Renal Failure In Rats Research Articles

Effect of Gum Arabic on Oxidative Stress and Inflammation in Adenine–Induced Chronic Renal Failure in Rats

Inflammation and oxidative stress are known to be involved in the pathogenesis of chronic kidney disease in humans, and in chronic renal failure (CRF) in rats. The aim of this work was to study the role of inflammation and oxidative stress in adenine-induced CRF and the effect thereon of the purported nephroprotective agent gum arabic (GA). Rats were divided into four groups and treated for 4 weeks as follows: control, adenine in feed (0.75%, w/w), GA in drinking water (15%, w/v) and adenine+GA, as before. Urine, blood and kidneys were collected from the rats at the end of the treatment for analysis of conventional renal function tests (plasma creatinine and urea concentration). In addition, the concentrations of the pro-inflammatory cytokine TNF-α and the oxidative stress markers glutathione and superoxide dismutase, renal apoptosis, superoxide formation and DNA double strand break frequency, detected by immunohistochemistry for γ-H2AX, were measured. Adenine significantly increased the concentrations of urea and creatinine in plasma, significantly decreased the creatinine clearance and induced significant increases in the concentration of the measured inflammatory mediators. Further, it caused oxidative stress and DNA damage. Treatment with GA significantly ameliorated these actions. The mechanism of the reported salutary effect of GA in adenine-induced CRF is associated with mitigation of the adenine-induced inflammation and generation of free radicals.

Heat-processed ginseng saponin ameliorates the adenine-induced renal failure in rats

To evaluate the effect of the saponin of heat-processed ginseng (Sun ginseng, SG), we investigated the protective effect of SG total saponin fraction against adenine-induced chronic renal failure in rats. SG saponin significantly decreased the levels of urea nitrogen and creatinine in the serum, but increased the urinary excretion of urea nitrogen and creatinine, indicating an improvement of renal function. SG saponin also inhibited adenine-induced kidney hypertrophy and edema. SG saponin reduced serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and lactate dehydrogenase activities increased by adenine. Based on these findings, the ameliorating effect of SG on chronic renal failure may result from its saponin.

Urinary chemokine (C-C motif) ligand 2 (monocyte chemotactic protein-1) as a tubular injury marker for early detection of cisplatin-induced nephrotoxicity

Because of the difficulty in detecting segment-specific response in the kidney, we investigated the molecular events underlying acute kidney injury in the proximal tubules of rats with cisplatin (cis-diamminedichloroplatinum II)-induced nephrotoxicity. Microarray analysis revealed that mRNA levels of several cytokines and chemokines, such as interleukin-1beta, chemokine (C-C motif) ligand (CCL) 2, CCL20, chemokine (C-X-C motif) ligand (CXCL) 1, and CXCL10 were significantly increased after cisplatin treatment in both isolated proximal tubules and whole kidney. Interestingly, tubular CCL2 mRNA levels increased soon after cisplatin administration, whereas CCL2 mRNA levels in whole kidney first decreased and then increased. Levels of both CCL2 and kidney injury molecule-1 (KIM-1) in the whole kidney increased after cisplatin administration. Immunofluorescence analysis revealed CCL2 changes in the proximal tubular cells initially and then in the medullary interstitium. Urinary CCL2 excretion significantly increased approximately 3-fold compared with controls the day after cisplatin administration (5mg/kg), when no changes were observed plasma creatinine and blood urea nitrogen levels. Urinary levels of KIM-1 also increased 3-fold after cisplatin administration. In addition, urinary CCL2 rather than KIM-1 increased in chronic renal failure rats after administration of low-dose cisplatin (2mg/kg), suggesting that urinary CCL2 was selective for cisplatin-induced nephrotoxicity in renal impairment. These results indicated that the increase in cytokine and chemokine expression in renal epithelial cells might be responsible for kidney deterioration in cisplatin-induced nephrotoxicity, and that urinary CCL2 is associated with tubular injury and serves as a sensitive and noninvasive marker for the early detection of cisplatin-induced tubular injury.

