噬菌体生物扩增法检测尿液结核分枝杆菌对肾结核的诊断价值探讨

目的利用噬菌体生物扩增法检测尿液结核分枝杆菌,评价其对肾结核诊断价值。方法对肾结核患者63例应用涂片抗酸染色法检测结核分枝杆菌、结核分枝杆菌培养、噬菌体生物扩增法进行尿液结核分枝杆菌检测,聚合酶链反应法检测结核菌DNA。同时选正常人群21人作为对照组行尿液噬菌体生物扩增法检测结核分枝杆菌,聚合酶链反应法检测结核分枝杆菌DNA。结果肾结核患者尿液行噬菌体生物扩增法检测结核分枝杆菌阳性率明显高于涂片抗酸染色法检测结核分枝杆菌及结核分枝杆菌培养(P<0.01)。与PCR法比较差异无统计学意义(P>0.05),噬菌体生物扩增法检测尿液中结核分枝杆菌对肾结核诊断有较高的特异度(95.2%)和灵敏度(69.8%)。结论噬菌体生物扩增方法检测尿液结核分枝杆菌对肾结核诊断具有重要的参考价值。

尿液γ-谷氨酰转移酶的检测在鉴别肾病与泌尿系感染中的价值

【目的】探讨尿中γ-谷氨酰基转移酶(GGT)的检测在肾病中的意义。【方法】用连续监测法在AU-640全自动生化分析仪测定正常对照组、肝胆疾病组、肾小球肾炎组及尿路感染组患者尿中的GGT活性。【结果】正常对照组尿液GGT活性高于血液,有显著性差异(P<0.01)。肝胆疾病组血清GGT升高而尿液此酶与对照组相比无差异(P>0.05)。肾小球肾炎组尿GGT活性明显高于对照组(P<0.01),也明显高于尿路感染组,而血清中GGT值与对照组无差异(P>0.05)。尿路感染组血、尿GGT,与对照组相比无统计学意义(P>0.05)。肾小球肾炎组阳性数为47例,阳性率为90.4%,尿路感染组阳性数为2例,阳性率为3.6%。肾小肾炎组阳性率明显高于尿路感染组。【结论】测定尿液中GGT的活性有利于肾病和尿路感染的鉴别。

原发性肾病综合征患儿尿TGF-β_1检测的临床意义

【目的】检测原发性肾病综合征患儿尿液转化生长因子β1(TGFβ1)水平并评价其临床意义。【方法】对38例接受治疗的原发性肾病综合征患儿治疗前及缓解后检测尿液TGFβ1水平,并与30例健康对照组相比较。【结果】22例激素敏感型患儿治疗后尿TGFβ1水平明显下降[(363.8±187.6)vs(234.5±113.2)ng/mgCr,(P<0.01)]。16例激素抵抗型患儿治疗后尿TGFβ1水平无明显变化[(374.5±193.5)vs(353.9±173.3)ng/mgCr,(P>0.05)],但加用环磷酰胺冲击治疗后10例病情缓解,尿TGFβ1水平明显下调[(376.6±180.3)vs(208.5±102.7)ng/mgCr,(P<0.05)]。TGFβ1水平与尿白蛋白(r=0.480,P<0.01)、24h尿蛋白(r=0.419,P<0.01)呈正相关。【结论】尿TGFβ1水平可作为反映肾病综合征患儿病情、评价治疗效应的指标。

高尿酸血症与肾虚的临床流行病学调查──附1986例检查结果分析

高尿酸血症与肾虚的临床流行病学调查──附１９８６例检查结果分析深圳市中医院（５１８００１）黄涛主题词肾虚／流行病学，尿酸，肾虚／尿为了探讨高尿酸血症与中医肾虚的关系，我们对１９９４年深圳市１９８６例干部体检结果进行了临床流行病学调查分析，现报告如下：...

