尿结石患者体重指数对血尿生化及结石成分的影响

目的 分析尿路结石患者体重指数（BMI）对24h尿液、血液生化指标及结石成分的影响。方法 对2017年1月~2018年7月我院收治的尿路结石患者150例进行血尿生化分析,按照BMI分为体重正常组45例、超重组65例,肥胖组40例,检测24h尿钙、磷、尿酸、血钙、血磷、血尿酸及尿pH等指标,同时收集患者结石标本进行红外光谱结石成分分析。比较组间各指标及结石成分的差异性;根据结石成分不同分为四组（草酸钙组、磷酸钙组、尿酸组和磷酸镁铵组）,比较组间各指标的差异性。结果 超重组和肥胖组尿液pH均低于正常组（P＜0.05）;体重正常组患者24h尿钙、尿磷、尿酸和血磷、尿酸明显低于超重或肥胖组（P＜0.05）。磷酸镁铵组患者尿液pH高于其它组（P＜0.05）。尿酸组和磷酸钙组24h尿磷高于草酸钙组和磷酸镁铵组（P＜0.05）。尿酸组24h尿酸高于其它组,磷酸镁铵组24h尿酸低于其它组（P＜0.05）。尿酸组血尿酸高于其它组,磷酸镁铵组血尿酸低于磷酸钙组和尿酸组（P＜0.05）。磷酸镁铵组BMI低于其它组（P＜0.05）。肥胖组、超重组草酸钙、尿酸结石比例均高于正常组（P＜0.05）,而磷酸镁铵比例则低于正常组（P＜0.05）。BMI与尿液pH的相关性分析表明两者高度相关（r=-0.725,P＜0.05）。结论 肥胖及超重对血尿生化、血生化、尿pH及结石成分比例有一定影响,且存在性别差异,建议肥胖或超重的尿结石患者行血尿生化、结石成分等评估,注意饮食控制、减重等措施。     

维生素D受体基因启动子Fok I多态性与尿钙浓度的关系

目的 研究维生素D受体（VDR）基冈启动子Fok Ⅰ多态性与尿钙浓度之间的关系.方法 应用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）对50例泌尿系结石（结石组）及50例非泌尿系结石患者（对照组）的外周血进行Fok I多态性检测,分析两组间基因型和等位基因的频率分布,并用常规尿生化分析仪比较两组的24 h尿钙浓度.结果 结石组基因型分布：FF 28%（14/50）,Ff 52%（26/50）,ff 20%（10/50）;对照组：FF 34%（17/50）,Ff 56%（28/50）,ff10%（5/50）,其中FF和ff基因型分布在两组中差异有统计学意义（P〈0.05）.结石组与对照组等位基因F分布频率分别为54%（54/100）和62%（62/100）（P〉O.05）;f分别为46%（461100）和38%（381100）（P〈0.05）.结石组FF、Ff、ff基因型的24 h尿钙浓度分别为（0.030±0.008）mmol/kg、（0.037±0.009）mmol/kg和（0.081±0.013）mmol/kg,对照组分别为（0.028±0.006）mmol/kg、（0.036±0.002）mmol/kg和（0.043＋0.003）mmol/kg,FF和Ff基因型在两组中尿钙浓度之间差异没有统计学意义（P〉0.05）,而ff基因型差异有统计学意义（P〈0.05）.结论 VDR基因起始密码子中Fok I多态性与泌尿系结石患者尿钙浓度升高有关系.     

