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At least 433 records · Page 24Linked to original sources
PubMed2005

Cardiac troponins and renal function in nondialysis patients with chronic kidney disease.

BACKGROUND: Serum cardiac troponin concentrations are commonly increased in end-stage renal disease (ESRD) in the absence of an acute coronary syndrome (ACS). The data on cardiac troponin I (cTnI) are more variable than those for cardiac troponin T (cTnT). There is little information on cardiac troponin concentrations in patients with chronic kidney disease (CKD) who have not commenced dialysis. METHODS: We studied 222 patients: 56 had stage 3 (moderate CKD); 70 stage 4 (severe CKD); and 96 stage 5 (kidney failure). Patients underwent echocardiography and were followed prospectively for a median of 19 months; all-cause mortality was recorded. RESULTS: Overall, serum cTnT was increased above the 99th percentile reference limit in 43% of all CKD patients studied, compared with 18% for cTnI. Serum cTnT and cTnI concentrations were more commonly increased in the presence of more severe CKD (11 and 6 patients in stage 3, 27 and 8 in stage 4, and 57 and 24 in stage 5 (P < 0.0001 and <0.02, respectively). Among 38 patients with detectable cTnI, 32 had detectable cTnT (r(s) = 0.67; P < 0.0001). There was evidence that decreasing estimated glomerular filtration rate increased the odds of having detectable cTnT (P < 0.001) but not cTnI (P = 0.128). There was no evidence to support an adjusted association of detectable cardiac troponins with increasing left ventricular mass index. Increased cTnT (P = 0.0097), but not cTnI, was associated with decreased survival. CONCLUSIONS: Increased cTnT and cTnI concentrations are relatively common in predialysis CKD patients, in the absence of an ACS, including among those with stage 3 disease. The presence of left ventricular hypertrophy alone does not explain these data. Detectable cTnT was a marker of decreased survival.

Aged↗
PubMed2003

The role of renin-angiotensin-aldosterone system inhibition in chronic kidney disease.

Chronic kidney disease (CKD) is emerging as a new health pandemic. Underlying the global rise in CKD is an increase in diabetes, hypertension and other cardiovascular risk factors leading to progressive renal dysfunction. Emerging evidence strongly suggests that achieving target blood pressure goals via inhibition of the renin-angiotensin-aldosterone system confers significant renal and cardioprotection for patients with CKD. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) lower blood pressure, reduce proteinuria and reduce both the progression of CKD and adverse cardiovascular events. The role of aldosterone inhibition and combination therapy, such as ACEI/ARB, in CKD are under investigation. As our understanding of the basic mechanisms underlying CKD progression advances, novel therapies targeting post-translational endothelial and mesangial messengers downstream from angiotensin II and aldosterone may become available for clinical use.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Traditional and nontraditional risk factors predict coronary heart disease in chronic kidney disease: results from the atherosclerosis risk in communities study.

Some risk factors for coronary heart disease (CHD) incidence in the general population are not associated with CHD incidence among patients with ESRD but have not been well characterized in chronic kidney disease (CKD). The association of several risk factors with CHD incidence was studied among participants with CKD in the population-based Atherosclerosis Risk in Communities (ARIC) Study. CHD risk factors and estimated GFR using serum creatinine were measured among 807 ARIC participants with CKD (estimated GFR between 15 and 59 ml/min per 1.73 m(2)). The incidence of CHD during 10.5 yr of follow-up was 6.3, 8.5, and 14.4 per 1000 person-years among ARIC participants with an estimated GFR of >/=90, 60 to 89, and 15 to 59 ml/min per 1.73 m(2), respectively. After adjustment for age, race, gender, and ARIC field center, among those with CKD, the relative risk (95% confidence interval) of CHD was 1.65 (1.01 to 2.67) for current smoking, 2.02 (1.27 to 3.22) for hypertension, 3.06 (2.01 to 4.67) for diabetes, and 1.96 (1.14 to 3.36) for anemia. The comparably adjusted relative risks of CHD for each standard deviation higher total and HDL cholesterol were 1.50 (1.25 to 1.71) and 0.79 (0.62 to 1.01), respectively, and 1.38 (1.13 to 1.69), 1.24 (1.06 to 1.46), 0.65 (0.54 to 0.79), and 1.38 (1.19 to 1.59) for waist circumference, leukocyte count, serum albumin, and fibrinogen, respectively. CHD risk factors in the general population remain predictive among patients with CKD. Given the high risk for CHD among patients with CKD, control of these risk factors may have a substantial impact on their excess burden of CHD.

