Lupus glomerulonephritis in 788 Chinese children: a multi-centre clinical and histopathological analysis based on 549 renal biopsies.

BACKGROUND: System lupus erythematosus (SLE) is a severe multisystem autoimmune disease. OBJECTIVE: To describe the clinical and pathological features, treatment, and renal outcome in children under 18 years with lupus nephritis (LN). METHODS: The study was undertaken by a questionnaire completed in 26 Grade 3A hospitals' paediatric renal units in China. The study comprised 788 children (619 girls, 169 boys) diagnosed with SLE by the American College of Rheumatology criteria (1997) during 2005-2010. Results of renal biopsies were classified according to the guidelines of The International Association of Nephrology and the Renal Pathology Society (2003). Guidelines by the Chinese Society of Paediatric Nephrology were applied for the diagnosis and treatment (for trial implementation) in 2010 to determine inclusion. The data included the prevalence of acute kidney injury (AKI), SLE disease activity index (SLEDAI), renal histopathology and the induction of therapy mode. RESULTS: The mean (SD) age of onset of SLE was 10.9 (2.90) years (range 1-18) and at diagnosis was 11.3 (2.9) years. The mean (SD) SLEDAI score was 13.5 (5.53). The clinical classification was as follows: about 36 (4.6%) patients had isolated haematuria, 99 (12.6%) isolated proteinuria, 60 (7.6%) isolated haematuria and proteinuria, 157 (19.9%) acute glomerulonephritis, 392 (49.7%) nephrotic syndrome, 20 (2.5%) rapidly progressive glomerulonephritis, 15 (1.9%) chronic nephritis, 2 (0.3%) tubule-interstitial damage and 7 (0.9%) subclinical LN. A total of 549 children (69.7%) underwent renal biopsy. The most frequent renal histopathological findings of LN were Class IV, followed by Class II and Class V + IV. There were no significant differences between the age groups in either renal pathological types or prognosis. In 242 (30.7%) patients, LN was complicated by AKI. Those with AKI had an older mean (SD) age at onset than the non-AKI patients [11.5 (2.8) years vs 10.7 (2.9) years, respectively, p < 0.0001] and a higher SLEDAI score [14.3 (5.8) vs 13.1 (5.4), respectively, p = 0.003]. In the induction phase, cyclophosphamide (CTX) and mycophenolate mofetil (MMF) were equally effective in the patients with the same pathological type. Follow-up records were only available for 482 (61.2%) patients, with a mean (SD) follow-up time of 21.5 (18.4) months. Six of the 35 patients who deteriorated required dialysis and seven died. CONCLUSION: In LN, AKI is a risk factor for poor outcome. Owing to different times of onset and remission, the pathological types of LN cannot be estimated by clinical manifestation alone, and therefore renal biopsy should be undertaken in all LN children with AKI. In the induction phase, there was no significant difference in efficacy between CTX and MMF. Follow-up of children with LN in China needs to be improved.

[Effect of Homeobox A13 transfection on epithelial-mesenchymal transition and bone morphogenetic protein-7 expression in kidney tubular epithelial cells].

OBJECTIVE: To examine the transfection of Homeobox A13 (HOXA13) on epithelial-mesenchymal transition (EMT) and the expression of bone morphogenetic protein-7 (BMP-7) induced by albumin-overload in human kidney tubular epithelial cells (HKCs). METHODS: The cultured HKCs were treated with 20 mg/mL human serum albumin (HSA) for 48 hours. Protein expression of cytokeratin (CK), vimentin and HOXA13 in the HKCs was assessed by Western blot. Protein expression of CK, vimentin, and BMP-7 was also detected in HKCs transfected with lipofectamine contained HOXA13 DNA. RESULTS: HSA induced EMT in HKCs, presented by decreased CK expression (P<0.01) and increased vimentin expression (P<0.01). The up-regulated expression of HOXA13 transfected by lipofectamine inhibited the level of EMT induced by HSA in HKCs (P<0.05). The decreased rate of BMP-7 protein expression induced by HSA was inhibited by over-expressed HOXA13 in HKCs (P<0.05). CONCLUSIONS: Transfection of HOXA13 in HKCs could inhibit the degree of EMT induced by albumin-overload, possibly by increasing BMP-7 expression.