L-Citrulline Protects against Rhabdomyolysis -Induced Acute Renal Failure in Rats

There is increasing evidence indicating that oxidative stress plays an important role in the pathogenesis of rhabdomyolysis-induced myoglobinuric acute renal failure (ARF). In this study, protective effects of L-citrulline on glycerol-induced acute renal failure (ARF) in rats were investigated. Six groups of rats were employed in this study, after seven days of glycerol injections, the blood samples and kiney tissues were harvested for future biochemical and pathology analysis. The levels of creatinine (Cr) and urea nitrogen (BUN) in plasma, the content of malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), the activity of total nitric oxide synthase (TNOS), inducible nitric oxide synthase (iNOS), endothelial NO synthase (eNOS) and superoxide dismutase (SOD) were evaluated in kiney tissues. Consequently, treatment with L-citrulline improved an impaired intrarenal oxygenation and kidney function compare with the glycerol group, and prevented the renal oxidative stress damage as well as severe functional and morphological renal deterioration.

Fenugreek seeds reduce aluminum toxicityassociated with renal failure in rats

Despite the reports on safety concerns regarding the relationship between aluminum salts and neurological and bone disease, many countries continue to use aluminum as phosphate binders among patients with renal failure. In search for a diet supplement that could reduce aluminum toxicity related to renal failure, we carried out this prospective animal study in which the fenugreek seeds were assessed for their effects on rats nephrotoxicity induced by aluminum chloride (AlCl3). Oral AlCl3 administration during 5 months (500 mg/kg bw i.g for one month then 1600 ppm via drinking water) led to plasma biochemical changes, an inhibition of alkaline phosphatase (ALP), a decrease of total antioxidant status (TAS), and an induction of lipid peroxidation (LPO) in the blood and brain, in addition to kidney atrophy and morphological alterations at the level of Bowman's capsule, the glomerulus and different sorts of tubules, reminiscent of some known kidney disease. The treatment with the whole fenugreek seed powder (FSP) (5% in the diet) during the last 2 months showed its effectiveness in restoring normal plasma values of urea, creatinine, ALP and glucose, as well as re-increasing the TAS, inhibiting LPO and alleviating histopathological changes in the injured kidneys. This study highlights the induced nephrotoxicicity, as well as the related toxicity in the brain and bone, by chronic oral ingestion of the aluminum salts. However, the maintenance of a diet supplemented with fenugreek seeds could offer protection for the kidney, bone and brain, at the same time.

Protective Effect of Lactoferrin on Cisplatin-Induced Nephrotoxicity in Rats

Although cisplatin (cis-diamminedichloroplatinum II) is one of the most effective chemotherapeutic agents, its clinical use is limited because of its strong side effects on the kidneys. The aim of this study was to investigate the renoprotective effect of bovine lactoferrin (bLf) in cisplatin-induced renal failure in rats. To assess the renoprotective effect of bLf, oral bLf (300 mg/kg) was administered from the day before to the fifth day after cisplatin (7 mg/kg, i.p.) injection. Daily administration of bLf histologically reduced renal tubular injury induced by cisplatin and suppressed the deterioration of renal function. Accumulated platinum content in the kidney was significantly decreased by the daily administration of bLf. Moreover, the administration of intravenous bLf caused a significant increase in urine volume in a dose-dependent manner. These results suggest that pretreatment with bLf produces a protective effect against cisplatin-induced nephrotoxicity. This protective effect of bLf involves the reduction of accumulated cisplatin in the kidney.

Protective effect of Hygrophila spinosa against cisplatin induced nephrotoxicity in rats

Objective:To evaluate the nephroprotective effect of methanolic extract of Hygrophila spinosa (HSME) (Acanthaceae) in (CP)-induced acute renal failure in rats.Materials and Methods:HSME (250 mg/kg and 500 mg/kg body weight), were administered orally to male wistar albino rats.CP was used to induce acute renal failure. The parameters studied included blood urea and serum creatinine and malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and GSH peroxidase activities. Histopathological examination was also carried out.Results:The results revealed that HSME pretreatment signiûcantly reduced blood urea and serum creatinine levels elevated by CP administration. Furthermore, HSME signiûcantly attenuated CP-induced increase in MDA and decrease in reduced GSH, and CAT and SOD and GSH peroxidase activities in renal cortical homogenates. Additionally, histopathological examination showed that HSME markedly ameliorated CP-induced renal tubular necrosis.Conclusion:The results indicate that the aerial parts of H. spinosa are endowed with nephroprotective activity.