Cohort Studies↗
PubMed2005

High prevalence of occult coronary artery stenosis in patients with chronic kidney disease at the initiation of renal replacement therapy: an angiographic examination.

The prevalence of coronary artery stenosis (CAS) at the initiation of renal replacement therapy (RRT) in patients with chronic kidney disease (CKD) and no previous history of angina and/or myocardial infarction (MI) has not been fully elucidated. The prevalence of significant CAS was evaluated in 30 asymptomatic stage 5 CKD patients without a history of angina and/or MI by coronary angiography at the initiation of RRT. The correlations of various parameters with the prevalence of CAS were also examined. Atherosclerotic surrogate markers, including intima-media thickness of carotid artery and ankle-brachial BP index (ABI), were also evaluated. Significant CAS (>50% stenosis) was seen in 16 (53.3%) of 30 asymptomatic CKD patients on coronary angiography at the start of RRT. Stress cardiac scintigraphy was not effective for detecting hidden cardiac ischemia among the CKD patients. Univariate analysis showed that diabetes (P = 0.01), left ventricular mass index (P = 0.04), hyperlipidemia (P = 0.04), total cholesterol (P = 0.02), LDL cholesterol (P < 0.01), intima-media thickness (P = 0.04), and fibrinogen (P = 0.01) were positively correlated with the presence of CAS, whereas ABI (P < 0.01) showed a negative correlation with CAS. Stepwise logistic regression analysis revealed that diabetes and fibrinogen were significant and independent risk factors for CAS in asymptomatic CKD patients who started RRT. The results clearly demonstrated that despite the absence of cardiac events, stage 5 CKD patients are already in a very high risk group for CAS at the initiation of RRT, which was also closely associated with a significant decrease in ABI.

Adult↗
PubMed2006

Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy.

Complications of chronic kidney disease (CKD) include depressed responses to insulin/IGF-1 and accelerated muscle proteolysis as a result of activation of caspase-3 and the ubiquitin-proteasome system. Experimentally, proteolysis in muscle cells occurs when there is suppression of phosphatidylinositol 3-kinase (PI3-K) activity. Postreceptor signaling through the insulin receptor substrate (IRS)/PI3-K/Akt pathway was evaluated in muscles of acidotic, CKD and pair-fed control rats under physiologic conditions and in response to a dose of insulin that quickly stimulated the pathway. Basal IRS-1-associated PI3-K activity was suppressed by CKD; IRS-2-associated PI3-K activity was increased. The basal level of activated Akt in CKD muscles also was low, indicating that the higher IRS-2-associated PI3-K activity did not compensate for the reduced IRS-1-associated PI3-K activity. Insulin treatment overcame this abnormality. The low IRS-1-associated PI3-K activity in muscle was not due to a decrease in IRS-1 protein, but there was a higher amount of the PI3-K p85 subunit protein without a concomitant increase in the p110 catalytic subunit, offering a potential explanation for the lower IRS-1-associated PI3-K activity. Eliminating the acidosis of CKD partially corrected the decrease in basal IRS-1-associated PI3-K activity and protein degradation in muscle. It is concluded that in CKD, acidosis and an increase in the PI3-K p85 subunit are mechanisms that contribute to suppression of PI3-K activity in muscle, and this leads to accelerated muscle proteolysis.

