Monoterpene linalool restrains gentamicin-mediated acute kidney injury in rats by subsiding oxidative stress, apoptosis, and the NF-κB/iNOS/TNF-α/IL-1ß pathway and regulating TGF-ß.

The clinical use of gentamicin (GM) is restricted by its nephrotoxic effects. This study aimed for the first time to elucidate the ameliorative effects of the monoterpene linalool (Lin) against GM-mediated acute kidney injury in rats. A total of thirty-two rats were subdivided into four equal groups: control (saline), Lin (100 mg/kg/day), GM (100 mg/kg/day), and GM + Lin (100 and 100 mg/kg/day). Lin and GM were intraperitoneally administered for 12 days. Our results illustrated that Lin ameliorated GM-mediated renal histopathological abnormalities and reduced serum urea and creatinine levels in rats exposed to GM. Lin treatment mitigated oxidative stress in nephrotoxic animals as manifested by reducing serum and renal levels of malondialdehyde and increasing the activities of serum and renal glutathione peroxidase and renal catalase. Moreover, Lin markedly inhibited GM-triggered inflammation by downregulating NF-κB, iNOS, TNF-α, and IL-1ß and reducing renal myeloperoxidase activity and nitric oxide levels. Interestingly, Lin repressed GM-induced apoptosis, as reflected by a marked downregulation of Bax and caspase-3 expression, concurrent with the upregulation of Bcl2 expression. Finally, Lin administration led to a significant downregulation of TGF-ß expression in nephrotoxic animals. In summary, Lin ameliorated GM-mediated nephrotoxicity in rats, at least through its antioxidant, anti-inflammatory, and anti-apoptotic activities and by modulating TGF-ß.

Cytotoxic and epigenetic effects of berberine-loaded chitosan/pectin nanoparticles on AGS gastric cancer cells: Role of the miR-185-5p/KLF7 axis, DNMTs, and global DNA methylation.

Poor bioavailability, solubility, and absorption of berberine (Ber) limit its widespread application. Here, we formulated novel chitosan/pectin nanoparticles (NPs) loaded with Ber to address delivery problems and promote the anticancer properties of Ber in AGS gastric cancer cells. The ionic gelification method was used to synthesize NPs-Ber. Physicochemical characterization of NPs-Ber was performed using FE-SEM, DLS, PDI, ζ potential, and FTIR. The cytotoxic effects of NPs-Ber on AGS cells were evaluated using the MTT assay. Apoptosis and cell cycle arrest were examined by flow cytometry. The gene expression levels of miR-185-5p, KLF7, caspase-3, and DNMTs were determined using RT-qPCR. In addition, the 5-methylcytosine level in the genomic DNA was quantified using ELISA. FE-SEM images revealed a denser and more packed matrix for NPs-Ber, and FTIR analysis confirmed the formation of NPs-Ber. The size (550.39 nm), PDI (0.134), and ζ potential (-16.52 mV) confirmed the stability of the prepared NPs-Ber. NPs-Ber showed a continuous release pattern following the Korsmeyer-Peppas model such that 81.36 % of Ber was released from the formulation after 240 min. Compared to NPs and free Ber, NPs-Ber was found to possess higher anticancer activity in AGS cells. This result was indicated by the viability test and further clarified by augmented apoptosis and cell cycle arrest at the G0/G1 phase. The IC50 value of NP-Ber against AGS cells was significantly lower than those of free Ber and NPs. Interestingly, our results showed that NPs-Ber considerably changed the expression levels of miR-185-5p, KLF7, caspase-3, and DNMTs (DNMT1, 3A, and 3B) compared with unloaded NPs and free Ber. Additionally, 5-methylated cytosine (5-mC) levels in cells treated with NPs-Ber were significantly higher than those in cells treated with unloaded NPs or free Ber. In summary, the present study demonstrated that Ber encapsulation in NPs enhances its cytotoxic and epigenetic effects on AGS cells, suggesting the promising potential of NPs-Ber in GC therapy.

Regulation of HIF-1 by MicroRNAs in Various Cardiovascular Diseases.

