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PubMed2005

Cinacalcet: An oral calcimimetic agent for the management of hyperparathyroidism.

BACKGROUND: Uncontrolled hyperparathyroidism (HPT), particularly HPT resulting from chronic kidney disease (CKD), is associated with significant morbidity and cardiovascular mortality. Traditional medical therapy (eg, vitamin D sterols, calcium, phosphate binders) has been inadequate for the management of HPT and its vascular and skeletal complications. OBJECTIVE: : The goal of this article was to review the efficacy and safety profile of cinacalcet, a second-generation calcimimetic, in the management of HPT secondary to CKD, primary HPT, and parathyroid carcinoma. METHODS: MEDLINE, Web of Science, and International Pharmaceutical Abstracts were searched from 1995 to July 2005 using the terms cinacalcet, AMG 073, KRN 1493, calcimimetics, hypercalcemia, and hyperparathyroidism. RESULTS: Compared with placebo, cinacalcet significantly reduced parathyroid hormone levels within 2 to 4 hours after administration (P < 0.05). In Phase III trials involving 1136 patients with secondary HPT, 56% of those who received cinacalcet achieved the National Kidney Foundation Kidney Disease Outcomes Quality Initiative target of a reduction in parathyroid hormone to <300 pg/mL, 65% achieved a calcium-phosphorus product <55 mg2/dL2, and a respective 49% and 46% achieved normalized serum calcium and phosphorus levels (P < 0.001). Cinacalcet's effects were similar regardless of patients' demographic characteristics, duration or mode of dialysis, severity of HPT, or use of concomitant medical therapy. Preliminary evidence suggests that cinacalcet may reverse cortical bone loss. Cinacalcet was well tolerated, with nausea (31%) and vomiting (27%) being the most commonly reported adverse effects. Hypocalcemia was transient in 5% of patients, was usually asymptomatic, and was corrected by dose reduction. CONCLUSIONS: Based on the available evidence, cinacalcet is effective and well tolerated in the treatment of secondary HPT and refractory parathyroid carcinoma. Its use in primary HPT appears promising. Further investigations are needed to determine if cinacalcet can prevent the long-term complications of HPT and reduce mortality.

Animals↗

PubMed2006

Open-label pilot study comparing quantitative ultrasound and dual-energy X-ray absorptiometry to assess corticosteroid-induced osteoporosis in patients with chronic kidney disease.

BACKGROUND: Patients with chronic kidney disease (CKD) might be at high risk for bone disease. Decreased functional kidney mass contributes to renal osteodystrophy, which might be exacerbated by certain drug therapies. Long-term (> or = 6 months) corticosteroid treatment is commonly prescribed in patients with glomerular disease, possibly causing bone loss both indirectly and directly, putting the patient at increased risk for fracture. The dual-energy x-ray absorptiometry (DXA) is the current "gold standard" for measuring osteoporosis-related fractures and works by passing ultrasound waves through bone to determine the structural anisotropy in the heel. OBJECTIVE: This pilot study was designed to determine whether there is a correlation between DXA and quantitative ultrasound (QUS) in detecting corticosteroid-induced osteoporosis. METHODS: This open-label pilot study was conducted at the Medical Center Nephrology Clinic, Albany Medical College, Albany, New York. Female patients aged > or = 18 years with a diagnosis of CKD and/or a history of kidney transplantation and who were receiving long-term corticosteroid treatment were enrolled. Each patient served as her own control and underwent DXA of the hip and spine (DXA-hip and DXA-spine, respectively) and QUS of the dominant and nondominant heels (QUS-dominant and QUS-nondominant, respectively), within 1 week so that conditions were similar in each patient. RESULTS: Eight patients were included in the study (mean [SD] age, 50.2 [11.2] years). A positive correlation was found between DXA-hip and QUS-nondominant (r2=0.76; P=0.009); however, no correlation was found with DXA-spine. Similarly, a positive correlation was found between DXA-hip and QUS-dominant (r2=0.75; P=0.009), but no correlation with DXA-spine was found (r2=0.22). CONCLUSION: In this small, selected population, QUS showed a fair correlation with DXA-hip but no correlation with DXA-spine. Further studies are needed to determine the effectiveness in other populations.

