Chronic Renal Insufficiency Cohort (CRIC) GWAS
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ABSTRACT:
PROVIDER: PRJNA171879 | ENA |
REPOSITORIES: ENA
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Project description:<p>The Chronic Renal Insufficiency Cohort (CRIC study) was established in 2001 by the National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK) to improve the understanding of the relationship between chronic kidney disease and cardiovascular disease. The goals of the CRIC Study are to examine risk factors for progression of chronic kidney disease and cardiovascular disease among patients with chronic kidney disease and to develop predictive models to identify high-risk subgroups, informing future treatment trials and increasing application of available preventive therapies.</p>
| phs000524 | dbGaP
Project description:<p>The Chronic Renal Insufficiency Cohort (CRIC study) was established in 2001 by the National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK) to improve the understanding of the relationship between chronic kidney disease and cardiovascular disease. The goals of the CRIC Study are to examine risk factors for progression of chronic kidney disease and cardiovascular disease among patients with chronic kidney disease and to develop predictive models to identify high-risk subgroups, informing future treatment trials and increasing application of available preventive therapies.</p>
| phs000524.v1.p1 | EGA
Project description:Biomarkers for early detection of chronic kidney disease are needed, as millions of patients suffer from chronic diseases predisposing them to kidney failure. Protein microarrays may hold utility in the discovery of auto-antibodies in other conditions not commonly considered auto-immune diseases. We hypothesized that proteins are released as a consequence of damage at a cellular level during end-organ damage from renal injury, not otherwise recognized as self-antigens, and an adaptive humoral immune response to these proteins might be detected in the blood, as a non-invasive tracker of this injury. The resultant antibodies (Ab) detected in the blood would serve as effective biomarkers for occult renal injury, enabling earlier clinical detection of chronic kidney disease than currently possible, due to the redundancy of the serum creatinine as a biomarker for early kidney injury. To screen for novel autoantibodies in chronic kidney disease, 24 protein microarrays were used to compare serum Ab from patients with chronic kidney disease against matched controls. From a panel of 38 antigens with increased Ab binding, 4 were validated in 71 individuals, with (n=50) and without (n=21) renal insufficiency. Significant elevations in the titer of novel auto-Ab were noted against Angiotensinogen (AGT) and PRKRIP1 in renal insufficiency. Current validation is underway to evaluate if these auto-Ab can provide means to follow the evolution of chronic kidney disease in patients with early stages of renal insufficiency, and if these rising titers of these auto-Ab correlate with the rate of progression of chronic kidney disease. Serum antibodies were profiled for 7 healthy individuals and 17 patients with chronic kidney disease, using the Invitrogen ProtoArray® Human Protein Microarray v3.0 platform (Invitrogen, Carlsbad, CA). This platform contains 5,056 non-redundant human proteins expressed in a baculovirus system, purified from insect cells and printed in duplicate onto a nitrocellulose-coated glass slide. Each protein is spotted twice on each array, to measure the quality of the signal intensity. Details for experiment processing and analysis follow the previous publication from our group (Li et al Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4148-53). Prospector software was used to retrieve the expression based on immune response profiling of the .gal files.
2010-08-12 | E-GEOD-23609 | biostudies-arrayexpress
Project description:Biomarkers for early detection of chronic kidney disease are needed, as millions of patients suffer from chronic diseases predisposing them to kidney failure. Protein microarrays may hold utility in the discovery of auto-antibodies in other conditions not commonly considered auto-immune diseases. We hypothesized that proteins are released as a consequence of damage at a cellular level during end-organ damage from renal injury, not otherwise recognized as self-antigens, and an adaptive humoral immune response to these proteins might be detected in the blood, as a non-invasive tracker of this injury. The resultant antibodies (Ab) detected in the blood would serve as effective biomarkers for occult renal injury, enabling earlier clinical detection of chronic kidney disease than currently possible, due to the redundancy of the serum creatinine as a biomarker for early kidney injury. To screen for novel autoantibodies in chronic kidney disease, 24 protein microarrays were used to compare serum Ab from patients with chronic kidney disease against matched controls. From a panel of 38 antigens with increased Ab binding, 4 were validated in 71 individuals, with (n=50) and without (n=21) renal insufficiency. Significant elevations in the titer of novel auto-Ab were noted against Angiotensinogen (AGT) and PRKRIP1 in renal insufficiency. Current validation is underway to evaluate if these auto-Ab can provide means to follow the evolution of chronic kidney disease in patients with early stages of renal insufficiency, and if these rising titers of these auto-Ab correlate with the rate of progression of chronic kidney disease.