Animals↗
PubMed2005

Chronic kidney disease and cognitive impairment in the elderly: the health, aging, and body composition study.

Previous studies suggest a link between chronic kidney disease (CKD) and cognitive impairment. Whether the longitudinal course of cognitive impairment differs among people with or without CKD is unknown. Data collected in 3034 elderly individuals who participated in the Health, Aging, and Body Composition study were analyzed. Cognitive function was assessed with the Modified Mini-Mental State Exam (3MS) at baseline and then 2 and 4 yr after baseline. Cognitive impairment was defined as a 3MS score <80 or a decline in 3MS >5 points after 2 or 4 yr of follow-up among participants with baseline 3MS scores > or =80. Participants with CKD, defined as an estimated GFR (eGFR) <60 ml/min per 1.73 m2, were further divided into two eGFR strata. Unadjusted mean baseline 3MS scores and mean declines in 3MS scores over 4 yr were significantly more pronounced for participants with lower baseline eGFR. More advanced stages of CKD were associated with an increased risk for cognitive impairment: Odds ratio (OR) 1.32 (95% confidence interval [CI] 1.03 to 1.69) and OR 2.43 (95% CI, 1.38 to 4.29) for eGFR 45 to 59 ml/min per 1.73 m2 and <45 ml/min per 1.73 m2, respectively, adjusted for case mix, baseline 3MS scores, and other potential confounders. CKD is associated with an increased risk for cognitive impairment in the elderly that cannot be fully explained by other well-established risk factors. Studies aimed at understanding the mechanism(s) responsible for cognitive impairment in CKD and efforts to interrupt this decline are warranted.

Age Factors↗
PubMed2006

Regional arterial stiffness in patients with type 2 diabetes and chronic kidney disease.

Increased arterial stiffness is an independent predictor of death from cardiovascular disease, and aortic stiffness is more predictive than stiffness of other arterial regions. Because little is known about the effect of chronic kidney disease (CKD) on regional arterial stiffness, pulse wave velocity (PWV) of four different arterial segments was measured in patients who had type 2 diabetes with and without various stages of CKD. A total of 434 patients had type 2 diabetes, and there were 192 healthy control subjects who were comparable in age and gender. GFR was estimated by the abbreviated Modification of Diet in Renal Disease equation. The patients with diabetes were classified into CKD stages by the definition of the Kidney Disease Outcomes Quality Initiative guidelines. PWV was measured in the heart-femoral, heart-carotid, heart-brachial, and femoral-ankle segments simultaneously using an automatic pulse wave analyzer. PWV of each arterial region was increased in patients who had diabetes without kidney damage and was increased further in a stepwise manner with the advanced stages of CKD. The increase in PWV was greater in the heart-femoral and heart-carotid regions than in the heart-brachial and femoral-ankle segments. However, after adjustment for age, BP, and other confounding factors using a multiple regression model, decreased GFR was independently associated with increased PWV of the heart-femoral region but not with PWV of other arterial segments. In type 2 diabetes, CKD was associated with increased stiffness of arteries, particularly of the aorta. The cross-sectional result may explain the increased risk for cardiovascular disease in CKD, although longitudinal studies are needed to confirm it.

Arteries↗
PubMed2007

Kidney function and risk of peripheral arterial disease: results from the Atherosclerosis Risk in Communities (ARIC) Study.

