Third, it was later found that, in T cells, the protein kinase general control nonderepressing-2 (GCN2), with a putative binding site for free acyl-tRNAs, acts as a molecular sensor for intracellular tryptophan, participating in the integrated stress response (ISR) pathway, which controls cell growth and differentiation (reviewed in [[2]]). It was further demonstrated that this pathway, in the presence of kynurenines, leads to induction of Foxp3+ Treg SB203580 mw cells [[7]]. Finally, IDO was found to possess signaling activity in dendritic cells (DCs),

which are stably turned into regulatory DCs by its activation, thus presiding over long-term immune homeostasis and immune-related functions not only in pregnancy, but also in infectious, allergic, autoimmune, chronic inflammatory diseases, as well as in transplantation and immune-escaping Torin 1 manufacturer tumoral mechanisms ([[8]] and reviewed in [[5, 9, 10]]). Normally expressed at low basal levels, IDO is rapidly induced by IFN-γ in DCs (Fig. 1) [[11]]. The combined actions of IFN-γ and IDO represent a phylogenetically conserved and coevolved means of restricting infection and, at the same time, preventing eventually harmful, exaggerated inflammatory responses in the host, inflammation being often a dangerous necessity for the host to cope with infectious challenges [[12]]. However, IDO’s long-term regulatory function in pregnancy [[4]]

and in preventing different forms of autoimmunity and/or immunopathology [[13]] cannot be accounted for by IFN-γ alone. Some insight into this issue came from the observation that autocrine or paracrine signaling in DCs through transforming growth factor β (TGF-β) can initiate an alternative Mannose-binding protein-associated serine protease form of IDO-driven immunoregulation in a feedforward loop (reviewed in [[3]]). Much like other metabolic enzymes, IDO is endowed with a second (“moonlighting”)

function, which allows IDO to meet different functional challenges within local tissue microenvironments [[14]]. We have recently provided evidence that IDO in plasma-cytoid DCs (pDCs) can meet apparently disparate environmental needs; in particular, locally produced cytokines can turn IDO’s functional mode from one characterized by an intense but short course of Trp degradation (e.g. in IFN-γ-dominated innate or inflammatory responses) to a condition whereby IDO mediates a TGF-β-driven, self-maintaining form of intracellular signaling activity, which — independently of Trp degradation — contributes to sustaining a stable regulatory phenotype in pDCs, as required by tolerance [[15]]. While IFN-γ may be instrumental in generating Treg cells via IDO’s enzymatic functions, TGF-β sustains a constitutive form of IDO expression at the interface between DCs and regulatory T cells. It is generally thought that each cytokine exerts either immune stimulatory (proinflammatory) or immune inhibitory (antiinflammatory or regulatory) biological activities.

These cysts are frequently associated with vertebral or spinal cord abnormalies and dual malformation with mediastinal or abdominal cysts. Collectively, they are called split notochord syndrome. The authors describe their experience in the treatment of a 57-year-old man having an endodermal cyst mimicking an intramedullary tumor at the level of Th1-2. He was admitted to our institution for evaluation of an intraspinal mass diagnosed by MRI at a local hospital after experiencing temporary numbness and weakness of the lower left extremity. T1-weighted sagittal MRI demonstrated the lesion with signal intensity iso- to slightly hypointense RG7420 chemical structure to

the spinal cord without enhancement after administration of gadolinium. Although T2-weighted sagittal images demonstrated as hyperintense to the spinal cord,

axial images revealed a passage between the mass and subarachnoid space. We could not completely rule out the presence of an intramedullary tumor and undertook a laminectomy with a posterior approach. Histopathological analysis revealed an endodermal cyst and the authors found syringomyelia, which was clearly separated from the cyst in the preoperative sagittal MRI and intraoperative ultrasonography study. To the selleck chemical best of our knowledge, this is the first report in the English literature of a thoracic endodermal cyst requiring differential diagnosis from a spinal cord tumor. “
“Cribriform neuroepithelial tumor (CRINET) is a very rare and recently described entity of INI1-deficient intraventricular neuroepithelial tumor of primitive non-rhabdoid cells with distinct cribriform

