Chronic Renal Failure Group Research Articles

Importance of neutrophil gelatinase-associated lipocalin in differential diagnosis of acute and chronic renal failure.

Background:Neutrophil Gelatinase-associated Lipocalin (NGAL) protein is easily detected in the blood and urine soon after acute renal injury. NGAL gains features of an early, sensitive and noninvasive biomarker for acute renal injury. Recent evidences suggest that its expression is also increased in CRF reflecting the severity of disease.Objectives:In the present study, we aimed to investigate whether blood NGAL level plays a role in the differential diagnosis of acute and chronic renal failure.Patients and Methods:This was a prospective case-control study. Fifty patients presented to emergency department with acute renal failure (ARF), 30 with chronic renal failure (CRF) and 20 healthy individuals as control group were included in this study. Blood pH, HCO3-, BUN, creatinine and potassium values were evaluated in all patients. Blood NGAL values were evaluated in all groups. BUN, serum creatinine and NGAL values were statistically compared between patients and controls.Results:Median NGAL levels in patients was 304.50 (29), and 60 (0) in control, which was statistically significant between the two groups (Z = -6.477, P < 0.001). The median NGAL values were 261.50 ± 291 in ARF group and 428.50 ± 294 in CRF group. There was a significant difference in NGAL level between ARF and CRF groups (Z = -2.52, P = 0.012). Median BUN values were 153.46 ± 82.47 in ARF group and 169.40 ± 93.94 in CRF group. There was no significant difference in BUN value between ARF and CRF groups (P > 0.05). Median creatinine values were 2.84 ± 2.95 in ARF group and 4.78 ± 4.32 in CRF group. In serum creatinine values, a significant difference was found between ARF and CRF groups (P < 0.05).Conclusions:Serum NGAL levels of ARF and CRF patients were significantly higher than healthy individuals. In addition, NGAL values of patients with CRF were significantly higher than those of ARF. Serum NGAL values can be used to detect renal injury and differentiate ARF and CRF.

Ocular Surface Findings in Chronic Renal Failure

The purpose of this study was to describe the ocular surface findings in chronic renal failure (CRF). Sixty eyes of 30 patients with CRF group and 70 eyes of 35 healthy subjects were evaluated. Schirmer-I, tear film break-up time tests and conjunctival impression cytology were performed in addition to complete ophthalmologic examination. The presence of dry eye symptoms and conjunctival calcification were noted. The groups were age and gender matched. The mean break-up time was 10.3±3.1 in group-1 and 11.2±1.7 seconds in the group-2 (p=0.03). The mean Schirmer score was 11.2±2.8 mm and 12.0±1.7 mm in the CRF and control group (p=0.095), respectively. In CRF group, conjunctival impression cytology was revealed as grade-0 findings in 16 eyes, grade 1 findings in 41 eyes and grade 2 findings in 3 eyes, in control group, it was revealed grade-0 findings in 48 eyes, grade 1 findings in 22 eyes and showed no changed in grade 2 (p<0.001). In CRF group, conjunctival calcification was regarded as grade 0 findings in 18 eyes, grade 1 findings in 34 eyes and grade 2 findings in 8 eyes. Grade 0 changes were seen in all subjects in group 2 (p<0.001). Itching (45%), redness (95%) and foreign body sensation (83%) were observed more frequently in the CRF group and also in all eyes with conjunctival calcification in both groups (p<0.001). Chronic renal failure patients suffer more than normal subjects from ocular surface complaints because of conjunctival calcifications and tear film instability although they have the same tear production with their contemporaries.