Chronic kidney disease (CKD) is associated with an increased risk for cardiovascular disease, but its association with peripheral arterial disease (PAD) is unclear. With the use of data from the Atherosclerosis Risk in Communities (ARIC) Study, 14,280 middle-aged adults were categorized on the basis of estimated GFR >/=90, 60 to 89, and 15 to 59 ml/min per 1.73 m(2) for normal kidney function, mildly decreased kidney function, and stages 3 to 4 CKD, respectively. Incident PAD was defined as a new onset of ankle-brachial index <0.9 assessed at regular examinations, new intermittent claudication assessed by annual surveillance, or PAD-related hospital discharges. Incidence rates and relative risks (RR) for PAD were compared across these categories. During a mean follow-up time of 13.1 yr (186,616 person-years), 1016 participants developed PAD. The incidence rates per 1000 person-years were 4.7, 4.9, and 8.6 for the normal kidney function, mildly decreased kidney function, and CKD groups, respectively. Compared with participants with normal kidney function, the age-, gender-, race-, and ARIC field center-adjusted RR for PAD was 1.04 (95% confidence interval [CI] 0.91 to 1.18) for those with mildly decreased kidney function and 1.82 (95% CI 1.34 to 2.47) for those with CKD. After additional adjustment for cardiovascular disease risk factors, an increase in risk for incident PAD still was observed in participants with CKD, with a multivariable adjusted RR of 1.56 (95% CI 1.13 to 2.14). Patients with CKD are at increased risk for incident PAD. Development of strategies for screening and prevention of PAD in this high-risk population seems warranted.

Aging↗
PubMed2006

The endothelin system and its antagonism in chronic kidney disease.

The incidence of chronic kidney disease (CKD) is increasing worldwide. Cardiovascular disease (CVD) is strongly associated with CKD and constitutes one of its major causes of morbidity and mortality. Treatments that slow the progression of CKD and improve the cardiovascular risk profile of patients with CKD are needed. The endothelins (ET) are a family of related peptides, of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both CVD and CKD. ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness and more novel cardiovascular risk factors such as oxidative stress and inflammation. Through these, ET also contributes to endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists may reduce cardiovascular risk. In particular relation to the kidney, antagonism of the ET system may be of benefit in improving renal hemodynamics and reducing proteinuria. ET likely also is involved in progression of renal disease, and data are emerging to suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in slowing CKD progression.

Animals↗
PubMed2006

Medical costs of untreated anemia in elderly patients with predialysis chronic kidney disease.

The objective of this study was to quantify the incremental medical costs that are associated with untreated anemia among elderly patients with predialysis chronic kidney disease (CKD). An analysis of claims and laboratory data between January 1999 and February 2005 was conducted. Inclusion criteria were age >/=65 yr, two or more hemoglobin readings, one or more claims for CKD, and two or more GFR values of <60 ml/min per 1.73 m(2) (stages 3 to 5 CKD). Patients were excluded when they had cancer or lupus, had received organ transplantation, or were treated for anemia. An open-cohort design was used to classify patients' observation periods into anemia and nonanemia. Both univariate and multivariate analyses were conducted to compare periods of anemia and nonanemia for average monthly medical costs; the latter was adjusted for age, gender, GFR, diabetes, hypertension, liver cirrhosis, coronary artery disease, myocardial infarction, and left ventricular hypertrophy. A subset analysis of patients with moderate CKD (stage 3) was conducted. A total of 2001 patients were identified. Untreated anemia was associated with a significant increase in medical costs, with an unadjusted incremental monthly cost of $1089 (P < 0.0001) and a cost ratio of 1.8:1 relative to nonanemia. After controlling for covariates, untreated anemia remained significantly associated with a cost increase (adjusted incremental monthly cost $503; cost ratio 1.4:1; P < 0.0001). Similar significant cost burden was observed in the subset of patients with moderate CKD. The retrospective observational design may be more susceptible to bias than a randomized, controlled trial. This large study, which was based on real-life practice data, demonstrated that untreated anemia in elderly patients with predialysis CKD was associated with a significant increase in medical costs.

Aged↗
PubMed2006

Role of pulse pressure on cardiovascular risk in chronic kidney disease patients.