Today, we see an increase in death due to cardiovascular diseases all over the world, which has a lot to do with the regulation of oxygen homeostasis. Also, hypoxia-inducing factor 1 (HIF-1) is considered a vital factor in hypoxia and its physiological and pathological changes. HIF- 1 is involved in cellular activities, including proliferation, differentiation, and cell death in endothelial cells (ECs) and cardiomyocytes. Similar to HIF-1α, which acts as a protective element against various diseases in the cardiovascular system, the protective role of microRNAs (miRNAs) has also been proved using animal models. The number of miRNAs identified in the regulation of gene expression responsive to hypoxia and the importance of investigating the involvement of the non-coding genome in cardiovascular diseases is increasing, which shows the issue's importance. In this study, the molecular regulation of HIF-1 by miRNAs is considered to improve therapeutic approaches in clinical diagnoses of cardiovascular diseases.

Global and Regional DNA methylation silencing of PPARγ Associated with Glioblastoma Multiforme Pathogenesis.

BACKGROUND: The relationship between peroxisome proliferator-activated receptor gamma (PPARγ) expression level and epigenetic modifications occurring in glioblastoma multiforme (GBM) pathogenesis is largely unknown. Herein, we examine the association of PPARγ expression with its promoter and genomic global DNA methylation status, as well as DNA methyltransferases (DNMTs) gene expression in GBM patients. METHODS: We examined the patterns of promoter methylation and PPARγ expression in 26 GBM tissues and 13 adjacent non-tumor tissues by methylation-specific PCR (MSP), real-time PCR, and ELISA, respectively. Also, we examined the genomic global 5-methyl cytosine levels and DNMTs gene expression using ELISA and real-time PCR methods, respectively. RESULTS: We found that hypermethylation on a specific region of the PPARγ promoter is significantly associated with the downregulation of the PPARγ gene and protein level in GBM patients. Interestingly, the amount of 5-methyl cytosine level was significantly reduced in GBM patients and positively correlated with PPARγ protein expression. Furthermore, the expression level of DNMT1, DNMT3A, and 3B were upregulated in GBM patients and the average expression level of all three DNMTs was positively correlated with tumor area. Also, we found that tumors from cortical regions exhibited a higher global DNA hypomethylation and PPARγ hypermethylation was related to the increase in GBM risk. CONCLUSION: Our study demonstrated that global DNA methylation and PPARγ epigenetic silencing is associated with the GBM risk. Our data provide a novel molecular mechanistic insight into epigenetic silencing of PPARγ in GBM patients that may be relevant as a key tumor marker for GBM pathogenesis.

Gene therapy: A promising approach for breast cancer treatment.

Breast cancer (BC) is the most prevalent malignancy and the second leading cause of death among women worldwide that is caused by numerous genetic and environmental factors. Hence, effective treatment for this type of cancer requires new therapeutic approaches. The traditional methods for treating this cancer have side effects, therefore so much research have been performed in last decade to find new methods to alleviate these problems. The study of the molecular basis of breast cancer has led to the introduction of gene therapy as an effective therapeutic approach for this cancer. Gene therapy involves sending genetic material through a vector into target cells, which is followed by a correction, addition, or suppression of the gene. In this technique, it is necessary to target tumour cells without affecting normal cells. In addition, clinical trial studies have shown that this approach is less toxic than traditional therapies. This study will review various aspects of breast cancer, gene therapy strategies, limitations, challenges and recent studies in this area.

Effect of folic acid and vitamin E on promoter DNA methylation and expression of TGF-ß1, ESR-1 and CDH-1 in the uterus of STZ-induced diabetic rats.

The present study is the first attempt made to investigate the effects of diabetes on expression and promoter DNA methylation of TGF-ß1, ESR-1, and CDH-1 genes and also the effects of folic acid (FA) and vitamin E (Vit E) supplementations on improving diabetes mellitus. STZ-induced diabetic rats were treated with Vit E (200 mg/kg/day) and FA (25 mg/kg/day) for 8 weeks and expression and DNA methylation of TGF-ß1, ESR-1, and CDH-1 genes in uterus were analysed. Data indicated that diabetes increases the expression of TGFß-1 and ESR-1 and decreases CDH-1 expression and TGFß-1 promoter methylation in the uterus of rats. Vit E and FA improved the negative effects of diabetes by decreasing the expression of TGFß-1 and ESR-1 and increasing that of CDH-1 in diabetic rats. In conclusion, these findings emphasise that Vit E and FA supplementations could improve negative effects caused by diabetes on uterus function and fertility in diabetic rats.

Cinnamic acid ameliorate gentamicin-induced liver dysfunctions and nephrotoxicity in rats through induction of antioxidant activities.