[Expression of urinary neutrophil gelatinase-associated lipocalin and its clinical significance in children with idiopathic nephrotic syndrome].

OBJECTIVE: To investigate the urinary neutrophil gelatinase-associated lipocalin (NGAL) concentration in children with idiopathic nephrotic syndrome (INS) and its clinical significance. METHODS: Thirty-four children newly diagnosed with INS received oral prednisone for 4 weeks. Patients whose urinary protein did not become negative were classified as steroid-resistant nephrotic syndrome (SRNS) group, while those whose urinary protein did become negative were classified as steroid-sensitive nephrotic syndrome (SSNS) group. Morning midstream urine specimens were collected from all patients before use of prednisone and after 1, 2, 3, and 4 weeks of treatment with prednisone. Enzyme-linked immunosorbent assay was used to measure the urinary NGAL concentration. Meanwhile, urinary creatinine (Cr) concentration was measured, and urinary NGAL concentration in a single urine collection was adjusted according to the urinary Cr excretion. The two groups were compared in terms of urinary NGAL/Cr ratio. RESULTS: Compared with the SRNS group, the SSNS group had significantly decreased urinary NGAL/Cr ratios after 3 and 4 weeks of prednisone treatment (P < 0.05). Compared with the SRNS group, the SSNS group had a significantly decreased urinary ß2-MG/Cr ratio after 4 weeks of prednisone treatment (P < 0.05). In both groups, urinary NGAL/Cr ratio was positively correlated with urinary protein/Cr ratio (r = 0.510, P < 0.01). The results of ROC curve analysis showed when diagnostic cut-off point of urinary NGAL/Cr was 0.043 by 3 weeks after treatment, sensitivity and specificity achieved 100% and 79.2% respectively. CONCLUSIONS: Urinary NGAL/Cr ratio remains high in children with SRNS, while this ratio decreases gradually during prednisone treatment in children with SSNS, and it falls ahead of urinary ß2-MG/Cr ratio. These results suggest that dynamic monitoring of urinary NGAL/Cr ratio is useful for early judgment of response to prednisone in patients with INS.

Nephroprotective effects of subcapsular transplantation of metanephric mesenchymal cells on gentamicin-induced acute tubular necrosis in rats.

BACKGROUND: The subcapsular transplantation of metanephric mesenchymal cells (MMCs) may be a new therapeutic approach for the treatment of acute tubular necrosis (ATN). To investigate this hypothesis and provide evidence for its possible use in the clinic, we evaluated the nephroprotective effects of transplanting MMCs into the renal subcaspsule of rats with ATN induced by gentamicin. METHODS: MMCs were expanded in culture. After gentamicin-induced ATN was established, fluorescently-labeled cells were transplanted and traced in kidney tissues by fluorescence microscopy. Serum creatinine (Cr), urea nitrogen (BUN), and N-acetyl-b-D-glucosaminidase (NAG) levels were determined at different time points. Kidney pathology was studied by hematoxylin-eosin staining. Apoptosis was examined by the TUNEL assay. RESULTS: In the MMCs-treated group, the mortality rate decreased; BUN, Cr, and NAG levels peaked at 8 days, and were significantly lower than those in the other groups at 11 and 14 days. RIMM-18 cells locally recruited through precise tropism to sites of injury had the ability to migrate into the tubuli from the renal subcapsule. Damage to the cell-treated kidneys was reduced. The pathologic lesion scores of tubular damage reached the highest values at 8 days in the treated kidneys and 11 days in the untreated ones. The apoptotic index showed that the peaks of apoptosis occurred at earlier stages of the injury process in cell-treated than in untreated kidney and thereafter declined in a time-dependent manner. CONCLUSION: The subcapsular transplantation of MMCs could ameliorate renal function and repair kidney injury.