晨尿蛋白/尿肌酐比和24h尿蛋白定量的相关性分析与临床评价

目的探讨晨尿蛋白/尿肌酐比值可否替代24h尿蛋白定量,监测尿蛋白的排泄情况。方法选取住院肾脏病患者136例,共272例尿标本,将晨尿蛋白/尿肌酐与24h尿蛋白定量进行相关性分析;采用ROC曲线分析确定晨尿蛋白/尿肌酐比值相对于24h尿蛋白定量≥0.15g、≥1.00g和≥3.00g最佳诊断点。结果晨尿蛋白/尿肌酐比值与24h尿蛋白定量呈显著正相关(r=0.83;P<0.001);24h尿蛋白定量≥0.15g,≥1.00g和≥3.00g时,临床诊断敏感性和特异性最佳点分别为晨尿蛋白/尿肌酐比值≥0.20g/gcr,≥0.95g/gcr和≥2.92g/gcr。结论晨尿蛋白/尿肌酐比值可替代24h尿蛋白定量,监测肾脏病患者尿蛋白排泄情况。

Linggui Zhugan Decoction Improves High Glucose-Induced Autophagy in Podocytes

Objective To explore the influence of Linggui Zhugan Decoction(LGZGD)on high glucose induced podocyte autophagy Methods LGZGD containing serum were prepared by intragastric administation of 4.2 g·kg^(-1)(low dose),8.4 g·kg^(-1)(medium dose),and 12.6 g·kg^(-1)(high dose)LGZGD into SD rats respectively.MPC5 and AB8/13 cells were treated with 60 mmol/L glucose to establish diabetic nephropathy podocyte model in vitro.Podocytes,MPC5 and AB8.13,were divided into control group,high glucose group,low dose LGZGD group,medium dose LGZGD group,and high dose LGZGD group,respectively.For the three LGZGD groups,before LGZGD intervention,podocytes were treated with 60 mmol/L glucose for 3 days.After treated with LGZGD containing serum,cells were collected to analyze cell migration using Transwell assay,proliferation using CCK8,apoptosis and cell cycle using flow cytometry,,autophagosome formation using transmission electron microscopy,and expression levels of Beclin-1,Atg5,LC3II/I,and P62 proteins using western blot.Results Compared with the control group,the proliferation and migration of MPC5 and AB8.13 cells in high glucose group showed slightly decreased,whereas these parameters restored after intervention with low and medium concentrations of LGZGD,with the medium dose LGZGD having the best effect.Flow cytometry analysis showed that the medium dose LGZGD group had a lower apoptosis rate(P<0.05)and higher survival rate(P>0.05)compared to the high dose group.High glucose arrested podocytes in G1 phase,whereas LGZGD shifted podocytes from being predominant in G1 phase to increasing into G2.High dose LGZGD significanly reduced increased autophagosome formation due to high glucose in both podocytes(P<0.05).Western blot analysis showed that Beclin-1,Atg5,LC3Ⅱ/Ⅰ,and P62 expressions were increased in MPC5 cells treated with high glucose,and reversed after adminstration of low and medium doses of LGZGD(P<0.05).Conclusion LGZGD reduced apoptosis and enhanced autophagy in high glucose treated podocytes via regulating Beclin-1/LC3II/I/Atg5 expression.

养阴活血方对CsA慢性肾毒性大鼠肾功能的保护作用

目的:观察养阴活血方对环孢素A(CsA)慢性肾毒性大鼠肾功能的保护作用。方法:将40只SD大鼠随机分为高剂量组、低剂量组,阳性对照组及模型组,钠耗竭法建立CsA慢性肾毒性大鼠模型,分别以养阴活血方20倍、5倍成人剂量,依那普利10倍成人剂量及自来水灌胃4周,分别于第1、2、3、4周末检测24小时尿蛋白定量、血肌酐、肌酐清除率,并对各组结果进行比较。结果:模型组24小时尿蛋白定量4周后稍有上升,但差别无显著性意义(P>0.05),其余各用药组均有下降。模型组血肌酐呈上升趋势但差别无显著性意义(P>0.05)。各用药组治疗后第4周血肌酐值较第1周有明显下降,差别均有显著意义(P<0.05),与模型组差别有非常显著性意义(P<0.01)。模型组后肌酐清除率无明显变化(P>0.05),对照组及高、低剂量组治疗后肌酐清除率呈上升趋势,差别无显著性意义(P>0.05)。结论:中药养阴活血方对CsA慢性肾毒性大鼠的肾脏功能有一定的保护作用。