Epidemiologic studies have emphasized the close relationship between high BP and cardiovascular disease (CVD). Recently published prospective studies have focus on systolic and pulse pressure (PP). Systolic BP seems to be a more important factor than diastolic BP on cardiovascular and all-cause mortality in older patients. PP reflects stiffness of the large arteries and increases with age. Increasingly, PP is recognized as an independent predictor of myocardial infarction, congestive heart failure, and cardiovascular death, even in hypertensive patients who undergo successful antihypertensive drug therapy, especially in older individuals. Chronic kidney disease (CKD) is a major public health problem. The progression of kidney disease and its associated cardiovascular complications are the major causes of morbidity and mortality. This holds true for all stages of kidney disease, including ESRD that requires renal replacement therapy. Most of the traditional CVD risk factors are highly prevalent in CKD, and several nontraditional factors also are associated with atherosclerosis in CKD. The burden of hypertension is present at all stages of CKD. Several studies have shown that PP is a reliable prognostic factor for mortality and CVD in patients who have CKD and are on hemodialysis and in renal transplant patients. The purpose of this review is to show the importance of PP on cardiovascular risk in patients with CKD, including kidney transplant recipients.

Blood Pressure↗
PubMed2006

Anemia and cardiovascular risk: the lesson of the CREATE Trial.

Anemia has received increasing attention as an independent cardiovascular risk factor in patients with chronic kidney disease (CKD); a number of studies have highlighted its clear relationship with CKD mortality, because its impact on cardiac function leads to the development of left ventricular hypertrophy. However, despite the association between higher hemoglobin levels and better outcomes, a number of clinical studies have failed to demonstrate that fully correcting anemia has a positive effect on morbidity and mortality in patients with CKD. The Cardiovascular Reduction Early Anemia Treatment Epoetin beta (CREATE) study was designed from the hypothesis that, as anemia develops early in the course of CKD and nearly at the same time as cardiovascular disease, its earlier correction may provide better protection against the development of cardiovascular abnormalities. This randomized, multicenter, open-label, parallel-group trial involved 603 patients who had moderate anemia (hemoglobin 11 to 12.5 g/dl) and stage 3 to 4 CKD (estimated GFR 15 to 35 ml/min) and were randomly assigned to attain complete or partial anemia correction. The final results are due to be published within a few months, but the preliminary analyses do not show that complete anemia correction leads to any cardiovascular advantage, although the cardiovascular event rate was half that expected, possibly as a result of patient selection, trial effect, and improved medical care. The baseline findings also indicated that the burden of cardiovascular disease already is very high even in relatively early stages of CKD.

Anemia↗
PubMed2006

Effects of atorvastatin on inflammatory and fibrinolytic parameters in patients with chronic kidney disease.

Although substantial evidence suggests that treatment of dyslipidemia with statins reduces mortality and morbidity that are associated with cardiovascular disease, only a few studies have examined the efficacy of statins on inflammatory and fibrinolytic status in patients with chronic kidney disease (CKD). A 6-mo, prospective, randomized study was designed to assess the efficacy of atorvastatin in reducing circulating inflammatory and fibrinolytic parameters in patients with CKD. Sixty-six patients with CKD (stages 2, 3, and 4) and LDL cholesterol levels > or =100 mg/dl were randomly assigned (2:1) to receive 20 mg/d atorvastatin (n = 44) or nonatorvastatin therapy (n = 22). Lipid profile, renal function, fibrinolytic balance (tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1), and inflammatory markers (C-reactive protein [CRP], IL-1 beta, IL-6, and TNF-alpha) were measured before and 6 mo after atorvastatin was added to the treatment. Twenty-five age-matched individuals with normal renal function (estimated GFR >90 ml/min) were used as healthy control subjects. Patients with CKD had higher CRP, IL-1 beta, TNF-alpha, and IL-6 levels than age-matched population with normal renal function. t-PA concentration was higher in patients with CKD (P = 0.000). Plasminogen activator inhibitor-1 values were comparable in all patients. Total cholesterol and LDL cholesterol were significantly reduced only in patients who received atorvastatin. In addition to the hypolipidemic effect, atorvastatin treatment significantly reduced inflammatory parameters: CRP (median 4.1 to 2.9; P = 0.015), TNF-alpha (6.0 +/- 2.7 to 4.7 +/- 2.4; P = 0.046), and IL-1 beta levels (1.9 +/- 0.7 to 1.2 +/- 0.7; P = 0.001). These parameters remained unchanged in patients who were not treated with atorvastatin. Fibrinolytic parameters were not modified by atorvastatin treatment. Patients with CKD showed higher levels of inflammatory parameters and t-PA levels than age-matched healthy control subjects. Atorvastatin treatment, in addition to its beneficial effect on cholesterol levels, improved the inflammatory state of these patients without modifying fibrinolytic balance.

