Hyperphosphatemia is prevalent among children with nephrotic syndrome and normal renal function

The aim of the study was to analyze systematically our observation that children with severe nephrotic syndrome (NS) have hyperphosphatemia despite normal kidney function. Forty-seven children with NS and normal glomerular filtration rate (GFR) were studied [26 with steroid-sensitive nephrotic syndrome (SSNS) and 21 with persistent NS]. The plasma phosphate level was expressed as the number of standard deviations (SDs) from the mean levels in age- and gender-matched controls. In SSNS plasma phosphate concentration was elevated (+3.7±2.0 SDs) during relapse and normalized (−0.7±1.7 SDs) in remission. In persistent NS the phosphate level was +4.0±2.1 SDs. Patients with marked hyperphosphatemia (>4 SDs) were younger (p<0.001), had lower plasma albumin (p<0.001), and had higher urinary protein levels (p<0.05). Hyperphosphatemia did not correlate with GFR, plasma calcium, or urinary sodium levels. Children with persistent NS had decreased serum 25(OH)D₃ and insulin-like growth factor 1 (IGF-1) concentrations. Hyperphosphatemia is prevalent among children with persistent nephrotic syndrome and normal renal function, correlates with its severity, and may result from increased urinary IGF-1 wasting.     

Bone histology in patients with nephrotic syndrome and normal renal function

BACKGROUND: The prevalence of metabolic bone disease in patients with nephrotic syndrome (NS) at normal level of renal function remains uncertain. METHODS: To address this issue, we studied 30 patients (20 men and 10 women, mean age 27.3 +/- 11.7 years) with NS who had normal renal function (mean creatinine clearance 103 +/- 4 ml/min). We evaluated their serum calcium, phosphorus, alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), vitamin D metabolites, urinary calcium, and skeletal survey. The extent of bone mineralization was analyzed by histomorphometric analysis of iliac crest bone biopsy specimens in all patients. The findings on bone histology were correlated with biochemical parameters. RESULTS: The mean duration of NS was 35.5 +/- 26.9 months, with a protein excretion of 7.3 +/- 3.2 g/24 hr and a serum albumin of 2.2 +/- 0.8 g/dl. Total serum calcium was 7.8 +/- 0.8 mg/dl, whereas ionized calcium was 5.7 +/- 0.7 mg/dl, phosphorus 3.2 +/- 1.2 mg/dl, and alkaline phosphatase 149 +/- 48.6 U/liter. Serum iPTH levels were normal in all except two patients. The mean serum 25-hydroxyvitamin D [25(OH)D] level was 3.9 +/- 1.2 ng/ml (normal 15 to 30 ng/ml), whereas 1,25-dihydroxyvitamin D was 24 +/- 4.7 pg/ml (normal 16 to 65). There was an inverse correlation between serum levels of 25(OH)D and the magnitude of proteinuria (r = -0.42, P < 0.05). The mean 24-hour urinary calcium excretion was 82 +/- 21 mg/day. The skeletal survey was normal in all patients. Bone histology was normal in 33.3% of the patients, whereas 56.7% had isolated osteomalacia (OSM), and 10% had an increased bone resorption in association with defective mineralization. The severity of OSM measured by mineralization lag time correlated linearly with the duration (r = 0.94, P < 0.0001) and the amount (r = 0.97, P < 0.0001) of proteinuria. All patients with NS for more than three years had histological changes. Patients with OSM had lower 25(OH)D and serum albumin as compared with those with normal histology (P < 0.005). Bone mineralization had no significant correlation with serum iPTH, divalent ions, or vitamin D levels. CONCLUSIONS: OSM is a frequent finding in adult patients with NS, even at a normal level of renal function. Its severity correlates with the amount and duration of proteinuria.     

Insulin resistance, dyslipidaemia, inflammation and endothelial function in nephrotic syndrome.