Comparison of the Immunogenicity of a Monovalent Influenza A/H1N1 2009 Vaccine Between Healthy Individuals, Patients With Chronic Renal Failure, and Immunocompromised Populations

BackgroundData on the immunogenicity (IG) of the influenza vaccine among patients at high risk of influenza-related complication are limited. MethodsWe studied the antibody titer following a single dose of monovalent 2009 influenza A (H1N1) vaccine between groups of adult patients who were healthy, those with chronic renal failure (CRF), kidney transplant (KT) recipients, and human immunodeficiency virus (HIV)-infected patients. The IG (primary endpoints) was accessed at 4 weeks after vaccination. The secondary endpoint was safety of the vaccine. ResultsA total of 293 patients were studied. Patients' mean age was 41(standard deviation [SD], 13.3) years old. At baseline, mean age (P < .001), history of vaccination in a prior year (P < .001), and geometric mean titers (GMT; P < .001) significantly differed between each groups and the majority (70%) of participants had the hemagglutination inhibition titer <1:10. The IG of the vaccine was highest in the healthy group (71.4 %). The response rate among CRF, KT, and HIV groups was 42.4% (risk ratios [RR], 0.72; 95% confidence interval [CI], 0.5–1.02), 31.9% (RR, 0.51; 95% CI, 0.34–0.76), and 29.7% (RR, 0.42; 95% CI, 0.3–0.6), respectively. The vaccine was well-tolerated in all studied groups. Thirty (10.2%) patients experienced at least 1 adverse reaction but systemic reaction was uncommon (3.4%). ConclusionsA single dose of monovalent 2009 influenza A (H1N1) vaccine result in poor IG among high-risk populations, including CRF, KT and HIV patients.

Effects of sodium citrate on salt sensitivity and kidney injury in chronic renal failure.

Metabolic acidosis, which is observed in salt-sensitive hypertension, is also associated with kidney injury. Alkali therapy in chronic renal failure (CRF) may ameliorate the progression of kidney disease; however, few studies have examined the effects of alkali therapy on salt sensitivity and kidney injury in CRF. We randomly administered standard diet (SD), sodium chloride with 20% casein diet (NACL), or sodium citrate with 20% casein diet (NACT) to Sprague-Dawley rats after a CRF or a sham operation. Four weeks after 5/6 nephrectomy, serum bicarbonate levels were higher in the NACT-treated group. On the pressure-natriuresis curve, NACT-treated CRF rats were more salt-resistant than NACL-treated CRF rats. Additionally, the NACT-treated CRF group showed less tubulointerstitial damage than the NACL-treated CRF group. The expression and immunoreactivity of NHE3 in the kidney in the NACT-treated CRF group were lower than those in the NACL-treated CRF group. We observed that dietary NACT as alkali therapy in CRF might improve the altered salt-sensitivity and ameliorate the progression of kidney injury compared to the NACL diet, which may be related to reduced renal NHE3 expression.

Effect of chronic renal failure on the hepatic, intestinal, and renal expression of bile acid transporters

Although the kidney is believed to play a minor role in bile acid (BA) excretion, chronic renal failure (CRF) has been reported to be associated with increased serum bile acid levels and alterations in BA homeostasis. The mechanisms for elevated BA levels are poorly understood in both clinical and experimental studies. This study was designed to examine the effects of naturally progressing CRF of longer duration on the hepatic and renal mRNA and protein levels of the BA-synthesizing enzyme Cyp7a1 and the BA transporters Ntcp, Bsep, Mrp3, Ost-α, and Ost-β. Sprague-Dawley rats were randomized to the CRF group (&frac56; nephrectomy) or to the sham-operated control group and were analyzed 8 wk after surgery. Results obtained in the CRF rats were compared with those obtained in rats that had undergone uninephrectomy (UNX). The CRF group exhibited significantly increased plasma cholesterol and BA concentrations. Hepatic Cyp7a1 mRNA and protein levels were almost identical in the two groups. Hepatic Mrp3, Ost-α, and Ost-β expression was increased, suggesting increased basolateral efflux of bile acids into the blood. However, no such changes in BA transporter expression were observed in the remnant kidney. In UNX rats, similar changes in plasma BA levels and in the expression of BA transporters were found. We hypothesize that the increase in plasma BA is an early event in the progression of CRF and is caused by increased efflux across the basolateral hepatocyte membrane.

