Chronic Kidney Disease: A Clinical Model of Premature Aging

Stenvinkel, Peter; Larsson, Tobias E.

doi:10.1053/j.ajkd.2012.11.051

Cited by 257 publications

(228 citation statements)

References 165 publications

(153 reference statements)

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“…This hypothesis was initially proposed as the precipitation-calcification hypothesis, and is currently being reconsidered in the field of renal failure progression and premature aging. [27][28][29] T 50 might be of clinical use for the early detection of patients at high mortality risk. Furthermore, serum T 50 may be of use as a guide for the treatment of renal patients.…”

Section: Discussionmentioning

confidence: 99%

Calcification Propensity and Survival among Renal Transplant Recipients

Keyzer

Borst

Berg

et al. 2016

Journal of the American Society of Nephrology

121

108

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Calciprotein particle maturation time (T 50 ) in serum is a novel measure of individual blood calcification propensity. To determine the clinical relevance of T 50 in renal transplantation, baseline serum T 50 was measured in a longitudinal cohort of 699 stable renal transplant recipients and the associations of T 50 with mortality and graft failure were analyzed over a median follow-up of 3.1 years. Predictive value of T 50 was assessed for patient survival with reference to traditional (Framingham) risk factors and the calcium-phosphate product. Serum magnesium, bicarbonate, albumin, and phosphate levels were the main determinants of T 50 , which was independent of renal function and dialysis vintage before transplant. During follow-up, 81 (12%) patients died, of which 38 (47%) died from cardiovascular causes. Furthermore, 45 (6%) patients developed graft failure. In fully adjusted models, lower T 50 values were independently associated with increased all-cause mortality (hazard ratio, 1.43; 95% confidence interval, 1.11 to 1.85; P=0.006 per SD decrease) and increased cardiovascular mortality (hazard ratio, 1.55; 95% confidence interval, 1.04 to 2.29; P=0.03 per SD decrease). In addition to age, sex, and eGFR, T 50 improved prognostication for all-cause mortality, whereas traditional risk factors or calcium-phosphate product did not. Lower T 50 was also associated with increased graft failure risk. The associations of T 50 with mortality and graft failure were confirmed in an independent replication cohort. In conclusion, reduced serum T 50 was associated with increased risk of all-cause mortality, cardiovascular mortality, and graft failure and, of all tested parameters, displayed the strongest association with all-cause mortality in these transplant recipients.

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Section: Discussionmentioning

confidence: 99%

Calcification Propensity and Survival among Renal Transplant Recipients

Keyzer

Borst

Berg

et al. 2016

Journal of the American Society of Nephrology

121

108

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“…Sulforaphane treatment also led to a significant reduction of DNA damage in the comet assay and DSBs (c-H2AX-foci) compared to aldosterone-treated rats. DNA damage has long been recognized as an important factor in aging and cellular senescence (53), but lately, it has also been considered a contributor to disease progression due to the generation of dysfunctional cells (25). Furthermore, the DNA damage response was recently connected to progressive loss-of-kidney function (31).…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

Queisser¹,

Oteiza²,

Hey³

et al. 2013

Free Radical Biology and Medicine

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“…It can therefore be debated whether a diagnosis of CKD in the elderly truly represents a disease process rather than part of normal ageing. [10][11][12][13] Although CKD is most often identified in cats over the age of 12 years, there is evidence that tubulointerstitial inflammation may be identified in the renal parenchyma of young cats that have died for other reasons and as such it has been proposed that the development of CKD may also be part of a normal aging process in cats. 14 Ageing is a programmed biological process, which is regulated by many genes.…”

Section: Ageing and The Kidneymentioning

confidence: 99%

Current Understanding of the Pathogenesis of Progressive Chronic Kidney Disease in Cats

Jepson

2016

Veterinary Clinics of North America: Small Animal Practice

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Abstract:In cats with chronic kidney disease (CKD), the most common histopathological finding is tubulointerstitial inflammation and fibrosis. However, these changes reflect a non-specific response of the kidney to any inciting injury. The risk of development of CKD in a patient is likely to reflect genetic predispositions, ageing, environmental and individual factors that influence decline in renal function over the course of a cat's life. However, there is still relatively little information about exactly which risk factors predispose a cat to develop CKD and these will be explored. Whilst many cats diagnosed with CKD have stable disease for many years, some cats show overtly progressive disease.

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Chronic Kidney Disease: A Clinical Model of Premature Aging

Cited by 257 publications

References 165 publications

Calcification Propensity and Survival among Renal Transplant Recipients

Calcification Propensity and Survival among Renal Transplant Recipients

Aldosterone Activates Transcription Factor Nrf2 in Kidney Cells both In Vitro and In Vivo

Current Understanding of the Pathogenesis of Progressive Chronic Kidney Disease in Cats

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