尿NGAL联合L-FABP水平对脓毒症急性肾损伤早期的诊断价值

目的分析探讨尿液中中性粒细胞明胶酶相关脂质运载蛋白(NGAL)联合肝型脂肪酸结合蛋白(L-FABP)对脓毒症患者是否发生急性肾损伤(AKI)提供早期诊断的价值,为脓毒症急性肾损伤的治疗提供参考依据。方法以本院2015年3月至2017年3月间收治的77例脓毒症患者作为研究对象,按入院是否发生AKI分为对照组(37例)和观察组(40例)。观察组患者自确诊AKI时起记为0 h,对照组患者以入院后同时间点记为0 h,记录两组患者0、12、24、48 1h时的血肌酐(Scr)、血尿素氮(BUN)、尿NGAL、L-FABP水平,比较尿NGAL与L-FABP在脓毒症AKI早期的变化,分析其与传统指标Scr、BUN在诊断早期AKI时的相关性、准确性和敏感度。结果对照组患者在入院后48 h Scr、BUN内未发生显著变化(P>0.05);观察组则在24 h后出现显著升高(P<0.05)。对照组患者在入院后48h内尿NGAL、L-FABP未发生显著变化(P>0.05);观察组患者确诊12 h时尿NGAL、L-FABP显著增高(P<0.05)。相关性分析发现尿NGAL与L-FABP在诊断脓毒症AKI早期时与传统指标Scr和BUN呈正相关(r均>0.7,P<0.05),且与Scr和BUN相比,尿NGAL和L-FABP发生显著变化的时间更早,提升幅度显著,更便于检测。联合应用尿NGAL与L-FABP在确诊脓毒症AKI时具有更高的准确性和精确度(P<0.05)。结论尿NGAL与L-FABP在脓毒症急性肾损伤早期即可检测出显著升高,较传统指标Scr和BUN能更早检测出急性肾损伤的发生。两种指标联合使用能够更加提高诊断的准确度和精确度,有望在临床推广运用。

Experimental Study on Prevention and Treatment of Rat Passive Hermann Nephritis (PHN) with Ligustrazine

Objective: To explore the effects of ligustrazine on proteinuria, serumcreati-nine, urinary thromboxane A_2(TxA_2), metabolism of prostacyclinI_2(PGI_2)―6-keto-PGF_(1α), and renal pathological changes of SD rats with passive Hermannnephritis (PHN). Methods: The PHN model was induced by intravenous injection of rabbit anti-ratrenal tubular epithelial antigen (Tub―Ag) an-tiserum to SD rats. I. P. administration ofligustrazine to rats was given every 2 d for 1 to 5 weeks. The proteinuria, creatinine, TxA_2 and6-keto-PGF_(1α) were measured by sulfosaticylic acid, picric acid, and direct radioimmunoassayrespectively. The renal pathological changes were observed under light microscope, electronicmicroscope and by direct immunofluorescence staining rabbit and rat IgG. Results: The PHN ratstreated with ligustrazine had significantly less proteinuria, serum creatinine, urinary TxA_2 andpathological changes of kidney, and more urinary 6-keto-PGF_(1α) than those without administrationof ligustrazine. Conclusion: Ligustrazine decreases proteinuria, urinary TxA_2, and renal tissueinjury and increases urinary 6-keto-PGF_(1α). These data indicate that ligustrazine may modulatethe balance of TxA_2 and PG I_2 in rat PHN model and can be used for preventing and treatingmembranous glomerulonephritis.