BACKGROUND: Nephrotic syndrome (NS) is associated with an increased risk of cardiovascular disease (CVD). We have shown previously that endothelial function, measured by post-ischaemic flow-mediated dilatation (FMD) of the brachial artery, is impaired in NS. In this study our aim was to assess the potential roles of insulin resistance, plasma non-esterified fatty acids (NEFAs) and inflammation in endothelial dysfunction in NS patients. METHODS: FMD was compared between NS patients (n=19) and controls (CS, n=19). Plasma glucose, insulin and NEFAs were measured. Insulin resistance was calculated using the Homeostasis Model Assessment (HOMA) score. C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor alpha (TNFalpha) and fibrinogen were measured as markers of inflammation. RESULTS: FMD was significantly lower in the NS group (mean+/-standard error, NS 5.1+/-0.7%, CS 7.3+/-0.7%, P=0.02). Fasting insulin (NS 12.5+/-1.5 mU/l, CS 6.8+/-0.7 mU/l, P<0.01), fasting glucose (NS 5.3+/-0.2, CS 4.8+/-0.1, P=0.02) and the HOMA score (NS 3.0+/-0.4, CS 1.5+/-0.2, P=0.001) were significantly higher in NS. These differences persisted after adjusting for waist circumference. Of the inflammatory markers, only fibrinogen (P<0.01) and IL-6 (P=0.01) were significantly increased in NS. Despite significantly lower plasma NEFAs in NS, the NEFA:albumin ratio showed a non-significant trend to higher levels in NS (NS 10.7+/-0.1 micro mol/g, CS 8.7+/-0.1 micro mol/g, P=0.06). Within the NS group, multivariate backward regression analysis showed that NEFAs (P<0.01) and low-density lipoprotein (LDL) cholesterol (P=0.05) were significant negative independent predictors of FMD. CONCLUSION: Endothelial function in NS is inversely correlated with plasma concentrations of NEFAs and LDL cholesterol. Dyslipoproteinaemia and NEFAs probably contribute to the increased risk of CVD seen in NS. We also postulate that in NS, hypoalbuminaemia increases the delivery of NEFAs to endothelial cells thereby impairing the synthesis and release of nitric oxide.     

Thyroid function in children with nephrotic syndrome

The thyroid function of seven children with untreated nephrotic syndrome who had a normal serum creatinine concentration was compared with that of the same patients in remission and age-matched controls. There was a significant decrease in serum thyroxine (T₄), tri-iodothyronine (T₃) and thyroid-binding globulin (TBG) concentrations in untreated nephrotic children compared with the same patients in remission and age-matched controls. Most values for serum free T₄, free T₃ and thyroid-stimulating hormone (TSH) in the patients with nephrosis were within the normal range. However, the mean serum free T₄ and free T₃ concentrations were significantly (P<0.05) lower in the untreated patients than in the same patients in remission, and the mean serum TSH concentrations were significantly (P<0.05) higher in the untreated patients than in the same patients in remission. There were massive urinary losses of T₄, T₃, TBG. free T₄ and free T₃ in the untreated nephrotic children compared with the same patients in remission and age-matched controls. The daily urinary protein excretion showed a positive correlation with the urinary T₄, T₃, free T₄, free T₃ and TBG excretion. Furthermore, the urinary protein excretion showed a negative correlation with the serum T₄, T₃, free T₄, free T₃ and TBG levels. There was a negative correlation between serum albumin and serum TSH. These findings provide evidence of mild hypothyroidism in children with untreated nephrotic syndrome, partly because of losses of T₄, T₃, free T₄, free T₃ and TBG into the urine.     

Glomerular volume and renal function in children with different types of the nephrotic syndrome

Glomerular hypertrophy has been suggested to be an important factor in the pathogenesis of focal glomerular sclerosis. The aim of the present study was to analyse retrospectively the renal biopsies of 58 children (0.2–16.1 years of age) with different types of the nephrotic syndrome, minimal change nephrotic syndrome (MCNS), diffuse mesangial proliferation (DMP) and focal segmental glomerulosclerosis (FSGS). Glomerular surface area was measured and glomerular volume was calculated and related to steroid responsiveness and to renal function, measured by clearances of inulin and para-aminohippuric acid. Glomerular volume correlated with body surface area (BSA) and age. Because of this, patients with FSGS and DMP were matched according to BSA and age, with corresponding MCNS patients. Glomerular volumes of FSGS and DMP patients were significantly larger than those of MCNS patients. In the MCNS patients, significant correlations were found between glomerular volumes and glomerular filtration rate and effective renal plasma flow. Steroid-dependent and steroid-resistant patients showed larger glomeruli than the steroid-responsive children. We suggest that hyperfiltration and hyperperfusion, among other factors, may contribute to glomerular hypertrophy, mesangial proliferation and glomerulosclerosis.     

Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.     

