The burden of kidney disease: Improving global outcomes

Eknoyan, Garabed; Lameire, Norbert; Barsoum, Rashad S.; Eckardt, Kai‐Uwe; Levin, Adeera; Levin, Nathan W.; Locatelli, Francesco; MacLeod, Alison Murray; Vanholder, Raymond; Walker, Rowan G.; Wang, Haiyan

doi:10.1111/j.1523-1755.2004.00894.x

Cited by 433 publications

(316 citation statements)

References 22 publications

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“…(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.…”

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

234

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: 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

234

224

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“…Renal function impairment has many negative effects on cardiovascular, hematopoietic, and gastrointestinal system as well as bone metabolism [1]. Changes in mineral metabolism and bone structure develop early in the course of CKD and worsen with progressive loss of kidney function.…”

Section: The European Research Journal Volume 5 Issue 3 May 2019mentioning

confidence: 99%

Comparison of laboratory and imaging methods associated with bone metabolism in patients with or without renal failure under the age of 45 years with elevated parathyroid hormone levels

Peynirci

Ersoy

Gürsoy

et al. 2019

The European Research Journal

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Objectives: Although bone biopsy is considered the gold standard for the definitive diagnosis of renal osteodystrophy; it is not suitable for routine clinical practice due to its invasive nature. The present study was aimed to evaluate and compare the bone mineral status using dual energy X-ray absorptiometry of patients with or without chronic kidney disease in young population with elevated parathyroid hormone levels. Methods: This was a single center, cross-sectional, retrospective study conducted in patients younger than 45 years of age. The study was performed in the outpatient clinic of a university hospital. Patients with elevated parathyroid hormone levels were included. Results: Among them, 29 had renal insufficiency, 158 had normal renal function. Measured bone mineral density with dual energy X-ray absorptiometry and laboratory values were collected from patient files. The primary end point was to assess the efficiacy of dual energy X-ray absorptiometry in patients with or without renal failure. Except Z score at Ward's triangle, all of the T and Z scores at lomber, femur neck, trochanteric, and intertrochanteric areas were found significantly lower in patients with chronic kidney disease compared to those without (p < 0.001). Conclusion: Dual energy X-ray absorptiometry seemed to be a reliable method for detection of osteoporosis in premenopausal female and male patients younger than 45 years of age with or without renal failure with elevated parathyroid hormone levels.

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“…Najčešći etiološki faktori HBI u razvijenim zemljama su hipertenzija i dijabetes, a u zemljama u razvoju inflamatorne bolesti [1]. Anemija je jedan od prvih znakova HBI.…”

Section: Uvodunclassified

Uticaj korekcije anemije bolesnika sa hroničnom bubrežnom insuficijencijom na kardiovaskularni sistem

Radović¹,

Kešelj²,

Pejović³

2011

Biomedicinska istraž.

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Kratak sadržajUvod. Anemija je česta komplikacija hronične bubrežne insuficijencije, a njen glavni uzrok je nedovoljno stvaranje eritropoetina. Anemija predstavlja značajan faktor rizika za nastanak kardiovaskularnih bolesti. Cilj rada je bio da se ispita oporavak anemije tokom primjene humanog rekombinovanog eritropoetina kod bolesnika sa hroničnom bubrežnom insuficijencijom u predijaliznom periodu i uticaj korekcije anemije na kardiovaskularne promjene.Metode. U prospektivnoj studiji praćeno je 20 bolesnika (13 muškaraca i sedam žena) sa hroničnom bubrežnom insuficijencijom u predijaliznoj fazi tokom jedne godine. Bolesnici su podijeljeni u tri grupe prema jačini glomerulske filtracije (JGF) i u dvije podgrupe -bolesnici sa i bez dijabetesa. JGF je procjenjena pomoću Cockroft-Gault formule. Težina anemije određivana je na osnovu vrijednosti hemoglobina i hematokrita. Kardiovaskularni status je praćen EKG i EHO pregledima srca na početku studije i poslije godinu dana. Statistička obrada rađena je primjenom Studentov-og t-test, analize varijanse, Pearson-ovog koeficijenta korelacija uz korišćenje programa SPSS 12.Rezultati. Prije započinjanja liječenja anemije kod svih bolesnika vrijednosti hemoglobina (Hb) i hematokrita (Hct) su ukazivale na težak stepen anemije. Bolesnicima je ordiniran eritropoetin-beta. Poslije mjesec dana liječenja kod svih je došlo do statistički značajnog porasta Hb i Hct, a poslije tri mjeseca postignuta je ciljna vrijednost Hb i Hct. U ispitanoj grupi bolesnika, svi su sem jednog, imali značajnu hipertofiju lijeve komore koja je utvđena ehosonografski prije početka ispitivanja. Poslije godinu dana liječenja anemije postignuta je statistički značajna regresija mase lijeve komore (MLK) od 267,2g/m 2 do 212,5g/m 2 pri prosječnoj promjeni koncentracije Hb od 9 g/l na 12,5 g /dl. Kod bolesnika koji nisu imali dijabetes, prosječan Hb bio je 8,9 g /dl i povećao se na 12,2g /dl, a prosječna MLK se smanjila od 293,3 g/1,73 m 2 na 222,9 g/1,73 m 2 , dok je kod dijabetičara prosječna vrijednost Hb porasla sa 9,0 g / dl na 12,6 g /dl, a MLK se smanjila od 231,1 g/1,73 m 2 do 198,1 g/1,73 m 2 .Zaključak. Liječenje eritropoetinom u predijaliznom periodu omogućilo je statistički visoko značajnu korekciju anemije. Oporavak anemije pratilo je smanjenje hipertrofije lijeve komore, smanjenje manifestacija ishemije srca i normalizacija EKG nalaza.Ključne riječi: hronična bubrežna insuficijencija, anemija , eritropoetin, hipertrofija lijeve komore.

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The burden of kidney disease: Improving global outcomes

Cited by 433 publications

References 22 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

Comparison of laboratory and imaging methods associated with bone metabolism in patients with or without renal failure under the age of 45 years with elevated parathyroid hormone levels

Uticaj korekcije anemije bolesnika sa hroničnom bubrežnom insuficijencijom na kardiovaskularni sistem

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