This study was the first to evaluate the possible protective effects of cinnamic acid (CA) against Gentamicin (GM) induced liver and kidney dysfunctions in rats. Adult male Wistar rats were randomly assigned to 4 equal groups (n = 8): Control group (saline, 0.5 ml/day), CA group (CA, 50 mg/kg/day), GM group (GM, 100 mg/kg/day), and GM + CA group (100 & 50 mg/kg/day). Following 12 days of treatments, blood and 24 h urine samples were collected and kidneys were taken out for biochemical, histopathological, and molecular studies. Following CA treatment, renal function markers and transaminases activities including serum urea (59.92%) and creatinine (50.41%), protein excretion rate (43.67%), and serum activities of aspartate aminotransferase (AST) (54.34%) and alanine aminotransferase (ALT) (47.26%) significantly reduced in the treated group as compared with the GM group (P < 0.05). Also, CA could significantly ameliorate the levels of triglyceride (29.70%), cholesterol (13.02%), very low-density lipoprotein (29.69%) and high-density lipoprotein-cholesterol (7.28%). CA could also attenuate oxidative stress through a decrease of serum malondialdehyde (MDA) (50.86%) and nitric oxide (NO) (0.85%) and an increase of renal catalase (CAT) (196.14%) and glutathione peroxidase (GPX) activities (45.88%) as well as GPX mRNA expression (44.42-fold) as compared with the GM group (P < 0.05). Moreover, histopathological evaluations revealed attenuated tubular damages and reduced inflammatory cellular infiltration in CA treated animals. Overall, CA alleviates GM-induced nephrotoxicity and alterations in transaminases activities in rats through its antioxidant activities.

Protective effects of quercetin against hyperglycemia-induced oxidative stress in hepatic HepG2 cell line.

OBJECTIVE: Hyperglycemia is a severe consequence of diabetes mellitus (DM). Throughinduction of oxidative stress, it plays a major role in the pathogenesis of several complications in DM. Therefore, new strategies and antioxidants should be implemented inthe treatment of DM. Quercetin is a flavonoid with strong antioxidant capacity found dominantly in vegetables, fruits, leaves, and grains. The current study aimed to investigate quercetin protective effects under D-glucose-induced oxidative stress by assessing antioxidant defense enzymes inHepG2 cells as an in vitro model. MATERIALS AND METHODS: HepG2 cells were cultured with different concentrations of D-glucose (5.5, 30 and 50 mM) and/or 25 µM quercetin for 48 and 72 hr, respectively. The effect of treatments on cellular integrity, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) activity, andcellular levels of glutathione (GSH) and malondialdehyde (MDA) wasdetermined. RESULTS: D-glucose had various effects on intracellular antioxidant defense atdifferent doses and time-points and quercetin could attenuate oxidative stress and modulate antioxidant defenses. CONCLUSION: The results of this study indicated that flavonoid quercetin could be proposed as an agent protecting hepatic HepG2 cells against oxidative stress associated with hyperglycemia.

Molecular determinants of response to 5-fluorouracil-based chemotherapy in colorectal cancer: The undisputable role of micro-ribonucleic acids.

5-flurouracil (5-FU)-based chemotherapy is the main pharmacological therapy for advanced colorectal cancer (CRC). Despite significant progress in the treatment of CRC during the last decades, 5-FU drug resistance remains the most important cause of failure in CRC therapy. Resistance to 5-FU is a complex and multistep process. Different mechanisms including microsatellite instability, increased expression level of key enzyme thymidylate synthase and its polymorphism, increased level of 5-FU-activating enzymes and mutation of TP53 are proposed as the main determinants of resistance to 5-FU in CRC cells. Recently, micro-ribonucleic acids (miRNA) and their alterations were found to have a crucial role in 5-FU resistance. In this regard, the miRNA-mediated mechanisms of 5-FU drug resistance reside among the new fields of pharmacogenetics of CRC drug response that has not been completely discovered. Identification of the biological markers that are related to response to 5-FU-based chemotherapy is an emerging field of precision medicine. This approach will have an important role in defining those patients who are most likely to benefit from 5-FU-based chemotherapy in the future. Thereby, the identification of 5-FU drug resistance mechanisms is an essential step to predict and eventually overcome resistance. In the present comprehensive review, we will summarize the latest knowledge regarding the molecular determinants of response to 5-FU-based chemotherapy in CRC by emphasizing the role of miRNAs.