Cinacalcet attenuates the renal endothelial-to-mesenchymal transition in rats with adenine-induced renal failure

Elevated serum parathyroid hormone (PTH) is an important complicated phenomenon in patients with chronic kidney disease (CKD). Emerging evidence indicates the involvement of PTH in organ fibrosis, and suppression of PTH by cinacalcet (CINA) ameliorates the progression of fibrotic disorders. However, the underlying mechanisms are largely unknown. The endothelial-to-mesenchymal transition (EndMT) has been shown to be an important mechanism involved in renal fibrosis. The present study aimed to investigate whether CINA treatment attenuated renal EndMT in rats with adenine-induced chronic renal failure (CRF). Compared with the control group, serum PTH was significantly higher in the CRF group and was suppressed after CINA treatment. Serum calcium, phosphorus, and calcium × phosphorus product levels were similar in the CRF group and CINA-treated CRF group. Renal collagen accumulation was significantly increased in the CRF group, which was markedly ameliorated by CINA treatment. Expression of the endothelial marker CD31 was significantly downregulated in rats with CRF, whereas expression of the mesenchymal markers fibroblast specific-protein 1 and α-smooth muscle actin was markedly upregulated. These changes were inhibited by CINA treatment. The protein levels of these EndMT-related markers were strongly correlated with serum PTH concentrations. Furthermore, the in vitro study showed that PTH could significantly increase the expression of fibroblast specific-protein 1 and α-smooth muscle actin and decrease CD31 in mRNA and protein levels in a concentration- and time-dependent manner. In conclusion, our study suggests that reducing serum PTH by CINA treatment could attenuate renal fibrosis via suppression of EndMT in the adenine-induced CRF rat model.

Changes of adiponectin and its receptors in rats following chronic renal failure

Objective: To investigate changes of adiponectin and its receptors (Adipo R) in rats following chronic renal failure. Methods: Male SD rats were randomly divided into two groups: control group and chronic renal failure (CRF) group. The CRF group were gavaged with adenine (300 mg/kg/d) for 4 weeks and the control group with drinking water. All rats were anesthetized at 2nd or 4th week and blood and urine samples were collected for detection of renal function, 24 h urine protein and adiponectin concentration. Renal tissues were also collected for HE staining, immunohistochemistry and RT-PCR screening. Results: Compared with control group, the serum concentrations of urea and creatinine, 24 h urine protein excretion in the CRF group were significantly higher at 2nd week and further increased at 4th week (p < 0.05). The adiponectin levels in serum and urine in the CRF group were significantly higher than those of control group (p < 0.01). The renal expressions of Adipo R1 and Adipo R2 in CRF group were also significantly increased compared to control group (p < 0.01). The increased expressions of Adipo R1 and Adipo R2 were positively related to the adiponectin levels in serum, urine, and 24 h urine protein. Conclusion: The significant changes in expression of adiponectin and its receptors in rat CRF model could be an adaptive response that may provide the basis to understand pathological changes in chronic kidney disease.

PA21, a New Iron-Based Noncalcium Phosphate Binder, Prevents Vascular Calcification in Chronic Renal Failure Rats