[Application of stem cell transplantation in kidney diseases].

This paper summarizes the current literature on the potential therapeutic role of stem cell transplantation for kidney injury and repair and focuses on the choice of types of stem cells, the method of transplantation, and the mechanisms of stem cell homing to injured renal tissues and its protective effects. The application of umbilical cord mesenchymal stem cells (UC-MSCs) shows wide prospects, but the approach and optimal dose of cell transplantation are under intensive investigation. Signals that regulate stem cell homing to injured renal tissues may be related to chemokines or factors released in the target site. Several studies have pointed out that paracrine and endocrine of stem cells are the most likely mechanism of action in the injured nephron. Many questions remain unanswered but stem cell-based therapy is a promising new strategy for acute and chronic kidney diseases.

Does injection of metanephric mesenchymal cells improve renal function in rats?

Chronic kidney disease (CKD) is a massive global health-care problem. Cell therapy offers a potential treatment for CKD. The aim of this study was to investigate whether the administration of a population of stem cells could be used to treat adriamycin (ADR)-induced glomerulopathy in rats, a form of CKD. We intravenously transplanted metanephric mesenchymal cells (MMCs) into rats treated with ADR. We also induced MMC differentiation in vitro using a medium derived from serum and homogenates of ADR-induced glomerulopathy rats. We detected the induction of an early epithelial phenotype (cytokeratin-18 expression) and a proximal tubule phenotype (vitamin D receptor expression) in vitro, and MMC-derived epithelial cells corresponding to the proximal tubule and glomeruli in vivo. Transplantation of MMCs after induction of glomerulopathy significantly increased the creatinine clearance rate (Ccr), a marker for glomerular filtration rate, but had no significant effect on other parameters (24-hour urinary protein excretion, serum albumin, total cholesterol). In addition, there was no significant difference in blood urea nitrogen or serum creatinine levels in rats with and without ADR administration. Our results indicate that MMCs might survive, engraft and differentiate into renal epithelia in vivo when transplanted into ADR-treated rats. However, further studies are needed to determine whether MMC transplantation improves renal function and causes renal repair in this model.

[Expression of vascular endothelial growth factor is related to microvessel injury of renal interstitium in children with Henoch Schönlein purpura nephritis].

OBJECTIVE: To investigate the relationship between vascular endothelial growth factor (VEGF) expression and microvessel injury of renal interstitium in children with Henoch-Schönlein purpura nephritis (HSPN). METHODS: Thirty-two children with HSPN and who had not received glucocorticoid or immunodepressants treatment before hospitalization were enrolled. Five children undergoing nephrectomy due to renal trauma were used as the control group. Renal samples were stained by hematoxylin and eosin and renal pathological changes were evaluated semi-quantitatively. CD34 and VEGF expression was detected by immunohistochemistry. CD34 was used as the marker for endothelial cells of renal microvessels. The microvessel density (MVD) was calculated by CD34 immunostaining. RESULTS: Compared with the control and the renal pathological grade II HSPN groups, MVD in the grade III and above HSPN groups decreased significantly, with an obvious reduction in MVD with the increased renal pathological grade (p<0.05). The renal microvessel score in the grades IIIa, IIIb, IV, and V HSPN groups decreased obviously compared with that in the control group. The renal microvessel score decreased with the increased renal pathological grade (p<0.05). VEGF expression in the grade II HSPN group was higher (p<0.05), while that in the grades IV and V HSPN group was lower than that in the control group (p<0.05). VEGF expression in the HSPN group showed a significant reduction with the increased renal pathological grade (p<0.05). There was a positive correlation between VEGF expression and MVD in renal tissue in the HSPN group (r=0.935, p<0.01). CONCLUSIONS: The decreased expression of VEGF may be responsible for the renal pathological damage and microvessel injury in HSPN.

[Protective effects of catechin on apoptosis of endothelial progenitor cells induced by H2O2 in rats].

