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Objective To investigate the association between stem cell factor (SCF) expression and tubulointerstitial fibrosis in the kidney of rat model with uric acid nephropathy. Methods Thirty-six Wistar rats were randomly divided into model group and control group. The rats in the model group were fed with adenine by lavage at a dose of 150 mg·kg-1·d-1, and the rats in the control group were fed with normal saline by lavage at equal volume. Six rats from each group were sacrificed respectively at week 4, 8 and 12. The mRNA levels of SCF and ColⅠin the kidney were detected by real-time fluorescence quantitative polymerase chain reaction (PCR), and their protein levels and infiltrated Mast cell (MC) were measured by immunohistochemistry. The difference and correlation of each index among different time points and groups were compared. The differences between the two groups were tested by t-test, multiple data were tested by one-way analysis of variance (ANOVA) and the correlation was analyzed by Pearson's correlation. Results ①The serum uric acid (SUA) [week 4, 8, 12: (302 ±41))μmol/L, (424 ±61) μmol/L, (518 ±57) μmol/L], creatinine[week 4, 8, 12:(151±9)μmol/L, (219±15)μmol/L, (299±21)μmol/L], urea nitrogen [week 4, 8, 12:(26.7±3.7) mmol/L, (40.3 ±5.7) mmol/L, (61.9 ±9.4) mmol/L], urine protein/creatinine (Up/Ucr) [week 4, 8, 12: (0.71 ±0.10) mmol/L, (1.18 ±0.11) mmol/L, (1.78 ±0.13) mmol/L] and the expressions of SCF mRNA [week 4, 8, 12: (1.19 ± 0.41), (1.69 ±0.63), (2.21 ±0.97)} and SCF protein [week 4, 8, 12: (1.42 ±0.33), (6.02 ±1.81), (10.03 ±2.69)] in nephridial tissue of model group's rats were significantly higher compared to the control group (all of t value>4.59, P<0.01), and the indexes were increasing gradually as the lavage going on. ②The expression of SCF was correlated with collagenⅠ, degree of renal interstitial injury, urine nitrogen, serum creatinine and UP/Ucr(At week 4, r=0.53, 0.42, 0.40 and 0.51 respectively;at week 8, r=0.60, 0.59, 0.41 and 0.39 respectively;at week 12, r=0.74, 0.61, 0.56 and 0.39 respectively, all of P value<0.05). ③ Compared with control group, the number of infiltrated MC was significantly higher in the model group, and was positively correlated with the expression of SCF (r=0.91, P<0.01). Conclusion Compared with the control group, the expression of SCF and the number of infiltrated MC in the renal interstitium are evidently increased, and are increasing gradually as the lavage going on and the deteriorating of renal interstitial damage. These results suggest that both may play important roles in the occurrence and development of uric acid nephropathy.
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To summarize the clinical experience of Professor WANG Meng-yong in the treatment of uric acid nephropathy. Professor WANG believes that the disease is mainly caused by spleen and kidney deficiency, disorder of function of Sanjiao, and pathological products, such as phlegm dampness and blood stasis and other metabolic disorders. Therefore, the treatment should distinguish symptoms and essence. Starting from pathogenesis and pathological features of spleen and kidney deficiency and phlegm dampness and blood stasis, the treatment should flexibly apply the methods of nourishing spleen and kidney, reducing phlegm and dispelling humidity, and activating blood and using diuretic of hydragogue to alleviate water retention, which can greatly reduce side effects caused by the long-term use of Western medicine and the onset of gout, and then to help disease recovery.
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[Objective] To summarize professor SUN Wei's clinical thinking and experience of using Chinese medicine to treat uric acid nephropathy. [Methods] The following professor SUN Wei clinical records, related medical records, typical case analysis, summarized professor SUN Wei on the treatment of uric acid nephropathy clinical medicine ideas and experience from the aspects of etiology and pathogenesis, clinical treatment, and a case was presented. [Results] Professor SUN Wei thinks that the etiology of uric acid nephropathy is dampness stasis, pathogenesis is spleen and kidney, phlegm stasis toxin blacking collaterals, creating "Yishen Xiezhuo method" is the basic treatment principle, specific treatment that tonifying kidney and spleen in a solid first day after tomorrow, clearing the pain to treat the symptoms, detoxification to clear the root of turbidity. [Conclusion] Professor SUN Wei uses the method of benefiting kidney and clearing turbidity to treat uric acid nephropathy. It is effective in the practice and has the function of reducing uric acid and improving renal function effectively. It is worth popularizing.
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This study was aimed to investigate the effect of Rheum tanguticum on expression of serum endothelial nitric oxide synthase (eNOS), endothelin (ET) and 6-keto-prostaglandin F1α (6-Keto-PGF1α) in uric acid nephropathy rat model. After 3 weeks of treatment with different extractions of Rheum tanguticum on uric acid nephropathy rat model, levels of serum BUN, Cr and UA were measured by biochemical analyzer. ELISA method was used to measure the expression of serum eNOS, ET and 6-Keto-PGF1α. Meanwhile, pathological changes of renal tissues were observed by light microscope. The results showed that compared with the normal control group, the levels of serum BUN, Cr, UA and renal index were higher in the model group (P< 0.05). Compared with the model group, the concentration of eNOS in the model group was obviously higher in the rhubarb ethanol extraction group, rhubarb water extraction group, and allopurinol group (P< 0.05). Concentration of ET was obviously reduced in the rhubarb water extraction group and allopurinol group (P< 0.05). There was no statistical difference with the rhubarb ethanol extraction group. There was no significant difference in the concentration of 6-Keto-PGF1α among groups. Lots of inflammatory cells and uratic crystallization were observed by light microscope in renal tissues among rats in the model group. Damages of renal tissues in medication groups were alleviated than the model group. It was concluded that Rheum tanguticumcan alleviate the damage of uratic crystallization and inflammatory cell infiltration, increase the concentration of serum eNOS, and decrease the concentration of serum ET. Thus, it can reduce the damage of renal endothelial cells and protect renal functions. The effect of rhubarb ethanol extraction on reducing ET expression was less than the water extraction.