Absorptiometry, Photon↗

PubMed2005

Renal osteodystrophy: a pediatric perspective, 2005.

Renal osteodystrophy (ROD) associated with chronic kidney disease (CKD) involves a complex interrelationship of the loss of divalent mineral homeostasis, hyperparathyroidism, and gene modulation. In affected children, ROD leads to impaired linear growth as well as to the development of other significant skeletal and extraskeletal manifestations. Despite the success of kidney transplantation, many ROD complications cannot be completely reversed; and thus, patients with CKD and ROD require long-term follow-up. Although the availability of vitamin D analogues has advanced ROD management, it has also created new issues for clinicians to address, motivating future investigations of calcimimetic therapies. An algorithmic approach to the management of ROD in children is presented; to be most effective, this approach requires close and frequent surveillance to prevent side effects related to potent therapies.

Calcitriol↗

PubMed2006

A potential evidence to explain the reason behind the devastating prognosis of coronary artery disease in uraemic patients: renal insufficiency is associated with poor coronary collateral vessel development.

The potential of individuals to develop coronary collateral circulation is often neglected but is of potential major importance in myocardial vulnerability. Likewise, the effect of chronic kidney disease (CKD) on collateral vessel development is not known. The purpose of this study was to evaluate the effect of CKD on collateral development in patients with advanced coronary artery disease. A total of 171 uraemic patients (serum creatinine > or = 1.5 mg/dl, creatinine clearance < 80 mL)/min) who underwent coronary angiography were evaluated in this study. A total of 134 patients met the criteria for the uraemic group and 134 consecutive non-uraemic patients who constituted the control group. The collateral score (CS) was graded according to the Rentrop classification and the collateral score was calculated by summing the Rentrop numbers of every patient. Collateral vessels have also been categorized according to their anatomic locations and collateral connection grades (CC). CC2 collaterals were observed less frequently in the uraemic patients than in the control subjects (11% versus 26%, p=0.03) and CC0 more frequently (31% versus 22%, p<0.05). Epicardial pathway was detected more frequently in the control subjects than in the uraemic patients (31% versus 12%, p=0.03) and septal pathway less frequently (37% versus 54%). There was a significant negative correlation between CS and creatinine (r=-0.68, p<0.01). The mean CS in the uraemic group was significantly lower than the non-uraemic group (1.29+/-0.88 versus 2.18+/-1.3, p<0.001). These results altogether showed that besides the quantity, quality (functional, haemodynamic and anatomic features) of the uraemic collaterals and a network that they constitute is also impaired and different from the collaterals of the patient with normal renal function.

Aged↗

PubMed2005

Racial disparities in the optimal delivery of chronic kidney disease care.

This article provides evidence that the current and growing burden of CKD in racial and ethnic minority populations is likely to be multifactorial involving the interplay of biologic, clinical, social, and behavioral determinants. To eliminate these disparities, crafting successful solutions requires more attention to the constellation of contributing factors not only by specialists, primary care physicians, and other health care providers involved in CKD care, but also clinical and behavioral scientists, payers of health care, and patients.

Delivery of Health Care↗

PubMed2005

Measurement of kidney function.

Accurate estimation of kidney function is central to the detection, evaluation, and treatment of chronic kidney disease (CKD). Glomerular filtration rate (GFR) is widely accepted as the best overall measure of kidney function and as such it forms the basis of definition and classification system for CKD. GFR cannot be measured directly in clinical practice and multiple methods are used to estimate GFR, all of which have their strengths and limitations. The current recommended method is to use estimating equations based on serum creatinine and which incorporate demographic and clinical variables.

Biomarkers↗

PubMed2005

Multiple risk factor intervention in chronic kidney disease: management of cardiac disease in chronic kidney disease patients.

This article describes the relationship between CVD and CKD, the current state of knowledge regarding medical interventions, and underscores the importance of attending to both CVD and kidney disease aspects in each individual. The burden of cardiac disease in CKD patients is high with severe LVH, dilated cardiomyopathy and coronary artery disease occurring frequently. This predisposes to congestive heart failure, angina, myocardial infarction, and death. Multiple risk factors for cardiac disease exist and include hypertension, diabetes, smoking, anemia, abnormal calcium and phosphate metabolism, inflammation, and LVH. The efficacy of risk factor intervention has not been established in these populations, although there is good evidence for good blood pressure control, partial correction of anemia, treatment of dyslipidemia, cessation of tobacco use, correction of divalent abnormalities, and aspirin us. Appropriate use of ACE inhibitors, beta-blockers, and statins should be encouraged.