Biocompatibility, Cytotoxicity, Antimicrobial and Epigenetic Effects of Novel Chitosan-Based Quercetin Nanohydrogel in Human Cancer Cells.

BACKGROUND: Previous studies have reported that quercetin (Q) has a potential antibacterial and anticancer activity. However, its application is limited by many important factors including high hydrophobicity and low absorption. METHODOLOGY: In the current study, we synthesized and characterized (Patent) a novel chitosan-based quercetin nanohydrogel (ChiNH/Q). Encapsulation efficiency was confirmed by UV/VIS spectrophotometer. Physicochemical characterization of ChiNH/Q was assessed by PDI, DLS, SEM, FTIR, and XRD. The toxicity of the ChiNH/Q against five strains of the pathogen and HepG2 cells was examined. Moreover, the quantification of ChiNH/Q on genomic global DNA methylation and expression of DNMTs (DNMT1/3A/3B) in HepG2 cancer cells were evaluated by ELISA and real-time PCR, respectively. RESULTS: Under the SEM-based images, the hydrodynamic size of the ChiNH/Q was 743.6 nm. The changes in the PDI were 0.507, and zeta potential was obtained as 12.1 mV for ChiNH/Q. The FTIR peak of ChiNH/Q showed the peak at 627 cm-1 corresponded to tensile vibrational of NH2-groups related to Q, and it is the indication of Q loading in the formulation. Moreover, XRD data have detected the encapsulation of ChiNH/Q. The ChiNH/Q showed a potent antimicrobial inhibitory effect and exerted cytotoxic effects against HepG2 cancer cells with IC50 values of 100 µg/mL. Moreover, our data have shown that ChiNH/Q effectively reduced (65%) the average expression level of all the three DNMTs (p<0.05) and significantly increased (1.01%) the 5-methylated cytosine (5-mC) levels in HepG2 cells. CONCLUSION: Our results showed for the first time the bioavailability and potentiality of ChiNH/Q as a potent antimicrobial and anticancer agent against cancer cells. Our result provided evidence that ChiNH/Q could effectively reduce cellular DNMT expression levels and increase genomic global DNA methylation in HepG2 cancer cells. Our results suggest a potential clinical application of nanoparticles as antimicrobial and anticancer agents in combination cancer therapy.

Nicotine attenuates global genomic DNA methylation by influencing DNMTs gene expression in human endometrial stromal cells.

BACKGROUND: There is increasing evidence indicating an incidence of infertility and also the risk of endometrial cancers among smokers. However, the mechanism underlying nicotine adverse effect on female reproduction remains unclear. Growing evidence has suggested that environmental exposures such as nicotine could modulate the epigenome. No study has yet been published to evaluate the direct effect of nicotine on the epigenome profiling of human endometrial stromal cells (HESC). Herein, we decided to examine the direct effects of nicotine on global genomic DNA methylation status and DNA methyl- transferases (DNMTs) gene expression in HESC. HESC were treated with different doses of nicotine (0 or control, 10- 11, 10- 8 and 10- 6) M for 24 h and their genomic global DNA methylation and gene expression of DNMTs (DNMT1, DNMT3A, and DNMT3B) were investigated using ELISA and real-time PCR, respectively. RESULTS: Nicotine treatments reduced the average level of DNMTs gene expression by 90, 79, and 73.4% in 10- 11, 10- 8 and 10- 6 M of nicotine treated cells as compared to control cells, respectively (p < 0.05). Also, 10- 8 and 10- 6 M of nicotine concentrations effectively reduced the amounts of 5-methylated cytosine (5-mC) by 1.09 and 1.87% compared to control cells, respectively (p < 0.05). The 5-mC percentages were positively correlated with the relative cellular DNMTs expression in HESC as verified by the Pearson correlation test. CONCLUSION: An interesting possibility raised by the current study is that the reduced genomic global DNA methylation level in HESC may be partly due to the suppression of DNMTs gene expression caused by nicotine in these cells.

Polyunsaturated fatty acids and DNA methylation in colorectal cancer.