维生素D受体基因启动子Fok Ⅰ多态性与尿钙浓度的关系

目的 研究维生素D受体(VDR)基冈启动子Fok Ⅰ多态性与尿钙浓度之间的关系.方法 应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)对50例泌尿系结石(结石组)及50例非泌尿系结石患者(对照组)的外周血进行Fok I多态性检测,分析两组间基因型和等位基因的频率分布,并用常规尿生化分析仪比较两组的24 h尿钙浓度.结果 结石组基因型分布:FF 28%(14/50),Ff 52%(26/50),ff 20%(10/50);对照组:FF 34%(17/50),Ff 56%(28/50),ff10%(5/50),其中FF和ff基因型分布在两组中差异有统计学意义(P<0.05).结石组与对照组等位基因F分布频率分别为54%(54/100)和62%(62/100)(P>O.05);f分别为46%(461100)和38%(381100)(P<0.05).结石组FF、Ff、ff基因型的24 h尿钙浓度分别为(0.030±0.008)mmol/kg、(0.037±0.009)mmol/kg和(0.081±0.013)mmol/kg,对照组分别为(0.028±0.006)mmol/kg、(0.036±0.002)mmol/kg和(0.043+0.003)mmol/kg,FF和Ff基因型在两组中尿钙浓度之间差异没有统计学意义(P>0.05),而ff基因型差异有统计学意义(P<0.05).结论 VDR基因起始密码子中Fok I多态性与泌尿系结石患者尿钙浓度升高有关系.     

从化地区尿石症患者结石成分及代谢异常的研究

目的分析从化地区尿石症患者的尿路结石成分及尿液代谢异常的关系。方法将200例尿路结石进行结石成分测定,并对其中的153例进行24 h尿液分析,对其结果进行综合评价。结果从化地区尿路结石以含草酸盐结石为主（90.5%）,其中单纯草酸钙结石占42.5%;其次为含尿酸结石（26.5%）,其中纯尿酸结石占5.5%;多数结石患者合并各种尿液代谢异常,其中高尿钙症36例（23.5%）、高尿磷症64例（41.8%）、高尿酸尿55例（35.9%）、低镁尿51例（33.3%）、高草酸尿39例（25.4%）、低枸橼酸尿症100例（65.3%）。结论尿路结石成分分析及尿液代谢分析对了解结石病因与预防有重要的指导意义。     

NMP22在泌尿系统肿瘤中的临床应用研究

为了探讨尿液中核基质蛋白(NMP22)对泌尿系统恶性肿瘤诊断的临床意义.本文应用ELISA测定271例泌尿系恶性肿瘤患者和43例泌尿系良性病变患者尿液NMP22含量.结果表明: 检测NMP22对尿路上皮恶性肿瘤的敏感性为89.2%,特异性为93.3%.尿路上皮恶性肿瘤、非尿路上皮恶性肿瘤和泌尿系良性病变患者, 尿NMP22阳性率分别为: 89.2%、37.2%和34.5%, 其中膀胱移行细胞癌89.5%.泌尿系恶性肿瘤比良性病变阳性率明显增高(P＜0.05),尿路上皮恶性肿瘤比非尿路上皮恶性肿瘤阳性率增高(P＜0.05).另外, 尿中NMP22含量与膀胱移行细胞癌分期、分级和肿瘤生长方式以及瘤体数目均无显著差异(P＞0.05).提示尿液NMP22检测对诊断尿路上皮恶性肿瘤有较高的敏感性, NMP22对泌尿系肿瘤良、恶性鉴别诊断也有一定意义.     

URAT1基因在尿酸结石患者肾脏的表达及其临床意义

目的探讨尿酸结石患者尿酸代谢特征以及肾脏URAT1表达改变的意义。方法回顾性分析2012年1月至2013年10月我院收治的24例结石患者的临床资料,按结石成分分为尿酸结石患者9例(A组)、非尿酸性结石患者15例(B组),另选取7例因其他疾病操作而取材做m RNA测定的患者为C组,10例健康体检者为D组(仅用作收集其血尿酸检验结果以及24 h尿液标本)。采集各组参与者一般临床资料以及血液、24 h尿液的尿酸代谢相关指标结果,并应用Real-time PCR技术检测其肾脏URAT1表达情况,所得数据进行组间统计分析比较。结果 A组患者血尿酸水平、体重指数、年龄显著高于B组及C组(P0.05),而尿PH值显著降低。24 h尿量及尿酸定量分析各组间无明显差异(P0.05)。Real-time PCR实验结果提示尿酸结石患者肾脏URAT1表达较其他组显著增高(P0.05)。结论尿酸结石患者与高尿酸血症密切相关,而肾脏尿酸排泄无明显改变,URAT1在肾脏高表达可能是这一临床特征的重要分子机制。     