Cardiovascular Diseases↗

PubMed2006

Predicting the impact of population level risk reduction in cardio-vascular disease and stroke on acute hospital admission rates over a 5 year period--a pilot study.

UNLABELLED: The brief for this study was to produce a practical, evidence based, financial planning tool, which could be used to present an economic argument for funding a public health-based prevention programme in coronary heart disease (CHD) related illness on the same basis as treatment interventions. OBJECTIVES: To explore the possibility of using multivariate risk prediction equations, derived from the Framingham and other studies, to estimate how many people in a population are likely to be admitted to hospital in the next 5-10 years with cardio vascular disease (CVD) related events such as heart attacks, strokes, heart failure and kidney disease. To estimate the potential financial impact of reductions in hospital admissions, on an 'invest to save' basis, if primary care trusts (PCTs) were to invest in public health based interventions to reduce cardiovascular risk at a population level. STUDY DESIGN: The populations of five UK PCTs were entered into a spreadsheet based decision tree model, in terms of age and sex (this equated to around 620,000 adults). An estimation was made to determine how many people, in each age group, were likely to be diabetic. Population risk factors such as smoking rates, mean body mass index (BMI), mean total cholesterol and mean systolic blood pressure were entered by age group. The spreadsheet then used a variant of the Framingham equation to calculate how many non-diabetic people in each age group were likely to have a heart attack or stroke in the next 5 years. In addition heart failure and dialysis admission rates were estimated based upon risk factors for incidence. The United Kingdom Prospective Diabetes Study (UKPDS) risk engines 56 and 60 were used to calculate the risk of CHD and stroke, respectively, in people with type 2 diabetes. The spreadsheet deducted the number of people likely to die before reaching hospital and produced a predicted number of hospital admissions for each category over a 5-year period. The final part of the calculation attached a cost to the hospital activity using the UK Health Resource Grouping (HRG) tariffs. The predicted number of events in each of the primary care trusts was then compared with the actual number of events the previous year (2004/2005). METHODOLOGY: The study used a decision tree type model, which was populated with data from the research literature. The model applied the risk equations to population data from five primary care trusts to estimate how many people would suffer from an acute CVD related event over the next 5 years. The predicted number of events was then compared with the actual number of acute admissions for heart attacks, strokes, heart failure, acute hypoglycaemic attacks, renal failure and coronary bypass surgery the previous year. RESULTS: The first outcome of the model was to compare the estimated number of people in each PCT likely to suffer from a heart attack, a stroke, heart failure or chronic kidney failure with the actual number the previous year 2004/2005. The predicted number was remarkably accurate in the case of heart attack and stroke. There was some over-prediction of chronic kidney disease (CKD) which could be accounted for by known under-diagnosis in this illness group and the inability of the model to pick up, at this stage, the fact that many CKD patients die of a CHD related event before they reach the stage of requiring renal replacement. The second outcome of the model was to estimate the financial consequence of risk reduction. Moderate reductions in risk in the order of around 2-4% were estimated to lead to saving in acute admission costs or around pounds sterling 5.4 million over 5 years. More ambitious targets of risk reduction in the order of 5-6% led to estimated savings of around pounds sterling 8.7 million. CONCLUSIONS: This study is not presented as the definitive approach to predicting the economic consequences of investment in public health on the cost of secondary care. It is simply a logical, systematic approach to quantifying these issues in order to present a business case for such investment. The research team do not know if the predicted savings would accrue from such investments; it is theoretical at this stage. The point is, however, that if the predictions are correct then the savings will accrue from over 4000 people, from an adult population of around 185,000 not having a heart attack or a stroke or an acute exacerbation of heart failure.

Adolescent↗

PubMed2005

Effects of vitamin D analogs on the expression of plasminogen activator inhibitor-1 in human vascular cells.