Giant Hydroureteronephrosis Associated with Ipsilateral Inguinal Hernia and Contralateral Hydronephrosis:a Case Study

GIANT hydronephrosis is a rare urological entity. It was first defined as the presence of more than 1000 mL of fluid in the collecting sys-tem.1 That disease is seen more often in males

The inhibitory effect of lotus leaf extract on hyperuricemia and its potential mechanism

Objective:Lotus leaf is a traditional Chinese herb that has been used successfully for centuries for relieving edema by inducing diuresis.Based on its good clinical evidence and anti-hypertensive effectiveness,this study aimed to investigate the potential mechanism of the hyperuricemic inhibitory effects of lotus leaf crude extract(LL)and lotus leaf total alkaloids fraction(LA).Methods:The xanthine oxidase(XOD)inhibitory effect of LL and LA was analyzed in vitro by determining mRNA expression and protein expression levels of hepatic XOD.The hyperuricemic inhibitory effect of the lotus leaf was analyzed in vivo in a potassium oxonate(PO)-induced rat model by determining mRNA expression for renal urate transporters.Results:At a concentration of 40mg/mL,LL and LA suppressed XOD enzymatic activity by 37.35%±9.50%and 47.73%±8.32%,respectively.Both LL and LA administration significantly reduced the concentration of uric acid in the serum and liver of PO-induced hyperuricemic rats.Both LL and LA administration could inhibit XOD mRNA and protein expression,activate renal organic anion transporter 1/3 mRNA expression,and inhibit renal urate reabsorption by decreasing renal GLUT9 and renal urate transporter 1.Conclusions:Insight was gained into the mechanism behind the hyperuricemic inhibitory effects of LL and LA.Our results suggest that they act on two targets:decreasing the production of uric acid by inhibiting mRNA and protein expression of XOD in the liver,and regulating the mRNA expression of renal urate transporters in the kidneys.

Correlation between podocyte excretion and proteinuria in diabetic nephropathy patients

Objective： To observe the podocyte injury in diabetic nephropathy （DN） patients by identifying the urinary podocytes and the situation of detached podocytes in glomeruli and to demonstrate the correlation between podocyte excretion and proteinuria, blood glucose, serum creatinine in different phases in DN patients. Methods： Urinary podocytes and the podocalyxin （PCX） expression state of podocytes in glomeruli were identified and observed by indirect immunofluorescent method. The DN patients were divided into three groups according to the volume of proteinuria, namely small, medium and large volume proteinuria groups. The podocytes in the urine of every group were calculated. The DN patients were divided into five groups according to the chronic kidney disease （CKD） phases, then the positive podocytes in urine were calculated. Meanwhile, the 24-hour protein in urine, fasting blood glucose （FBG） and the serum creatinine of DN patients were tested. The correlations among the proteinuria, serum creatinine, FBG and the number of positive podocytes in the urine of DN patients were statistically analyzed. Results： Urinary positive podocytes were found in 88% of the patients with DN, whereas podocytes were found in 0% of patients with minimal changed disease （MCD） and healthy cases. The expression of PCX was absent in DN patients. In contrast, PCX was expressed integrally in MCD patients. The positive podocytes was 1.49±0.95/ml in small-volume proteinuria group, 2.15±0.70/ml in the medium-volume proteinuria group, and 3.48±1.27/ml in the large-volume proteinuria group. There was no significant difference between the small- and medium- volume proteinuria groups, and there were significant differences between other groups （P〈0.05）. The positive podocyte number tended to increase as proteinuria was increased. By Pearson analysis, the correlation between podocyte number and proteinuria was podocytes in urine from different groups of DN patients, CKD pc I sitive statistically. The difference of the number of positive -V group was significant statistically. The correlation between serum creatinine of CKD Ⅰ -Ⅲ group and positive podocytes in urine was positive statistically. The correlation between serumcreatinine of CKD Ⅳ- Ⅴ group and positive podocytes in urine was not significant statistically. The correlation between FBG and positive podocytes in urine was not significant either. Conclusion： The mechanism of the podocyte injury in DN patients is present. The podocyte injury in DN may positively correlate to proteinuria and serum creatinine of CKD Ⅰ -ⅢDN patients, but not to the FBG and serum creatinine of CKD Ⅳ-Ⅴ patients.