Chronic renal failure (CRF) is associated with the development of secondary hyperparathyroidism and vascular calcifications. We evaluated the efficacy of PA21, a new iron-based noncalcium phosphate binder, in controlling phosphocalcic disorders and preventing vascular calcifications in uremic rats. Rats with adenine-diet-induced CRF were randomized to receive either PA21 0.5, 1.5, or 5% or CaCO3 3% in the diet for 4 weeks, and were compared with uremic and nonuremic control groups. After 4 weeks of phosphate binder treatment, serum calcium, creatinine, and body weight were similar between all CRF groups. Serum phosphorus was reduced with CaCO3 3% (2.06 mM; P ≤ 0.001), PA21 1.5% (2.29 mM; P < 0.05), and PA21 5% (2.21 mM; P ≤ 0.001) versus CRF controls (2.91 mM). Intact parathyroid hormone was strongly reduced in the PA21 5% and CaCO3 3% CRF groups to a similar extent (1138 and 1299 pg/ml, respectively) versus CRF controls (3261 pg/ml; both P ≤ 0.001). A lower serum fibroblast growth factor 23 concentration was observed in the PA21 5%, compared with CaCO3 3% and CRF, control groups. PA21 5% CRF rats had a lower vascular calcification score compared with CaCO3 3% CRF rats and CRF controls. In conclusion, PA21 was as effective as CaCO3 at controlling phosphocalcic disorders but superior in preventing the development of vascular calcifications in uremic rats. Thus, PA21 represents a possible alternative to calcium-based phosphate binders in CRF patients.

Su1684 Adenosine Regulates Cholangiocyte IL-6 Secretion via the A2B Receptor

Background. Although the kidney is believed to play a minor role in bile acid (BA) excretion, chronic renal failure (CRF) has been reported to be associated with increased serum bile acid levels and alterations in BA homeostasis. According to a recent report, rats studied 3 weeks after 5/6 nephrectomy and fed a high-protein diet exhibited increased activities of hepatic HMG-CoA reductase (HMG-CoAR) and cholesterol 7 alpha-hydroxylase (Cyp7a1), despite normal corresponding mRNA levels. Design and Methods. This study was designed to examine the effects of naturally progressing CRF of longer duration on the hepatic and renal mRNA and protein levels of the bile acid synthesizing enzyme Cyp7a1 and the bile acid transporters, Ntcp, Bsep, Mrp3, Ost-alpha and OST-beta. Sprague-Dawley rats were randomized to the CRF group (5/6 nephrectomy) or to the sham-operated, placebo-treated normal control group. They were allowed free access to regular rat chow and were analyzed 8 weeks after surgery. Results obtained in CRF rats were compared to those obtained in rats that had undergone uninephrectomy (UNX). Results. The CRF group exhibited significantly increased plasma cholesterol and bile acid concentrations. Hepatic Cyp7a1 mRNA, and protein levels were almost identical in the two groups. Hepatic Mrp3, Ostα and Ost-β expression was increased at both the mRNA and protein levels, suggesting increased basolateral efflux of bile acids into basolateral blood. However, no such changes in bile acid transporter expression were observed in kidney. In UNX rats, similar changes in plasma bile acid levels and in the expression of bile acid transporters were found. We hypothesize, that the increase in plasma bile acids is an early event in the progression of CRF and is caused by increased efflux across the basolateral hepatocyte membrane.

Su1681 Hypoxia Induces Dysregulation of Lipid Metabolism in HEPG2 Cells via Activation of HIF-2a

Background. Although the kidney is believed to play a minor role in bile acid (BA) excretion, chronic renal failure (CRF) has been reported to be associated with increased serum bile acid levels and alterations in BA homeostasis. According to a recent report, rats studied 3 weeks after 5/6 nephrectomy and fed a high-protein diet exhibited increased activities of hepatic HMG-CoA reductase (HMG-CoAR) and cholesterol 7 alpha-hydroxylase (Cyp7a1), despite normal corresponding mRNA levels. Design and Methods. This study was designed to examine the effects of naturally progressing CRF of longer duration on the hepatic and renal mRNA and protein levels of the bile acid synthesizing enzyme Cyp7a1 and the bile acid transporters, Ntcp, Bsep, Mrp3, Ost-alpha and OST-beta. Sprague-Dawley rats were randomized to the CRF group (5/6 nephrectomy) or to the sham-operated, placebo-treated normal control group. They were allowed free access to regular rat chow and were analyzed 8 weeks after surgery. Results obtained in CRF rats were compared to those obtained in rats that had undergone uninephrectomy (UNX). Results. The CRF group exhibited significantly increased plasma cholesterol and bile acid concentrations. Hepatic Cyp7a1 mRNA, and protein levels were almost identical in the two groups. Hepatic Mrp3, Ostα and Ost-β expression was increased at both the mRNA and protein levels, suggesting increased basolateral efflux of bile acids into basolateral blood. However, no such changes in bile acid transporter expression were observed in kidney. In UNX rats, similar changes in plasma bile acid levels and in the expression of bile acid transporters were found. We hypothesize, that the increase in plasma bile acids is an early event in the progression of CRF and is caused by increased efflux across the basolateral hepatocyte membrane.