Effects of Dietary Protein Sources on the Progression of Renal Failure without Dialysis in Rats

The quality and quantity of protein are essential factors that determine nutritional significance of a protein. The aim of this study was to compare the effects of several animal and plant proteins on the progression of renal failure in rats. Ninety male rats were allocated into nine groups and were fed with a basal diet containing different protein sources for 12 weeks. Two groups comprised of a negative control group and a positive control group (with induced renal failure) fed on the basal diet. Rats in the remaining seven groups were fed using different diets containing 10% protein derived from fish, meat, chicken, egg, soybean, lentil, and white bean. Biological, biochemical and histological studies were done at the end of the study. Protein content was highest for the chicken extract (87.36%), followed by meat (85.67%), egg (78.85%), and fish (78.55%). Body weight gain increased as food intake decreased in all groups other than the positive control group, and the food efficiency ratio paralleled food intake. Rats fed the fish protein diet had lower blood urea nitrogen (28.0 mg/dL), uric acid (3.5mg/dL) levels compared with the other groups. There were no significant differences in creatinine levels between rats fed the animal protein (fish and meat) or the plant protein (soy and white bean) diets. Histological studies revealed no abnormal renal features in rats fed the fish or soybean protein diets. Therefore, the results of the study suggest that a diet containing fish protein may delay the progression of chronic renal failure relative to other protein diets.

Ratlarda Gliserol ile İndüklenen Miyoglobinürik Akut Böbrek Yetmezliği Üzerine Losartanın Etkileri

Ratlarda Gliserol ile İndüklenen Miyoglobinürik Akut Böbrek Yetmezliği Üzerine Losartanın Etkileri

Serial MR Imaging of Magnetically Labeled Humen Umbilical Vein Endothelial Cells in Acute Renal Failure Rat Model

Purpose : To evaluate the usefulness of in vivo magnetic resonance (MR) imaging for tracking intravenously injected superparamagnetic iron oxide (SPIO)-labeled human umbilical vein endothelial cells (HUVECs) in an acute renal failure (ARF) rat model. Materials and Methods: HUVECs were labeled with SPIO and poly-L-lysine (PLL) complex. Relaxation rates at 1.5-T MR, cell viability, and labeling stability were assessed. HUVECs were injected into the tail vein of ARF rats (labeled cells in 10 rats, unlabeled cells in 2 rats). Follow-up serial T2*-weighted gradient-echo MR imaging was performed at 1, 3, 5 and 7 days after injection, and the MR findings were compared with histologic findings. Results: There was an average of 98.4±2.4% Prussian blue stain-positive cells after labeling with SPIOPLL complex. Relaxation rates (R2*) of all cultured HUVECs at day 3 and 5 were not markedly decreased compared with that at day 1. The stability of SPIO in HUVECs was maintained during the proliferation of HUVECs in culture media. In the presence of left unilateral renal artery ischemia, T2*-weighted MR imaging performed 1 day after the intravenous injection of labeled HUVECs revealed a significant signal intensity (SI) loss exclusively in the left renal outer medulla regions, but not in the right kidney. The MR imaging findings at days 3, 5 and 7 after intravenous injection of HUVECs showed a SI loss in the outer medulla regions of the ischemically injured kidney, but the SI progressively recovered with time and the right kidney did not have a significant change in SI in the same period. Upon histologic analysis, the SI loss on MR images was correspondent to the presence of Prussian blue stained cells, primarily in the renal outer medulla. Conclusion: MR imaging appears to be useful for in vivo monitoring of intravenously injected SPIO-labeled HUVECs in an ischemically injured rat kidney. Index words : Magnetic resonance imaging (MRI)∙Superparamagnetic iron oxide (SPIO) Human umbilical vein endothelial cells (HUVECs)∙Cell tracking

Diosgenin prevents hepatic oxidative stress, lipid peroxidation and molecular alterations in chronic renal failure rats