OBJECTIVE: To study the effect of H2O2 on the proliferation and apoptosis of endothelial progenitor cells (EPCs) and the antogonistic effects of catechin on the cell apoptosis induced by H2O2 in rats. METHODS: Immuno-fluoreascence assay was applied to detect CD34, CD133 and VEGFR-2 expression. EPCs of generation 2 were divided into control cells, H2O2-treated cells and catechin-H2O2-treated cells (H2O2: 100 mg/L; catechin: 10 mg/L). Genomic DNA was extracted by the conventional method after intervention for the analysis of apoptosis ladder pattern. The MTT assay was applied to detect proliferation rate of EPCs. RESULTS: The cultured cells at day 10 expressed CD34, CD133 and VEGFR-2. DNA apoptosis ladder pattern appeared in H2O2-treated cells 2 days after intervention. After 3 days of intervention DNA apoptosis ladder pattern appeared in both H2O2-treated cells and H2O2-catechinjtreated cells, with more ladders and grayer scale in H2O2 -treated cells. Compared with the controls, H2O2-treated cells and H2O2-catechin-treated cells showed significantly decreased proliferation rate (p<0.01), with the lowest proliferation rate at the 2nd day (p<0.05). The H2O2-catechin-treated cells showed increased proliferation rate than H2O2-treated cells at the 1st, 2nd and 3rd days. CONCLUSIONS: H2O2 may impair EPCs proliferation and induce EPCs apoptosis. Catechin may increase the capacity of EPCs for the resistance to apoptosis induced by H2O2.

[Relationship between leukotrienes and clinical, pathological features of Henoch-Schoenlein purpura nephritis in children].

OBJECTIVE: To investigate the role of leukotrienes (LTs) in the progress of children's Henoch-Schoenlein purpura (HSP) nephritis (HSPN), and to provide an experimental basis for clinical application of leukotrienes antagonists in treatment of HSPN. METHODS: The serum and urine samples were collected from 34 patients with HSPN 18 of them received renal biopsy, 27 cases with HSP and 16 healthy children as control. The level of LTB4 in the serum and urine was tested by enzyme-linked immunosorbent assay (ELISA) and LTE4 in urine in each group by enzyme immunoassay (EIA). The extent of expression of LTC4 synthase was detected by indirect immune fluorescence (IIF) in the renal tissue of 18 HSPN cases who received renal needle biopsy. Meanwhile, 3 cases with thin basement membrane nephropathy (TBMN) and 4 cases with simple hematuria were enrolled as controls. The results of pathological examination of the 4 cases with simple hematuria was normal by light microscope or electron microscope. At the same time, total urine protein in 24 hours was determined in 24 HSPN patients. RESULT: (1) The level of serum and urinary LTB4 in the children with HSPN was (1164.33 +/- 300.28) ng/L and (841.19 +/- 115.23) ng/L, respectively. The level of serum and urinary LTB4 in those with HSP was (559.60 +/- 180.23) ng/L and (574.42 +/- 101.17) ng/L, respectively. The level of serum and urinary LTB4 in the control group was (211.95 +/- 67.72) ng/L and (227.33 +/- 76.12) ng/L, respectively. There was significant difference in the LTB4 level between HSPN group and HSP group (P < 0.01) while there was statistically significant difference in the LTB4 level between HSPN group and control group (P < 0.01). The urinary LTE4 was (1252.31 +/- 251.62) ng/L, (805.93 +/- 185.52) ng/L and (149.51 +/- 33.66) ng/L for HSPN group, HSP group and control group, respectively, and the differences were significant (P < 0.01). (2) The increase of serum and urinary LTB4 and urinary LTE4 was closely relative to the severity of histopathological changes. (3) Serum and urinary LTB4, urinary LTE4 increased in parallel to the enhancement of urine protein in HSPN patients (P < 0.01 or P < 0.05). (4) Markedly significant difference of LTC4 synthase by IIF existed between HSPN groups and control group. CONCLUSION: LTs can promote the progress of children's HSPN. There is a close relationship between LTs expression in renal tissues, the pathological severity of HSPN and proteinuria.

