Association of serum fetuin-A and fetuin-A gene polymorphism in relation to mineral and bone disorders in patients with chronic kidney disease

Maharem, Dalia Aly; Gomaa, Salwa H.; Ghandor, Marwa K. El; Mohamed, Ehab I.; Matrawy, Khaled; Zaytoun, Sameh; Nomeir, Hanan Mohamed

doi:10.1016/j.ejmhg.2013.07.003

Cited by 9 publications

(24 citation statements)

References 82 publications

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“…These results came in agreement with the findings of Zeidan et al 18 and Maharem et al 36 who conducted their study on Egyptian chronic kidney disease patients(CKD) and found no statistically significant difference between CKD patients and control groups regarding the frequencies of the three fetuin-A genotypes (C→G), and no significant difference was found between fetuin-A genotypes as regards vascular calcification and atherosclerosis assessed by measurement of intimamedia thickness. However, Ma et al, 8 found that frequencies of the GG genotype and the G allele in fetuin-A (rs4918) were significantly higher in patients with ischemic stroke or atherosclerotic cerebral infarction than those in the control group.…”

Section: Discussionsupporting

confidence: 92%

Preliminary Study of Biochemical Role of Serum Fetuin-A Level and its Gene Polymorphism in Diabetic Patients with Microalbuminuria

Hamouda¹

2015

JDMDC

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Background: Microalbuminuria (MA) is a risk factor for cardiovascular disease. Fetuin-A is a hepatokines involved in insulin resistance (IR) and type 2diabetes. The aim of this study was to evaluate the possible association between both serum level and (Thr256Ser) gene polymorphism of fetuin-A and the pathogenesis of MA in type 2 diabetic patients, and determine its correlation with some vascular and oxidative stress markers. Methods: 50 patients with type 2 diabetes divided into two equal groups (normoalbuminuria and microalbuminuria groups) and 25 healthy subjects as controls. ELISA was used to measure serum fetuin-A and insulin levels, then assessment of IR. Fetuin-A gene (Thr256Ser) polymorphism was done using PCR-RFLP technique. Serum nitric oxide (NO) and ischemia modified albumin (IMA) were measured, in addition to routine investigations. Results: Significant increase of serum IMA, NO, insulin and fetuin-A levels were documented in the microalbuminuric patient group as compared to the other two groups, with no statistically significant difference as regard the three fetuin-A genotypes either between both diabetic patient groups or between them and the control. By using multiple logistic regression analysis, Fetuin-A, is the most important predictor of MA. Conclusion: So, it could be concluded that the higher levels of fetuin-A may be an independent novel risk factor for MA in type 2 diabetic patients, in spite of the non significant difference either between normoalbuminuric and microalbuminuric diabetic or between them and control according to the frequencies of the three fetuin-A genotype.

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Section: Discussionsupporting

confidence: 92%

Preliminary Study of Biochemical Role of Serum Fetuin-A Level and its Gene Polymorphism in Diabetic Patients with Microalbuminuria

Hamouda¹

2015

JDMDC

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“…Our nding with regards to the association of fetuin-A level with eGFR is similar to a previous study by Ix et al (29), which showed negative association between fetuin-A and predominantly non-diabetic subjects with stage 3 or 4 CKD, i.e., high fetuin-A level and low eGFR. Contrastingly, previous observational studies (14,15,30) found positive association between fetuin-A and kidney function, i.e., decreasing serum fetuin-A would decrease eGFR. It is worth noting that the functions and regulatory mechanisms of fetuin-A are complex, and may seem to differ according to the pathophysiologic characteristics of the population being studied (14).…”

Section: Discussioncontrasting

confidence: 83%

“…(33,34) Therefore, in a sustained in ammatory response, circulating fetuin-A levels are progressively depleted and its protective role in halting further decline of kidney function is undermined. Moreover, though not consistently demonstrated (16), variations in fetuin-A levels may also be determined by genetic polymorphisms independent of in ammation (15,35).…”

Section: Discussionmentioning

confidence: 99%

“…Some evidences have also shown that in ammatory markers (e.g., high sensitivity C-Reactive protein (hsCRP), interleukin-1 (IL-1), endothelin-1 (ET -1), and tumor necrosis factor-α (TNF-α) (12,13)) are associated with eGFR decline. In addition, recent evidences from observational studies showed that fetuin-A was also associated with CKD morbidity (14,15) and mortality (16,17). Moreover, fetuin-A has been found to be associated with CKD risk including BMI (18), DM (19,20) and HT (21,22).…”

Section: Introductionmentioning

confidence: 99%

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Causal association pathways between fetuin-A and kidney function: A mediation Analysis