Aged↗
PubMed2005

Chronic kidney disease as a metabolic syndrome with malnutrition--need for strict control of risk factors.

Patients with chronic kidney disease (CKD) have an increased risk for death from cardiovascular disease (CVD). They have multiple metabolic abnormalities that may accelerate atherosclerosis, such as hypertension, insulin resistance, and dyslipidemia, along with other CKD-related risk factors. In addition, a considerable proportion of patients with advanced stages of CKD are malnourished, presenting "metabolic syndrome with malnutrition". The presence of malnutrition/inflammation dramatically changes the apparent relationship between CVD death risk and some risk factors. For example, in stage 5 CKD patients on hemodialysis, a higher body mass index and a higher plasma cholesterol are predictors of better survival. To understand the paradoxic epidemiology, we should recognize risk factors for occurrence of CVD events and risk factors of fatality after an event. In this article, we review the unique situation of CKD, emphasizing the need of more strict control of both types of risk factors to improve survival of CKD patients.

Chronic Disease↗
PubMed2005

Genetic and genomic approaches to glomerulosclerosis.

Chronic kidney disease (CKD) is common, progressive and expensive to manage. Although modifiable risk factors can be treated and outcomes improved, CKD remains a chronic disease with excessive morbidity and mortality. The completion of the human genome sequence and the advent of methodologies to define gene function provide new opportunities to manage and treat patients with CKD and other chronic diseases. Despite the lack of clear correspondence between genotype and phenotype and an obvious Mendelian inheritance pattern, CKD susceptibility has a genetic basis. In this review, we focus on recent studies of familial focal segmental glomerulosclerosis and the discoveries that have resulted from both genetic and genomic approaches used to understand its pathogenesis. Key slit diaphragm proteins were discovered using linkage analyses of these rare causes of glomerulosclerosis and subsequent work has characterized slit diaphragm function in health and disease. Podocyte dysfunction is now recognized as a key contributor to the functional and histologic derangements that characterize glomerular dysfunction in many common causes of CKD. In aggregate, these studies provide a paradigm for approaches to better define mechanisms of CKD and to identify novel therapeutic targets.

Animals↗
PubMed2006

Late referral of patients with chronic kidney disease: no time to waste.

The prevalence of patients with chronic kidney disease (CKD) in the US population is approximately 11%, and because of the increase in life expectancy and in diabetic nephropathy incidence, an exponential increase is predicted for the next decades. During the past decade, evidence that the progression of CKD can be attenuated by a multifactorial therapeutic approach has been increasing. However, a substantial percentage of patients with CKD will have progression to CKD stage V (ie, need for renal replacement therapy). Late referral of these patients (ie, <1 to 6 months before the start of renal replacement therapy) has been shown to be associated with higher mortality, morbidity, and costs. However, up to 64% of patients with CKD are still referred late. This review presents the available data on the epidemiology, causes, and consequences of late patient referral. Furthermore, it offers information to prevent late referral, improve CKD patient care, and change clinical practice.

Disease Progression↗
PubMed2004

High prevalence of low bone mineral density in pre-dialysis chronic kidney disease patients: bone histomorphometric analysis.