formation and has a relatively favorable prognosis. A 14-month-old boy had presented with gait imbalance and was crawling for the last 2 weeks. MRI revealed a large, complex solid and cystic mass with dimensions of 55 × 55 × 50 mm in the vicinity of the third ventricle. Histopathologically, the tumor was composed of relatively small undifferentiated neuroepithelial cells arranged in a cribriform pattern and intervening solid sheets with true rosettes. Immunohistochemically, the tumor cells showed complete loss of nuclear INI1 expression and distinct expression of epithelial membrane antigen Resveratrol (EMA) along the luminal borders of the tubules or glands. The typical rhabdoid feature of tumor cells was absent. Ultrastructurally, the tumor cells were neuroepithelial cells that contained short linear rough endoplasmic reticula and distinct intercellular junctions. Here, we describe a new case of CRINET and also discuss its clinicopathological, immunohistochemical, and ultrastructural features. “
“We aimed to characterize angiogenesis and proliferation and their correlation with clinical characteristics in a large brain metastasis (BM) series. Ki67 proliferation index, microvascular density (MVD) and hypoxia-inducible factor 1 alpha (HIF-1 alpha) index were determined by immunohistochemistry in BM and primary tumor specimens.

HEK-293-TLR4/MD2-CD14 (293-TLR4) cells (Invivogen) were cultured in DMEM supplemented with 10% FBS (Invitrogen), 1% penicillin/streptomycin (PAA) 10mg/ml of Blasticidin (Invivogen) and 50 mg/ml of HygroGoldTM (Invivogen). Human monocytes were obtained from the blood

of healthy donors by elutriation and differentiated in MDDCs as described [[39]]. TBK1/IKK-ε double KO cells were kindly provided by Dr. Toby Lawrence and cultured as described [[40]]. LPS was obtained from Alexis Biochemicals and PI3K inhibitor (LY294002) from Calbiochem. The following antibodies were used: Anti-HA (Roche), Anti-Flag (Sigma), Anti-FOXO3 and anti-p-FOXO3 (Thr32) (Millipore), anti-IKK-ε (Imegenex), anti-pan Ser (Sigma), Y 27632 anti-pan Thr (Cell Signaling), anti-Lamin A/C (BD), and anti-Tubulin and anti-β-actin (Santa Cruz biotechnology). HA-FOXO3 WT and HA-FOXO3-TM were amplified from plasmids provided by Dr. Eric Lam (Imperial College London, UK) using Phusion taq polymerase (Finnzymes Oy, Finland) and cloned in pENTR vector (Invitrogen). HA-FOXO3 construct was recombined into pAD/PL DEST vector (Invitrogen) for adenovirus production and subsequent delivery Anti-infection Compound Library nmr into human DCs. HA-FOXO3-S644A

and QM were generated by fusion PCR using external primers as above and internal primers containing the S644A mutation and cloned in pENTR vector. IKK-ε and IKK-ε-KA were subcloned from constructs provided by Dr. Tom Maniatis (Harvard Medical School, Boston, USA) PtdIns(3,4)P2 in the modified pENTR vector (pBent) [[25]]. IKK-β and IKK-β-KA were generated following the same procedure. Expression constructs encoding full-length human IRF3, IRF7, and NF-κB subunits tagged with FLAG in pBent vector were previously described [[25]]. For the GST-FOXO3 purification, human FOXO3 was amplified by PCR and sub-cloned in pGEX-4T1 vector (Promega) for bacterial production. NF-κB-luc was obtained from Promega, p27-luc and

ISRE-luc were a generous gift of Dr. B. M. Burgering (University Medical Center Utrecht, Netherlands) and Dr. Lynn Williams (Imperial College London, UK), respectively. IFN-β-luc and IFN-λ1-luc were previously described [[25]]. Luciferase assays were performed in triplicate and repeated at least two times using Dual-Glo Luciferase Assay System (Promega). Luciferase activity was normalized by intensity of Renilla luciferase produced from co-transfected pRL-TK construct (Promega). For WB, total protein extracts were prepared as described [[41]] and resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). For co-IP experiments, precleared total protein extracts were incubated overnight with anti-FOXO3 antibody for endogenous protein precipitation, or anti-HA coupled with sepharose beads (Roche) for HA-tagged proteins. Protein complexes were precipitated with protein G beads (GE Healthcare) and run on SDS-PAGE.