Uremic anorexia and gastrointestinal motility dysfunction correlate with the changes of ghrelin system in hypothalamus

Ghrelin can act as a signal for meal initiation and play a role in the regulation of gastrointestinal (GI) motility via hypothalamic circuit. This study investigated the correlation between changes of hypothalamic ghrelin system and GI motility dysfunction and anorexia in rats with chronic renal failure (CRF). Sprague-Dawley (SD) rats (male/female 1:1, 180 ± 20 g) were randomly classified into a CRF group and control group (n = 8 per group). 5/6 nephrectomy was used to construct the CRF model. When plasma creatinine concentration (PCr) and blood urea nitrogen (BUN) in the CRF group were twice higher than the normal, food intake (g/24 h) and gastrointestinal interdigestive myoelectric complex (IMC) were detected. Then all rats were killed for assessment of the mRNA expression of ghrelin and growth hormone secretagogue receptor (GHS-R) in hypothalamus using reverse transcription-polymerase chain reaction. Analysis of variance, Student-Newman-Keuls-q-test and Correlation Analysis were used to do statistical analysis. P < 0.05 was considered as statistically significant. Compared to the control group, the CRF group was obviously decreased in the food intake (g/24 h), the phase III duration and amplitude and the ghrelin and GHS-R expression in the hypothalamus (P < 0.05). There was a positive correlation between them (P < 0.05). Changes of ghrelin and GHS-R in the hypothalamus correlate with gastrointestinal motility dysfunction and anorexia in rats with CRF.

Effect of chronic renal failure medium on the ubiquitin-proteasome pathway of arterial muscle cells

The ubiquitin‑proteasome pathway (UPP) is involved in the occurrence and development of atherosclerosis through inhibitor of κB (IκB) degradation which activates nuclear factor-κB (NF‑κB). However, the correlation between UPP and vascular complications of uramia remains unknown. The aim of the present study was to determine whether the UPP is activated in aortic smooth muscle cells (ASMCs) when cultured with uremic serum and to examine the role of the UPP on the dysfunction of ASMCs in uremia. ASMCs were cultured with pooled normal sera or chronic renal failure sera. The mRNA expression levels for ubiquitin (Ub) and Ub-activating enzyme (E1) were analyzed using reverse transcription PCR and levels of the ubiquitinated proteins E1 and IκBα were measured using western blot analysis. The enzymatic activities of three 20S proteasomes were examined using specific fluorogenic peptide substrates. Compared with normal serum, chronic renal serum increased E1 mRNA and protein expression of rabbit ASMCs (both P<0.01). In addition, the mRNA expression of Ub also increased and the expression of IκBα was observed to decrease significantly (both P<0.01). Ubiquitinated proteins in the normal and chronic renal failure groups were not found to be significantly different, but the activity of proteasomes increased significantly (P<0.01). Chronic renal failure medium induced the activation of the UPP in ASMCs.