Experience of renal biopsy in children with nephrotic syndrome

Percutaneous renal biopsy (PRB) is useful in childhood renal diseases. This study was done to determine the indications for renal biopsy in nephrotic children, to correlate the indications with histology and to document the complications of PRB. This study included 250 nephrotic children younger than 18 years old who had renal biopsy from January 1988 to December 2002. Ultrasonographic guidance was used in the latter part of the study. Coagulation profile and renal function assessment and blood group testing were done prior to biopsy. Children were monitored clinically during and after the procedure. All children had local anesthesia and 202 children also had short-acting general anesthesia. All biopsies were done on the left kidneys. The specimens were studied under light and immunofluorescent microscopy. All had a post-biopsy ultrasonography at 24 h. Biopsy was diagnostic in 95.2% of children, with a failure rate of 4.8%. The most common indication for biopsy was steroid-resistant nephrotic syndrome (65.2%), and minimal change disease (52.1%) was the most common histology, irrespective of the indications for renal biopsy. Mild (16.0%) and gross (16.8%) hematuria and subcapsular hematoma (6.0%) were the common complications. Fifty-five percent of the children had no complications. Only two children (0.8%) had biopsy site infection.     

Acute renal failure in children with idiopathic nephrotic syndrome

Acute renal failure (ARF) is an uncommon but alarming complication of idiopathic nephrotic syndrome. The renal failure could be secondary to causes evident from the history and evaluation, such as severe intravascular volume depletion, acute tubular necrosis, allergic interstitial nephritis, bilateral renal vein thrombosis, acute pyelonephritis, or rapid progression of the original glomerular disease. It may be termed idiopathic if the underlying cause is undetermined. We present three children with idiopathic nephrotic syndrome who were admitted with acute renal failure. One case was due to drug-induced allergic interstitial nephritis. The other two were idiopathic in nature. Improvement in renal function occurred in the three patients over a variable period of 10 days to 4 weeks. After careful exclusion of well-known causes of acute renal failure, idiopathic acute renal failure (IARF) should be considered as a diagnostic possibility in these patients. The exact pathophysiology of IARF is not understood. Possible proposed explanations include interstitial edema, tubular obstruction, altered glomerular permeability, and unrecognized hypovolemia.     

Normal splenic function in children with the nephrotic syndrome

Children with the idiopathic nephrotic syndrome (NS) are known to be susceptible to bacterial infections. A recent report suggested that splenic hypofunction may be responsible for this immunological defect. We assessed splenic function by counting the circulating pocked red blood cells (PkRBCs) using interference phase contrast microscopy. PkRBCs are removed by the spleen, so that normal eusplenic individuals have less than 2% PkRBCs while asplenics have 15%–30%. Intermediate values are seen in hyposplenism. Thirty-three measurements of PkRBCs were made in 19 children with NS (mean age 7.5±0.8 years). PkRBCs were normal in all children tested (range 0–0.8%), including two patients with bacterial peritonitis associated with relapse. Thus we were unable to find evidence of hyposplenism in children with NS.     

儿童原发性肾病综合征中血管生成素样蛋白3的表达

目的 研究血管生成素样蛋白3 (angiopoietin-like 3 protein，ANGPTL3)在儿童原发性肾病综合征(PNS)患者肾组织中表达分布及其参与蛋白尿发生的机制。方法 ANGPTL3分别与足细胞核标记抗原(WT1)、基底膜标记抗原类肝素硫酸蛋白多糖perlecan进行双标记法免疫荧光染色。应用免疫组化的方法检测ANGPTL3和perlecan在不同病理类型的69例PNS及血尿患儿，包括微小病变(MCD)31例、膜性肾病(MN)6例、局灶节段硬化性肾小球肾炎(FSGS)6例、IgA肾病16例、薄基底膜肾病(TBMN)10例以及2例正常对照肾组织中表达，并以IMS彩色图像分析系统量化为免疫组化指数。在MCD病例中将尿蛋白肌酐比值分别与肾组织中ANGPTL3和perlecan肾小球内染色强度及电镜下平均足突宽度(FWP)进行相关分析。对不同病理诊断时间(发病至肾穿刺)分组患儿肾小球ANGPTL3和perlecan的表达进行比较。结果 (1)ANGPTL3在正常肾组织呈现微弱的沉积，而在不同病理类型的肾病综合征患儿的肾组织的肾小球和肾小管存在不同程度的表达。肾小球内ANGPTL3表达量在MCD(7.49±1.96)、MN(6.27±0.98)中显著高于正常对照(0.02±0.001)、TBMN(0.02±0.001)及FSGS(3.14±0.49)(均P < 0.05)。在IgA肾病(系膜增生型)中，蛋白尿组肾小球中ANGPTL3表达量显著高于单纯血尿组(1.90±0.81比0.03±0.01， P < 0.05)。(2) 在MCD肾组织中，WT1及perlecan荧光双标记染色显示， ANGPTL3在足细胞胞浆及沿肾小球血管袢表达。(3) ANGPTL3在肾小球表达量分别与尿蛋白肌酐比值及电镜下平均足突宽度正相关(r为0.86、0.84，P均<0.05)，并与perlecan在肾小球内表达量负相关(r为-0.83，P < 0.05)。(4)不同发病年限的MCD患儿肾组织中肾小球ANGPTL3及perlecan的表达无显著性差异。结论 在不同程度的蛋白尿及不同足突融合程度的肾组织中存在ANGPTL3的表达差异。在MCD中，ANGPTL3主要在足细胞胞浆表达，肾小球中ANGPTL3的表达与蛋白尿程度及足细胞融合程度呈正相关。     