Such an effect is also seen in patients with chronic lymphocytic leukaemia who receive RTX treatment.13 Here, a rapid clearance of malignant B cells from the bloodstream is observed, check details but a small fraction of uncleared cells and cells that are later released from lymphoid tissues seems to obtain a reduction in CD20 expression because of shaving, which occurs,

for example, by liver Kupffer cells when effector mechanisms such as CDC and ADCC have been saturated. As a result, a subsequent new bolus of RTX will have little effect on the remaining malignant B cells and so the shaving reaction has large clinical implications. Effector function of anti-CD20 antibodies varies

based on division into type I (RTX-like) and type II (tositumomab), where type II antibodies have increased B-cell depleting capacity in vivo.14 Until now, this difference between antibodies has not been explained in relation to affinity, opsonization, induction of phagocytosis, isotype or half life of the antibody, but they are known to have different abilities for redistributing CD20 in the plasma membrane. Hence, testing the effect on monocyte-mediated shaving would be important for a better understanding INCB024360 order of anti-CD20 antibody function. Here, we confirm, that in vitro co-culture of monocytes and RTX-labelled B cells results in reduced PJ34 HCl expression of RTX on the surface. We find that this reaction is dependent on the Fc part of RTX but is not the result of simple endocytosis. Instead, active protease activity is involved because EDTA and PMSF were able to partly inhibit the reaction. Also, we tested a series

of alternative type I and type II anti-CD20 antibodies for their ability to induce the shaving reaction and here the murine type I antibody AT80 showed reduced ability to initiate the shaving reaction compared with a series of other type I and type II anti-CD20 antibodies. Our findings demonstrate that a general strategy for developing novel antibodies against haematological malignancies is necessary and has to address the inhibitory functions of the shaving reaction. Peripheral blood mononuclear cells were isolated from buffy coats obtained from healthy donors from the Department of Clinical Immunology, Rigshospitalet using Lymphoprep (Axis-Shield, Oslo, Norway). They were washed in RPMI-1640 containing Glutamax. Monocytes were than separated by positive selection with anti-CD14 conjugated to paramagnetic beads using a commercial kit from Miltenyi Biotech (Bergisch Gladbach, Germany). Similarly, syngeneic B cells were isolated by negative selection with a commercial kit from Miltenyi Biotech.

Furthermore, BMDC treated with rHp-CPI before ovalbumin (OVA) antigen pulsing induced a weaker proliferation response and less interferon-γ production of OVA-specific CD4+ T cells compared with BMDC without rHp-CPI pre-treatment. Adoptive transfer of rHp-CPI-treated and OVA-loaded

BMDC to mice induced significantly lower levels of antigen-specific antibody response than the BMDC loaded with antigen alone. These results demonstrated that the CPI from nematode parasites is able to modulate differentiation and activation stages of BMDC. It also interferes with antigen and MHC-II molecule Selleckchem Gemcitabine processing and Toll-like receptor signalling pathway, resulting in functionally deficient DC that induce a suboptimum immune response. Nematode parasite infections are common in many parts of the world and cause significant health problems in humans.[1] Infections with this group of pathogens often undergo a chronic and asymptomatic course and induce a T helper type 2-dominated immune response.[2, 3] In addition, nematode infections often induce immunosuppression, which is believed to be an important strategy for the https://www.selleckchem.com/products/XL184.html survival of the parasite in the host.[4, 5] The immunosuppression associated with nematode infection is also demonstrated as the suppression of immune responses to unrelated

antigens and immune protection against concurrent infection with other pathogens.[6, 7] Epidemiological studies showed that helminth infections in human populations are also associated with decreased prevalence of autoimmune disorders and allergic diseases (hygiene hypothesis).[8, 9] Although nematode infections are known to elicit T helper type 2-dominant immune responses, which are required for immune protection against the nematode pathogens,[10] many

studies show that these pathogens also induce a regulatory T-cell response and cytokines that mediate the immunosuppression.[11-13] http://www.selleck.co.jp/products/Cisplatin.html In mice infected with the murine nematode parasite, Heligmosomoides polygyrus, we identified a subset of dendritic cells (DC) that are selectively expanded following H. polygyrus infection and induce interleukin-10 (IL-10) production by T cells and FoxP3+ CD4+ T-cell response.[14] Previous studies with H. polygyrus and other nematode species also demonstrated that the crude preparation or excretory–secretory (ES) products from the parasites are able to modulate the phenotypes and functions of immune cells.[15-17] It has been reported that the ES products from H. polygyrus can modulate the antigen presentation function of DC and specifically induce an IL-10-producing T-cell response.[15] However, the immunoregulatory molecule(s) produced by H. polygyrus have not been fully characterized. A number of studies in recent years have shown that cysteine proteases inhibitor (CPI; cystatin) is one of the major immune modulators produced by nematode parasites.