2型糖尿病患者尿Ⅳ型胶原和尿微量白蛋白联合测定的意义

为评价尿微量白蛋白与Ⅳ型胶原对2型糖尿病患者肾功能早期损伤的诊断价值, 取正常人30名与165例2型糖尿病患者24小时的尿液, 采用放射免疫法(RIA), 同时测定尿微量白蛋白和Ⅳ型胶原(浓缩法).结果显示: (1)正常组24h尿微量白蛋白为6.45±2.04mg/24h,尿Ⅳ型胶原为86.68±11.98μg/L.(2)根据2型糖尿病患者24h尿微量白蛋白含量分为两组,A组130例, 尿微量白蛋白大于或等于30mg/24h,尿Ⅳ型胶原为120.03±34.02μg/L; B组35例, 尿微量白蛋白小于30mg/24h, 尿Ⅳ型胶原为97.14±24.93μg/L.结论: 2型糖尿病患者在尿微量白蛋白还未超过正常上限时, 已经有部分人尿Ⅳ型胶原升高, 说明尿Ⅳ型胶原比尿微量白蛋白更能体现2型糖尿病患者肾功能早期损伤.     

尿内皮素在糖尿病患者肾脏微血管早期损害的诊断价值

目的探讨尿内皮素(ET)对糖尿病患者肾脏早期损害的诊断价值.方法选取常规尿蛋白阴性的2-型糖尿病患者68例,按微量蛋白排泄率(UAER)分为三组:DM1组(UAER＜30 mg/24 h);DM2组(UREA 30～300mg/24h);DM3组(UREA＞300mg/24 h).采用放射免疫检测法测定尿ET.结果糖尿病患者尿ET与对照组有显著差异(P＜0.01),且DM2组与DM1组有显著差异.尿α1微球蛋白与肌酐比(α1-MG/Cr),尿N-乙酰-β-D-氨基糖苷酶与肌酐比(NAG/Cr)与对照组有显著差异(P＜0.01),β2-MG/Cr除DM1组与对照组无显著差异外,其余两组均有显著差异.结论尿ET是诊断糖尿病早期肾脏微血管损害的敏感指标,对于糖尿病肾病的早期诊断、肾功能损害程度判断具有一定价值.     

草酸钙肾结石大鼠模型肾组织中Klotho的表达及其意义

目的:初步探究Klotho在草酸钙肾结石大鼠模型肾组织中的表达及其意义.方法:将30只6～8周龄雄性SD大鼠随机分为结石组和对照组,每组15只,结石组采用乙二醇和氯化铵诱导法构建草酸钙肾结石模型.28 d造模完成后采集大鼠24 h尿液、血清标本,比较两组血肌酐(Cr)、尿素氮(BUN)、血Ca2+、24 h尿Ca2+及草酸(Ox)指标;采集肾组织标本,HE染色比较各组肾脏病理改变及草酸钙结晶的沉积情况,荧光定量PCR、Western印迹及免疫组织化学染色检测两组肾组织中Klotho mRNA及蛋白表达,并对肾脏氧化应激相关指标总抗氧化能力(total antioxidant capacity,T-AOC)、丙二醛(malondialdehyde,MDA)、过氧化氢酶(catalase,CAT)进行测定.结果:结石组在光学显微镜观察下可见草酸钙结石晶体沉积并有伴肾小管病理性改变,血清Cr,BUN,24 h尿Ca2+及Ox较对照组升高,差异有统计学意义(P＜0.01),血Ca2+差异无统计学意义(P＞0.05);结石组Klotho mRNA及蛋白表达较对照组下降,差异有统计学意义(P＜0.01);肾脏氧化应激相关指标中,结石组T-AOC,CAT较对照组降低,MDA较对照组升高,差异均有统计学意义(P＜0.01).结论:草酸钙肾结石的形成与Klotho表达异常及氧化应激反应有关;Klotho可能通过调控Ca2+代谢和氧化应激反应参与草酸钙肾结石的发病过程.     

尿路草酸钙结石形成的相对危险期——尿液成分昼夜改变的观察

作者将一天分为10段收集尿液,研究尿路草酸钙精石患者与非结石者尿液成分的昼夜变化规律。结果发现:两组尿离子钙排泄峰值均出现在09:00～11:00时,谷值出现在22:00～06:00时,07:00～09:00时和17:00～21:00时是结石组尿总钙排泄峰值的两个时相,而对照组尿总钙排泄峰值在06:00～07:00时,从     

Is magnesium a marker of disordered mineral metabolism in males with idiopathic recurrent calcium urolithiasis? Observations focussing on fasting magnesiuria and magnesiemia, protein and other substances in urine and plasma.

