This paper describes the clinical epidemiologic features, main pathogenesis, early diagnostic biomarkers and managements of septic acute kidney injury in children. It is suggested that pediatric clinicians should increase awareness of the treatment of septic acute kidney injury in children.

Objective To investigate the effects of malnutrition,nephrosis itself and glucocorticoid therapy on serum thyroid hormone,illustrate the relationship between serum thyroid hormone and renal IGF-I/IGFBPs autocrine/paracrine in nephrotic rats.Methods Twenty-four male Sprague-Dawley(SD) rats were randomly divided into control,pair-fed,doxorubicin(5mg/kg)-induced nephrotic and dexamethasone treated nephrotic(des-treated) rats.Serum T 3,T 4 and GH were measured by RIA,renal GHR and IGF-I/IGFBPs mRNA were analyzed by radioreceptor assay and RT-PCR respectively.Results ⑴Serum thyroid hormone levels were decreased by degrees according normal rats,pair-fed rats,nephrotic rats and lowest in des-treated rats except for high serum T 4 in pair-fed rats showed increasing trendency.⑵Reduced serum thyroid hormone was parallel well with decreased renal GHR and IGFBP-2 mRNA,and correlated negatively with increased renal IGFBP-3 mRNA.⑶There was some significant correlation positively between nose-tail length or weight and serum thyroid hormone.Conclusions The hypothyroidism is a possible mechanism of IGFBPs autocrine/paracrine disorder and further growth retardation in nephrotic syndrome.

Objective To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on serum IGF-l and liver IGF-l mRNA, and illustrate relationship between growth failure in nephrotic rats and turbulence of serum IGF-l. Methods Twenty-four male SD rats were randomly divided into control, pair-fed, doxorubincin-induced nephrotic(nephrotic) and dexamethasone-treated nephrotic (des-treated) rats. Serum IGF-1 and liver IGF-l mRNA were measured by RIA and RT-PCR respectively. Results 1. Serum IGF-l was reduced and liver ICF-l mRNA was increased in pair-fed and nephrotic rats, but no significant difference was found between two groups. 2. Serum IGF-l and liver IGF-l mRNA were lower in des-treated rats than in nephritic rats. 3. There was a positive correlation of serum IGF-l with nose-tail length and weight. Conclusions Reduced serum IGF-1 induced by secondary malnutrition is the cause of growth failure in nephrotic syndrome. Glucocorticoid therapy deteriorates growth failure in nephrotic syndrome by further decreased liver IGF-1 synthesis.

Objective To explore the relationship between the pathological classification and clinical manifestations of lupus nephritis(LN)in children by renal biopsy and laboratory examination. Methods Renal biopsy and routine laboratory tests were performed in 35 cases of LN . The pathological classification of LN was made according to the criteria of WHO1982. Results Type Ⅳ of LN was most common(37.4%), and type Ⅴ(31.7%) and type Ⅲ(20.0%) were next. Type Ⅳ and type Ⅴ usually appeared as nephritic syndrome, while Type Ⅱ and Ⅲ mainly appeared as nephritis syndrome. The frequency of hypertension and renal dysfuction was the highest in type Ⅳ. Generally the renal interstitial injury of LN was mild, but that of type IV of LN was relatively obvious. There was a positive correlation between serum creatinine level and the degree of renal interstitial injury. Conclusion Lupus nephritis in childhood possessed some features in renal pathological change and clinical manifestations. Renal biopsy was important to diagnosis, treatment and prognosis evaluation of lupus nephritis.

Objective To observe the correlation between the C-myc expression and pathologic lesions of kidney to explore the role of C-myc re-expression in children's primary nephrotic syndrome(CPNS). Methods The C-myc expression of renal tissue in 30 cases of CPNS was detected using immunohistochemical method, and the correlation between C-myc expression and renal pathological lesions was analyzed. Results There were various degrees of C-myc positive staining in the renal tissue of all patients with CPNS, while no C-myc positive expression in the renal tissue of control group. C-myc expression was mainly located in podocytes and less in endothelial cells of glomeruli. There was high level of C-myc expression in nephric tubules, especially in proximate tubules. There was no C-myc expression in the Henle's loop,tubulous matrix and vessel areas. There was no obvious difference in C-myc expression level in the podocytes and proximate tubules among the different pathological types of CPNS. The level of focal segmental glomerulosclerosis(FSGS) in proximate tubules obviously reduced compared with mesangil proliferative glomerulonephritis(MsPGN) and minimal change disease(MCD)(P

catechin plus dexamethasone-treated group. Compared with nephrotic group, the renal pathologic score were significantly different among the nephrotic group and the catechin-treated group (6 80?0 84,P