Aim: Chronic renal failure (CRF) is one of the major contributors of cardiovascular pathological events and CRF associated uremic condition in rats elevates liver oxidative stress. The aim of the present study was to evaluate the preventive potential of diosgenin on antioxidant system and molecular protection potential in liver of CRF rats. Materials and Methods: CRF in rats was induced by feeding rats with diet containing 0.75% adenine for 5 weeks. Diosgenin was given orally at a dose of 40 mg/kg body weight (bw) of animal each and every day. The activities of antioxidant enzymes and lipid peroxidation level were determined by biochemical assays. Fourier transform infrared spectroscopy (FTIR) was employed to illustrate the molecular protection potential of diosgenin. Results: This study has shown adenine containing diet induced CRF in rats elevates liver oxidative stress by suppressing the activity of enzymatic antioxidant system, increased lipid peroxidation, and macromolecular structural alterations. In this study, treatment of diosgenin 40 mg/kg bw of rat significantly restores the enzymatic antioxidant system and reduces the lipid peroxidation level. Moreover, based on the FTIR study, we confirmed that diosgenin administration significantly protected the macromolecular changes including, the protein structural damage that occurred in liver. Conclusion: This study has proved the hepato protective action of diosgenin through antioxidant and molecular protection effect in CRF condition.

Ischemia/Reperfusion-Induced Renal Failure in Rats as a Model for Evaluating Cell Therapies

Chronic renal failure is a devastating disease that leads to a multitude of complications. Cell therapy has emerged as a potential treatment modality for renal failure. However, efficacy testing on systemic renal function has been challenging due to the limited availability of reliable models that are fully characterized. In this study, we investigated the possibility of using renal ischemia/reperfusion (I/R) injury as a viable model for testing cell therapies. We examined functional and pathological changes in rat kidneys that were exposed to different ischemia times. Male Lewis rats were divided into five groups. Renal failure was induced by clamping both renal pedicles for combinations of 60, 75, and 90 min, followed by reperfusion. Age-matched healthy rats served as controls. Blood was collected at regular intervals for serum chemistry, and kidneys were harvested at the same intervals for histomorphological assessment. Serum creatinine levels of the animals with I/R injury increased significantly after 3 days and returned to normal levels at 4 weeks. Histologically, kidney tissue showed progressive glomerular and tubular deterioration with varying degrees of fibrosis. Animals exposed to 75- and 90-min ischemia combination times consistently generated more severe injury than the 60-min ischemia period. However, these groups resulted in a high mortality rate. A model in which one kidney is exposed to a shorter ischemia time (60 or 90 min) resulted in sustained renal damage with a lower mortality rate. This study shows that kidneys exposed to I/R result in renal tissue damage as well as decreased renal function. This model can be used to study both the short-term and longer-term effects of kidney disease by varying the length of the ischemic time. In particular, the use of longer ischemic times (75 and 90 min) could be used to study new therapies for acute renal disease, whereas shorter ischemic times (60 min) could be used to study therapies for chronic renal insufficiency.

Establishment of a Blood Purification System for Renal Failure Rats Using Small‐Size Dialyzer Membranes

Hemodialysis techniques for small animals have not been established because no small dialysis apparatus has been available. We recently developed a small-size dialyzer and established an appropriate blood purification system for small animals. To confirm the appropriate dialysate flow rate, bovine blood was dialyzed for 60 min at a fixed blood flow rate of 1.0 mL/min and variable dialysate flow rates. Blood urea nitrogen and creatinine levels decreased significantly at a dialysate flow rate of 5 mL/min (from 13.7 ± 0.2 to 10.3 ± 1.2 mg/dL and 1.07 ± 0.15 to 0.61 ± 0.12 mg/dL, respectively, P < 0.05). To determine the appropriate in vivo conditions, extracorporeal circulation was performed in anesthetized male Sprague-Dawley rats at a dialysate flow rate of 0.0 mL/min, for 240 min, and at variable blood flow rates. Extracorporeal circulation was successful at a blood flow rate of 1.0 mL/min, but not 1.5 mL/min. To establish in vivo hemodialysis conditions, we used the animal model of end stage renal failure. Sprague-Dawley rats were fed a 0.75% adenine-containing diet for 3 weeks, after which they received hemodialysis for 120 min at a dialysate and blood flow rate of 5.0 and 1.0 mL/min, respectively. There were no significant changes in systolic blood pressure or heart rate during dialysis. Thus, this blood purification system can be safely used for small animals at a dialysate flow rate of 5.0 mL/min and a blood flow rate of 1.0 mL/min. This system provides a basis for further research on hemodialysis therapy.