INTRODUCTION: Vitamin D analogs such as paricalcitol and calcitriol have been shown to provide survival benefit for Stage 5 chronic kidney disease (CKD) patients, possibly due to their positive impact on the cardiovascular system. Plasminogen activator inhibitor-1 (PAI-1) is one of the risk markers for coronary artery disease. MATERIALS AND METHODS: Human coronary artery smooth muscle cells (SMC) and endothelial cells (CAEC) were treated with vitamin D analogs to assess the effects of the drugs on the expression of PAI-1 mRNA and protein. RESULTS: In SMC, both paricalcitol and calcitriol down-regulated the expression of PAI-1 mRNA and protein in a dose-dependent manner. The EC(50) values of paricalcitol and calcitriol on suppressing PAI-1 mRNA were 3.0 and 2.8 nM, respectively. Interestingly, these two drugs had no significant effect on the expression of PAI-1 protein or mRNA in CAEC. Further analysis showed that CAEC did not express functional vitamin D receptor (VDR) and paricalcitol failed to induce the expression of 25-hydroxyvitamin D-24-hydroxylase (CYP24A1) mRNA, a gene known to be regulated by VDR. As a comparison, SMC expressed VDR and paricalcitol induced CYP24A1 mRNA in SMC (>150-fold at 10 nM) dose-dependently. The effect of paricalcitol on suppressing PAI-1 in SMC was blocked by cycloheximide, suggesting that protein synthesis was involved. CONCLUSION: These results demonstrate that vitamin D analogs suppress PAI-1 in SMC, but not in CAEC. Suppression of PAI-1 in SMC may be one of the factors contributing to the survival benefits of vitamin D analog therapy in CKD patients.

Calcitriol↗

PubMed2006

TACE-dependent EGF receptor activation in angiotensin-II-induced kidney disease.

Angiotensin II (Ang II) has been implicated in the development of cardiovascular disorders and chronic kidney disease (CKD). Ang II causes renal lesions through the activation of tumor necrosis factor (TNF)-alpha-converting enzyme (TACE, also called a disintegrin and a metalloproteinase domain 17) and the release of transforming growth factor (TGF)-alpha, which binds to and activates the epidermal growth factor receptor. Renal lesions such as glomerulosclerosis, tubular atrophy, fibrosis, mononuclear cell infiltration and proteinuria following chronic Ang II infusion are substantially reduced in mice lacking TGF-alpha and those given a specific TACE inhibitor. These findings indicate that the selective inhibition of renal TACE could have therapeutic potential in the treatment of CKD.

ADAM Proteins↗

PubMed2006

Chronic kidney disease is still present after renal transplantation with excellent function.

According to a k/DOQI work group, chronic kidney disease (CKD) can be present also in subjects with glomerular filtration rate (GFR) >90 mL/min or a serum creatinine (sCr) below 1.3 mg/dL. The aim of this study was to document the prevalence of clinical or biologic abnormalities among 190 cadaveric renal transplant patients with excellent and stable renal function at 6 months after transplantation as well as 5 years later. The recipients were 82 women and 108 men of mean age at transplantation of 44.56 +/- 11.73 years. All patients were on Neoral-based immunosuppression with at least 5-year follow-up. Mean sCr was 1.18 +/- 0.2 mg/dL. Mean GFR was 78.57 +/- 27.06 mL/min. Systolic blood pressure was >130 mm Hg in 56.6%, although 78.3% of patients were on antihypertensive therapy; 34.3% were anemic; 75.4% had serum cholesterol >200 mg/dL; 62.2% had serum triglyceride levels >170 mg/dL. Serum intact parathyroid hormone >100 pg/mL was observed in 38% of patients and 43% were on vitamin D supplementation, and 11.4% had developed posttransplant diabetes mellitus. With respect to controls, von Willebrand factor was higher in 81.2% (P < .0001; RR = 11); serum homocysteine levels in 75% (P < 0.001; RR = 7.61); PAI-1 in 37.5% (P = .0009; RR = 4). At 5 years posttransplantation we observed an overall improvement in these abnormalities. The vast majority of renal transplant patients with excellent graft function belong to stage 1 of CKD being affected by hypertension, dyslipidemia, anemia, and residual hyperparathyroidism. Markers of endothelial dysfunction were largely abnormal, a condition that could predispose to cardiovascular events.