Colorectal cancer (CRC) has been designated a major global problem, especially due to its high prevalence in developed countries. CRC mostly occurs sporadically (75%-80%), and only 20%-25% of patients have a family history. Several processes are involved in the development of CRC such as a combination of genetic and epigenetic alterations. Epigenetic changes, including DNA methylation play a vital role in the progression of CRC. Complex interactions between susceptibility genes and environmental factors, such as a diet and sedentary lifestyle, lead to the development of CRC. Clinical and experimental studies have confirmed the beneficial effects of dietary polyunsaturated fatty acids (PUFAs) in preventing CRC. From a mechanistic viewpoint, it has been suggested that PUFAs are pleiotropic agents that alter chromatin remodeling, membrane structure and downstream cell signaling. Moreover, PUFAs can alter the epigenome via modulation of DNA methylation. In this review, we summarize recent investigations linking PUFAs and DNA methylation-associated CRC risk.

Effects of Dietary Polyunsaturated Fatty Acids on DNA Methylation and the Expression of DNMT3b and PPARα Genes in Rats.

BACKGROUND: Previous studies have suggested a protective role for Polyunsaturated Fatty Acids (PUFA) against cancer, cardiovascular, and other diseases. To provide new insights into the in vivo effects of PUFA on gene expression, the effects of dietary PUFA on DNMT3b and PPARα gene expression and global DNA methylation were investigated in selected rat tissues. METHODS: Thirty sprague-dawley rats were allotted into 3 dietary groups of ten animals each, received experimental diets containing PUFAs every day by gavages for 12 weeks as follows: control group fed a normal diet and water; n-3 PUFAs group received 300 mg/kg/day n-3 PUFAs supplementation; mixed-PUFAs group received 300 mg/kg/day of a mixture of n-3, -6, -9 PUFAs supplementations. The expressions of DNMT3b and PPARα genes were quantitated using real-time RT-PCR. The genome-wide 5-methylcytosine contents in rat tissues were determined by ELISA method. RESULTS: The average expression of the DNMT3b mRNA was 50% lower in the colon and liver of rats fed the n-3- or mixed-PUFAs supplemented diet than control group (p=0.00). However, PPARα expression was significantly upregulated both in the colon and liver of PUFAs-supplemented rats (p<0.001). No significant difference was observed in the blood, colon, and liver DNA methylation levels between PUFAs-supplemented and control animals. CONCLUSION: The results indicate that dietary PUFAs could modulate the expressions of PPARα and DNMT3b genes in various rat tissues. The findings of this study provide additional insights into the in vivo mechanism of PUFA-mediated regulation of gene expression and could provide an opportunity to develop personalized diets for related disease control.

The effects of dietary polyunsaturated fatty acids on miR-126 promoter DNA methylation status and VEGF protein expression in the colorectal cancer cells.

BACKGROUND: There is increasing evidence indicating an aberrant expression of miRNAs in colorectal cancer (CRC) development. Growing evidence has suggested that polyunsaturated fatty acids (PUFAs) could modulate the remodeling of the epigenome. No study has yet been published to examine the direct effect of PUFA on the promoter methylation of miRNAs. This study aimed to examine the potential clinical application of PUFA on the promoter DNA methylation of miR-126 and its angiogenic target molecule (VEGF) in the CRC cells. METHODS: We investigated the direct effect of 100 µM EPA, DHA, and LA for 24 h on promoter methylation status of miR-126 in a panel of five CRC cell lines (HCT116, HT29/219, Caco2, SW742, and LS180) by methylation-specific PCR (MSP). We also quantified the miR-126 and VEGF transcript expression levels in five CRC cell lines affected by PUFA by real-time PCR. Moreover, we analyzed the protein expression level of VEGF, as a target of miR-126, by western blotting assay. RESULTS: MSP analysis showed extensive DNA methylation of the miR-126 promoter in all five CRC cell lines, and among all three PUFAs, only DHA completely demethylated the promoter of miR-126 in HCT116 and Caco2 cell lines. We found that only DHA significantly induces the expression level of miR-126 in HCT116 and Caco2 cell lines, respectively, by 20.1-fold and 1.68-fold (p < 0.05). Our finding indicates that the downregulation of VEGF protein level is also effectively observed only in DHA-treated HCT116 and Caco2 cells compared to control cells (p < 0.05). CONCLUSIONS: Our results provide evidence that n-3 PUFAs are able to modulate cellular miR-126 DNA methylation and inhibit VEGF expression level in a cell-type specific manner in colorectal cancer cells. DHA always showed higher efficacy than EPA and LA in our experiment. Overall, our results suggest a potential clinical application of n-3 PUFAs as anti-angiogenic agents in CRC therapy.