2010-08-13 | GSE23609 | GEO
Project description:MicroRNAs (miRNAs) contribute to chronic kidney disease progression via negatively regulating mRNA abundance. However, their association with clinical outcome remains poorly understood. We performed large-scale miRNA and mRNA expression profiling on cryo-cut renal biopsy sections from a discovery (n=43) and a validation (n=29) cohort. In the discovery cohort (GEO Series accession number GSE45980), miRNAs differentiating stable and progressive cases were determined, and putative target mRNAs showing inversely correlated expression profiles were identified. We found a downregulation of 7 miRNAs in the progressive phenotype, and an upregulation of 29 target mRNAs that are involved in inflammatory response, cell-cell-interaction, apoptosis, and intracellular signaling. Reduced expression of miR-206 in progressive disease correlated with the upregulation of the target mRNAs CCL19, CXCL1, IFNAR2, NCK2, PTK2B, PTPRC, RASGRP1, and TNFRSF25, all participating in inflammatory pathways. Progressive cases also showed a lower expression of miR-532-3p and an increased expression of cognate target transcripts MAP3K14, TNFRSF10B/TRAIL-R2, TRADD, and TRAF2, all being involved in apoptosis pathways. In the independent validation cohort (this set of arrays), we confirmed the decreased expression of miR-206 and miR-532-3p, and the inverse correlation of these miRNAs with the expression of 9 of the 12 target genes. The levels of the identified miRNAs and the target mRNAs correlated to histological damage indices. These results suggest the involvement of specific miRNAs and mRNAs in biological pathways associated with the progression of chronic kidney disease.
2015-12-31 | GSE60860 | GEO
Project description:MicroRNAs (miRNAs) significantly contribute to chronic kidney disease (CKD) progression via regulating mRNA expression and abundance. However, their association with clinical outcome remains poorly understood. We performed large scale miRNA and mRNA expression profiling on cryo-cut renal biopsy sections from n=43 subjects. miRNAs differentiating stable and progressive cases were determined, and putative target mRNAs showing inversely correlated expression profiles were identified and further characterized. We found a downregulation of 7 miRNAs in the progressive phenotype, and an upregulation of 29 target mRNAs which are involved in inflammatory response, cell-cell-interaction, apoptosis, and intracellular signaling. Particularly a diminished expression of miR-206 in progressive disease correlated significantly with the upregulation of the target mRNAs CCL19, CXCL1, IFNAR2, NCK2, PTK2B, PTPRC, RASGRP1, and TNFRSF25, all participating in inflammatory pathways. Progressive cases also showed a decreased expression of miR-532-3p, and an increased expression of target transcripts MAP3K14, TNFRSF10B/TRAIL-R2, TRADD, and TRAF2, all being involved in apoptosis pathways. miR-206, miR-532-3p and all 12 mRNA targets correlated with the degree of histological damage. The identified renal miRNA- and mRNA-profiles, and biological pathways may represent regulatory mechanisms, which are commonly present in various kinds of progressive chronic kidney disease.
2015-12-31 | GSE45980 | GEO
Project description:Central pulse pressure (PP) can be noninvasively derived using the radial artery tonometric methods. Knowledge of central pressure profiles has predicted cardiovascular morbidity and mortality in several populations of patients, particularly those with known coronary artery disease and those receiving dialysis. Few data exist characterizing central pressure profiles in patients with mild-moderate chronic kidney disease who are not on dialysis. We measured central PP cross-sectionally in 2531 participants in the Chronic Renal Insufficiency Cohort Study to determine correlates of the magnitude of central PP in the setting of chronic kidney disease. Tertiles of central PP were <36 mm Hg, 36 to 51 mm Hg, and >51 mm Hg with an overall mean (+/-SD) of 46+/-19 mm Hg. Multivariable regression identified the following independent correlates of central PP: age, sex, diabetes mellitus, heart rate (negatively correlated), glycosylated hemoglobin, hemoglobin, glucose, and parathyroid hormone parathyroid hormone concentrations. Additional adjustment for brachial mean arterial pressure and brachial PP showed associations for age, sex, diabetes mellitus, weight, and heart rate. Discrete intervals of brachial PP stratification showed substantial overlap within the associated central PP values. The large size of this unique chronic kidney disease cohort provides an ideal situation to study the role of brachial and central pressure measurements in kidney disease progression and cardiovascular disease incidence.
| S-EPMC2941985 | biostudies-literature