Adult↗

PubMed2003

Early detection of kidney disease in community settings: the Kidney Early Evaluation Program (KEEP).

BACKGROUND: Early identification of persons at risk for kidney disease provides an opportunity to prevent or delay its progression and decrease morbidity and mortality. Our hypothesis was that implementation of a targeted screening program in communities with high-risk populations would detect previously unidentified persons with or at high risk for chronic kidney disease (CKD) with a prevalence that exceeds that predicted for CKD in the general population. METHODS: Persons with hypertension or diabetes or a first-order relative with hypertension, diabetes, or kidney disease were screened for kidney disease risk factors. Blood pressure, blood glucose level, serum creatinine level, hemoglobin level, microalbuminuria, hematuria, pyuria, body mass index, and estimated glomerular filtration rate (EGFR) were evaluated. RESULTS: Six thousand seventy-one eligible persons were screened from August 2000 through December 2001: of these persons, 68% were women, 43% were African American, 36% were white, 10% were Hispanic, and 5% were Native American. Most reported high-school education or more (84%) and health insurance coverage (86%). Twenty-seven percent met the screening definitions for diabetes; 64%, for hypertension; 29%, for microalbuminuria; 8%, for anemia; 18%, for hematuria; 13%, for pyuria; 5%, for elevated serum creatinine level; 16%, for reduced EGFR; and 44%, for obesity. Among participants without a reported history of specified conditions, screening identified 82 participants (2%) with diabetes, 1,014 participants (35%) with hypertension, 277 participants (5%) with elevated serum creatinine levels, 839 participants (14%) with reduced EGFRs, and 1,712 participants (29%) with microalbuminuria. Thirty-five percent of participants with a history of diabetes had elevated serum glucose levels at screening (> or =180 mg/dL [10 mmol/L]), and 64% with a history of hypertension did not have blood pressure controlled to less than 140/90 mm Hg. Only 18% of participants with a history of diabetes and 31% with a reduced EGFR had blood pressure controlled to less than 130/80 mm Hg and less than 135/85 mm Hg, respectively. CONCLUSION: Targeted screening is effective in identifying persons with previously unidentified or poorly controlled kidney disease risk factors, as well as persons with a moderately decreased EGFR.

Adolescent↗

PubMed2003

Predialysis psychoeducational intervention and coping styles influence time to dialysis in chronic kidney disease.

BACKGROUND: Consensus endorses predialysis intervention before the onset of end-stage renal disease. In a previous study, predialysis psychoeducational intervention (PPI) extended time to dialysis therapy by a median of 6 months. We undertook to replicate and extend this finding by examining hypothesized mechanisms. METHODS: We used an inception-cohort, prospective, randomized, controlled trial with follow-up to evaluate an intervention that included an interactive 1-on-1 slide-supported educational session, a printed summary (booklet), and supportive telephone calls once every 3 weeks. Participants were sampled from 15 Canadian (tertiary care) nephrology units and included 297 patients with progressive chronic kidney disease (CKD) expected to require renal replacement therapy (RRT) within 6 to 18 months. The main outcome was time to dialysis therapy (censored at 18 months if still awaiting RRT). RESULTS: Time to dialysis therapy was significantly longer (median, 17.0 months) for the PPI group than the usual-care control group (median, 14.2 months; Cox's proportional hazards analysis, controlling for general nonrenal health, P < 0.001). Coping by avoidance of threat-related information (called blunting) was associated with shorter times to dialysis therapy (P < 0.032). A group x blunting interaction (P < 0.069) indicated: (1) time to dialysis therapy was shortened in the usual-care group, especially when patients coped by blunting; but (2) time to dialysis therapy was extended with PPI, even among patients who coped by blunting. Knowledge acquisition predicted time to dialysis therapy (r = 0.14; P < 0.013). Time to dialysis therapy was unrelated to depression or social support. CONCLUSION: PPI extends time to dialysis therapy in patients with progressive CKD. The mechanism may involve the acquisition and implementation of illness-related knowledge. Routine follow-up also may be especially important when patients cope by avoiding threat-related information.

Adaptation, Psychological↗

PubMed2026

Effect of semaglutide on kidney outcomes in the SELECT, FLOW, and SOUL trials: a prespecified pooled analysis.