Intrarenal Metabolomic Investigation of Chronic Kidney Disease and its TGF-β1 Mechanism in Induced-adenine Rats using UPLC Q-TOF/HSMS/MSE

Chronic kidney disease (CKD) is becoming a worldwide public health problem. In this study, a kidney metabonomics method based on the ultra performance liquid chromatography/high-sensitivity mass spectrometry with MS(E) data collection technique was undertaken to explore the excretion pattern of low molecular mass metabolites in rat model of adenine-induced chronic renal failure (CRF). Coupled with blood biochemistry and kidney histopathology results, the significant difference in metabolic profiling between the adenine-induced CRF group and the control group by using pattern recognition analysis indicated that changes in global tissue metabolites were occurred. Some significantly changed metabolites like fatty acids, p-cresol sulfate, and indoxyl sulfate have been identified. The results showed that the most important CRF-related metabolites were polyunsaturated fatty acids, indoxyl sulfate, and p-cresyl sulfate. Indoxyl sulfate and p-cresyl sulfate (uremic toxins) were significantly increased in CRF rats. Indoxyl sulfate and p-cresyl sulfate stimulate progressive tubulointerstitial fibrosis by increasing the expression of transforming growth factor-β1 (TGF-β1). These biochemical changes in tissue metabolites are related to the perturbations of fatty acid metabolism and amino metabolism, which may be helpful to further understand the TGF-β1 mechanisms of tubulointerstitial fibrosis. This work shows that the metabonomics method is a valuable tool for studying the essence of CKD.

Nitric oxide levels in patients with chronic renal disease.

Nitric Oxide (NO), the L-arginine derivative, is tonically synthesised by the endothelium within the kidney and it plays a crucial role in the regulation of the blood pressure and the renal blood flow. NO regulates the renal function through the modulation of the vascular tone and sodium handling. With the progressive development of the renal insufficiency, it remains unclear whether the endogenous NO production is increased or decreased in the kidney. This study was carried out to determine whether there were any changes in the levels of NO and teir correlation with the routine parameters of the renal dysfunction in the patients of Chronic Renal Failure (CRF), as the disease progresses in conjunction with poor renal functions. Thirty patients with chronic renal disease which was caused by chronic glomerulonephritis and hypertension, who were on Maintenance Haemodialysis (MHD) with serum creatinine levels of > 2.5 mg/dl, were included in this study. Thirty healthy voluntary blood donors were taken as the controls. NO was estimated by a spectrophotometric method by using cadmium reduction. The routine renal function tests, BUN and Creatinine were performed by the standard clinical chemistry procedures. The serum NO levels were found to be significantly increased (p < 0.01) in the CRF on MHD (98.77 ± 35.40 μmol/l) as compared to the controls (22.03 ± 7.23 μmol/l). The NO output correlated with the serum creatinine (r = 0.8123, p < 0.01) and the urea concentration (r = 0.5166, p = <0.01) in the CRF group. The NO levels were markedly enhanced in the CRF patients who were on MHD. This was due to the dialysis procedure itself, which led to the stimulation of cytokine induced NO synthase and also due to the platelets which generated more NO due to uraemia. At high concentrations, NO is a cytotoxic molecule which is responsible for the complications of dialysis and it results in Nitrosative Stress in these patients, as it is a highly reactive free radical. Since the no output correlated with the serum creatinine and urea concentrations, a higher no production probably indicated insufficient blood purification, due to the common effect on their elimination pathways via the renal tract. Therefore, the alterations of the renal function, that are reflected in the changes of the creatinine concentration, will be accompanied by the changes in the serum NO. Thus, the determination of the NO levels in the peripheral blood may be useful in the assessment of the dialysis and they can also be used as markers in the follow up and the prognosis in these type of patients.