[Effect of triptergium wilfordii polyglycosidium on content of Th1 and Th2 in child recurrent nephrotic syndrome].

OBJECTIVE: To study the effect of triptergium wilfordii polyglycosidium on the content of Th1 and Th2 in the treatment child patients of rcurrent nephrotic syndrome. METHOD: Patients were randomized into treatment group and health group. Sixty-one patients in treatment group were treated with triptergium wilfordii polyglycosidium 1 mg x kg(-1) x d(-1) orally tid for 12 weeks. However, patients in health group was not treated with any drugs. Twelve weeks constituted one course of treatment and the content of IL-12, IL-2, TNF-alpha, IL-13, IL-6, IL-4 in peripheral blood was measured before and behind therapy. RESULT: In treatment group, the content of serum cytokines behind therapy was significantly lower than that before therapy, except for IL-12. CONCLUSION: Triptergium wilfordii polyglycosidium could reduce the cytokine level (except for IL-12) of Th1 and Th2, which could lead a therapeutic effect of in the child patients of RNS.

[Pathological features and clinical manifestations in 313 children with nephropathy under 6].

OBJECTIVE: To explore the relationship between pathological features and clinical manifestations in children with nephropathy under 6 years old. METHODS: Renal biopsy by rapid percutaneous puncturation was performed on 313 children under 6 who were all diagnosed clinically as kidney diseases of 14 different kinds. The specimens were divided into 3 parts for microscope, electron microscope and immuno fluorescence examination respectively and processed by HE, PAS, PASM, and Masson staining. Immunofluorescence was used to detect the deposition of IgG, IgM, IgA, C3, C4, C1q, and Fb in the renal tissues. Additional examinations were done to detect HBs-Ag, HBeAg and HBcAg deposition in some cases with positive serum HBs-Ag. Altogether 290 of the specimens (290/313, 92.65%) were examined by electron microscope. RESULTS: All the renal biopsy performances were successful. The clinical manifestations comprised of persistent haematuria (32.92%, 103/313), idiopathic nephritic syndrome (26.1%, 82/313), acute nephritic syndrome (20.14%, 63/313), Henoch Schonlein purpura nephritis (8.32%, 26/313), HBV-nephritis (4.79%, 15/313), and isolated proteinuria (2.56%, 8/313). The main pathological patterns of glomerular disease were identified as mesangial proliferation (51.75%, 162/313), IgM nephropathy (8.31%,26/313), minor and minimal change (7.99%, 25/313), IgA nephropathy (7.35%, 23/313), endocapillary proliferative glomerulonephritis (5.11%, 16/313), focus segmental glomerulosclerosis (4.47%, 14/313), thin basement membrane nephropathy (4.47%, 14/313), and membrane nephropathy (4.47%, 14/313). Alport syndrome, congenital nephrotic syndrome, and thin basement membrane nephropathy can be diagnosed by electron microscope, white IgA nephropathy, IgM nephropathy and C1q nephropathy by immunopathology. CONCLUSION: Similar clinical manifestations may differ in the pathology and the clinical features of one pathological diagnosis may vary greatly. Renal biopsy is of great help to the diagnosis, treatment and the prognosis evaluation for children with nephropathy under 6. Electron microscopes also play an important role in the diagnosis of nephropathy.

[Effects of astragalus on renal tubulointerestitial lesions and expression of NF-kappaB and MCP-1 in renal tissues in rat experimental IgA nephropathy].

