OBJECTIVE: To observe the variation of GH2IGF axis in children with the refractory nephrotic syndrome (RNS) . METHODS: Serum and urine levels of IGF2I and IGFBP23 and baseline serum levels of GH were assayed using
RIA and IRMA in 26 patients with RNS , and hight standard deviation score (HtSDS) was calculated. Eighteen healthy children of similar ages were used as the control group (NC group) . RESULTS: Serum IGF2I [ (152. 68 ±120. 95) ng/ ml ] and IGFBP23 [ (2 183. 33 ±1 711.33) ng/ ml ] levels in the RNS group were significantly lower than those of the NC group [ (255. 68 ±46. 92) ng/ ml, 4 333.87 ±1 122.00) ng/ ml ] (P<0.05), and urine IGF2I [ (5. 32 ±2. 84) ng/ mg creatinine ] and IGFBP23 [ (16. 38 ±8. 55) ng/ mg creatinine ] levels were higher than those of the NC group [ (0.90 ±0.37) ng/ mg creatinine, (5.13 ±1. 64) ng/ mg creatinine ] ( P<0.05). The serum GH level was lower than that of the NC group, but didn’t achieve any statistical significance. HtSDS (-0.42±0.75) of the RNS group was lower than that of the NC group (0.30±0.17) (P<0.05). CONCLUSIONS: A disorder of the GH2IGF axis was detected in children with RNS. This abnormality may contribute to the growth failure seen in RNS.
OBJECTIVE: To analyze the relationship between the clinical and pathological effects and longterm prognosis in children with Henoch Schonlein nephritis. METHODS: Changes of clinical pathology were studied in 32 children with Henoch Schonlein nephritis and 19 cases of them were followed over an 8 to 14 year period. RESULTS: Acute nephritis ranked first (50%) and the nephritic syndrome ranked second (40%) in the clinical classification of Henoch Schonlein nephritis; the majority had pathological changes of Grade Ⅱ～Ⅲ. The rate of recovery of acute nephritis and the nephritic syndrome was 55.6% and 28.6%, respectively. The rate of recovery and deterioration of Grade Ⅰ～Ⅲ pathological changes was 43.8% and 12.5%, respectively. Of the patients with Grade Ⅳ～Ⅴ pathological changes, 66.7% deteriorated or died. CONCLUSIONS: The prognosis of acute nephritis was better than that of the nephritic syndrome, and longterm prognosis is closely associated with the clinical classification and pathology
OBJECTIVE: To investigate the therapeutic effect of Duoxikang capsula (DXK) on hyperlipoidemia in children with the steroid sensitive nephrotic syndrome (SSNS). METHODS: Twenty SSNS children were randomly divided into a DXK treated group and a control group. DXK was then administered (45 mg/kg weight daily) in the DXK treated group and the same regular steroid therapeutic measurements were conducted in two groups of SSNS. Bloodlipoid compliments were determined, including total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) and low density lipoproteincholesterol (LDL-C) before the randomization, and again 2～3 weeks, 5～6 weeks, 8～10 weeks after the treatment. RESULTS: During the 2～3 weeks, levels of LDL-C ［(3.19±2.08) mmol and TC ［(6.42±2.04) mmol］ in the DXKtreated group were markedly lower than those in the control group ［(5.82±2.73) mmol, (10.0±4.75) mmol, respectively］ (both P<0.05). During the 5～6 weeks and 8～10 weeks, the level of LDL-C in the DXK treated group was also lower than that in the control group ［(2.83±1.50) mmol vs (4.94±2.04) mmol; (2.30±0.46) mmol vs (4.20±2.22) mmol, respectively. P<0.01 . CONCLUSIONS: DXK treatment reduced severe hyperlipoidemia, especially LDL-C in children with SSNS. It is suggested that DXK treatment may reduce the secondary renal injury in these children.