Thus by exclusion, there is some support for the proposal that these massively calcified LGGs are distinct from other paediatric LGGs. In conclusion, our findings suggest that massively calcified LGGs of childhood could represent a distinct entity with characteristic radiological and pathological features and a lack of genetic alterations to align them readily with other paediatric LGGs. Study concept and design: D.W.E. Data

collection and interpretation: K.G., J.H.H., N.D.S., I.Q., K.K., D.W.E. Manuscript writing: K.G., D.W.E. Manuscript editing: K.G., J.H.H., N.D.S., I.Q., K.K., D.W.E. All authors have read the final version of the manuscript. “
“World Health Organization (WHO) grade III meningiomas are subclassified on the basis of their RG7422 cost architectural

pattern into papillary and rhabdoid subtypes. Some meningiomas even combine papillary architecture with rhabdoid cytology. Additionally, they always show malignant histological features, follow an aggressive clinical course and tend to spread through the CSF after frequent local recurrence. We render the first series of rhabdoid papillary meningioma with review of the literature to further elucidate its biological behavior. From six patients (three male, three female), nine specimens of rhabdoid papillary meningioma were obtained between 1994 and 2010. Correlations of histologic parameters, immunohistochemical study, and clinical features were assessed. The Small molecule library clinical trial mean age of patients was 44.7 years at their first operation. The mean postoperative follow-up period was 63.2 months. Five

patients experienced tumor recurrence, and one of them died from the disease after diffuse leptomeningeal dissemination. The mean time to first recurrence was 28 months. Only one patient was free of tumoral recurrence after an 8-year follow-up. Immunohistochemically, all tumors were positive for vimentin and epithelial membrane antigen. MIB-1 labeling indices were higher following tumor recurrence. The present study expands the clinicopathologic horizon of rhabdoid papillary meningioma and suggests that it will behave aggressively based on its histology and concomitant features of atypia or malignancy or high MIB-1 labeling indices. Close follow-up and aggressive treatments of these tumors are warranted. “
“To assess the sensitivity of the FTDC Arachidonate 15-lipoxygenase revised criteria of behavioral variant frontotemporal dementia (bvFTD) in a pathological cohort and to determine their predictive values in a clinical context suggestive of bvFTD. To assess the influence of the age at onset and underlying pathology in the clinico-pathological correlations. Retrospective, blinded review of the clinical and neuropathological data from the Neurological Tissue Bank (NTB) of the Biobank-Hospital Clinic-IDIBAPS, Barcelona (Spain) assessing the fulfillment of the diagnostic criteria on a case-by-case basis.

4 The bladder, prostate, urethra and central nervous system can be etiological organs for LUTS caused by BPH, although it is not clear if hyperplasia of the prostate is a source of

LUTS.5 Prevalence of LUTS complex is 15–60% in men aged over 40 years and prevalence rises markedly with age.5–7 The prevalence of ED is also very high and rises with age; 17–40% of 40-year-old men experience some degree check details of ED, and the rate is as high as 70–84% in 70-year-old men.8,9 In many community-based studies, the prevalence of ED is associated with the presence and severity of LUTS and the severity of BPH-induced LUTS is proportional to the severity of ED. Both BPH and ED have a significant negative impact on health-related quality of life for ageing men.10 It has not yet been confirmed how much the two disorders influence each other and what is considered the main factor in the initiation of both disorders. There has been increasing interest in the nitric oxide (NO)-cGMP pathway as a promising pharmacological target for treating BPH/LUTS. The presence