OBJECTIVE: To investigate the effects of astragalus on tubulointerstitial lesions in rats with IgA nephropathy (IgAN) and to explore the possible mechanism. METHODS: Twenty-eight Sprague-Dawley rats were randomly assigned to three groups. The rat model of IgA nephropathy was induced by intragastric administration of bovine serum albumin and injections of LPS and CC14. Six weeks later, the rats with IgAN were randomly treated with oral astragalus (3 g/kg/d, for 6 weeks) or normal saline. Normal control rats which were not subjected to IgAN were treated with normal saline. The number of urinary erythrocytes and urinary protein and B-D-N-Acetyl glucosaminidase (NAG) contents were determined by Pan-automatic biochemistry analyzing meter. Expression of monocyte chemotactic protein-1 (MCP-1) and nuclear factor-kappa B (NF-kappaB) in tubulointerstitial tissues were analyzed by immunohistochemistry. A semiquantitative score was used to evaluate the degree of renal pathologic lesions. RESULTS: The number of urinary erythrocytes (74.02+/-16.58 / microL vs 383.23+/-4.94 /microL) and urinary protein (13.88+/-4.94 vs 59.82+/-14.73 mg/L) and NAG contents (2.84+/-0.31 vs 5.24+/-0.80 U/L) in the astragalus-treated IgAN rats decreased remarkably compared with those in the IgAN rats without astragalus treatment (P<0.01). Expression of the NF-kappaB and MCP-1 in the renal tissues in the IgAN rats without astragalus treatment was significantly higher than that in the astragalus-treated IgAN rats and normal control rats (P<0.01). There were significant differences in the scores of renal pathologic lesions between the IgAN rats with or without astragalus treatment (6.03+/-0.46 vs 10.57+/-1.23; P<0.01). CONCLUSIONS: Astragalus can decrease the number of urinary erythrocytes and urinary protein and NAG contents, and relieves tubulointerstitial lesions, possibly through the down-regulation of NF-kappaB and MCP-1 expression in rats with IgAN.

[Role of mast cells in the development of renal interstitial fibrosis in children with Henoch-Schonlein purpura nephritis].

OBJECTIVE: To investigate the role of mast cells in the development of renal interstitial fibrosis in children with Henoch-Schonlein purpura nephritis (HSPN) and possible mechanisms. METHODS: Paraffin-embedded renal biopsy tissue sections from 20 children with HSPN were examined for the levels of tryptase-beta and transforming growth factor-beta1 (TGF-beta1) by immunohistochemical staining. Mast cells were counted by toluidine blue staining. Masson staining was used to assess the level of renal interstitial fibrosis and renal histopathological scores. Normal renal tissue sections from 5 nephrectomized children for nephroma were used as control group. RESULTS: The percentages of positive tryptase-beta cellsand mast cells and the TGF-beta1 expression in the HSPN group were significantly higher than those in the control group (P < 0.05). The percentages of positive tryptase-beta cells and mast cells and the TGF-beta1 expression in renal tissue were positively correlated with the glomeruli histopathological score (r =0.940, 0.920, 0.937, respectively; P < 0.05) and were also positively correlated with the histopathological score of renal interstitium (r=0.903, 0.859, 0.948, respectively; P < 0.05). The level of renal interstitial fibrosis was positively correlated with the percentages of positive tryptase-beta cells and mast cells and the expression of TGF-beta1 (r =0.790, 0.766, 0.858, respectively; P < 0.05). There was a positive correlation between the percentages of positive tryptase-beta cells and mast cells (r =0.941, P < 0.05), between the percentage of positive tryptase-beta cells and the TGF-beta1 expression (r =0.897, P < 0.05) and between the percentage of positive mast cells and the TGF-beta1 expression (r=0.942, P < 0.05). CONCLUSIONS: Tubulointerstitial mast cell infiltration is associated with the development of renal interstitial fibrosis in children with HSPN. Mast cells together with TGF-beta1 and mast cell-derived tryptase-beta may be involved in the development of the renal interstitial fibrosis in HSPN.

[Mobilization effects of SCF along with G-CSF on bone marrow stem cells and endothelial progenitor cells in rats with unilateral ureteral obstruction].

