Application of Lipid Apheresis in Acute Lipogenic Pancreatitis.

INTRODUCTION: Recently, the incidence of hypertriglyceridemia-associated pancreatitis (HTG-AP) has been increasing. The pathogenesis of lipogenic pancreatitis is not fully understood. This study aimed to retrospectively analyze the laboratory data, clinical manifestations, and prognosis of patients with lipid-derived pancreatitis who received lipid purification, to explore whether lipid purification is a better treatment for acute hyperlipidemic pancreatitis. METHODS: In this study, we enrolled five subjects diagnosed with HTG-AP at the Second Xiangya Hospital of Central South University between 2021 and 2022. We collected demographic data, medical histories, clinical manifestations, and laboratory data. All patients received routine therapy. Blood lipid purification was conducted using the double filtration plasmapheresis (DFPP) method. Plasma was separated from blood cells and purified to remove cholesterol, triglycerides, and low-density lipoprotein (LDL). SPSS was used for statistical analyses. RESULTS: Following a single lipoprotein apheresis (LA) treatment, significant improvements in serum lipid levels were observed. Three patients achieved triglyceride levels below 5.65 mmol/L within 24 h, while the remaining 2 patients experienced reductions of 82% and 78%, respectively. The average triglyceride level decreased from 36.82 to 7.27 mmol/L, representing an 80% reduction from baseline. Total cholesterol decreased by 59% on average, and LDL levels decreased by 69%. Statistically significant differences were observed in triglyceride and cholesterol levels before and after treatment. Four patients exhibited increased HDL levels posttreatment, while 1 patient showed a decrease. The average HDL/TC level was 21% higher after treatment. CONCLUSION: LA in HTG-AP effectively improves clinical symptoms, rapidly lowers lipid levels, and achieves good therapeutic outcomes.

Oxalate crystal-related acute renal injury caused by orlistat: A case report. / å¥¥åˆ©å¸ä»–è‡´è‰é ¸ç›ç»“æ™¶ç›¸å ³æ€¥æ€§è‚¾æŸä¼¤1例.

We reported a case of oxalate crystal-related acute kidney injury caused by orlistat. The patient was admitted for nephrotic syndrome and acute kidney injury. The pathomorphological assessment of renal biopsy showed intratubular oxalate crystals. The patient reported that she had taken orlistat regularly to loss weight for more than a year. This patient had a habit of drinking vegetable soup and strong herbal tea daily. Orlistat, an intestinal lipase inhibitor, may cause secondary hyperoxaluria, that is, intestinal hyperoxaluria. Dietary habits could be a common precipitating factor for orlistat-relevant hyperoxaluria. It was comprehensively considered to be oxalate crystal-related acute renal injury, and the patient's renal function recovered gradually after drug withdrawal. Clinicians should pay attention to screening drug-related acute kidney injury including orlistat when observing patients with unexplained acute kidney injury, and renal biopsy should be performed if necessary. It is also important to warn people who take the orlistat for weight loss about the side effects of this drug so as to adjust the eating habits.

Mitochondria-Targeted Peptide SS31 Attenuates Renal Tubulointerstitial Injury via Inhibiting Mitochondrial Fission in Diabetic Mice.