Mg can theoretically play a role in renal calcium stone formation of IRCU patients, but the status of Mg is uncertain. The aim of this study was to investigate whether in IRCU variation of Mg in fasting urine and plasma is associated with altered urine Ca, Pi, oxalate, Ca/Pi ratio, supersaturation and other factors, the clinical severity of stone disease (metabolic activity; MA) included. This was a cross-sectional study (284 IRCU patients), comprising males with mean age in the fifth decade and unimpaired renal function. Patients had an unrestricted home diet, standardized laboratory procedures, including sample collection (daily and fasting urine, plasma), with classification of patients according to tertiles of fasting Mg-uria, keeping comparable age, the number of patients with renal stones present or absent, and normo- or idiopathic hypercalciuria. MA was scored. We found that the tertile I patients (= referent) exhibited sub-normal fasting Mg excretion (< 4 mg/2 h) and fractional excretion (< 3.5%), in daily urine the lowest Mg and oxalate, but highest Ca excretion rate; compared with tertile III, tertile I patients had significantly lower plasma total (not ultrafiltrable) Mg, blood bicarbonate and pH, and the lowest MA; fasting urinary excretion of Ca and citrate were also low, but urinary Pi, body weight, plasma glucose and insulin were increased. In tertile III not only was Mg-uria (excretion, FE) significantly elevated vs I, but so were urinary pH, excretion of sodium, Ca, potassium, protein (total and non-albumin) and citrate, FE sodium and Ca, the urinary molar ratios Ca/Pi and Mg/Potassium, hydroxyapatite supersaturation, bone resorption markers, and MA; in this environment urinary oxalate and Ca oxalate supersaturation were unchanged, plasma glucose, insulin and parathyroid hormone decreased. The tertile II patients, showing intermediate Mg excretion, also exhibited (vs. I) increase of FE Mg, urinary excretion and FE of sodium and Ca, excretion of protein, citrate and bone markers, the ratios Ca/Pi and Mg/Potassium, and MA. When urinary Ca/Pi was considered as the outcome of disordered metabolism, significant determinants (according to multiple regression analysis) were urinary Pi (negative), Ca and Mg/Potassium (positive); significant determinants of MA, the sum of stone-forming processes, were the urinary concentration of non-albumin protein, Mg/Potassium and sodium (all positive). Among IRCU patients 1) approx. one third is in need of Mg conservation by the kidney, associated with low plasma total Mg, modest metabolic acidosis, a trend towards overweight, high plasma insulin and glucose; 2) low Mg- or acidosis-induced increase of bone resorption may follow, attenuating glycemia and insulinemia but forcing the kidney to functional adaptation, manifesting as a rise of urinary sodium, Mg, Ca, Pi, Ca/Pi, pH and protein, together presumably aggravating MA; 3) larger controlled studies are justified, to decide whether Mg deficiency initiates renal Ca stones, and if urinary Mg loss exaggerates IRCU.     