Secondary resistance to cyclosporin A in children with nephrotic syndrome

We investigated the phenomenon of secondary resistance to cyclosporin (CsA) in children with steroid dependent (SD) or steroid resistant (SR) nephrotic syndrome. Secondary resistance was defined as an initial response to CsA with relapse on withdrawal of therapy and absent or diminished response on reinstitution of the drug. Thirty-two children with nephrotic syndrome who were treated with CsA were included in the study. Twenty-two of the children (15 of 15 SD and 7 of 17 SR) responded while ten demonstrated primary CsA resistance. Of these 22 responders, 20 relapsed when therapy was tapered or discontinued. Cyclosporin was reinstituted in 19. Ten responded, demonstrating CsA dependence, and nine exhibited secondary CsA resistance. Focal segmental glomerular sclerosis (FSGS) was present in one patient with CsA dependence on the initial biopsy and in two of six on a subsequent biopsy. In comparison, seven of nine patients with secondary CsA resistance and ten of ten with primary CsA resistance had FSGS on the initial or subsequent biopsy ( P=0.03). C4 and/or C1q were present on the initial biopsy in one patient with CsA dependence as compared to six of nine with secondary CsA resistance ( P=0.02). Four patients with secondary CsA resistance had an accelerated progression to end-stage renal disease (ESRD). We conclude that the presence of FSGS, or of C4 and/or C1q, appears to increase the risk of secondary CsA resistance and some of these children rapidly progress to ESRD.     

他克莫司在儿童原发性肾病综合征中的应用

目的 研究他克莫司（TAC,FK506）在儿童原发性肾病综合征中的临床应用。 方法 65例患儿入院后根据不同的临床类型联合激素或逐渐减用激素,同时给予口服他克莫司,剂量0.1～0.15 mg/kg,每12小时１次,疗程6～24个月,并监测血药浓度。 结果 65例患儿经他克莫司治疗1～2个月后,尿蛋白逐渐减少;血清白蛋白迅速增加并恢复正常;胆固醇、三酰甘油均有不同程度的改善;总缓解率83.1％;显效时间为7～54 d。随访中12例出现复发。细胞亚群CD4增高时缓解率高。他克莫司药物代谢基因型为3/3型或3/1型缓解率高。微小病变型肾病（MCN）缓解率为96.4％;系膜增生性肾炎（MsPGN）为90.0％;膜性肾病（MN）为2/3;膜增生性肾炎（MPGN）为3/5;局灶节段性肾小球硬化症（FSGS）为4/9。他克莫司起始剂量为0.1～0.15 mg/kg,每12小时１次,治疗浓度控制在5～10 g/L时,本组患儿可获得缓解。12例出现厌食、恶心、呕吐;1例腹痛;2例头痛;1例震颤;3例失眠;4例出现一过性Scr上升;8例N-乙酰氨基葡萄糖苷酶（NAG）轻微增加;6例C3与α-2巨球蛋白增加。部分患儿在1周内恢复正常,其他患儿在他克莫司减药后症状消失。 结论 他克莫司对原发性肾病综合征患儿有良好的疗效,即使患儿肝功能异常、并发结核感染或有严重激素不良反应。他克莫司可替代环孢素A作为新的治疗用药。     