OBJECTIVE: Renal tubular injury is an early characteristic of diabetic nephropathy (DN) that is related to mitochondrial dysfunction. In this study, we explore the effects and mechanisms of mitochondria-targeted peptide SS31 on renal tubulointerstitial injury in DN. METHOD: 40 C57BL/6 mice were randomly divided into control group, STZ group, STZ+SS31 group, and STZ+normal saline group. SS31 was intraperitoneally injected to the mice every other day for 24 weeks. Renal lesions and the expression of Drp1, Mfn1, Bcl-2, Bax, Caspase1, IL-1ß, and FN were detected. In in vitro studies, HK-2 cells were incubated with different concentrations of D-glucose (5, 30 mM) or combined with SS31 and Drp1 inhibitor Midivi1. Mitochondrial ROS, membrane potential, and morphology have been detected to evaluate the mitochondrial function. RESULTS: Compared with diabetic mice, the levels of serum creatinine and microalbuminuria were significantly decreased in the SS31 group. Renal tubulointerstitial fibrosis, oxidative stress, and apoptosis were observed in diabetic mice, while the pathological changes were reduced in the SS31-treatment group. SS31 could decrease the expression of Drp1, Bax, Caspase1, IL-1ß, and FN in the renal tissue of diabetic mice, while increasing the expression of Mfn1. Additionally, mitochondria exhibit focal enlargement and crista swelling in renal tubular cells of diabetic mice, while SS31 treatment could partially block these changes. An in vitro study showed that pretreatment with SS31 or Drp1 inhibitor Mdivi1 could restore the level of mitochondrial ROS, the membrane potential levels, and the expressions of Drp1, Bax, Caspase1, IL-1ß, and FN in HK-2 cells under high-glucose conditions. CONCLUSION: SS31 protected renal tubulointerstitial injury in diabetic mice through a decrease in mitochondrial fragmentation via suppressing the expression of Drp1 and increasing the expression of Mfn1.

Significance of serum procalcitonin as biomarker for detection of bacterial peritonitis: a systematic review and meta-analysis.

BACKGROUND: Bacterial peritonitis is serious disease and remains a diagnostic challenge for clinicians. Many studies have highlighted the potential usefulness of procalcitonin (PCT) for identification of bacterial peritonitis, however, the overall diagnostic value of PCT remains unclear. Therefore, we performed a meta-analysis to assess the accuracy of PCT for detection of bacterial peritonitis. METHODS: We performed a systematic searched in MEDLINE, EMBASE, SCOPUS, China Biology Medicine Database (CBM), China National Knowledge Infrastructure Database (CNKI) and Cochrane databases for trials that evaluated the diagnostic role of PCT for bacterial peritonitis. Sensitivity, specificity and other measures of accuracy of PCT were pooled using bivariate random effects models. RESULTS: Eighteen studies involving 1827 patients were included in the present meta-analysis. The pooled sensitivity and specificity of serum PCT for the diagnosis bacterial peritonitis were 0.83 (95% CI: 0.76-0.89) and 0.92 (95% CI: 0.87-0.96), respectively. The positive likelihood ratio was 11.06 (95% CI: 6.31-19.38), negative likelihood ratio was 0.18 (95% CI: 0.12-0.27) and diagnostic odds ratio (DOR) was 61.52 (95% CI: 27.58-137.21). The area under the receiver operating characteristic curve (AUROC) was 0.94. Use of a common PCT cut-off value could improve the DOR to 75.32 and the AUROC to 0.95. Analysis of the seven studies that measured serum C-reactive protein (CRP) indicated that PCT was more accurate than CRP for the diagnosis of bacterial peritonitis. CONCLUSIONS: Our results indicate that PCT determination is a relatively sensitive and specific test for the diagnosis of bacterial peritonitis. However, with regard to methodological limitations and significant heterogeneity, medical decisions should be based on both clinical findings and PCT test results.

Effect of L-carnitine therapy on patients in maintenance hemodialysis: a systematic review and meta-analysis.

