UK Consensus Conference on Early Chronic Kidney Disease 6 and 7 February 2007

Archibald, G. C.; Bartlett, William A.; Brown, A.; Christie, Bryan; Elliott, Alison M; Griffith, K.; Pound, S.; Rappaport, Irving; Robertson, D.; Semple, Yvonne; Slane, Peter W; Whitworth, Caroline; Williams, Bryan

doi:10.1093/ndt/gfm268

Cited by 49 publications

(27 citation statements)

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“…Because we did not use predefined GFR thresholds, this study provides reference values that may contribute to refining CKD staging, as suggested by others. 5,43 Only clinical trials such as those carried out for anemia can determine whether treating these abnormalities at these stages would prevent the excess risks for morbidity and mortality associated with them, and our study provides useful information to help design such trials.…”

Section: Discussionmentioning

confidence: 95%

Timing of Onset of CKD-Related Metabolic Complications

Moranne

Froissart²,

Rossert³

et al. 2009

Journal of the American Society of Nephrology

419

283

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Chronic kidney disease (CKD) guidelines recommend evaluating patients with GFR Ͻ60 ml/min per 1.73 m 2 for complications, but little evidence supports the use of a single GFR threshold for all metabolic disorders. We used data from the NephroTest cohort, including 1038 adult patients who had stages 2 through 5 CKD and were not on dialysis, to study the occurrence of metabolic complications. GFR was measured using renal clearance of 51 Cr-EDTA (mGFR) and estimated using two equations derived from the Modification of Diet in Renal Disease study. As mGFR decreased from 60 to 90 to Ͻ20 ml/min per 1.73 m 2 , the prevalence of hyperparathyroidism increased from 17 to 85%, anemia from 8 to 41%, hyperphosphatemia from 1 to 30%, metabolic acidosis from 2 to 39%, and hyperkalemia from 2 to 42%. Factors most strongly associated with metabolic complications, independent of mGFR, were younger age for acidosis and hyperphosphatemia, presence of diabetes for acidosis, diabetic kidney disease for anemia, and both male gender and the use of inhibitors of the renin-angiotensin system for hyperkalemia. mGFR thresholds for detecting complications with 90% sensitivity were 50, 44, 40, 39, and 37 ml/min per 1.73 m 2 for hyperparathyroidism, anemia, acidosis, hyperkalemia, and hyperphosphatemia, respectively. Analysis using estimated GFR produced similar results. In summary, this study describes the onset of CKD-related complications at different levels of GFR; anemia and hyperparathyroidism occur earlier than acidosis, hyperkalemia, and hyperphosphatemia.

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Section: Discussionmentioning

confidence: 95%

Timing of Onset of CKD-Related Metabolic Complications

Moranne

Froissart²,

Rossert³

et al. 2009

Journal of the American Society of Nephrology

419

283

View full text Add to dashboard Cite

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“…The study was approved by the Research and Ethics Committee of Guy's and St. Thomas' NHS Trust. Patients were divided into two groups according to the severity of kidney disease based on the estimated glomerular filtration rate (eGFR), calculated using the MDRD formula [21]: group 1, eGFR 30-45 mL/min (CKD stage 3B); group 2, eGFR \30 mL/min (CKD stage 4). Exclusion criteria included patients who had a history of previous parathyroidectomy or recent hospital admissions (\1 month), were on renal replacement therapy, or were on or had previously received treatment with active vitamin D metabolites (1-alfacalcidol, calcitriol), phosphate binders, or bisphosphonates.…”

Section: Subjectsmentioning

confidence: 99%

Circulating Sclerostin and Dickkopf-1 (DKK1) in Predialysis Chronic Kidney Disease (CKD): Relationship with Bone Density and Arterial Stiffness

et al. 2012

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Abnormalities of bone metabolism and increased vascular calcification are common in chronic kidney disease (CKD) and important causes of morbidity and mortality. The Wnt signaling pathway may play a role in the bone and vascular disturbances seen in CKD, termed collectively "CKD-MBD." The aim of the study was to investigate the possible association of circulating concentrations of the secreted Wnt signaling inhibitors DKK1 and sclerostin with BMD and arterial stiffness in predialysis CKD. Seventy-seven patients (48 M, 29 F), mean age 57 (SD = 14) years with CKD stages 3B (n = 32) and 4 (n = 45) were studied. Sclerostin, DKK1, PTH, and 1,25(OH)(2)D were analyzed. BMD was measured at the lumbar spine (LS), femoral neck (FN), total hip (TH), and forearm (FARM). Arterial stiffness index was determined by contour analysis of digital volume pulse (SI(DVP)). There was a positive correlation between sclerostin and age (r = 0.47, p < 0.000). Sclerostin was higher in men than women (p = 0.013). Following correction for age and gender, there was a negative association between GFR and sclerostin (p = 0.002). We observed a positive association between sclerostin and BMD at the LS (p = 0.0001), FN (p = 0.004), and TH (p = 0.002). In contrast, DKK1 was negatively associated with BMD at the FN (p = 0.038). A negative association was seen between DKK1 and SI(DVP) (p = 0.027). Our data suggest that the Wnt pathway may play a role in CKD-MBD. Prospective studies are required to establish the clinical relevance of sclerostin and DKK1 as serological markers in CKD.

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“…All patients gave informed consent in accordance with the ethical standards of the Research and Ethics Committee of Guy's and St Thomas' NHS Trust. The patients were divided into three groups according to the severity of kidney disease based on the estimated GFR (eGFR) calculated using the MDRD formula [19]-Group 1: eGFR >60 ml/min; CKD stage 1/2; Group 2: eGFR 30-59 ml/min; CKD stage 3; Group 3: eGFR <30 ml/min, CKD stage 4. Patients were excluded when they had a history of previous parathyroidectomy or recent hospital admissions (<1 month), were on renal replacement therapy or were on or had previously received treatment with 1-alphacalcidol, calcitriol, phosphate binders or bisphosphonates.…”

Section: Subjectsmentioning

confidence: 99%