Asymptomatic hyperuricemia following renal transplantation

in the genesis and progression of kidney disease, and a few studies are beginning to show a possible benefcial effect of urate-lowering therapy. Whether this holds true for renal allograft recipients is not clear. In this short review evidence from epidemiological as well as intervention studies is summarized and discussed, with some practical considerations presented at the end.

Effects of Houttuynia Cordata Thumb on Expression of BMP-7 and TGF-β_1 in the Renal Tissues of Diabetic Rats

Objective： To explore the effects of Houttuynia Cordata Thumb （HCT 鱼腥草 Yu Xing Cao） on expression of transforming growth factor-β1 （TGF-β1） and bone morphogenetic protein-7 （BMP-7） in the renal tissues of diabetic rats. Methods： The diabetic rats induced by intravenous injection of streptozotocin（STZ） were randomly divided into a model group, a HCT group and a lotensin group, with normal rats designated as the controls. 8 weeks later, the ratio of kidney weight to body weight, the glomerular area, the excretion of β 2-microglobin （β2-MG） in 24-hr urine, the albumin excretion in 24-hr urine, and creatinine clearance rate （CCR） were investigated. The expression of TGF- β 1, BMP-7 and collagen I in the renal tissues was observed with the immunohistochemical method and by the semi-quantitative assay. Results： The overgrowth of glomerulus, the excretion of β 2-MG in 24-hr urine, the albumin excretion rate in 24-hr urine and CCR in the HCT group significantly reduced （P〈0.05）, and the expression of TGF-β1 and collagen I significantly decreased （P〈0.05）, but BMP-7 significantly increased （P〈0.05） in the HCT group as compared with those in the model group, with no significant difference as compared with the lotensin group （P〉0.05）. Conclusion： HCT has a protective effect on the renal tissues in diabetic rats, which is probably correlated with the decrease of the expression of TGF-β1 and collagen I and with the increase of the expression of BMP-7 in the renal tissues.

Influence of astragalus polysaccharide on kidney status and fibrosis indices of a ratmodel of streptozotocin-induced diabetic nephropathy

Object： To examine the effect of astragalus polysaccharide （APS） on kidney status and fibrosis indices of rats withdiabetic nephropathy. Methods： 72 male rats were randomly divided into three groups： negative control group （NC, n =24）; diabetic nephropathy model group （DNM, n = 24）; and diabetic nephropathy model with APS group （DNM ＋ APS,n = 24）. Rats of the DNM and DNM ＋ APS groups were subjected to both unilateral nephrectomy and administeredstreptozotocin （STZ） injection （65 mg/kg）. DNM ＋ APS group rats were administered 50 IU/kg/d APS by subcutaneousinjection from the first week after operation until death. The NC and DNM group rats were subcutaneously injected withan identical volume of physiological saline. At weeks 3, 8, and 13 after the operation, 6 rats from each group wererandomly sacrificed and blood was collected to measure serum creatinine and blood urea nitrogen. On the day beforesacrifice, the rats were placed in a metabolic cage for 24 h to collect urine. At week 14 after the operation, 6 rats fromeach group were randomly selected to measure body weight and kidney index. Blood was collected to measure bloodglucose. The kidneys were harvested to detect pathological changes by hematoxylin and eosin staining. Results：Histological assessment of DNM rats suggested damage symptoms as evidenced by hyperplasia of the glomerularmesangial matrix, atrophia of the kidney tubules, and thickening of the basement membrane. In contrast, STZ-induceddiabetic nephropathy rats treated with APS （50 IU/kg/d） showed significantly improved histological results, suggestingthat APS has beneficial effect on renal tissues in STZ-induced DNM rats. Our results also indicated that APS relievedrenal injury and effectively improved body weight in DNM rats. The ratio of kidney weight to body weight was reducedand the early stage of renal function damage was improved after APS treatment. In the later stages of the disease, the 24h urinary protein significantly decreased. Moreover, APS down-regulated TGF-β1 and α-SMA expression of the kidney.Conclusion： APS significantly improved renal tubular interstitial injury in DNM rats and the early stage of renalfunction damage. The mechanism may be related to downregulation of the expression of TGF-β1 and α-SMA whichdelays the progression of renal interstitial fibrosis in DNM rats.