BACKGROUND: The GLP-1 receptor agonist semaglutide reduces clinically important kidney outcomes in people with type 2 diabetes and chronic kidney disease (CKD). We aimed to assess the pooled effects of semaglutide on kidney outcomes in prespecified analyses of participant-level data from the diverse populations of the SELECT, FLOW, and SOUL randomised placebo-controlled trials. METHODS: Participants with CKD (FLOW) or atherosclerotic cardiovascular disease (SELECT and SOUL) were randomly assigned semaglutide (once-weekly subcutaneous 1·0 mg [FLOW], once-weekly subcutaneous 2·4 mg [SELECT], or once-daily oral 14 mg [SOUL]) or matching placebo, added to standard of care. The primary outcome in this pooled analysis was time to first occurrence of a kidney composite, defined as onset of persistent 50% or greater reduction in estimated glomerular filtration rate (eGFR), kidney failure (persistent eGFR <15 mL/min per 1·73 m2, or initiation of kidney replacement therapy), kidney-related death, or cardiovascular-related death. Safety was also assessed. FINDINGS: The pooled participants from the trials (N=30 787) had a mean follow-up of 39·5-47·5 months. Among participants assigned to semaglutide, 973 first events of the primary kidney composite occurred compared with 1134 first events for placebo (hazard ratio [HR] 0·84 [95% CI 0·77-0·91]). First events of a narrower secondary kidney composite (excluding cardiovascular-related death from the primary outcome) were also reduced with semaglutide versus placebo (347 and 416, respectively; 0·80 [0·69-0·92]). Safety outcomes were overall similar between groups, and in line with other GLP-1 receptor agonist trials. Serious adverse events were numberically lower with semaglutide than with placebo. INTERPRETATION: Data pooled from three large phase 3 trials suggest that semaglutide reduces the risk of major kidney outcomes in a broad population with cardio-kidney-metabolic disease while having a favourable risk-benefit profile. In people with cardio-kidney-metabolic disease, with and without diabetes, semaglutide (oral or injected) prevents kidney-related and cardiovascular complications and induces adverse events in line with GLP-1 receptor agonist studies, regardless of baseline characteristics within the cardio-kidney-metabolic spectrum. This was a participant-level analysis conducted in a large database of three randomised controlled trials of similar design and examining the same treatment, but there were some differences in participants' baseline characteristics, and in the dose and route of administration of treatment. This pooled analysis adds evidence for the benefit of GLP-1 receptor agonists in general, and semaglutide in particular, in a broad population of people with cardio-kidney-metabolic disease, suggesting that the benefit of semaglutide might not be explained only by its glycaemic effects, weight-management effects, or both. FUNDING: Novo Nordisk.

Humans↗

PubMed1993

Insulin receptor autophosphorylation. II. Determination of autophosphorylation sites by chemical sequence analysis and identification of the juxtamembrane sites.

Autophosphorylation sites of the human insulin receptor were identified by microsequence analysis of 19 discrete tryptic [32P]phosphopeptides, purified from the autophosphorylated cytoplasmic kinase domain (CKD). Seventeen phosphopeptides were generated by cleavage at Arg and/or Lys, but two phosphopeptides were generated reproducibly by anomalous cleavages. Two new sites were identified in the juxtamembrane region of the intact insulin receptor beta-subunit (the amino terminus of the CKD), including phosphotyrosines 965 and 972. Three sites in the central region, including phosphotyrosines 1158, 1162, and 1163, were identified from six phosphopeptides; tyrosine at 1158 was the least phosphorylated. Monophosphopeptides contained phosphotyrosine at either residue 1158 or 1163, but not at 1162. Bisphosphorylation included phosphotyrosines only at 1162 and 1163. The two autophosphorylation sites near the carboxy terminus were found in seven phosphopeptides, including phosphotyrosines at 1328 and 1334. When mapped by reverse-phase high-performance liquid chromatography, these phosphopeptides eluted in the order central domain, first; carboxy-terminal region, second; and juxtamembrane (amino-terminal) domain, last.

Adenosine Triphosphate↗

PubMed2006

Assessment of glomerular filtration rate in addition to albuminuria is important in managing type II diabetes.