OBJECTIVE: To study the mobilization effects of stem cell factor (SCF) along with granulocyte colony-stimulating factor (G-CSF) on bone marrow stem cells and endothelial progenitor cells in rats with unilateral ureteral obstruction (UUO). METHODS: Fifty-six healthy male Wistar rats were randomly divided into seven groups: control, SCF, G-CSF, SCF+G-SCF, Sham-operated, UUO and UUO+SCF+G-CSF groups (n=8 each). The rats from the control, SCF, G-CSF and SCF+G-CSF groups were hypodermically injected with normal saline (2 mL/kg), SCF (200 microg/kg), G-CSF (200 microg/kg) and SCF along with G-CSF respectively for 5 days. The rats from the UUO and UUO+SCF+G-CSF groups were subjected to the ligation of right ureter and then were hypodermically injected with normal saline (2 mL/kg) and SCF (200 microg/kg)+G-CSF (200 microg/kg) respectively for 5 days. The sham-operated group had the same operative approach as the UUO and the UUO+SCF+G-CSF groups but the right ureter was not ligated. After operation they received a hypodermical injection of 2 mL/kg normal saline for 5 days. Five days later blood samples were collected. The percentages of CD34+ and CD34+/CD133+ cells in intravenous blood mononuclear cells were detected by flow cytometry. Serum contents of glutamate-pyruvate transaminase (GPT), glutamic oxalacetic transaminase (GOT), urea nitrogen and creatinin were measured. RESULTS: Except for the sham-operated group, the other five groups (SCF, G-CSF, SCF+G-SCF, UUO and UUO+ SCF+G-CSF groups) had significantly higher percentage of CD34+ cells and CD34+/CD133+ cells in intravenous blood mononuclear cells than the control group (P < 0.05). There were significant differences in the percentage of CD34+ cells and CD34+/CD133+ cells among the five groups (P < 0.05). The UUO+SCF+G-CSF group showed the highest percentage of CD34+ cells and CD34+/CD133+ cells, followed by the SCF+G-CSF group. There were no significant differences in serum contents of GPT, urea nitrogen and creatinin among the seven groups. Except the UUO group showed higher GOT contents, there were no significant differences in the GOT contents among the other six groups. CONCLUSIONS: The mobilization effects of SCF and G-CSF on bone marrow stem cells and endothelial progenitor cells were not always in paraller. A combination of SCF and G-CSF can effectively mobilize stem cells and endothelial progenitor cells, and side effects were not found in the liver and the kidney.

[Analysis of 94 cases of IgA nephropathy in children].

OBJECTIVE: To evaluate the clinical and pathological features of 94 children suffering from IgA nephropathy (IgAN) while estimating the prevalent situation in Hunan province. METHODS: To summarize the annual number of hospitalized children, those with kidney diseases, those accepted biopsy, and those confirmed as IgAN in both Xiangya Hospital and Second Xiangya Hospital undertaking kidney biopsy in Hunan province during 1995 and 2004. RESULTS: In the past 10 years, as the hospitalized population in both hospitals accrued to 9.98% each year. The rate of 7.5% was seen in those with kidney diseases. Among whom 56.3% accepted kidney biopsy and 94 of them were confirmed as IgAN. Hematuria was the main clinical presentation, seen in 71 cases, accounting to 76%, and even to 98% after excluding those with nephrotic syndrome and isolating proteinuria type of IgAN. Inflammation infiltration (91%), renal tubule degeneration (81%), and renal interstitial fibrosis (31%) were the major pathological features of 94 children, especially in nephrotic syndrome IgAN. CONCLUSION: The number of children with IgAN synchronously accrues as hospitalized population, those with kidney diseases, and those by kidney biopsy. Hematuria is the major symptom. To routinely perform urine analysis and kidney biopsy in asymptomatic hematuria may improve the diagnosis. Inflammation infiltration, renal tubule degeneration, and renal interstitial fibrosis are the major pathological features in IgAN children, especially in nephrotic syndrome IgAN, probably relating to continuous proteinuria. Early control of proteinuria may delay or decrease renal tubule fibrosis.

[Liver lesions in children with hepatitis B virus associated glomerulonephritis].

