Background: Despite current interest in the unfavourable impact of non-traditional lipid profiles on cardiovascular disease, information regarding its relations to reduced glomerular filtration rate (GFR) in H-type hypertension population has not been systemically elucidated.Methods: Analyses were based upon a cross-sectional study of 3259 participants with H-type hypertension who underwent assessment of biochemical, anthropometric and blood pressure values. Reduced GFR was considered if meeting estimated GFR <60?ml/min/1.73 m2.Results: A stepwise multivariate regression analysis indicated that non-traditional lipid parameters remained as independent determinants of estimated GFR (all p?.001). In multivariable models, we observed a 50%, 51%, 31%, and 24% higher risk for decreased GFR with each SD increment in TC/HDL-C, TG/HDL-C, LDL-C/HDL-C ratios and non-HDL-C levels, respectively. The highest quartile of TC/HDL-C, TG/HDL-C and LDL-C/HDL-C ratios carried reduced GFR odds (confidence intervals) of 5.50 (2.50 to 12.09), 6.63 (2.58 to 17.05) and 2.22 (1.15 to 4.29), respectively.Conclusions: The relative independent contribution of non-traditional lipid profiles, as indexed by TC/HDL-C, TG/HDL-C, LDL-C/HDL-C ratios and non-HDL-C, towards reduced GFR putting research evidence at the very heart of lipoprotein-mediated renal injury set a vital example for applying a clinical and public health recommendation for reducing the burden of chronic kidney disease.
KEY MESSAGES
Non-traditional lipid profiles has been linked with the occurrence of cardiovascular disease, but none of the studies that address the effect of non-traditional lipid profiles on reduced GFR risk in H-type hypertension population has been specifically established.
A greater emphasis of this study resided in the intrinsic value of TC/HDL-C, TG/HDL-C, LDL-C/HDL-C ratios and non-HDL-C that integrate atherogenic and anti-atherogenic lipid molecules to predict the risk of reduced GFR among H-type hypertension population and provide insight into the pathophysiology of subsequent cardio-cerebrovascular outcomes.
In a large Chinese H-type hypertension adults, the relative independent contribution of non-traditional lipid profiles, as indexed by TC/HDL-C, TG/HDL-C, LDL-C/HDL-C ratios and non-HDL-C, towards reduced GFR putting research evidence at the very heart of lipoprotein-mediated renal injury set a vital example for applying a clinical and public health recommendation for reducing the burden of CKD.
Background: Patients with hepatocellular carcinoma (HCC) often have coexisting cirrhosis, which may predispose to the development of diabetes mellitus (DM). Diabetic HCC patients may have renal insufficiency and a subsequent worse outcome. This study investigated the interaction between DM, cirrhosis and renal dysfunction and the impact of these factors on HCC. Methods: A prospective database of 1713 HCC patients was analysed. Results: A total of 392 (22.9%) patients were diabetic. Diabetic patients had a significantly higher Child–Turcotte–Pugh (CTP) score, model for end‐stage liver disease score and serum creatinine level, but had significantly lower serum albumin, sodium, alanine aminotransferase, aspartate aminotransferase and bilirubin levels. The serum creatinine level progressively increased and correlated well with increasing CTP class in both diabetic and non‐diabetic patients. After a mean follow‐up of 18 ± 16 months, DM was shown to be an independent predictor of mortality in the Cox proportional hazard model after adjusting for other predictors [hazard ratio (HR): 1.2, 95% confidence interval (CI): 1.02–1.42]. Diabetic patients more often had renal insufficiency, defined as serum creatinine >1.5 mg/dl (17.3 vs 8.3%, P<0.0001). Renal insufficiency was an independent prognostic predictor in diabetic patients (HR: 2.26, 95% CI: 1.57–3.24) but not in non‐diabetic patients, because it was significantly associated with the severity of cirrhosis in the non‐diabetic group (P<0.001) but not in the diabetic group (P=0.143). Conclusions: DM is associated with inadequate liver reserve and independently predicts decreased survival in HCC patients. Both advanced cirrhosis and DM are associated with renal insufficiency, which is a poor prognostic predictor for HCC. 相似文献
