd in sekundarni gozd) na krasu je bila uporabljena tehnologija verižne reakcije s polimerazo-denaturirajoča gradientna gelska elektroforeza (PCR-DGGE). Rezultati raziskave so pokazali, da: (1) je bila v vsaki sukcesiji vegetacije pestrost bakterijskih in glivnih združb na kraškem območju višja kot na nekraškem. V primerjavi z bakterijsko raznovrstnostjo (Shannonov indeks je bil 2,97 v primarnem gozdu, 2,91 v sekundarnem gozdu, 3,18 v tleh grmičevja, 3,14 v tleh travišč in 2,68 v nekraškem območju) je bila raznovrstnost gliv med kraškimi območji (Shannonov indeks je bil v primarnem gozdu 3,56, 3,78 v sekundarnem gozdu, 3,73 v tleh grmičevja in 3,70 v tleh travišč) in nekraškimi (Shannonov indeks je bil 3,08) jasneje izražena. To je lahko povezano s spremembami v sestavi rastlinske združbe in vira ogljika v tleh glede na stanje sukcesije v vegetaciji kraškega ekosistema. (2) Primerjava kazalnikov bakterijske raznovrstnosti in abundance je bila celostno ovrednotena in sledi takole: grmičevje > travišče > primarni gozd > sekundarni gozd. Kazalnika raznovrstnosti in abundance glivnih združb kažeta sledeči trend: sekundarni gozd > grmičevje > travišče > primarni gozd. Rezultati izkazujejo, da so se glivne združbe precej spremenile zaradi sukcesije v vegetaciji, vendar pa na drugi strani ni bilo bistvenega vpliva na kazalnika bakterijske raznovrstnosti in abundance. Rezultati med drugim dajejo tudi znanstveno podlago za razumevanje delovanja kraškega površinskega ekosistema, kar ključno prispeva k cilju zaščite krasa pred dezertifikacijo (širjenjem puščav)

Association Between Pre-operative BUN and Post-operative 30-Day Mortality in Patients Undergoing Craniotomy for Tumors: Data From the ACS NSQIP Database

ObjectiveThere is limited evidence to clarify the specific relationship between pre-operative blood urea nitrogen (BUN) and post-operative 30-day mortality in patients undergoing craniotomy for tumors. Therefore, we aimed to investigate this relationship in detail.MethodsElectronic medical records of 18,642 patients undergoing craniotomy for tumors in the ACS NSQIP from 2012 to 2015 were subjected to secondary retrospective analysis. The principal exposure was pre-operative BUN. Outcome measures were post-operative 30-day mortality. We used binary logistic regression modeling to evaluate the association between them and conducted a generalized additive model and smooth curve fitting (penalized spline method) to explore the potential relationship and its explicit curve shape. We also conducted sensitivity analyses to ensure the robustness of the results and performed subgroup analyses.ResultsA total of 16,876 patients were included in this analysis. Of these, 47.48% of patients were men. The post-operative 30-day mortality of the included cases was 2.49% (420/16,876), and the mean BUN was 16.874 ± 6.648 mg/dl. After adjusting covariates, the results showed that pre-operative BUN was positively associated with post-operative 30-day mortality (OR = 1.020, 95% CI: 1.004, 1.036). There was also a non-linear relationship between BUN and post-operative 30-day mortality, and the inflection point of the BUN was 9.804. For patients with BUN < 9.804 mg/dl, a 1 unit decrease in BUN was related to a 16.8% increase in the risk of post-operative 30-day mortality (OR = 0.832, 95% CI: 0.737, 0.941); for patients with BUN > 9.804 mg/dl, a 1 unit increase in BUN was related to a 2.8% increase in the risk of post-operative 30-day mortality (OR = 1.028, 95% CI: 1.011, 1.045). The sensitivity analysis proved that the results were robust. The subgroup analysis revealed that all listed subgroups did not affect the relationship between pre-operative BUN and post-operative 30-day mortality (P > 0.05).ConclusionOur study demonstrated that pre-operative BUN (mg/dl) has specific linear and non-linear relationships with post-operative 30-day mortality in patients over 18 years of age who underwent craniotomy for tumors. Proper pre-operative management of BUN and maintenance of BUN near the inflection point (9.804 mg/dl) could reduce the risk of post-operative 30-day mortality in these cases

Homocysteine Aggravates Intestinal Epithelial Barrier Dysfunction in Rats with Experimental Uremia