Oral Contraceptive Use May Modulate Global Genomic DNA Methylation and Promoter Methylation of APC1 and ESR1

Background: There are challenging reports in the public health sphere regarding associations between oral contraceptive (OC) use and cancer risk. Methods: To evaluate possible effects of OCs on cancer susceptibility, we quantified of global 5-methyl cytosine (5-mC) levels and assessed methylation patterns of CpG islands of two key tumor suppressor genes, APC1 and ESR1, in serum of users by enzyme-linked immunosorbent assay and methylation specific PCR methods, respectively. Results: Our results indicated that OCs significantly decrease the level of global DNA methylation in users relative to control non-users. However, our data revealed no significant differences between CpG island methylation patterns for ESR1 and APC1 in healthy control and OC-treated women. However, we did find a trend for hypermethylation of both tumor suppressor genes in OC users. Conclusion: Our data suggest that the level of 5-mC but not individual CpG island patterns is significantly influenced by OCs in our cross-section of adult users.

Effect of eicosapentaenoic acid on the expression of ABCG1 gene in the human monocyte THP-1 cells.

Cardiovascular disease (CVD) is the leading cause of death and disability in developed countries. Atherosclerosis is the major cause of CVD, accounting for about half of the attributed deaths. Cholesterol homeostasis is one of the most important factors in atherosclerosis. ATP-Binding cassette transporters cholesterol. Omega (ω) 3 fatty acids are important ligands for regulation of ABC transporters such as ABCG1. Concern has been raised that the low absolute intakes of EPA and high ratios of ω-6 polyunsaturated fatty acids (ω-6 PUFA) to EPA may predispose some individuals to CVD. Eicosapentaenoic acid (EPA) is the most abundant ω3 fatty acid in the diet. The objective of this study was to evaluate the effect of different concentrations of EPA on the expression of ABCG1 gene in the human monocyte THP-1 cells. In this study, THP-1 cells were cultured in RPMI 1640 medium, THP-1 monocytes were then differentiated to macrophages with PMA (phorbol myristic acid) and stimulated with 50, 75 and 100 µM of EPA for 24 h at 37°C. We examined the effects of EPA treatment on the expression of ABCG1 gene using Quantitative Real time RT-PCR (qRT-PCR). Our results, indicate that ABCG1 mRNA expression was significantly reduced by 50, 75 and 100 µM EPA fatty acid treatments as compared to the control cells (р = 0.009, р < 0.001 and р = 0.002, respectively). These results suggest that polyunsaturated fatty acids (PUFAs) such as EPA have an effect on the cholesterol homeostasis in macrophages, and they can change the expression of ABCG1 gene. It seems that EPA has different effects on gene expression and lipid metabolism.

Significance of albumin and C-reactive protein variations in 300 end stage renal disease patients in Tehran University of Medical Sciences Hospitals during year 2010.

Protein- energy malnutrition, wasting and inflammation are frequent complication among patients with end-stage renal disease (ESRD). Malnutrition is associated with cardiac co-morbidity, inflammation and poor survival in ESRD patients. Serum albumin is a well-known marker of nutrition in ESRD patients. Serum albumin is still the most commonly used nutritional marker in ESRD patients. C-reactive protein (CRP), the major acute phase response (APR) protein is elevated in these patients. High CRP levels are linked to the degree of atherosclerosis in coronary, peripheral, and extracranial brain arteries. The aim of the present study was to investigate nutritional factor (albumin) and CRP levels in ESRD patients. In this cross- sectional study a total of 300 patients who had ESRD and had been on hemodialysis treatment for at least 6 months were selected. The laboratory tests consisted of measurement of CRP and albumin using high sensitive ELISA kits. The study patients included 157 males (52.3%) and 143 females (47.7%) with average age of 41.5 ± 14.3 years. Mean CRP level was 7.96 mg/ dl (±1.52), mean serum albumin was 4.07 g/dl (±0.19).Of 300 patients, 21 died (7%). These were patients with serum albumin <4 g/dl and CRP>9.5 mg/dl. This study showed that low albumin and high CRP levels are the main predictors for death. There was a significant difference between CRP and albumin levels in ESRD patients (P<0.0001). Measuring CRP as a marker of inflammation can be helpful in managing these patients.