BACKGROUND: L-Carnitine has been used as adjuvant therapy in hemodialysis (HD) patients for many years. However, there is controversy whether L-carnitine supplementation is beneficial. Therefore we performed a meta-analysis of randomized controlled trials (RCTs) to assess the effect of L-carnitine on HD patients. METHODS: RCTs of L-carnitine versus placebo for HD patients were searched from Medline, EMBASE and the Cochrane Central Register of Controlled Trials. We screened relevant studies according to predefined inclusion and exclusion criteria, and performed meta-analyses using Revman 5.1 software. RESULTS: Meta-analysis showed L-carnitine could not increase the total score of 36-item Short-Form Health Survey Questionnaire (SF-36) (SMD 0.76, 95 % CI -0.13 to 1.65, P = 0.09), and L-carnitine therapy did not improve serum C-reactive protein (SMD -0.37, 95 % CI -0.88 to 0.14, P = 0.16), oxidized low-density lipoprotein (SMD 0.04, 95 % CI -0.43 to 0.50, P = 0.87), albumin (SMD 0.25, 95 % CI -0.31 to 0.81, P = 0.38;), hemoglobin (SMD 0.23, 95 % CI -0.23 to 0.68, P = 0.33), cholesterol (SMD -0.24, 95 % CI -0.71 to 0.24, P = 0.33), triglycerides (SMD 0.02, 95 % CI -0.4 to 0.44, P = 0.91) or parathyroid hormone (SMD 0.21, 95 % CI -0.35 to 0.76, P = 0.46) levels. CONCLUSIONS: There is no evidence that L-carnitine can improve the inflammation, oxidative stress, nutrition, anemia, dyslipidemia, hyperparathyroidism status or quality of life in HD patients. However, given methodological limitations and lack of hard endpoints, high-quality, long-term randomized trials are required to fully elucidate the clinical value of L-carnitine administration in hemodialysis patients.

Is lead chelation therapy effective for chronic kidney disease? A meta-analysis.

The heavy metal lead (Pb) is a major environmental and occupational hazard. Epidemiological studies have demonstrated a strong association between lead exposure and the presence of chronic kidney injury. Some studies have suggested that chelation therapy with calcium disodium ethylenediaminetetraacetic acid (calcium disodium EDTA) might help decrease the progression of chronic kidney disease among patients with measurable body lead burdens. However, calcium disodium EDTA chelation in lead exposure is controversial due to the potential for adverse effects such as acute tubular necrosis. Therefore, we investigated the available randomized controlled trials assessing the renoprotective effects of calcium disodium EDTA chelation therapy. Our meta-analysis shows that calcium disodium EDTA chelation therapy can effectively delay the progression of chronic kidney disease in patients with measurable body lead burdens reflected by increasing the levels of estimated glomerular filtration rate (eGFR) and creatinine clearance rate (Ccr). There appears to be no conclusive evidence that calcium disodium EDTA can decrease proteinuria.

[Role of PKCδ on the phosphorylation and mitochondrial translocation of p66Shc in HK-2 cells induced by high glucose].

OBJECTIVE: To observe the effect of PKCδ on the phosphorylation of p66Shc and its mitochondrial translocation in human proximal tubular cells (HK-2) under high glucose (HG). METHODS: HK-2 cells were incubated with different concentrations of D-glucose (5-45 mmol/L) for indicated time (0-48 h). Then the mRNA expressions of PKCδ and p66Shc and the phosphorylation levels of PKCδ (p-PKCδ) and p66Shc (p-p66Shc) were determined by real-time polymerase chain reaction (PCR) and Western blot analysis respectively. In addition, the effect of PKCδ inhibitor on the phosphorylation and mitochondrial translocation of p66Shc in HK-2 cells exposed to HG was also observed. HK-2 cells were divided into 3 groups of 5 mmol/L glucose, 30 mmol/L glucose and 30 mmol/L glucose + 1.0 µmol/L Rottlerin. Cell immunofluorescence and Western blotting were used to observe the phosphorylation and mitochondrial translocation of p66Shc. RESULTS: Both mRNA expression and phosphorylation level of p66shc and PKCδ significantly increased in HK-2 cells after exposure to HG (15, 30, 45 mmol/L). And it was in a concentration- and time-dependent manner as compared with control group (up-regulated 0.9, 1.3 and 1.6-fold in mRNA of PKCδ, 0.4, 1.5 and 2.0-fold in protein of p-PKCδ respectively (all P < 0.05). PKCδ inhibitor Rottlerin dramatically inhibited the phosphorylation and mitochondrial translocation of p66Shc induced by HG in HK-2 cells (down-regulated 3.1 folds in protein of p-p66Shc in mitochondria, P < 0.01). CONCLUSIONS: HG increases the transcription and phosphorylation of PKCδ and p66Shc in HK-2 cells. And PKCδ may modulate the phosphorylation and mitochondrial translocation of p66Shc under HG.