Longitudinal Follow-up and Outcomes Among a Population With Chronic Kidney Disease in a Large Managed Care Organization

Keith, Douglas S.; Nichols, Gregory A.; Gullion, Christina M.; Brown, Jonathan B.; Smith, David H.

doi:10.1001/archinte.164.6.659

Cited by 1,475 publications

(992 citation statements)

References 12 publications

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“…(28) Mice were maintained in a virus-and parasite-free barrier facility and exposed to a 12-hour light/dark cycle. WT animals were maintained on standard rodent chow diet (PicoLab Rodent Diet 20, #5053; LabDiet, St. Louis, MO, USA) containing 0.63% phosphate, 0.81% calcium, with 2.2 IU/g Vitamin D 3 . To promote the development of hyperphosphatemia, jck mice were maintained on a casein-based diet containing 0.4% calcium and 1.0% phosphate (Diet #D08112306; Research Diets, Inc., New Brunswick, NJ, USA) from 4 weeks of age.…”

Section: Micementioning

confidence: 99%

“…(1,2) Patients continue to die from comorbidities associated with renal dysfunction and the risk of dying far exceeds the risk of entering dialysis. (3) Vascular calcification and left ventricular hypertrophy (LVH), two pathological findings associated with cardiovascular disease and sudden cardiac death, are detected in early CKD and continue to increase in severity as renal failure advances. (4) Evidence suggests that vascular disease is at least partially related to poor bone health.…”

Section: Introductionmentioning

confidence: 99%

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Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Sabbagh

Graciolli

O’Brien

et al. 2012

Journal of Bone and Mineral Research

241

224

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Chronic kidney disease–mineral bone disorder (CKD‐MBD) is defined by abnormalities in mineral and hormone metabolism, bone histomorphometric changes, and/or the presence of soft‐tissue calcification. Emerging evidence suggests that features of CKD‐MBD may occur early in disease progression and are associated with changes in osteocyte function. To identify early changes in bone, we utilized the jck mouse, a genetic model of polycystic kidney disease that exhibits progressive renal disease. At 6 weeks of age, jck mice have normal renal function and no evidence of bone disease but exhibit continual decline in renal function and death by 20 weeks of age, when approximately 40% to 60% of them have vascular calcification. Temporal changes in serum parameters were identified in jck relative to wild‐type mice from 6 through 18 weeks of age and were subsequently shown to largely mirror serum changes commonly associated with clinical CKD‐MBD. Bone histomorphometry revealed progressive changes associated with increased osteoclast activity and elevated bone formation relative to wild‐type mice. To capture the early molecular and cellular events in the progression of CKD‐MBD we examined cell‐specific pathways associated with bone remodeling at the protein and/or gene expression level. Importantly, a steady increase in the number of cells expressing phosphor‐Ser33/37‐β‐catenin was observed both in mouse and human bones. Overall repression of Wnt/β‐catenin signaling within osteocytes occurred in conjunction with increased expression of Wnt antagonists (SOST and sFRP4) and genes associated with osteoclast activity, including receptor activator of NF‐κB ligand (RANKL). The resulting increase in the RANKL/osteoprotegerin (OPG) ratio correlated with increased osteoclast activity. In late‐stage disease, an apparent repression of genes associated with osteoblast function was observed. These data confirm that jck mice develop progressive biochemical changes in CKD‐MBD and suggest that repression of the Wnt/β‐catenin pathway is involved in the pathogenesis of renal osteodystrophy. © 2012 American Society for Bone and Mineral Research.

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Section: Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Sabbagh

Graciolli

O’Brien

et al. 2012

Journal of Bone and Mineral Research

241

224

View full text Add to dashboard Cite

show abstract

“…Approximately 50% of patients with CKD will die of cardiovascular complications 2. Indeed, patients with CKD are more likely to die of CVD than they are to reach end‐stage renal disease 3, 4. The increased risk of CVD in this patient population is only partially explained by traditional (Framingham)5, 6 risk factors, and “nontraditional” factors likely influence the risk of CVD 7.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Microparticles and Systemic Complement Activation in Patients With Chronic Kidney Disease

Jalal

Renner

Laskowski

et al. 2018

JAHA

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BackgroundEndothelial microparticles are associated with chronic kidney disease (CKD) and complement activation. We hypothesized that the complement pathway is activated in patients with CKD via endothelial microparticles and that complement activation correlates with endothelial dysfunction in CKD.Methods and ResultsWe analyzed complement data of 30 healthy subjects, 30 patients with stage III/IV CKD, and 30 renal transplant recipients with stage III/IV CKD, evaluating the potential correlation of complement fragments with brachial artery flow–mediated dilation, Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and urinary albumin/creatinine ratio. Endothelial microparticles were characterized via proteomic analysis and compared between study groups. Complement fragment Ba was significantly increased in CKD and post–kidney transplant CKD. Plasma Ba levels correlated significantly with lower brachial artery flow–mediated dilation, lower Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and higher urinary albumin/creatinine ratio. Factor D levels were significantly higher in the plasma microparticles of patients with CKD versus healthy controls. Plasma microparticles isolated from patients with CKD and containing factor D activated the alternative pathway in vitro.ConclusionThe alternative complement pathway is activated in CKD and correlates with endothelial dysfunction and markers of CKD. Future studies are needed to evaluate whether endothelial microparticles with increased factor D play a pathologic role in CKD‐associated vascular disease.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02230202.

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“…Early HD has failed to improve survival, 26,27 and many patients may die before reaching the point of inevitable HD. 28 Peritoneal dialysis is a viable option for many 29 that is underutilized in the US. 30 It awards patients more control and possibly better quality of life.…”

Section: Respect For Autonomy: Patients Are Often Provided Neither Inmentioning

confidence: 99%

Dialysis in the Frail Elderly — A Current Ethical Problem, an Impending Ethical Crisis

2013

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Longitudinal Follow-up and Outcomes Among a Population With Chronic Kidney Disease in a Large Managed Care Organization

Abstract: Our data suggest that efforts to reduce mortality in this population should be focused on treatment and prevention of coronary artery disease, congestive heart failure, diabetes mellitus, and anemia.

Cited by 1,475 publications

References 12 publications

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Repression of osteocyte Wnt/β-catenin signaling is an early event in the progression of renal osteodystrophy

Endothelial Microparticles and Systemic Complement Activation in Patients With Chronic Kidney Disease

Dialysis in the Frail Elderly — A Current Ethical Problem, an Impending Ethical Crisis

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