OBJECTIVE: To investigate the pathological changes of liver in children with hepatitis B virus associated glomerulonephritis (HBV-GN). METHODS: Thirteen children with HBV-GN (aged from 2-14 years) underwent renal and liver biopsy. The biopsy findings were analyzed. RESULTS: Different degrees of hepatic lesions were seen in all of the 13 patients, mild lesions accounting for 69.2% (9/13). HBSAg positive was the most common in the liver tissue [76.9% (10/13)]. Among the renal lesions, membranous glomerulopathy accounted for 69.2%( 9/13), followed by membranoproliferative glomerulonephritis 30.8% (4/13). HBsAg and HBcAg positive were presented in all patients' kidney tissues. HBV antigens were detected in stroma between nephric tubule in all samples. Four patients presented with HBcAg positive in both live and kidneys. CONCLUSIONS: The children with HBV-GN couple with liver lesions. The severity of the renal lesions is not always accord with that of the liver lesions. The appearance of HBcAg in both kidneys and liver indicates severe lesions of the two organs. It is suggested that a liver-kidney holistic treatment is necessary for children with HBV-GN.

[Pathologic features and prognosis of 21 children with isolated proteinuria].

OBJECTIVE: To discuss the pathologic features, treatment and prognosis of the children with isolated proteinuria (IP). METHODS: Twenty-one children with IP were enrolled according to their renal biopsy and were followed up for 0.5 to 10 years. RESULTS: Renal biopsy was performed in all children. Among them 13 were mesangial proliferation glomerulonephritis (MsPGN) (including 3 minor, 6 moderate, and 4 severe ones), 2 minimal change nephritis (MCN), 3 IgA nephropathy (IgAN) (1 in Grade I and 2 in Grade II), 2 focal segmemtal glomerulosclerosis (FSGS) and 1 endocapillary proliferative glomerulonephritis (EnPGN). Interstitial changes could be found in MsPGN and FSGS mostly, presenting interstitial fibrosis, infiltration of inflammatory cells, atrophy of renal tubule, and the vacuolar degeneration of epithelia. All children accepted the medical treatment except the EnPGN case. Fifteen children recovered with no relapse; proteinuria persisted in 3 severe MsPGN and FSGS cases; 2 got the impaired renal function accompanied by persistent proteinuria; and 1 had hypertension. CONCLUSION: The different degrees of renal damage can be found in all IP children who have persistent proteinuria. Most patients can get good outcome after aggressive therapies. However, the prognosis of those with severe MsPGN and FSGS was not so optimistic, and some reno-protective treatments should be given to postpone the deterioration of the renal function.

[Pax2 expression in children with steroid-resistant primary nephrotic syndrome].

OBJECTIVE: To investigate the difference of Pax2 and P53 expressions in children with primary nephritic syndrome (PNS) and the effect of Pax2 on glucocorsteroid (GC)-resistance. METHODS: Renal Pax2 and P53 expressions in children with PNS (40 patients) were detected by immunohistochemistry. A semiquantitative score was used to evaluate the injury degree of the glomeruli and the tubulointerstitium, and correlation analysis was done among Pax2, P53 and pathologic score. RESULTS: Pax2 and P53 expressions were not found in the control group. Pax2 expression of renal tubule epithelia exsisted in children with PNS and there was weak or no expression of Pax2 in the podocytes. Pax2 expressions in the proximal tubule and the distal tubule in the GC-resistant group were more intense than those in the GC-intensive group (P <0.01). The more the Pax2 expression in the tubule, the more abnormal structure such as dilation and atrophy. Pax2 expression in the tubule epithelia was positively correlated with pathologic score of tubulointerstitium (P < 0.01). There was no P53 expression in the GC-intensive group, but there exsisted P53 expression in parts of the patients from the GC-resistant group, mainly distributing in the renal tubular epithelia. P53 expression was positively correlated with P53 expression and the pathologic score of tubulointerstitium (P < 0.01). CONCLUSION: Over-expression of Pax2 in the renal tubule epithelia may improve P53 expression to a certain degree, which may aggravate the lesion of the renal tubule. It may be one of the mechanisms resulting in GC-resistant in children with PNS.