Differences in pathological characteristics and laboratory indicators in adult and pediatric patients with Henoch-Schönlein purpura nephritis / 华中科技大学学报（医学）（英德文版）

We aimed to investigate the differences in renal histopathological changes and laboratory parameters between adult and pediatric patients with Henoch-Schönlein purpura nephritis (HSPN), and to analyze the correlation between laboratory parameters and renal histopathological grading. A total of 139 patients diagnosed with HSPN between September 2010 and December 2014 at the First Hospital of Jilin University, China, were retrospectively reviewed. The clinical and pathological characteristics were examined and compared between the adult and the pediatric patients. A majority of adult (75.0%) and pediatric (66.2%) patients were categorized as pathological grade III HSPN. Adults having crescent lesions, interstitial fibrosis and renal artery involvement significantly outnumbered child counterparts (all P<0.05). Pathological grading showed a positive correlation with 24-h urine protein (r=0.307, P=0.009), microalbuminuria (r=0.266, P=0.000) and serum globulin (r=0.307, P=0.014), and a negative correlation with serum albumin (r=0.249, P=0.037) in pediatric patients with HSPN. Among adult patients with HSPN, histopathological grading showed a positive correlation with 24-h urine protein (r=0.294, P=0.015), microalbuminuria (r=0.352, P=0.006), α1-microglobulin (r=0.311, P=0.019) and immunoglobulin G (r=0.301, P=0.023) in urine, and serum creatinine (r=0.292, P=0.018). Further, a negative correlation between serum albumin and pathological grading was also observed (r=0.291, P=0.018). In conclusion, the severity of renal pathological lesions in HSPN patients is well reflected by the levels of proteinuria. Adult patients have more severe renal histopathological changes than pediatric patients.

Decreased number of CD14+TLR4+ monocytes and their impaired cytokine responses to lipopolysaccharide in patients with chronic kidney disease / 华中科技大学学报（医学）（英德文版）

This study aimed to examine the number of circulating Toll-like receptor 4 (TLR4) + CD14+ monocytes in patients with different stages of chronic kidney disease (CKD), their responses to lipopolysaccharide (LPS), and to explore the potential association of the number of TLR4+CD14+ monocytes with clinical laboratory measures. The numbers of TLR4+CD14+, LPS-stimulated TNF-α+CD14+ and interleukin (IL)-6+CD14+ monocytes were determined by flow cytometry in 9 patients with stage 3 CKD, 11 with stage 4 CKD, 16 with stage 5 CKD, and 19 healthy controls (HCs). Their laboratory tests were performed by routine methods and the potential association among these measures was analyzed by Pearson's correlation analysis. The numbers of CD14+, CD14+TLR4+, LPSstimulated TNF-α+CD14+ and IL-6+CD14+ monocytes in patients with CKD were significantly less than those of HCs (all P<0.05), and were negatively associated with patient disease severity. The number of CD14+TLR4+ monocytes was positively correlated with estimated glomerular filtration rate (eGFR, P<0.001) and the levels of hematocrit (P<0.01), but negatively correlated with the levels of blood urine nitrogen, serum creatinine, and C-reactive protein (P<0.001 for all), in the CKD patients. Our data indicate that significant reduction in the number of TLR4+ monocytes and their impaired responses to LPS may be associated with the progression of CKD in Chinese patients.

Decreased number of CD14+TLR4+ monocytes and their impaired cytokine responses to lipopolysaccharide in patients with chronic kidney disease / 华中科技大学学报（医学）（英德文版）

This study aimed to examine the number of circulating Toll-like receptor 4 (TLR4) + CD14+ monocytes in patients with different stages of chronic kidney disease (CKD), their responses to lipopolysaccharide (LPS), and to explore the potential association of the number of TLR4+CD14+ monocytes with clinical laboratory measures. The numbers of TLR4+CD14+, LPS-stimulated TNF-α+CD14+ and interleukin (IL)-6+CD14+ monocytes were determined by flow cytometry in 9 patients with stage 3 CKD, 11 with stage 4 CKD, 16 with stage 5 CKD, and 19 healthy controls (HCs). Their laboratory tests were performed by routine methods and the potential association among these measures was analyzed by Pearson's correlation analysis. The numbers of CD14+, CD14+TLR4+, LPSstimulated TNF-α+CD14+ and IL-6+CD14+ monocytes in patients with CKD were significantly less than those of HCs (all P<0.05), and were negatively associated with patient disease severity. The number of CD14+TLR4+ monocytes was positively correlated with estimated glomerular filtration rate (eGFR, P<0.001) and the levels of hematocrit (P<0.01), but negatively correlated with the levels of blood urine nitrogen, serum creatinine, and C-reactive protein (P<0.001 for all), in the CKD patients. Our data indicate that significant reduction in the number of TLR4+ monocytes and their impaired responses to LPS may be associated with the progression of CKD in Chinese patients.