Effects of fenofibrate, a PPAR-α ligand, on the haemodynamics of glycerol-induced renal failure in rats

The modulating effect of peroxisome proliferator-activated receptor α ligand on haemodynamic effects of phenylepherine (PE), angiotensin II (AII), endothelin 1 (ET1), acetylcholine (Ach), sodium nitroprusside (SNP) and isoproterenol (ISO) were evaluated in glycerol-induced acute kidney injury in rats. The effect of PE on fenofibrate-treated animals was a dose-dependent increase in mean arterial blood pressure (MAP). For AII and ET1, MAP was also increased for the fenofibrate group but not in a dose-dependent fashion. On the medullary blood flow (MBF), while the lower doses of PE and AII increased the perfusion unit on the fenofibrate-treated group, the higher doses decreased the perfusion unit. The ET1 increased the perfusion unit on this group but not in dose-dependent fashion. The effects of PE and AII on the cortical blood flow (CBF) of fenofibrate-treated group is similar to that of MBF for the same group but not for ET1. The effect of Ach, SNP and ISO in all the groups was the decrease in MAP. ISO caused dose-dependent increase in MBF of fenofibrate-treated group. The effect of Ach, SNP and ISO on the CBF perfusion unit was that of the increase for the fenofibrate-treated group. The study showed that fenofibrate did not attenuate increased blood pressure induced by PE, AII and ET1 but caused enhanced vasodilation by Ach, SNP and ISO.

Urinary metabonomics study on the protective effects of ergosta-4,6,8(14),22-tetraen-3-one on chronic renal failure in rats using UPLC Q-TOF/MS and a novel MSE data collection technique

Ergosta-4,6,8(14),22-tetraen-3-one (ergone), isolated from the medicinal fungus Polyporus umbellatus, has been proven to prevent the progression of renal injury and the subsequent renal fibrosis. UPLC Q-TOF/MS was employed to investigate the metabonomic characteristics of adenine-induced chronic renal failure (CRF) and the proactive effects of ergone. The significant difference of the metabolic profiling was observed from ergone-treated group compared with the CRF model group during the 10-day and 20-day study periods by using the principal components analysis (PCA). The significant difference of the ergone-treated group in metabolic profiling was also observed between 10-day and 20-day study periods. The time-dependent tendency in ergone-treated group from day 10 to 20 was obtained, indicating the time-dependent recovery effect of ergone on CRF rats. Some significantly changed metabolites like creatinine, proline, adrenosterone, taurine, creatine, phenylalanine, ornithine, dopamine, kynurenine, kynurenic acid and 3-O-methyldopa have been identified during the 20-day study period. These biochemical changes are related to the disturbance in energy metabolism and amino acid metabolism, which are helpful to further understand the CRF and the therapeutic mechanism of ergone. This work suggests that this metabonomic approach could be used as a potentially powerful tool to investigate the biochemical changes of certain physiopathological conditions, such as metabolic syndrome, as an early diagnostic measure.

Protective Effect of Heat-processed Ginseng (Sun Ginseng) in the Adenine-induced Renal Failure Rats

The effect of orally administered sun ginseng (SG), which is a ginseng processed by steaming, was examined in adenine-induced chronic renal failure rat. SG significantly decreased both blood urea nitrogen and serum creatinine levels, indicating an improvement of renal function. Also, SG significantly increased the urinary excretion of both urea and creatinine. Furthermore it lowered the blood pressure, and inhibited adenine-induced kidney hypertrophy and edema. Based on these findings, SG may ameliorate chronic renal failures.

The effects of the hydroalcohol extract of Rosa canina L. fruit on ischemic acute renal failure in Wistar rats

This research evaluated the possible therapeutic potential of Rosa canina as a preventive agent in ischmia/reperfusiom induced acute renal failure in rats. There were three groups (n = 10), in which rats received orally 7 days before induction of ischemia, hydroalcoholic extract of R. canina (500 mg/kg) in R. canina + ischmia/reperfusiom (I/R) group and distilled water in I/R group. In sham group, the renal arteries were not occluded and distilled was administered orally 7 days before surgery. Renal ischemia was induced by both renal arteries occlusion for 45 min followed by 24 h of reperfusion. Blood samples were collected for biochemical analysis, and finally both kidneys were preserved for future histological examination. R. canina treatment reduced total renal histopathological score as well plasma creatinine and blood urea nitrogen levels in R. canina + I/R group in comparison to I/R group. According to these results, R. canina can be useful as a preventive agent against renal damages induced by ischemia/reperfusion injury in rat.