of nitric oxide synthase (NOS) has been described in detail in the human prostate by biochemical, immunohistochemical and molecular biological methods.11 In the human prostate, endothelial NOS (eNOS) is related to the maintenance of local vascular perfusion, whereas neuronal NOS (nNOS) is mainly involved in the initiation of the relaxation of smooth muscle and in the control of glandular function, including the proliferation of epithelial and subepithelial YAP-TEAD Inhibitor 1 purchase cells.12 Inducible NOS (iNOS) has not been detected in normal prostate tissue, although there is evidence that iNOS is expressed in hyperplastic and malignant prostatic tissues.13 Expression of phosphodiesterase (PDE) isoenzymes in the human prostate were verified by molecular biology and protein chemistry.14 Research next has shown that mRNA transcripts encoding for PDE types 1, 2, 4, 5, 7, 8, 9 and 10 in different anatomic

regions of the human prostate, and demonstrated hydrolytic activities of PDE types 4 and 5 in cytosolic fractions of prostatic tissue.15 Smooth muscle in the corpus cavernosum, prostate and bladder are relaxed by NO.14–16 Phosphodiesterase type 5 inhibitors (PDE5 I), such as mirodenafil, sildenafil, tadalafil, and udenafil increase the concentration of cGMP in smooth muscle by blocking PDE type 5 (PDE5) enzyme, inducing erection of the penis and relaxation of the bladder neck and prostate leading to voiding. Considering the high incidence of ED and BPH in aging men, the capacity to treat both disorders simultaneously with a single agent, such as a PDE5 I, would be very valuable.17 Recently, several PDE5 I have produced statistically significant improvements in various measures of sexual function and urinary symptoms.18,19 Therefore, we evaluated the relationship between BPH/LUTS and ED, and the role of PDE5 I on BPH/LUTS. Recent large-scale epidemiological studies disclosed a powerful association between BPH/LUTS and ED.

Cases included 131 women who had at least one tooth with a

probing depth of 3.5 mm or deeper. Controls included 1019 women without periodontal disease. Adjustment was made for age, region of residence, education, toothbrushing frequency and use of an interdental brush. Compared with the AA genotype of SNP rs731236, the GG genotype had a significantly increased risk of periodontal disease: the adjusted OR was 3.68 (95% confidence Alvelestat order interval: 1.06–12.78). There were no significant relationships between SNPs rs7975232, rs1544410 or rs2228570 and periodontal disease. None of the haplotypes were significantly related to periodontal disease. Compared with subjects with the AA or AG genotype of SNP rs731236 who had never smoked, those with the GG genotype who had ever smoked had a significantly increased risk of periodontal disease; nevertheless, neither multiplicative nor additive interaction was significant. The additive interaction between SNP rs7975232 and

smoking was significant, although the multiplicative interaction was not statistically significant. No multiplicative or additive interactions were observed between the other SNPs and smoking. Our results indicated that VDR SNP rs731236 might be associated with periodontal disease. In addition, we present new evidence for a biological interaction between VDR SNP rs7975232 and smoking that affects periodontal disease. Periodontal disease is a chronic inflammatory condition of the periodontium that is initiated by microbial plaque PF-01367338 ic50 that accumulates in the gingival crevice region and induces an inflammatory response [1, 2]. This inflammatory response of the periodontal tissues to infection is influenced by environmental factors as well as by genetic factors [1]. A key feature of periodontal disease is the loss of alveolar bone. As it is accepted that the immune system Cyclooxygenase (COX) plays an important role

in the pathogenesis of periodontal disease, most genes that are considered to be responsible for the development of periodontal disease are also linked to the immune response [1]. Vitamin D receptor (VDR) is involved in a variety of biological processes, including bone metabolism and the modulation of immune response [3]. Therefore, polymorphisms of VDR gene may have roles in the pathogenesis of periodontal disease. Many previous studies have examined the association between VDR polymorphisms and combinations of these variants and periodontal disease at TaqI, ApaI, BsmI and FokI restriction sites [4-18]. The results have been inconsistent, however, and it remains unclear which VDR gene polymorphisms may influence susceptibility to periodontal disease. Several case–control studies have found a significant association between TaqI polymorphism and periodontal disease [4-12], though other studies have failed to find significant associations of this type [13-16].