Protective effects of erythropoietin on endotoxin-related organ injury in rats / 华中科技大学学报（医学）（英德文版）

The protective effect of erythropoietin (EPO) on tissues following ischemia and reperfusion injuries remains poorly understood. We aimed to investigate the effect of EPO in preventing endotoxin-induced organ damage. Rat model of multiple organ failure (MOF) was established by tail vein injection of 10 mg/kg lipopolysaccharide (LPS). Recombinant human EPO treatment (5000 U/kg) was administered by tail vein injection at 30 min after LPS challenge. Twenty-four h after EPO treatment, changes in serum enzyme levels, including aspartate aminotransferase (AST), alanine transaminase (ALT), blood urea nitrogen (BUN) and creatinine (Cr), were evaluated by biochemical analysis. Serum levels of tumor necrosis factor-α (TNF-α) were determined by using immunoradiometric assay. Histological examination of tissue sections was carried out by hematoxylin and eosin staining, while ultrastructure evaluation of organ tissues was assessed by transmission electron microscopy. Protein expression levels were detected by using Western blotting. EPO treatment showed a modest effect in preventing LPS-induced elevation of AST, ALT, BUN, Cr, and TNF-α levels, and in protecting against LPS-induced tissue degeneration and injured ultrastructure in the lung, liver, and kidney. Moreover, LPS promoted phosphorylation of alanine aminotransferase (AKT) and increased nuclear factor-κB (NF-κB) activation in the lung, liver, and kidney (P<0.05 vs. control). However, EPO treatment significantly decreased the LPS-induced pAKT up-regulation in these tissues (P<0.05 vs. LPS treatment alone). The present study demonstrates that EPO may play a protective role against LPS-induced MOF by reducing the inflammatory response and tissue degeneration, possibly via the phosphatidylinositol 3-kinase/AKT and NF-κB signaling pathways.

Protective effects of erythropoietin on endotoxin-related organ injury in rats / 华中科技大学学报（医学）（英德文版）

The protective effect of erythropoietin (EPO) on tissues following ischemia and reperfusion injuries remains poorly understood. We aimed to investigate the effect of EPO in preventing endotoxin-induced organ damage. Rat model of multiple organ failure (MOF) was established by tail vein injection of 10 mg/kg lipopolysaccharide (LPS). Recombinant human EPO treatment (5000 U/kg) was administered by tail vein injection at 30 min after LPS challenge. Twenty-four h after EPO treatment, changes in serum enzyme levels, including aspartate aminotransferase (AST), alanine transaminase (ALT), blood urea nitrogen (BUN) and creatinine (Cr), were evaluated by biochemical analysis. Serum levels of tumor necrosis factor-α (TNF-α) were determined by using immunoradiometric assay. Histological examination of tissue sections was carried out by hematoxylin and eosin staining, while ultrastructure evaluation of organ tissues was assessed by transmission electron microscopy. Protein expression levels were detected by using Western blotting. EPO treatment showed a modest effect in preventing LPS-induced elevation of AST, ALT, BUN, Cr, and TNF-α levels, and in protecting against LPS-induced tissue degeneration and injured ultrastructure in the lung, liver, and kidney. Moreover, LPS promoted phosphorylation of alanine aminotransferase (AKT) and increased nuclear factor-κB (NF-κB) activation in the lung, liver, and kidney (P<0.05 vs. control). However, EPO treatment significantly decreased the LPS-induced pAKT up-regulation in these tissues (P<0.05 vs. LPS treatment alone). The present study demonstrates that EPO may play a protective role against LPS-induced MOF by reducing the inflammatory response and tissue degeneration, possibly via the phosphatidylinositol 3-kinase/AKT and NF-κB signaling pathways.