Protective Effect of Crocetin on Hemorrhagic Shock–Induced Acute Renal Failure in Rats

Multiple organ failure is a common outcome of hemorrhagic shock followed by resuscitation, and the kidney is one of the prime target organs involved. The main objective of the study was to evaluate whether crocetin, a natural product from Gardenia jasminoides Ellis, has beneficial effects on renal dysfunction caused by hemorrhagic shock and resuscitation in rats. Anesthetized rats were bled to reduce mean arterial blood pressure to 35 (SD, 5) mmHg for 60 min and then were resuscitated with their withdrawn shed blood and normal saline. Crocetin was administered via the duodenum at a dose of 50 mg/kg 40 min after hemorrhage. The increase in creatinine and blood urea nitrogen was significantly reduced at 2 h after hemorrhage and resuscitation in crocetin-treated rats. The increases in renal nitric oxide, tumor necrosis factor α, and interleukin 6 were also attenuated by crocetin. Hemorrhagic shock resulted in a significant elevation in malondialdehyde production and was accompanied by a reduction in total superoxide dismutase activity, activation of nuclear factor κB, and overexpression of inducible nitric oxide synthase. These changes were significantly attenuated by crocetin at 2 h after resuscitation. These results suggested that crocetin blocks inflammatory cascades by inhibiting production of reactive oxygen species and restoring superoxide dismutase activity to ameliorate renal dysfunction caused by hemorrhage shock and resuscitation.

A modified model of gentamicin induced renal failure in rats: Toxicological effects of the iodinated X-ray contrast media ioversol and potential usefulness for toxicological evaluation of iodinated X-ray contrast media

Contrast-induced nephropathy (CIN) remains a serious complication in patients exposed to iodinated X-ray contrast media (ICM). Animal models of CIN are useful to further understand the mechanisms involved, identify novel biomarkers and evaluate potential differences between ICM. The current investigation was undertaken to modify the rat-gentamicin model for potential usefulness for toxicological evaluation of ICM. A dose-range finding study (50, 60 and 70 mg/kg body weight (bw)) of gentamicin was conducted over 4 consecutive days. Based on the kidney histopathology findings, a gentamicin dose of 70 mg/kg bw was chosen to investigate whether ICM would cause further renal damage. Following gentamicin treatment, this group was given a single administration of ioversol (6 gI/kg bw). Blood and urine samples were taken from all animals 3 days before the start of the study and at the end of treatment. Serum and urinary creatinine, urinary N-acetyl-β-D-glucosaminidase (NAG), γ-glutamyl transferase (GGT), total protein, and urine cytology were evaluated as biomarkers of renal damage. Histopathological examination of kidneys was performed. Histopathological examination of the kidneys revealed vacuolation, dilatation, and necrosis of the proximal tubules in the gentamicin-ioversol treatment group. These changes were not seen in the gentamicin-only treatment groups. Data on GGT and urinary epithelial cells show clear differences between rats treated with gentamicin alone versus gentamicin plus ioversol. These findings show that the modified rat-gentamicin model was able to demonstrate the nephrotoxic effect of ioversol.

Effect of ergosta-4,6,8(14),22-tetraen-3-one (ergone) on adenine-induced chronic renal failure rat: A serum metabonomic study based on ultra performance liquid chromatography/high-sensitivity mass spectrometry coupled with MassLynx i-FIT algorithm

BackgroundErgosta-4,6,8(14),22-tetraen-3-one (ergone) has been proven to prevent the progression of renal injury and the subsequent renal fibrosis. We investigated the therapeutic effects and mechanism of ergone on a chronic renal failure model of rats induced by adenine. MethodsA serum metabonomic method based on the UPLC Q-TOF/MS was undertaken to explore the excretion pattern of low molecular mass metabolites. ResultsCoupled with blood biochemistry and kidney histopathology results, the significant difference in metabolic profiling between adenine-induced chronic renal failure group and the ergone treated group by using pattern recognition analysis indicated that changes in global serum metabolites occurred. Some significantly changed metabolites like lysophosphatidylcholines, adenine, dopamine, creatinine, aspartic acid and phenylalanine have been found and identified. These biochemical changes in serum metabolites are related to the perturbations of amino acid metabolism and lecithin metabolism, which may be helpful to further understand the chronic renal failure and therapeutic mechanisms of ergone. ConclusionThe work shows that the metabonomic method is a valuable tool for studying the essence of chronic kidney disease and therapeutic effect mechanism of preclinical or clinical drug.