UNLABELLED: Chronic kidney disease (CKD) leads to reduced bone mineral density (BMD) in pre-dialysis and dialysis patients. A few studies have used dual-energy x-ray absorptiometry (DEXA) to assess BMD in pre-dialysis CKD patients and have shown low BMD to be highly prevalent. Until now there have been no studies reporting the histological features of low BMD in pre-dialysis CKD patients. AIM: To determine the prevalence and histological features of low BMD in pre-dialysis CKD patients. METHOD: Pre-dialysis CKD patients (n = 103, 46 females/57 males), median creatinine clearance of 29 (10 - 78) ml/min/ 1.73 m2, were evaluated using biochemical analysis and DEXA. Bone biopsies were obtained from those with low BMD. RESULTS: Fifty (48.5%) out of the 103 patients had low BMD (LBD group) and 53 (51.5%) had normal BMD (NBD group). The risk for low BMD was increased in those patients with alkaline phosphatase levels above 190 U/l and intact-PTH (iPTH) below 70 pg/ml (p < 0.05). Demographic and biochemical parameters from both groups were comparable, except for lower body mass index (BMI) in LBD subjects (p = 0.04). Women who had been post-menopausal for at least 1 year comprised 65% (13/20) and 50% (13/26) of the LBD and NBD groups, respectively (p = NS). In 40 LBD patients, bone histomorphometry revealed adynamic bone disease (ABD, 52.5%), osteomalacia (OM, 42.5%) and mixed bone disease (MBD, 5%). Trabecular bone volume (BV/TV) was lower in ABD and OM patients. A nearly significant association was found between ABD and iPTH < or = 150 pg/ml (p = 0.056), whereas higher values of iPTH were associated with OM. Total alkaline phosphatase < or = 190 U/l was significantly associated with ABD, whereas higher values were associated with OM. No correlation was observed between BV/TV and BMD. CONCLUSION: Low BMD is frequent in pre-dialysis CKD patients, and low turnover bone disease, manifesting as ABD and OM, was the hallmark of this bone loss.

Absorptiometry, Photon↗
PubMed2006

Changes in total parathyroid hormone (PTH), PTH-(1-84) and large C-PTH fragments in different stages of chronic kidney disease.

INTRODUCTION: Loss of renal function is accompanied by progressive increase in serum levels of intact parathyroid hormone (iPTH) in patients with end-stage renal disease (ESRD). There is a paucity of data regarding levels of PTH-(1-84) and its large carboxyl-terminal fragments (large C-PTH fragments) and progressive loss of kidney function in patients with chronic kidney disease (CKD). The current study was undertaken to describe the glomerular filtration rate (GFR)-dependent plasma concentrations of PTH-(1-84) and related large C-PTH fragments in adult patients with CKD by using different commercially available PTH assays. METHODS: We studied 80 Caucasian patients with CKD stages 1-5 without renal replacement therapy. Creatinine clearance was calculated by the Modification of Diet in Renal Disease (MDRD) formula. Levels of iPTH were determined by second-generation assays (iPTH Elecsys system, Roche Diagnostics; DUO total iPTH, Scantibodies Laboratory, Inc.; iPTH, Nichols Institute Diagnostics). Third-generation assays were used to measure PTH-(1-84) (CAP (cyclase activating PTH), Scantibodies; Bio-Intact PTH, Nichols). Levels of large C-PTH fragments and ratios of PTH-(1-84)/large C-PTH fragments were calculated and statistical analyses performed. RESULTS: Levels of iPTH and PTH-(1-84) showed CKD stage-dependent increases. Variations among the assays increased with progressive loss of kidney function. The assay from Scantibodies showed a GFR-dependent decrease of the ratio 1-84 PTH / large C-PTH fragment that was not observed with the Nichols assay. CONCLUSION: Increasing variations among the assays with progression of CKD emphasize the fact that the interpretation of measurements must take into consideration the specific assay. We found evidence for a possible preferential increase of the level of large C-PTH fragments over 1-84 PTH in a CKD stage-dependent manner (Scantibodies). The clinical implications of this finding have to be further evaluated by bone biopsy studies.

Adult↗