The effects of oral estriol on the endometrium in postmenopausal women

BACKGROUND: Recent studies showed that postmenopausal women lost less bone mass when supplemented with calcium or estrogen therapy. However, the safety of the treatments in terms of the risk of calcium oxalate stone formation is unknown. We therefore conducted this study to determine the alteration in calcium oxalate supersaturation after calcium supplement or after combined calcium and estrogen therapy in postmenopausal osteoporotic women. METHODS: Fifty-six postmenopausal women were enrolled in this study. All subjects were more than 10 years postmenopausal with vertebral or femoral osteoporosis by bone mineral density criteria. They were randomly allocated to receive either 625 mg of calcium carbonate (250 mg of elemental calcium) at the end of a meal three times a day (group A, n=26) or calcium carbonate in the same manner plus 0.625 mg/day of conjugated equine estrogen and 5 mg medrogestone acetate from day 1-12 each month (group B, n=30). The age (mean +/- S.E.M.) was 66.3 +/- 1.2 and 65.1 +/- 1.1 years, weight 54.1 +/- 1.2 and 55.3 +/- 2.1 kg, in group A and group B, respectively. Urine specimens (24-h) were collected at baseline and 3 months after treatment for the determination of calcium oxalate saturation by using Tiselius's index (AP(CaOx)) and calcium/citrate ratio. RESULTS: After 3 months of treatment, there was no significant alteration from baseline for urinary excretion of calcium, citrate and oxalate. Urinary phosphate excretion was significantly reduced (6.3 +/- 0.7 vs. 5.1 +/- 0.7 mmol/day for group A and 8.2 +/- 0.9 vs. 5.8 +/- 0.7 mmol/day for group B, P<0.05), whereas net alkaline absorption was significantly elevated (10.1 +/- 3.6 vs. 20.1 +/- 4.4 meq/day for group A and 4.8 +/- 3.2 vs. 19.9 +/- 3.6 meq/day for group B, P<0.05). Calcium/citrate ratio and AP(CaOx) determined at baseline were not different from the corresponding values after treatment in both groups; calcium/citrate: 10.1 +/- 3.1 vs. 10.1 +/- 2.5 for group A and 9.3 +/- 1.8 vs. 11.9 +/- 2.5 for group B and AP(CaOx): 1.1 +/- 0.1 vs. 1.3 +/- 0.2 for group A and 1.2 +/- 0.2 vs. 1.1 +/- 0.1 for group B. There were eight and nine patients with high AP(CaOx), or >2, at baseline and after treatment, respectively. CONCLUSIONS: Calcium supplement with a meal or combined calcium supplement and estrogen therapy is not associated with a significant increased risk of calcium oxalate stone formation in the majority of postmenopausal osteoporotic patients. Determination of urinary saturation for calcium oxalate after calcium and estrogen supplements, especially at the initial phase of treatment, may be helpful in the avoidance of nephrolithiasis.     

Renal tubular impairment in children with idiopathic hypercalciuria

Idiopathic hypercalciuria (IH) is defined as hypercalciuria that persists after correction of dietary inbalances and has no detectable cause. The excretion of urinary N-acetyl-beta-D-glucosaminidase (U-NAG), a marker of proximal tubular damage, has been previously reported as either increased or normal in children with IH. We evaluated U-NAG in 20 children (13 boys and 7 girls, mean age 10.3 years +/- 5.7 SD) with IH (urinary calcium excretion above 0.1 mmol/kg/24 hours, with no detectable cause) and with otherwise normal renal function tests. Ultrasound examination revealed urolithiasis (n=4) and nephrocalcinosis (n=1). The U-NAG values were evaluated in the spot urine collected from the second morning void and calculated as the urinary NAG/creatinine ratio (U-NAG/Cr) and expressed in nkat/mmol. The 24-hour urinary calcium excretion (U-Ca/24h) was assessed in a urinary sample from 24-hour collected urine and calculated in mmol/kg. The obtained results of U-Ca/24h and U-NAG/Cr were expressed as Z-scores. When compared to the reference data, the U-Ca/24h and U-NAG/Cr were significantly higher (p = 0.0004 and p = 0.006, respectively). There was no correlation between the U-NAG/Cr and U-Ca/24h (r = 0.18, p = 0.20). The U-NAG/Cr values were significantly higher in the 5 patients with urolithiasis/nephrocalcinosis, whether compared to the rest of the group (p = 0.02), or to the reference data (p = 0.01). The U-NAG/Cr activity was higher in 15 children without urolithiasis/nephrocalcinosis when compared to reference data (p < 0.01). There was no difference in U-Ca/24h between the children with and without urolithiasis/nephrocalcinosis (p = 0.58). These findings suggest that tubular impairment, as reflected by U-NAG/Cr, might occur in children with IH, especially in patients with urolithiasis/nephrocalcinosis. There doesn't seem to be a direct relationship between the U-NAG/Cr activity and the degree of calcium leakage.     