OBJECTIVES: To evaluate the diagnostic performance of procalcitonin (PCT) in elderly patients with bacterial infection in the emergency department (ED). DESIGN: Prospective. SETTING: ED of a tertiary care hospital. PARTICIPANTS: Elderly patients with systemic inflammatory response syndrome (SIRS) enrolled from September 2004 through August 2005. MEASUREMENTS: A serum sample for the measurement of PCT, two sets of blood cultures, and other cultures of relevant specimens from infection sites were collected in the ED. Two independent experts blinded to the PCT results classified the patients into bacterial infection and nonbacterial infection groups. RESULTS: Of the 262 patients with SIRS enrolled, 204 were classified as having bacterial infection and 48 as having bacteremia. PCT levels were significantly higher in patients with bacteremia than in those without. The area under the receiver operating characteristic curve for identification of bacteremia according to PCT was 0.817 for the old‐old group (≥75), significantly higher than 0.639 for the young‐old group (65–74); P=.02). The diagnostic sensitivity, specificity, positive predictive value, and negative predictive value of PCT for bacteremia in patients aged 75 and older were 96.0%, 68.3%, 33.8%, and 98.8%, respectively, with a PCT cutoff value of 0.38 ng/mL. CONCLUSION: PCT is sensitive for diagnosing bacteremia in elderly patients with SIRS at ED admission but is helpful in excluding bacteremia only in those aged 75 and older. PCT is not an independent predictor of local infections in these patients. 相似文献
The effects of Phx-3 on changes in intracellular pH (pHi) in the MKN45 and MKN74 human gastric cancer cell lines were evaluated in order to determine the mechanism for the proapoptotic effects of 2-aminophenoxazine-3-one (Phx-3) on these cells. Phx-3 (100 μM) reduced pHi in MKN45 from 7.45 to 5.8, and in MKN74 from 7.5 to 6.2 within 1 min of engagement with these cells. Such a decrease of pHi was closely correlated with the dose of this phenoxazine and continued for 4 h. The activity of Na+/H+ exchanger isoform l (NHE1), which is involved in H+ extrusion from the cells, was dose-dependently suppressed by Phx-3 in these cells, and was greatly suppressed in the presence of 100 μM Phx-3. This result indicates that the decrease of pHi in MKN45 and MKN74 cells is closely associated with the inhibition of NHE1 in these cells. The morphology of these cells at 24 h after treatment with Phx-3 indicated shrinkage of the cells and condensation of the nuclear chromatin structure, which are characteristic of the apoptotic events in these gastric cancer cells. Cytotoxicity of Phx-3 against MKN45 and MKN74 cells was extensive because almost all MKN45 cells lost viability at 24 h in the presence of 20 μM Phx-3, and nearly 50% of the MKN74 cells lost viability in the presence of 50 μM Phx-3. These results suggest that rapid and extensive decrease of pHi in human gastric cancer MKN45 and MKN74 cells caused by Phx-3 might disturb intracellular homeostasis, leading to apoptotic and cytotoxic events in these cells. Phx-3 is a good candidate for therapeutics of gastric cancer that is intractable to conventional chemopreventive therapies. 相似文献
In osteoarthritis, angiogenesis, which occurs in the osteochondral junction and synovium, may accelerate inflammation and contribute to the severity of the disease. We used anterior cruciate ligament‐transection (ACLT) to investigate the therapeutic effect of an angiogenesis inhibitor, thrombospondin‐1 (TSP‐1), in a rat model of osteoarthritis. Osteoarthritis was induced in Wistar rats in the knee of one hind leg. After ACLT, AdTSP‐1 (adenoviral vector encoding mouse TSP‐1) was intraarticularly injected into the knee joints. Transgene expression, angiogenesis, and inflammatory responses in the knee joints were examined. They were also assessed morphologically, radiographically, and histologically for manifestations of disease. The levels of TSP‐1 peaked on day 3 and were substantially maintained for at least 9 days after AdTSP‐1 infection. Adenovirus‐mediated gene expression was detected in the synovial membrane and chondrocytes. TSP‐1 gene transfer induced transforming growth factor‐β (TGF‐β) production, but it reduced microvessel density, macrophage infiltration, and interleukin‐1β (IL‐1β) levels. Gross morphological and histopathological examinations revealed that rats treated with AdTSP‐1 had less severe osteoarthritis than controls. In vivo adenovirus‐mediated TSP‐1 gene transfer significantly reduced microvessel density, inflammation, and suppressed the progression of osteoarthritis. This study provides potential applications of TSP‐1 gene delivery for treating osteoarthritis. Published by Wiley Periodicals, Inc. J Orthop Res 28:1300–1306, 2010 相似文献