RSS is a great way

to keep up to date, and to access information that is not easily accessible by email, and the saves the busy Nephrologist from having to make a conscious decision to go out and find current information. Figure 2 shows an example of RSS feeds appearing in Google Reader. The advent of the Internet in the 1990s, also known as Web 1.0, revolutionized the way doctors were able to access information. Searching by hand through print indexes such as Index Medicus to locate articles in their area of research or clinical practice, taking sometimes days to do a complete search, became a distant memory. Instead they could search online databases such as Medline in less than half the BMN 673 concentration time. While this was good progress, doctors and researchers were essentially approaching the problem in the same way, doing the same things they had done before,

albeit in a much shorter time frame.2 Web 2.0 has changed the way information can be retrieved. MG-132 solubility dmso Web 2.0, with Blogs, RSS Feeds (see boxed text), Auto-Alerts and eTOC makes it possible for the modern doctor to keep up to date with professional news and research without making a conscious decision to seek it out. Instead, by organizing information sources to deliver content directly to a specified location via automated feeding, pertinent information presents itself regularly. With some organization, nephrologists do not need science to seek out clinical updates, clinical updates come to nephrologists. This information management can be personalized to suit an individual’s preference; it can be delivered via email or RSS (see boxed text), depending on what technology the doctor is most comfortable with. Online medical databases are the ideal place to search for the latest research in nephrology. Databases such as Medline provide easy access to the scholarly literature,

and also provide tools to tailor searches to a specific topic. Most of the major databases allow you to search using subject headings, keywords, author or journal names, and can be limited to English language or review articles. If you are interested in research in a particular field or topic area, you can set up an ‘auto-alert’. Auto-alerts are search strategies saved within the database, which are run automatically each time that database is updated. If your search retrieves any new articles, not previously identified by prior searches, you will be sent the citations by either email or RSS (see boxed text). You can customize the amount of information that is sent through, but typically the default format contains the article citation and abstract. The US National Library of Medicine’s PubMed (http://www.ncbi.nlm.nih.

This study aimed to clarify the effect of sodium restriction on prolonging the duration between the time when eGFR is 15 mL/min/1.73 m2 Enzalutamide purchase to hemodialysis (HD) induction (G5 spans). Methods: Seventy-seven type 2 DKD patients (61 men and 16 women, mean age 58.6 ± 11.2 years) were recruited. All patients underwent frequent nutritional therapy and 24-h urine collection. Sodium intake was calculated using the 24-h urine collection. Patients

were divided into the following 2 groups: adequate group (AG: n = 39) defined as patients with sodium intake < 8.0 g/day, and over-intake group (OG: n = 32) defined as sodium intake ≧ 8.0 g/day. We retrospectively evaluated the G5 span between the 2 groups. Results: The www.selleckchem.com/products/sotrastaurin-aeb071.html glycated hemoglobin value was 6.4 ± 1.8% when eGFR was firstly 15 mL/min/1.73 m2. In all patients, the G5 span was 556 ± 372 days, and the sodium intake was 7.9 ± 3.2 g/day. The G5 was significantly

longer in AG than in OG (660 ± 403 days vs. 487 ± 314 days, p < 0.05). Conclusion: Sodium restriction ameliorates the progression of renal dysfunction in type 2 advanced DKD patients (CKD stage G5). RAVI RAMA1,2, RAVI RAJALAKSHMI1,2, KURIEN ABRAHAM1,2, NAIR SANJEEV1,2, YUVARAJ ANAND1,2, ABRAHAM GEORGI1,2, RAVICHANDRAN SANGEETHA2, PANDIAN DEVI1,2 1Madras Medical Mission; 2Tamilnad Kidney Research Foundation Introduction: The current scenario of global burden of diseases comprise of a triple burden of diseases of which non communicable diseases form a huge proportion. Among the non communicable diseases, chronic kidney disease has emerged a major threat in terms of complications, accessibility and availability of treatment, especially in developing countries like India. There are a few studies done on prevalence of kidney disease and our programme targets early detection of kidney disease in the form of awareness and screening programmes directed at different segments of the society. Methods: The awareness programme

comprises of powerpoint presentation on basics of kidney functions and symptoms for early detection of kidney disease. The screening programme consists of brief history of medical illness, followed by measurement Fluorometholone Acetate of body mass index and blood pressure and urine examination to look for proteinuria. Results: We have so far conducted a total of 447 programmes of which 93.5% of the programmes were targeted to urban areas and we covered 79.2% of students through our awareness programmes. Our programme identified prehypertension in 38.7% of the population screened and 24.% were identified with proteinuria. Individuals who were above 45 years of age, and those with proteinuria were found to be significantly associated with abnormal serum creatinine and eGFR.