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Objective To observe the effect of Compoud Qingqin Liquids on renal function of rat model of uric acid nephropathy, and to discuss its protection of renal function. Methods The rat model was induced by gavaging adenine and feeding yeast. SD rats were randomly divided into control group, model group, positive group, and high-, medium-, low-dose groups of Chinese medicine. Blank control group and model group were daily gavaged with distilled water, positive control group was daily gavaged with allopurinol by 9.33 mg/kg, and high-, medium-, low-dose group of Chinese medicine was daily gavaged with Compound Qinggin Liguids by 3.77, 1.89, 0.09 g/(kg·d) respectively for 6 weeks. General condition of rats were observed, renal pathological changes were observed with light and electron microscope. Urine protein concentration, blood uric acid, blood urea nitrogen, creatinine and kidney weight index were respectively tested before and after treatment. Results There were no significant differences in eating, drinking and body weight between before and after modeling. Compoud Qingqin Liquids can obviously decrease the concentration of urine protein, blood uric acid, serum creatinine, blood urea nitrogen, and kidney weight index (P<0.05) of rats with uric acid nephropathy. Renal tubular epithelial cells atrophy and renal interstitial fibrosis of high-dose group of Chinese medicine were not evident. Conclusion Compoud Qingqin Liquids can protect the rats renal function against uric acid renal injury.
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[Objective]To observe the effect and mechanism of cortex phellodendron on uric acid nephropathy.[Methods]32 male SD rats were divided into four groups including control group,model group,cortex phellodendron treated group and allopurinol treated group.Uric acidnephropathy model rats were established by using yeast and adenine,then treated with Sodium Chloride,cortex phellodendron or allopurinol respectively for 30 days.Blood urea nitrogen(BUN),creatinine(Cr),uric acid(UA)in blood were examined,and the expressions of tumor necrosis factor alpha(TNF-?)and cyclooxygenase 2(COX-2)in renal tissue were detected by immunohistochemistry technique.[Results]Compared with model group,the levels of BUN,Cr,UA in blood and the expression of COX-2 and TNF-? in renal tissue in cortex phellodendron treated group decreased significantly.[Conclusion]Cortex phellodendron has a beneficial effect on uric acid nephropathy in rats.It could decrease the expression of TNF-? and COX-2 in renal tissue of uric acid nephropathy rats so as to alleviate the damage of kidney and protect renal function.
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Chronic deposition of uric acid in the kidney can lead to progressive tubulointerstitial injury with granuloma formation. We hypothesized that uric acid crystal deposition may induce granuloma formation by stimulating local expression of macrophage migration inhibitory factor(MIF), which is a known mediator of delayed type hypersensitivity(DTH). A model of acute uric acid nephropathy was induced in rats by the administration of oxonic acid (an inhibitor of uricase) together with uric acid supplements. Kidney tissue examined at 35 days showed widespread tubulointerstitial damage with intratubular uric acid crystals deposition and granuloma formation. Tubules within the areas of granuloma showed a six-fold increase in MIF mRNA compared to uninvolved areas by in situ hybridization. Moreover, the areas of increased MIF mRNA expression correlated with sites of dense accumulation of macrophages and T cells. Control rats fed a normal diet had no discernible evidence of renal disease by routine light microscopy and minimal tubular expression of MIF mRNA and protein. These data suggest that intrarenal granulomas in urate nephropathy may be the consequence of a crystal induced DTH-like reaction mediated by MIF.
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Rats , AnimalsABSTRACT
Acute uric acid nephropathy is a kind of acute renal failure and results from uric acid crystal deposition within the collecting ducts and the distal tubules due to rapid increase of serum uric acid concentration. Hyperuricemia can be, in the relation to the underlying physiology, clas sified into the three categories. i.e., increased urate pro duction, decreased uric acid excretion, or a combination of the two. It is most commonly presented in the lympho proliferative or myeloproliferative disorders after effective cytolytic chemotherapy in the form of tumor lysis syn drome. But we have recently experienced a case of a 73 year-old female patient with acute lymphoblastic leuke mia whose first presentation was acute uric acid nephrop athy, spontaneously developed without chemotherapy and so report it with review of related literatures.
Subject(s)
Aged , Female , Humans , Acute Kidney Injury , Drug Therapy , Hyperuricemia , Myeloproliferative Disorders , Physiology , Precursor Cell Lymphoblastic Leukemia-Lymphoma , Uric AcidABSTRACT
AIMTo evaluate the influence of serum UA level and ren al function of hyperuricemic rats administrated Hus. METHODSHype ruricemia and uric acid nephropathy in rats were induced by adenine ig feeding f eeds containing 10% yeast Drug therapy was given Simultaneously. After 18 d, blo od of rats was drawn from the hearts. Total protein, albumin(A), A/G ratio, uric acid(UA), creatinine(Cr), urea nitrogen(BUN), triglycerides (TG), high density lipoprotein (HDL), and Cholesterol of serum were detected by automatic biochemis try analyzer. Ultrastructural alteration and UA crystal were observed. R ESULTSSerum UA, Cr, BUN of Hus groups and All group were significantly r educed compared with model group(P