OBJECTIVE: To study the relationship between the nephrotic syndrome(NS) and active infection with human cytomegalovirus (HCMV). METHODS: HCMV-DNA in peripheral leukocytes from 36 cases of NS was detected with the polymerase chain reaction (PCR) technique. HCMV-IgM antibody detection was done using ELISA simultaneously. RESULTS: The positive rates of active HCMV-IgM antibody and HCMV-DNA were 30.5% and 38.9%, respectively, higher than those of the control group (both P<0.01). HCMV-IgM and HCMV-DNA were found simultaneously positive in 8 cases. CONCLUSIONS: Some children with NS have HCMV infection.
OBJECTIVE: To study the relationship between hyperlipidemia and pathologic renal changes in children with the primary nephrotic syndrome(NS). METHODS: Forty five children with no minimal change glomerulopathy (NMCD) (clinical type: steroidresistent NS) and 10 children with minimal change glomerulopathy (MCD) (clinical type: steroid sensitive NS) were compared with 80 healthy children. Seven lipoprotein metabolism parameters including serum total cholestero1 (TC), triglyceride (TG), highdensity lipoprotein cholesterol (HDL-C), lowdensity lipoprotein cholesterol (LDL-C), apolipoprotein AI (ApoAI), apolipoprotein B (ApoB) and lipoprotein (a) ［Lp (a)］ were detected using enzyme methods. RESULTS: After the treatment of the children with prednisone for 2 months, lipoprotein metabolism parameters remained significantly higher in the NMCD group compared to the controls: serum TC ［(6.54±4.33) mmol/L (NMCD) vs (3.94±0.67) mmol/L (control)］, TG ［(3.45±2.56) mmol/L vs (0.91±0.32) mmol/L］, HDL-C ［(1.62±0.79) mmol/L vs (1.31±0.32) mmol/L］, LDL-C［ (2.69±0.87) mmol/L vs (2.15±0.58) mmol/L］, ApoAI ［(1.51±0.54) g/L vs (1.30±0.58) g/L］, ApoB ［(1.45±0.54) g/L vs (0.67±0.16) g/L］, Lp(a) ［(360.6±179.4) g/L vs (162.5±128.5) g/L］ (P<0.05 or 0.01). In contrast, all abnormal lipoprotein metabolism parameters in the MCD cases recovered after prednisone treatment. CONCLUSIONS: There are obvious and long-term abnormialities of serum lipoprotein metabolism parameters in the NMCD group. NMCD cases should be treated with lipidlowering drugs early, while MCD cases should not be treated with lipid lowering drugs.
OBJECTIVE: To review the etiology of fever of unknown origin (FUO) and the methods used to establish a diagnosis. METHODS: A retrospective review of the medical records of 317 patients with FUO admitted between January, 1996 and December, 2000 was performed. RESULTS: Of the 317 children, 298 cases (94.0%) had a definitive etiology established. Of the 298 cases, 160 (53.7%) had infectious diseases and non infectious diseases, such as collagen vascular disease, and neoplasm which accounted for a large fraction of the remainder. A diagnosis was established in 140 (47.0%) by comprehensive clinical analysis alone. Culture of bacteria in serum and biopsy specimens established a diagnosis in 64 cases (21.5%) and 37 cases (12.4%), respectively. Noninvasive imaging techniques (35 cases; 11.7%), autopsy (11 cases; 3.7%), bone marrow examination (6 cases; 1.9%) and retrospective diagnosis (5 cases; 1.7%) accounted for the remainder of the diagnosis. CONCLUSIONS: Most cases of FUO can be diagnosed by clinical characteristics of the patients and by essential laboratory studies. Pathological examination is very important in diagnosing the etiology of FUO. Infectious diseases, collagen vascular disease and neoplasm are the major causes of FUO in children.