Objective To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on serum growth hormone binding protein(GHBP) and liver growth hormone receptor(GHR), and elucidate the relationship between growth failure in nephrotic rats and serum GHBP or liver GHR. Methods Twenty-four male Sprague-Dawley(SD) rats were randomly divided into control, pair-fed, doxoruhincin-induced nephrotic (nephrotic) and dexamethasone-treated nephrotic (des-treated ) rats. Serum GHB P, GHB P- 1 and liver GHR were measured by dextran-coated charcoal technique, gel filtration and radioreceptor assay respectively. Results (1) Serum GHBP and liver GHR were reduced in nephrotic and des-treated rats compared with control and pair-fed rats, but no significant difference was found between control and pair-fed rats or between nephrotic and des-treated rats. (2)Serum GHBP-1 was lower in pair-fed rats, even lower in nephrotic rats and lowest in des-treated rats than in control. (3) There was some significantly positive correlations between nose-tail length or weight and serum GHBP or liver GHR. Conclusion GH resistance, due to decreasd liver GHR, is an important cause of growth failure induced by secondary malnutrition and nephrosis itself Glucocorticoid therapy deteriorates growth failure by further decreased hepatic GHR.

A homozygous A to G transition (AGT to GGT) in codon 16 of growth hormone receptor (GHR) gene was found in one patient with idiopathic short stature(ISS), resulting in an amino acid change(Ser16Gly). This may be a novel GHR gene mutation; and another novel Arg43Gln GHR gene polymorphism was found in Chinese people.

To investigate the effects of catechin on angiotensin-converting enzyme (ACE) activity, angiotensin II(Ang II) content and microvessel density (MVD) in renal tissues of 5/6 nephrectomized rats.

ObjectiveStudy the relationship among CaSR expression, tubulointerstitial damage,metabolic disturbance of calcium and phosphorus and microvascular density around the tubulointerstitium in children with steroid-resistant nephrotic syndrome.Methods36 cases of children with primary nephrotic syndrome were divided into hormone-sensitive group and steroid-resistant group.Semi-quantitative scores for tubulointerstitial pathological evaluation of the extent of damage, automatic biochemical analyzer for the determination of serum calcium (Ca), phosphorus (P) concentration of renal tubular epithelial CaSR expression and microvessel microvascular density around the tubulointerstitium were determined by immunohistochemical assay.ResultsMore severe the tubulointerstitial damage, lower level of serum Ca and higher level of serum P were observed [(2.26 ± 0.15) mmol/L]in children of the steroid-resistant group and the steroid-sensitive group [(1.90 + 0.12) mmol/L, P ＜ 0.05].CaSR expression (4.63 + 0.78) of renal tubular epithelial cells in the steroid- sensitive group was significantly lower than that in the steroid-resistant group (6.56 + 1.22, P ＜ 0.05), but microvascular density was significantly higher in the steroid- sensitive group(2.98 +0.35 vs 2.02 +0.24, P ＜0.05).When the tubulointerstitial damage was mild, CaSR expression (4.15 +0.58) in renal tubular epithelial cells in the steroid- sensitive group (4.26 ±0.61) was lower than the steroid-resistant group(3.12 ± 0.33; 3.01 ± 0.21), and microvascular density was higher,but the difference was not significant(P ＞0.05).In the moderate tubulointerstitial damage, CaSR expression in renal tubular epithelial cells in the steroid- sensitive group (5.35 ± 0.64) was significantly lower than the resistant group (7.37 +0.81, P ＜0.01), and microvascular density was significantly higher than the resistant group (2.81 ±0.16, 2.02 ±0.14, P ＜0.05).Compared by mild and moderate tubulointerstitial damage in children with the steroid-resistant, CaSR expression (11.46 ± 1.38) in children with severe tubulointerstitial damage was significantly increased, and microvascular density (1.15 ± 0.11) was significantly decreased (all P ＜ 0.01).ConclusionsCaSR expression was increased and microvascular density around the tubulointerstitium was decreased in children with steroid-resistant nephrotic syndrome.Dut to steroid resistance, the cytotoxic of steroid damaged the renal tubular epithelial cells, the metabolic disturbance of calcium and phosphorus and the damage of blood vessel endothelium finally resulted in severe tubulointerstitial damage.