Bassey¹,

Numthavaj²,

Rattanasiri³

et al. 2020

Preprint

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BackgroundBody mass index (BMI), uric acid (UA) diabetes mellitus (DM) and hypertension (HT) are known risk factors of declined kidney function, and are associated with fetuin-A. However, the causal pathways of these associations are unclear. We therefore used cohort data to explore possible causal pathways of fetuin-A and kidney function. MethodologyWe used data of the Electricity Generating Authority of Thailand cohort 2009 (n= 2305). A causal pathway was constructed, which considered fetuin-A as study factor, BMI, UA, DM, and HT as mediators, and eGFR as the outcome. A generalized-structural equation model (GSEM) with 1000-replication bootstrapping was applied to assess the causal effects adjusting for covariates. ResultsThe fetuin-A → eGFR pathway showed a direct association of fetuin-A on eGFR with the coefficient of -0.0072 (95% CI: -0.0119, -0.0025). In addition, the indirect effects of fetuin-A→ BMI → eGFR was also significant with the coefficient of 0.00086 (0.00025, 0.0016; implying that every one unit of BMI increased, resulting from increasing fetuin-A, would significantly increase eGFR 0.00086 (0.00025, 0.0016) mL/min/1.73m2. There was a negative effect of fetuin-A on eGFR through BMI and UA pathway (Fetuin-A→BMI→UA→eGFR ) as well as the HT pathway (Fetuin-A→BMI→HT→eGFR ) with average casual mediation effects (ACME) of -0.00132 (-0.00177, -0.00092) and -0.00139 (-0.00237, -0.00069). Fetuin-AàDMàHTàeGFR was also statistically significant with the ACME of -0.00223 (-0.00535, -0.00066).ConclusionOur study has shed some light on the possible role of fetuin-A in the etiology of declining renal function through the mediatory roles of BMI, UA, DM and HT in the various complex causal pathways leading to declining kidney function in our study cohort. Further studies are however recommended to examine the pathomechanisms involved in the mediational processes of these studied risk factors in the etiology of declining kidney function.

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“…Es miembro de la superfamilia de inhibidores de la cistein proteasa. Es un transportador de factores de crecimiento, que se une al factor de crecimiento transformante-(TGF-b) y a la proteína morfogenética (44,45) . Disminuye la activación de macrófagos y la liberación de citokinas proinflamatorias.…”

Section: Ercunclassified

Metabolismo mineral óseo en pacientes con enfermedad renal crónica: revisión sobre su fisiopatología y morbimortalidad

Bernuy

Gonzáles

2015

Rev Peru Med Exp Salud Publica

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RESUMENLa enfermedad mineral ósea (EMO) es un término amplio que incluye a las alteraciones séricas del calcio, fósforo, vitamina D, paratohormona, anormalidades en el crecimiento, mineralización ósea y/o a las calcificaciones extraesqueléticas que acompañan al paciente con enfermedad renal crónica (ERC). Está presente en casi la totalidad de pacientes en diálisis y con el trasplante renal puede no siempre mejorar. Se han identificado nuevos factores y hormonas; como klotho y factor de crecimiento de fibroblastos-23 (FGF-23) que interactúan con la vitamina D y con la paratohormona en el manejo renal del calcio y fósforo. Ciertos reportes indican que son marcadores precoces del desarrollo de EMO, incluso cuando la función renal está levemente disminuida y los niveles de paratohormona son normales. La EMO ha sido asociada con mayor mortalidad, principalmente por su vinculación con la calcificación vascular. Este proceso conlleva a un incremento de eventos cardiovasculares que constituyen la principal causa de morbimortalidad en pacientes con ERC, sobre todo aquellos que se encuentran en diálisis, independientemente de la modalidad que los pacientes sigan. La forma de presentación de la EMO puede ser de alto o bajo recambio. Aunque no está completamente definido qué es lo que determina que se exprese una en particular, se ha encontrado que la enfermedad de bajo recambio se relaciona con malnutrición, uso inadecuado de calcitriol y diálisis ineficiente. El conocimiento de la EMO es relevante por su asociación con las complicaciones mencionadas y porque constituye un parámetro para evaluar la terapia instalada. Palabras clave: Hormona paratiroidea; Deficiencia de vitamina B; Enfermedad renal crónica; Trastornos del metabolismo del calcio (fuente: DeCS BIREME). BONE MINERAL METABOLISM IN PATIENTS WITH CHRONIC KIDNEY DISEASE: REVIEW OF ITS PATHOPHYSIOLOGY AND MORBIMORTALITY ABSTRACTMineral Bone Disorder (MBD) is a broad term that includes abnormal serum calcium, phosphorus, vitamin D, parathyroid hormone, growth abnormalities, bone mineralization and/or extraskeletal calcifications in patients with chronic kidney disease (CKD ). It is present in almost all patients on dialysis and may not always improve with a kidney transplant. New factors and hormones have been identified, such as Klotho and fibroblast growth factor-23 (FGF-23) that interact with vitamin D and the parathyroid hormone in the renal management of calcium and phosphorus. Some reports indicate that they are early markers of the development of MBD, even when kidney function is slightly decreased and parathyroid hormone levels are normal. MBD has been associated with higher mortality, mainly because of its link with vascular calcification. This process leads to an increase in cardiovascular events which are the leading cause of morbidity and mortality in CKD patients, especially those who are on dialysis, regardless of the modality that the patients follow. The presentation of the BMD can be of high or low turnover. Although it is not completely defined wha...

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Association of serum fetuin-A and fetuin-A gene polymorphism in relation to mineral and bone disorders in patients with chronic kidney disease

Cited by 9 publications

References 82 publications

Preliminary Study of Biochemical Role of Serum Fetuin-A Level and its Gene Polymorphism in Diabetic Patients with Microalbuminuria

Preliminary Study of Biochemical Role of Serum Fetuin-A Level and its Gene Polymorphism in Diabetic Patients with Microalbuminuria

Causal association pathways between fetuin-A and kidney function: A mediation Analysis

Metabolismo mineral óseo en pacientes con enfermedad renal crónica: revisión sobre su fisiopatología y morbimortalidad

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