OBJECTIVE: To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on IGF-I/IGFBPs mRNA expressions in the rat liver and kidney, and serum peptides. METHODS: Twenty four male SpragueDawley (SD) rats were randomly grouped into control, pair fed, doxorubincininduced nephrotic and examethasonetreated nephrotic rats. IGF-I/IGFBPs mRNA in the rat liver and kidney, and serum peptides were measured by RT-PCR, RIA and Western ligand blot respectively. RESULTS: ①Reduced serum IGF-I was caused by malnutrition and glucocorticoid therapy rather than nephrosis itself, but IGF-IA mRNA in rat liver and kidney was increased during malnutrition, reduced during glucocorticoid therapy, and unchanged during nephrosis. ②IGFBP-2 mRNA in the rat liver and serum peptides decreased during malnutrition, and were elevated during nephrosis, but serum IGFBP-2 was not changed during glucocorticoid therapy despite its diminished gene expression in the rat liver and kidney. However, IGFBP-2 mRNA in the rat kidney was unchanged during malnutrition, and reduced during nephrosis. ③Serum IGFBP-3 decreased during malnutrition and nephrosis, and increased during glucocorticoid therapy, but reduced IGFBP-3 mRNA in the rat liver was observed during nephrosis and glucocorticoid therapy rather than malnutrition. IGFBP-3 mRNA in the rat kidney was only detectable during glucocorticoid therapy. CONCLUSIONS: The regulation of nutrition, nephrosis and glucocorticoid on IGF-I/IGFBPsd mRNA expressions in the rat liver and kidney is organspecific. The disturbance of serum IGFBPs in the nephrotic syndrome are mainly due to altered liver synthesis except that low serum IGF-I is partly caused by reduced renal synthesis. IGFBPs might regulate the action of IGF-I at different levels in the nephrotic syndrome.
OBJECTIVE: To investigate the role of nuclear factor kappa B (NF-κB) in the pathogenesis of glomerulonephritis and to determine whether glucocorticoids can inhibit the activation of NF-κB in vivo. METHODS: Nephrotoxic sera nephritis (NTN) was induced by the injection of antiGBM antibody into the tail veins of rats. Glucocorticoidtreated rats received dexamethasone (0.125 mg/kg weight) daily for 14 days. Untreated and steroidtreated rats were killed on day 14 and NF-κB activation and monocyte chemoattractant protein1 (MCP-1) expression were assessed in glomerulus and renal tubules of rats. RESULTS: Significant upregulation of NF-κB activation was observed in glomerulus and renaltubules of untreated NTN rats compared to the control group ［(38.27±8.83)% vs (1.82±0.68)%; (68.46±12.94)% vs (16.89±4.47)%, repsectively］ (P<0.01), and so was the expression of MCP-1 ［(24.37±7.06) cells/gcs vs 0; (54.78±11.49)% vs (11.26±6.88)%］ (P<0.01). NF-κB activation and MCP-1 expression were associated with monocyte cell infiltration and the degree of proteinuria. Significant downregulation of NF-κB activation and MCP-1 expression were observed in the glucocorticoidtreated rats. CONCLUSIONS: The activated NF-κB may play a pivotal pathogenic role in glomerulonephritis and the antinephritic action of glucocorticoids may be mediated through the suppression of the activation of NF-κB.
OBJECTIVE: To explore the protective effects of nerve growth factor (NGF) on hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHODS: Forty 7day postnatal rats were randomly divided into NGFtreated (n=16), control (n=16) and sham surgery groups (n=8). Immediately after hypoxicischemic (HI) injury, 100 U NGF or normal saline solution was injected intraperitoneally; the sham surgery group was not injected. The effects on body weights, macro and microscopical changes were then assessed. The effect on apoptosis of neurons was observed by terminal deoxynucleotidyl transferase mediated dUTPbiotin nick end labelling (TUNEL) staining. RESULTS: The increased body weight in the NGF treatedgroup was significantly higher than that in the control group ［(4.16±0.24) g and (2.86±0.17) g, respectively (P<0.01)］. The average number of positive cells in the left hippocampus and cortex in the NGFtreated group at 24 h after HIBD were much lower than those in the control group (199.75±19.61 vs 285.50±32.67, 182.75±19.12 vs 271.00±28.36, respectively, P<0.01). At 48 h after HIBD, they were also much lower than those in the control group (77.75±15.76 vs 106.50±16.96; 82.50±19.15 vs 122.75±16.56, respectively, P<0.01). CONCLUSIONS: It is suggested that intraperitoneal administration on NGF has protective effects on neuronal apoptosis associated with hypoxicischemic injury.
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