Background/Aims: Previous studies have shown that homocysteine (Hcy) is an important intestinal-derived uremic toxin. However, whether Hcy is involved in the epithelial barrier dysfunction observed in uremia remains unclear. This study aimed to investigate the effect of Hcy on intestinal permeability and intestinal barrier structure and function in adenine-induced uremic rats. Methods: Sprague-Dawley rats were divided into five groups: normal control (group NC), Hcy (group H), uremia (group U), uremia + Hcy (group UH), and uremia + Hcy + VSL#3 (group UHV). Experimental uremia was induced by intragastric adenine administration, and Hcy was injected subcutaneously. The animal models were assessed for renal function and pathological tissue staining. The pathological changes of intestinal tissue were observed by hematoxylin and eosin staining and electron microscopy. The serum and intestinal tissue levels of Hcy, interleukin (IL)-6, tumor necrosis factor (TNF)-α, superoxide dismutase (SOD), and malondialdehyde (MDA) as well as serum endotoxin and intestinal permeability were assessed. The levels of the tight junction proteins claudin-1, occludin, and zonula occludens-1 (ZO-1) were assessed by western blotting. Results: Blood analyses and renal pathology indicated that experimental uremia was induced successfully. Pathological damage to intestinal structure was most obvious in group UH. Serum and tissue Hcy, serum endotoxin, and intestinal permeability were significantly elevated in group UH. The protein levels of claudin-1, occludin, and ZO-1 were decreased to various degrees in group UH compared with groups NC, H, and U. The serum and tissue levels of IL-6, TNF-α, and MDA were significantly increased, while SOD activity was markedly decreased. Supplementation with the probiotic VSL#3 improved these parameters to various degrees and up-regulated the abundance of tight junction proteins, which indicated a role for Hcy in the increase of intestinal permeability and destruction of the epithelial barrier in uremia. Conclusion: Hcy aggravates the increase of intestinal permeability and destruction of the epithelial barrier by stimulating inflammatory and oxidative damage. Probiotic administration can ameliorate this damage by reducing the levels of Hcy-induced inflammation and oxidation

Common variants at 2q11.2, 8q21.3, and 11q13.2 are associated with major mood disorders

Bipolar disorder (BPD) and major depressive disorder (MDD) are primary major mood disorders. Recent studies suggest that they share certain psychopathological features and common risk genes, but unraveling the full genetic architecture underlying the risk of major mood disorders remains an important scientific task. The public genome-wide association study (GWAS) data sets offer the opportunity to examine this topic by utilizing large amounts of combined genetic data, which should ultimately allow a better understanding of the onset and development of these illnesses. Genome-wide meta-analysis was performed by combining two GWAS data sets on BPD and MDD (19,637 cases and 18,083 controls), followed by replication analyses for the loci of interest in independent 12,364 cases and 76,633 controls from additional samples that were not included in the two GWAS data sets. The single-nucleotide polymorphism (SNP) rs10791889 at 11q13.2 was significant in both discovery and replication samples. When combining all samples, this SNP and multiple other SNPs at 2q11.2 (rs717454), 8q21.3 (rs10103191), and 11q13.2 (rs2167457) exhibited genome-wide significant association with major mood disorders. The SNPs in 2q11.2 and 8q21.3 were novel risk SNPs that were not previously reported, and SNPs at 11q13.2 were in high LD with potential BPD risk SNPs implicated in a previous GWAS. The genome-wide significant loci at 2q11.2 and 11q13.2 exhibited strong effects on the mRNA expression of certain nearby genes in cerebellum. In conclusion, we have identified several novel loci associated with major mood disorders, adding further support for shared genetic risk between BPD and MDD. Our study highlights the necessity and importance of mining public data sets to explore risk genes for complex diseases such as mood disorders

Common variants at 2q11.2, 8q21.3, and 11q13.2 are associated with major mood disorders

Bipolar disorder (BPD) and major depressive disorder (MDD) are primary major mood disorders. Recent studies suggest that they share certain psychopathological features and common risk genes, but unraveling the full genetic architecture underlying the risk of major mood disorders remains an important scientific task. The public genome-wide association study (GWAS) data sets offer the opportunity to examine this topic by utilizing large amounts of combined genetic data, which should ultimately allow a better understanding of the onset and development of these illnesses. Genome-wide meta-analysis was performed by combining two GWAS data sets on BPD and MDD (19,637 cases and 18,083 controls), followed by replication analyses for the loci of interest in independent 12,364 cases and 76,633 controls from additional samples that were not included in the two GWAS data sets. The single-nucleotide polymorphism (SNP) rs10791889 at 11q13.2 was significant in both discovery and replication samples. When combining all samples, this SNP and multiple other SNPs at 2q11.2 (rs717454), 8q21.3 (rs10103191), and 11q13.2 (rs2167457) exhibited genome-wide significant association with major mood disorders. The SNPs in 2q11.2 and 8q21.3 were novel risk SNPs that were not previously reported, and SNPs at 11q13.2 were in high LD with potential BPD risk SNPs implicated in a previous GWAS. The genome-wide significant loci at 2q11.2 and 11q13.2 exhibited strong effects on the mRNA expression of certain nearby genes in cerebellum. In conclusion, we have identified several novel loci associated with major mood disorders, adding further support for shared genetic risk between BPD and MDD. Our study highlights the necessity and importance of mining public data sets to explore risk genes for complex diseases such as mood disorders