UPLC-Q-TOF/HSMS/MSE-based metabonomics for adenine-induced changes in metabolic profiles of rat faeces and intervention effects of ergosta-4,6,8(14),22-tetraen-3-one

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. Ultra performance liquid chromatography coupled with quadrupole time-of-flight high-sensitivity mass spectrometry and a novel mass spectrometryElevated Energy (MSE) data collection technique was employed to investigate metabonomic characters of chronic renal failure (CRF) induced adenine and the protective effects of ergosta-4,6,8(14),22-tetraen-3-one (ergone). Coupled with blood biochemistry and kidney histopathology results, the significant difference in metabolic profiling between adenine-induced CRF group and ergone-treated CRF group by using pattern recognition analysis indicated that changes in global faecal metabolites were occurred. Seven endogenous metabolites were identified by using metabonomic method combined with multivariate data analysis, the accurate mass, isotopic pattern, MSE fragments information and MassLynx i-FIT algorithm. These biochemical changes in faecal metabolites are related to the perturbations of bile acid metabolism and phospholipid metabolism, which may be helpful to further understand the CRF and therapeutic mechanisms of ergone. This research proved that MSE can simultaneous acquire precursor ion information and fragment ion data at high and low collision energy in one analytical run, which facilitated the fast structural characterization of metabolites.

Evaluation urinary trehalase in patients with renal proximal tubular damage

Objective To investigate the value of urinary trehalase（T） in patients with renal proximal tubular damage. Methods 134 patients with kidney disease (male:66 female:68 age:18-59; 31 cases with acute renal failure, 30 cases with chronic renal failure, 20 cases with drug-induced renal impairment, 21 cases with renal transplantation and 32 cases with nephritic syndrome) and 101 healthy controls (58 males and 43 females) were selected.Urinary T, N-acetyl-D-glucosaminidase (NAG), β2-MG, gamma-glutamyl transferase(GGT) were detected.Data were analyzed by SPSS 11.5, including non-parametric rank test, ROC analysis. Results The level of urinary trehalase in control group was normally distributed （7.1±4.1） μmol/h·g Cr (0-25 μmol/h·g Cr). There was no significant difference between men and women (t=0.63, P=0.53).Urinary T levels were significant higher in all kidney disease groups than in control group (Z=6.80,5.90, 5.23, 6.00, 8.04，P＜0.01).According to ROC curve, the area of urinary T under the ROC curve (AUC) in 134 patients was 0.9, significantly different with NAG, β2-MG, GGT area （P＜0.01），the AUCs of T were 0.94,0.85, 0.90,0.90,0.91 in acute and chronic renal failure group, drug-induced renal impairment group, renal transplantation group and nephritic syndrome group, respectively; Youden index were 0.85,0.65,0.77,0.66,0.72 respectively.Corresponding to the Youden index，sensitivity and specificity were 90.3% and 95.1%, 73.3% and 92.1%, 85.0% and 92.1%, 81.0% and 85.2%, 87.5% and 84.2% respectively. Conclusions The Urinary trehalase is better than other markers in the diagnosis of the proximal renal tubular damage.It was better to evaluate the proximal tubular function early in time.The diagnostic value of urinary trehalase played a key role in diagnosis, treatment and prognosis of kidney diseases.（Chin J Lab Med，2012,35：1135-1138） Key words: Kidney diseases; Kidney tubules; proximal; Trehalase; Urinalysis

Evaluating the utility of plasma Atherogenic Index among several atherogenic parameters in patients with chronic renal Failure on maintenance hemodialysis

