Variability and Risk Factors for Kidney Disease Progression and Death Following Attainment of Stage 4 CKD in a Referred Cohort

Levin, Adeera; Djurdjev, Ognjenka; Beaulieu, Monica; Er, Lee

doi:10.1053/j.ajkd.2008.06.023

Cited by 245 publications

(195 citation statements)

References 23 publications

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“…Upregulation of phosphorus, FGF-23, and parathyroid hormone is associated with worsening kidney disease and a higher likelihood of death [17,18]. This study demonstrated a marked decrease in adenineinduced increases in serum phosphorus, FGF-23, and parathyroid hormone levels in rats, suggesting the preventative effects of resveratrol against adenine-mediated kidney disorders.…”

Section: Discussionsupporting

confidence: 50%

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Zhang¹,

Yang²,

Li³

et al. 2017

Trop. J. Pharm Res

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Section: Discussionsupporting

confidence: 50%

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Zhang¹,

Yang²,

Li³

et al. 2017

Trop. J. Pharm Res

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“…For example, hyperphosphatemia, high serum parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) levels, and vitamin D deficiency were reported to be risk factors for mortality and cardiovascular events in patients with CKD, especially in dialysis patients (2)(3)(4)(5)(6)(7). Recently, these derangements were reported to be associated with CKD progression (8)(9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

“…Given the difficulties of evaluating phosphate exposure in clinical practice, clinicians have routinely measured serum phosphate in CKD patients. Clinical studies have revealed that higher phosphate levels were linked to CKD progression in many settings (9,10,12). High PTH levels, which were also induced by phosphate load (15), were reported to be associated with CKD progression in a large retrospective cohort study (9).…”

Section: Introductionmentioning

confidence: 99%

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Nakano

Hamano

Fujii

et al. 2012

Clinical Journal of the American Society of Nephrology

114

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SummaryBackground and objectives Hyperphosphatemia, vitamin D deficiency, hyperparathyroidism, and high serum fibroblast growth factor 23 (FGF23) levels, when studied separately, were found to predict the progression of CKD. However, studies with simultaneous measurement of mineral bone disorder (MBD)-related factors were scarce. This study aimed to identify factors predicting renal outcome independent of other factors.Design, setting, participants, & measurements This was a prospective cohort study of 738 Japanese predialysis outpatients in the nephrology departments of two hospitals. The outcome was defined as a doubling of serum creatinine or initiation of dialysis.Results Mean estimated GFR (eGFR) was 35 ml/min per 1.73 m 2 . At enrollment, the increase in intact FGF23 with decreasing eGFR was the earliest among changes in MBD-related factors, followed by 1,25-dihydroxyvitamin D decrease, parathyroid hormone increase, and phosphate increase. Conclusions Combined use of two markers is useful for the risk stratification of renal outcome.

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“…1 To do so, determining the factors mediating the progression of CKD is the key. 2, 3 Chronic ischemic nephropathy is thought to be one of the major determining factors in progression of CKD. 4 Approximately, 15% of end-stage renal disease is attributed to chronic ischemic nephropathy from renovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Aliskiren reduced renal fibrosis in mice with chronic ischemic kidney injury—beyond the direct renin inhibition

et al. 2011

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Chronic renal ischemia leads to renal fibrosis and atrophy. Activation of the renin-angiotensin-aldosterone system is one of the main mechanisms driving chronic renal ischemic injury. The aim of the present study was to define the effect of aliskiren in chronic ischemia of the kidney. Two-kidney, one-clip mice were used to study chronic renal ischemia. Aliskiren significantly lowered the blood pressure in mice with renal artery constriction (92.1±1.1 vs. 81.0±1.8 mm Hg, Po0.05). Renin expression was significantly increased in ischemic kidneys when treated with aliskiren. In addition, (Pro)renin receptor expression was decreased by aliskiren in ischemic kidneys. Aliskiren treatment significantly increased klotho expression and reduced the expression of fibrogenic cystokines, caspase-3 and Bax in ischemic kidneys. Histological examination revealed that aliskiren significantly reduced the nephrosclerosis score (4.5±1.9 vs. 7.3±0.4, Po0.05). Immunofluorescence staining also showed that aliskiren decreased the deposition of interstitial collagen I in ischemic kidneys. In conclusion, direct renin inhibition significantly reduced renal fibrosis and apoptosis following chronic renal ischemia.

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Variability and Risk Factors for Kidney Disease Progression and Death Following Attainment of Stage 4 CKD in a Referred Cohort

Cited by 245 publications

References 23 publications

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Prevention of injury by resveratrol in a rat model of adenine-induced chronic kidney disease

Combined Use of Vitamin D Status and FGF23 for Risk Stratification of Renal Outcome

Aliskiren reduced renal fibrosis in mice with chronic ischemic kidney injury—beyond the direct renin inhibition

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