Although much emphasis has been placed on screening for albuminuria in type II diabetic patients, less attention has been focused on the role of glomerular filtration rate (GFR) in the assessment of risk. Herein, we examined the association between GFR and vascular complications in a consecutive cohort of 5174 type II diabetic patients between 1995 and 2000. Renal function was assessed by GFR (estimated by Modification of Diet in Renal Disease equation). The frequency of chronic kidney disease (CKD) as defined by GFR <60 ml/min/1.73 m(2), micro- and macrovascular complications, and their associations were analyzed. In this study cohort, 6% had serum creatinine > or =150 micromol/l and 15.8% had CKD. After adjustment for potential confounders, including urinary albumin excretion, odds ratios [95% confidence interval (CI)] across different stages of estimated GFR (> or =90, 60-89, 30-59, 15-29, <15 ml/min/1.73 m(2)) for macrovascular disease were 1.00, 1.42 [1.12-1.80], 1.80 [1.32-2.45], 2.74 [1.64-4.56], and 4.05 [1.77-9.26], respectively (P for trend <0.001); for retinopathy were 1.00, 1.23 [1.04-1.46], 1.80 [1.40-2.30], 2.05 [1.25-3.37], and 4.12 [1.56-10.90], respectively (P for trend <0.001); for sensory neuropathy were 1.00, 1.53[1.27-1.85], 2.09 [1.58-2.76], 4.32 [2.41-7.77], and 3.16 [1.25-8.02], respectively (P for trend <0.001); and for microalbumuria (with GFR <15 ml/min/1.73 m(2) excluded from the analysis) were 1.00, 1.51 [1.30-1.75], 5.80 [4.52-7.44], and 52.5 [16.4-168.2] respectively (P for trend <0.001). Measurement of serum creatinine alone without GFR may underestimate renal impairment in type II diabetic patients. Decreasing GFR was significantly associated with increasing frequency of micro- and macrovascular complications.

Adult↗

PubMed2006

Hypertension in renal parenchymal disease: why is it so resistant to treatment?

The association between hypertension and chronic renal disease is well known. The pathogenesis of hypertension in patients with chronic kidney disease (CKD) is complex and multifactorial, which may explain why it is resistant to treatment. The traditional paradigm is that hypertension in CKD is due either to an excess of intravascular volume (volume dependent) or to excessive activation of the renin-angiotensin system in relation to the state of sodium/volume balance (renin-dependent hypertension). This review focuses on the importance of less established mechanisms, such as increased activity of the sympathetic nervous system, increased endothelin production, decreased availability of endothelium-derived vasodilators and structural changes of the arteries, renal ischemia, and sleep apnea.

Antihypertensive Agents↗

PubMed2006

Blockade of Angiotensin II type-1 receptor reduces oxidative stress in adipose tissue and ameliorates adipocytokine dysregulation.

Dysregulated production of adipocytokines may be involved in the development of atherosclerotic cardiovascular disease in metabolic syndrome and chronic kidney disease (CKD) associated with metabolic syndrome. The aim of this study was to determine the effects of treatment with angiotensin II (Ang II) type-1 receptor blocker (ARB) on the regulation of adipocytokines. Olmesartan, an ARB, significantly blunted the age- and body weight-associated falls in plasma adiponectin both in genetically and diet-induced obese mice, without affecting body weight, but had no effect on plasma adiponectin levels in lean mice. Olmesartan also ameliorated dysregulation of adipocytokines in obesity, such as tumor necrosis factor-alpha, plasminogen activator inhibitor-1, monocyte chemotactic protein-1, and serum amyloid A3. Olmesartan significantly reduced reactive oxygen species originating from accumulated fat and attenuated the expression of nicotinamide adenine dinucleotide phospho hydrogenase oxidase subunits in adipose tissue. In cultured adipocytes, olmesartan acted as an antioxidant and improved adipocytokine dysregulation. Our results indicate that blockade of Ang II receptor ameliorates adipocytokine dysregulation and that such action is mediated, at least in part, by targeting oxidative stress in obese adipose tissue. Ang II signaling and subsequent oxidative stress in adipose tissue may be potential targets for the prevention of atherosclerotic cardiovascular disease in metabolic syndrome and also in metabolic syndrome-based CKD.

Adiponectin↗