Background: Patients with chronic renal failure undergoing longterm hemodialysis (HD) are prone to atherosclerosis and at increased risk of developing cardiovascular diseases.Objective: The objective of this study is to compare atherogenic index of plasma (AIP) in predicting the risk of cardiovascular disease (CVD) in patients with chronic renal failure (CRF) on regular hemodialysis, when associated with other chronic diseases.Patients and methods: A total of forty male patients with CRF on hemodialysis, matched in, age, body mass index BMI, and duration of hemodialysis were enrolled. They were grouped as group 1 (G1) includes eleven subjects with CRF without (hypertension and / or diabetes) groups 2 (G2) fourteen CRF subjects with hypertension and group 3 (G3) fifteen CRF subjects with diabetes. As a control group, eighteen healthy male subjects were included with special exclusion criteria. The plasma total cholesterol TC, triglyceride TG, and high density lipoprotein-cholesterol HDL-C were estimated using spectrophotometry methods. While low density lipoprotein-cholesterol LDL-c, and AIP were calculated using special formulas. Statistical analysis was performed by the student t-test.Results: The results of the study revealed significant increase in TC and TG, with significant decrease in HDL-c for all patient groups compared to control. No significant difference in LDL-c of G1 compared to control was found, while significant increase in LDL-c of G2 and G3 was found when compared to G1 or control. The AIP values were (0.42 ± 0.19 vs 0.43 ± 0.17; P&gt;0.05) for G1 and G2 respectively, that showed no significant difference of atherogenic risk between these groups.Conclusions: These results concluded that AIP seems to be superior to LDL-c in predicting the risk for CVD in CRF groups on hemodialysis and those at the highest risk when CRF coupled with diabetes.

Uremic anorexia and ghrelin expression in the amygdala

Background/aimsGhrelin can act as a signal for mealtime hunger and meal initiation. Amygdala is indispensable in appetitive behavior motivated by learned emotions. This study was to investigate the alteration of ghrelin in the amygdala of rats with chronic renal failure (CRF) and its relation with uremic anorexia. MethodsSD rats were randomly classified into CRF group and control group (n=16 per group). The CRF model was constructed using 5/6 nephrectomy. When plasma creatinine (PCr) and blood urea nitrogen (BUN) in the CRF group were twice more than the normal level, food intake (g/24h) was measured and then all rats were killed for detection of ghrelin protein expression in the amygdala using immunohistochemical analysis and mRNA expression using RT-PCT. Statistics was conducted with one-way analysis of variance, Student–Newman–Keuls-q test and correlation analysis. ResultsBy the 8th week after the surgery, the BUN and PCr of CRF rats exceeded double the normal level, and their food intake was obviously decreased compared with the controls (P<0.05). The protein and mRNA expression of ghrelin in the amygdala of CRF group were significantly reduced, and there was a positive correlation between this reduction and the decrease in food intake (P<0.05). ConclusionThe reduction of amygdala's ghrelin in CRF rats may be associated with uremic anorexia.

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.

Prevalence of Aspirin Resistance in Patients of Chronic Kidney Disease

Background: Chronic renal failure (CRF) is associated with increased risk of cardiovascular morbidity and mortality. Antiplatelets especially low dose aspirin becomes mandatory for prevention of primary and secondary prevention of cardiovascular events in patients of CKD. The aim of this study was to explore the prevalence of aspirin resistance in CRF. Methods: A prospective clinical study was conducted in which 130 patients suffering from CRF with concomitant cardiovascular risk factors were recruited and were on aspirin (100 mg daily) for 4 weeks. Aspirin non-responder status was identified by PFA-100 system. Results: Aspirin resistance was detected in 53 patients undergoing hemodialysis, 32 patients with stage 3-4 CKD and 22 controls. The frequency of aspirin resistance was significantly higher in the CRF group compared with controls (34.7% vs. 16.9%, P &lt; 0.001) and in hemodialysis patients (46.1%) compared with stage 3-4 CKD patients (24.6%, P &lt; 0.001) and controls (16.9%, P &lt; 0.001). Multivariate analysis revealed female sex (odds ratio (OR) = 2.201; 95% confidence interval (95% CI), 1.173 - 4.129; P = 0.014), hemodialysis (OR = 3.636; 95% CI, 1.313 - 10.066; P = 0.013) and HDL cholesterol (OR = 0.974; 95% CI, 0.950 - 0.999; P = 0.043) as independent predictors of aspirin resistance in this cohort of patients. Conclusion: Patients with CRF have higher frequency of aspirin resistance. This might further increase the risk of cardiovascular morbidity and mortality in these patients. doi:10.4021/wjnu4w