Urinary factors of kidney stone formation in patients with Crohn's disease

Summary An increased frequency of kidney stone formation is reported in patients with inflammatory bowel disease. In order to investigate its pathogenesis, the concentrations of factors known to enhance calcium oxalate stone formation (oxalate, calcium, uric acid) as well as of inhibitory factors for nephrolithiasis (magnesium, citrate) were determined in the urine of 86 patients with Crohn's disease and compared with those of 53 metabolically healthy controls. Six patients with Crohn's disease already had experienced calcium oxalate nephrolithiasis. Patients with Crohn's disease had significantly higher urinary oxalate and lower magnesium and citrate concentrations. Among all patients magnesium and citrate were significantly lower in those with a positive history of kidney stones. Our results demonstrate that the increased propensity for renal stone formation in patients with Crohn's disease is a result not only of increased urinary oxalate, but also of decreased urinary magnesium and citrate concentrations.Abbreviations CDAI Crohn's disease activity index Dedicated to Professor Dr. N. Zöllner on the occasion of his 65th birthday     

Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet.

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.     

Effect of Renal Insufficiency on Stone Recurrence in Patients with Urolithiasis

The study was designed to assess the relationship between glomerular filtration rate (GFR) and urinary stone-forming constituents, and to assess the effect of renal insufficiency on stone recurrence risk in first stone formers (SF). Baseline serum creatinine levels were obtained, and renal insufficiency was defined as creatinine clearance ≤60 mL/min (Cockroft-Gault). This retrospective case-control study consists of 342 first SF; 171 SF with normal renal function were selected with 1:1 propensity scores matched to 171 SF with renal insufficiency. Urinary metabolic evaluation was compared to renal function. GFR was positively correlated with urinary calcium, uric acid, and citrate excretion. Subjects with renal insufficiency had significantly lower urinary calcium, uric acid, and citrate excretion than those with normal renal function, but not urine volume. With regard to urinary metabolic abnormalities, similar results were obtained. SF with renal insufficiency had lower calcium oxalate supersaturation indexes and stone recurrence rates than SF with normal renal function. Kaplan-Meier curves showed similar results. In conclusion, GFR correlates positively with urinary excretion of stone-forming constituents in SF. This finding implies that renal insufficiency is not a risk factor for stone recurrence.

Graphical Abstract

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不同时期微生态肠内营养对急性胰腺炎患儿血清淀粉酶、hs-CRP及胃肠功能的影响

目的 探究不同时期微生态肠内营养对急性胰腺炎患儿血清淀粉酶、hs-CRP及胃肠功能的影响.方法 选取在2012年5月至2016年6月期间在我院接收治疗的急性胰腺炎患儿120例作为研究对象,按照给予微生态肠内营养时间对患儿分组,分为超早期组和早期组,超早期组于入院后24h进行微生态肠内营养支持干预治疗,早期组于入院后72h进行微生态肠内营养支持干预治疗,治疗结束后对患儿的血清淀粉酶、hs-CRP及胃肠功能进行比较和分析.结果 早期组患儿的营养耐受良好率明显低于超早期组,两组患儿组间比较差异具有统计学的意义(P＜0.05);两组患儿的病死率组间比较没有显著差异;早期组患儿的住院时间28.8±5.9d显著高于超早期组36.9 ±7.2d,两组患儿组间比较差异具有统计学的意义(P＜0.05).在接受治疗后超早期组患儿的hs-CRP水平89.5±38.2mg/L显著低于早期组110.5 ±20.2mg/L,组间数据差异比较差异具有统计学的意义(P＜0.05);治疗前后两组患者AMY水平均无明显差异(P＞0.05).早期组患儿的并发症发生率与超早期组相比较没有显著的差异,两组患儿各项数据比较差异不具有统计学的意义(P＞0.05).治疗后两组患儿胃肠功能评分显著低于治疗前,治疗前后数据比较差异具有统计学的意义(P＜0.05);治疗后超早期组患儿的评分0.26±0.03分显著低于早期组的患儿0.69±0.20分,两组数据比较差异具有统计学的意义(P＜0.05).结论 对急性胰腺炎患儿实施超早期微生态肠内营养能够有效地提高患儿的肠道耐受性,满足患儿的代谢和营养的需求,缩短住院的时间,有利于患儿早日康复.     

Investigation of relationship between idiopathic hypercalciuria and urinary enzyme activities

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