Epidemiology of primary nephrotic syndrome in Egyptian children

Background: Primary nephrotic syndrome is a common renal problem in pediatrics, with great variation in patients' characteristics in different regions of the world. The aim of this study was to define these characteristics in Egyptian children with primary nephrotic syndrome. Methods: Records of 100 primary nephrotic syndrome patients were retrospectively reviewed. Demographic, clinical, histopathological data and response to therapy were analyzed. Results: The mean age of onset was 4.43 ± 2.7 years. Thirty-four percent of patients were steroid resistant, and 66% showed initial steroid response; 46 of the latter were steroid dependent. Forty patients underwent a renal biopsy with minimal change nephrotic syndrome occurring in 30%, mesangioproliferative glomerulonephritis in 37.5% and focal segmental glomerulosclerosis in 30%. Nine percent of cases developed chronic renal insufficiency. Response to cyclophosphamide and cyclosporine occurred in 37.5% and 33.3% of steroid-resistant nephrotic syndrome patients, respectively. Conclusions: A greater percentage of steroid-resistant patients were found in our patients compared with those in other studies. Response to immunosuppressives was different from other studies, probably due to differences in the priority of selection for immunosuppressive therapy.     

Predictive value of repeat renal biopsies in children with nephrotic syndrome

In children who exhibit a frequently relapsing course of minimal change disease (MCD), treatment is often difficult and frustrating to the physician and the family since the goal of a sustained remission remains elusive. The progression of the disease is often unpredictable from its clinical presentation since the lesion of MCD may evolve into a more severe form, such as mesangial IgM nephropathy or focal segmental glomerulosclerosis (FSGS), without alteration in signs and symptoms. Alkylating agents such as cyclophosphamide, or immunosuppressives such as cyclosporine can induce a more sustained remission, but are fraught with inherent toxicity, which makes difficult the decision to use these drugs in patients with MCD. Over a 10-year period we studied 49 patients who had more than one renal biopsy. Repeat biopsies were performed either to delineate the morphological lesion prior to change in therapy, or to confirm suspected drug toxicity, which would necessitate discontinuation of therapy. A total of 83 repeat biopsies were performed in these 49 patients. Of the 49 patients, 25 had MCD, and in 21 of these the lesion evolved into either IgM nephropathy (n = 7) or FSGS (n = 14). Of patients with IgM nephropathy (n = 12), 50% evolved into FSGS. The clinical diagnosis made prior to the repeat biopsy did not confirm with the histological diagnosis in 43% of cases, and a change in therapy or cessation of therapy was carried out in 43 of 83 repeat biopsy instances. Since the complications were mild and the ability of clinical findings to accurately predict the histological lesion limited, we conclude that repeat renal biopsies are a useful tool to fashion optimal therapy in children with frequently relapsing nephrotic syndrome.     

Characterisation of renal immune cell infiltrates in children with nephrotic syndrome

There is increasing evidence that not only T cells but also B cells may play an important role in the pathogenesis of idiopathic nephrotic syndrome (NS). We have evaluated the infiltrating immune cells found in renal biopsies from 38 children with NS using immunohistochemistry techniques involving antibodies against T cells (CD3, CD4, CD8, FoxP3), B cells (CD20), macrophages (CD68) and follicular dendritic cells (CD21). Kidney biopsies with thin basement membrane disease were used as controls. We found higher numbers of interstitial CD3-positive T cells and macrophages in patients with focal segmental glomerulosclerosis (FSGS) than in those with minimal change glomerulopathy (MCGN) and in the controls, and significantly lower FoxP3-positive cells in patients with FSGS, MCGN and steroid-dependent NS than in the controls. Significantly higher numbers of glomerular B cells were found in FSGN patients than in MCGN patients and controls. Of note, in three patients who were later successfully treated with anti-CD20 antibody rituximab, the number of renal B cells was negligible in the preceding biopsy. In conclusion, the higher numbers of interstitial CD3-positive T cells in renal biopsies of pediatric patients with FSGS argue for a higher inflammatory activity. The significantly higher number of glomerular B cells in FSGS patients may indicate a particular pathogenetic role or epiphenomenon in this disease. However, patients with no interstitial or glomerular B cells could also benefit from rituximab treatment.     