Uric acid and chronic kidney disease: A time to act?

A role for uric acid in the pathogenesis and progression of renal disease had been proposed almost a century ago, but, too hastily dismissed in the early eighties. A body of evidence, mostly accumulated during the last decade, has led to a reappraisal of the infuence of uric acid on hypertension, cardiovascular, and renal disease. The focus of this review will be solely on the relationship between serum uric acid and renal function and disease. We will review experimental evidence derived from ani-mal and human studies, evidence gathered from a num-ber of epidemiological studies, and from the few （up to now） studies of uric-acid-lowering therapy. Some space will be also devoted to the effects of uric acid in special populations, such as diabetics and recipients of kidney allografts. Finally we will briefy discuss the challenges of a trial of uric-acid-lowering treatment, and the recent suggestions on how to conduct such a trial.

Tissue distribution and excretion of ^(125)I-lidamycin in mice and rats

AIM: To investigate the tissue distribution, urinary and fecal excretions of 125I-lidamycin (125I-C-1027) in mice and its biliary excretion in rats. METHODS:The total radioactivity assay (RA method) and the radioactivity assay after precipitation with 200 mL/L trichloroacetic add (TCA-RA method) were used to dete-rmine the tissue distribution,and the urinary and fecal excretions of 125I-C-1027 in mice and its biliary excretion in rats. RESULTS:Tissue concentrations reached the peak at the fifth minute after administration of 125I-C-1027 to mice. The highest concentration was in kidney, and the lowest in brain at all test-time points. The organs of the concentrations of 125I-C-1027 from high to low were kidney, lung, liver, stomach, spleen, uterus, ovary, intestine, muscle, heart, testis, fat, and brain in mice. The accumulative excretion amounts of 0-24 h, and 0-96 h after administration of 125I-C-1027 were 68.36 and 71.64% in urine, and 2.60 and 3.21% in feces of mice, respectively, and the accumulative excretion amount of 0-24 h was 3.57% in bile in rats. CONCLUSION: Our results reflect the characteristics of the tissue distribution, urinary and fecal excretions of 125I-C-1027 in mice and the biliary excretion of 125I-C-1027 and its metabolites in rats, and indicate that 125I-C-1027 and its metabolites are mainly distributed in kidney, and excreted in urine.

Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report

A man with past lithium use for more than 15 years, but off lithium for two years and not carrying the diagnosis of diabetes mellitus or nephrogenic diabetes insipidus(NDI), presented with coma and hyperglycemic hyperosmolar state(HHS). Following correction of HHS, he developed persistent hypernatremia accompanied by large volumes of urine with low osmolality and no response to desmopressin injections. Urine osmolality remained < 300 m Osm/kg after injection of vasopressin. Improvement in serum sodium concentration followed the intake of large volumes of water plus administration of amiloride and hydrochlorothiazide. Severe hyperglycemia may trigger symptomatic lithium-induced NDI years after cessation of lithium therapy. Patients with newonset diabetes mellitus who had been on prolonged lithium therapy in the past require monitoring of their serum sodium concentration after hyperglycemic episodes regardless of whether they do or do not carry the diagnosis of NDI.