Serum osteoprotegerin (OPG) in children with primary nephrotic syndrome

A novel cytokine system secreted by osteoblast, osteoprotegerin (OPG) and its ligand (OPGL) regulates osteoclastogenesis. To determine the relation of the serum OPG levels in children with nephrotic syndrome (NS) to the renal disease, we studied 30 patients with NS in comparison with 30 healthy children serving as controls. The study patients were divided into three equal groups: group 1 included newly diagnosed patients who were studied before and after a short course (one month) of steroid therapy for the first time, group 2 included frequent relapsers (FR), and group 3 included infrequent relapsers (IFR). In addition to serum OPG (ELISA), osteocalcin (OC), parathormone (PTH), alkaline phosphatase (ALP), and 24- hour urinary Ca and proteins were measured. The NS patients revealed a significantly lower serum OPG and parameters of bone formation (ALP and OC) and a significantly higher 24- hour urinary Ca than controls. A short course of glucocorticoids therapy for one month resulted in a significant decrease of serum OPG, ALP and OC levels and a significant increase of 24- hour urinary Ca, while serum PTH levels were not significantly affected by this the- rapy; the FR revealed a significantly lower serum level and a significantly higher 24- hour urinary Ca and serum PTH than the IFR. OPG had significant negative correlations with markers of disease activity and severity (ESR, serum cholesterol, 24- hour urinary protein and cumulative steroid dose), PTH and 24- hour urinary Ca. On the other hand, OPG had significant positive correlations with ALP, OC, and serum albumin. Low serum OPG, which is attributed to the renal disease and/or steroid therapy, may be an important factor contributing to bone resorption in NS. Studies of the protective effect of OPG administration against bone loss in NS are warranted.     

原发性肾病综合征并发急性肾损伤患者甲状腺功能的变化

目的观察原发性。肾病综合征（PNS）并发急性肾损伤（AKI）患者甲状腺功能的变化及其影响因素。方法回顾性分析PNS患者77例,其中PNS并发AKI患者27例为PNS＋AKI组;PNS肾功能正常者50例为PNS组;同时设原发性慢性肾小球肾炎肾功能正常组（CGN1组）和CGN肾功能异常组（CGN2组）作为对照组,每组各40例。比较4组患者的血浆总蛋白（TP）、血清白蛋白（Alb）、血肌酐（SCr）、甘油三脂（TG）、胆固醇（TC）、24h尿蛋白定量及甲状腺功能指标游离三碘甲腺原胺酸（盯3）、游离四碘甲腺原胺酸（FT4）、促甲状腺素（TSH）。结果（1）PNS＋AKl组FT3、FT4值较各组明显降低（P〈0.05）;而TSH无明显差异（P〉0.05）。（2）PNS＋AKI组和PNS组TP、Alb、SCr有显著差异（P〉0.05）。（3）多元回归分析示Alb、SCr对FT3影响显著（P〈0.05）。结论PNS合并AKI时较PNS患者FT3、FT4明显降低,而TSH无明显变化,这种改变可能与Alb的进一步降低和肾功能损伤有关。     

儿童原发性肾病综合征与Th1/Th2细胞失衡

目的 探讨Th1/Th2细胞失衡在原发性肾病综合征（PNS）患儿发病中的作用。方法运用三色荧光标记法流式细胞术检测21例初发和16例缓解期NS患儿外周血Th1和Th2细胞百分率（％）,并以10例正常儿童作对照。结果 正常儿童外周血Th1、Th2和Th0细胞百分率分别为（13.42±4.36）％,（2.53±1.97）％和（1.25±0.92）％。初发的PNS患儿均明显减低,分别为（2.34±2.09）％,（1.02±0.96）％和（0.40±0.38）％（P<0.05）。缓解期PNS患儿,分别为（11.96±4.75）％,（2.87±2.46）％和（1.31±0.87）％,与正常儿童比,差异均无显著性意义。由于初发的PNS患儿Th1细胞减低相对于Th2细胞而言更显著,因而导致Th1/Th2比值也较缓解期PNS患儿和正常儿童明显下降（2.43±2.65比4.17±2.32和5.41±2.77,P均<0.05）。结论 儿童PNS是一种以Th2细胞占优势的免疫介导的肾小球疾病,源于Th1细胞减低所致的Th1/Th2细胞失衡在原发性肾病综合征发病过程中可能起着重要作用。