Chronic kidney disease prevalence in a UK residential care home population.
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BACKGROUND: Chronic kidney disease (CKD) is common ( approximately 30%) in non-institutionalized older people but little is known about the prevalence of CKD amongst older people living in residential care. METHODS: An observational study of older subjects [n = 250, median age 86 (range 67-100) years, 79% female, 100% Caucasian, 16% diabetic, 48% hypertensive, 5% known renal disease, mean number of medications 7] who were recruited over a 9-month period from 155 residential care homes in east Kent (total population 3811) using a randomization process. The estimated glomerular filtration rate (eGFR, ml/min/1.73 m(2)) was calculated using the Cockcroft and Gault equation corrected for the body surface area and the simplified Modification of Diet in Renal Disease (MDRD) Study equation. Serum cystatin C concentration was also measured. RESULTS: Using the MDRD equation 18% had eGFR >/=60, 39% stage 3A CKD (eGFR 45-59), 34% stage 3B CKD (eGFR 30-44) and 10% stage 4 CKD (eGFR 15-29). By the Cockcroft-Gault equation the equivalent figures were 3%, 18%, 48% and 31%, respectively. Agreement between the equations for staging of CKD was poor (kappa = 0.07). However, >80% of residents were categorized as having stage 3 CKD (>40% stage 3B) or worse whichever equation was used. Serum cystatin C concentration was increased in 92% of the population. Increasing age and higher body mass index were predictive of decreased renal function. CONCLUSION: Significant CKD is prevalent and unrecognized in this population. This may have important management implications particularly for treatment with renally excreted drugs, fracture prevention or managing cardiovascular risk. (+info)
Ghrelin treatment of chronic kidney disease: improvements in lean body mass and cytokine profile.
(58/1600)
Chronic kidney disease (CKD) is associated with an increase in inflammatory cytokines and can result in cachexia with loss of muscle and fat stores. We previously demonstrated the efficacy of treating a model of cancer cachexia with ghrelin and a ghrelin receptor agonist. Currently, we examine a surgical model of CKD in rats, resulting in uremia and decreased accrual of lean body mass. Treatment with ghrelin and two ghrelin receptor agonists (BIM-28125 and BIM-28131) resulted in increased food intake and an improvement in lean body mass accrual that was related in part to a decrease in muscle protein degradation as assessed by muscle levels of the 14-kDa actin fragment resulting from cleaved actomyosin. Additionally, there was a decrease in circulating inflammatory cytokines in nephrectomized animals treated with ghrelin relative to saline treatment. Ghrelin-treated animals also had a decrease in the expression of IL-1 receptor in the brainstem and a decrease in expression of prohormone convertase-2, an enzyme involved in the processing of proopiomelanocortin to the anorexigenic peptide alpha-MSH. We conclude that ghrelin treatment in uremia results in improved lean mass accrual in part due to suppressed muscle proteolysis and possibly related to antiinflammatory effects. (+info)
Chronic kidney disease mineral and bone disorder in children.
(59/1600)
Childhood and adolescence are crucial times for the development of a healthy skeletal and cardiovascular system. Disordered mineral and bone metabolism accompany chronic kidney disease (CKD) and present significant obstacles to optimal bone strength, final adult height, and cardiovascular health. Decreased activity of renal 1 alpha hydroxylase results in decreased intestinal calcium absorption, increased serum parathyroid hormone levels, and high-turnover renal osteodystrophy, with subsequent growth failure. Simultaneously, phosphorus retention exacerbates secondary hyperparathyroidism, and elevated levels contribute to cardiovascular disease. Treatment of hyperphosphatemia and secondary hyperparathyroidism improves growth and high-turnover bone disease. However, target ranges for serum calcium, phosphorus, and parathyroid hormone (PTH) levels vary according to stage of CKD. Since over-treatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardiovascular calcifications, therapy must be carefully adjusted to maintain optimal serum biochemical parameters according to stage of CKD. Newer therapeutic agents, including calcium-free phosphate binding agents and new vitamin D analogues, effectively suppress serum PTH levels while limiting intestinal calcium absorption and may provide future therapeutic alternatives for children with CKD. (+info)
Short-term treatment with sevelamer increases serum fetuin-a concentration and improves endothelial dysfunction in chronic kidney disease stage 4 patients.
(60/1600)
BACKGROUND AND OBJECTIVES: Vascular calcification and endothelial dysfunction contribute to the development of cardiovascular disease in patients with chronic kidney disease (CKD). Sevelamer, a non-calcium-based phosphate binder, has been shown to attenuate cardiovascular calcification in CKD patients, although the exact mechanism has not been clarified. This study was designed to investigate the effect of short-term sevelamer treatment on both serum fetuin-A concentrations and endothelial dysfunction seen in CKD patients. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Fifty nondiabetic stage 4 CKD patients whose phosphate levels were > or =5.5 mg/dl were enrolled in this 8-wk randomized prospective study. Thirty-six healthy volunteers served as matched controls. Patients were treated with either sevelamer (n = 25, 12 males) or calcium acetate (n = 25, 13 males). Fetuin-A, high-sensitivity C-reactive protein, Ca x PO4 product, flow-mediated dilation (FMD), insulin, and homeostasis model assessment (HOMA) were obtained at baseline and after the treatment period. RESULTS: As expected, CKD patients had significantly lower levels of fetuin-A and FMD, and significantly higher levels of intact parathyroid hormone, Ca x PO4 product, and high-sensitivity C-reactive protein than controls (P < 0.001 for all). The use of sevelamer led to a significant increase in the fetuin-A concentration with improvement in FMD, whereas no significant difference was observed in the calcium acetate group. In a multiple regression analysis, FMD levels were independently related to fetuin-A both before (beta = 0.63, P < 0.001) and after (beta = 0.38, P = 0.004) treatment. CONCLUSIONS: This small, randomized, prospective study shows that short-term sevelamer treatment significantly increases fetuin-A levels and improves FMD in nondiabetic stage 4 CKD patients. (+info)
Bone and mineral guidelines for patients with chronic kidney disease: a call for revision.
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Recent clinical studies of mineral metabolism in patients with chronic kidney disease have helped to verify and extend the Kidney Disease Outcomes Quality Initiative practice guidelines for bone metabolism and disease that were published in 2003. In particular, investigations that examined calcium loading, vitamin D therapy, and mortality risk associated with serum calcium and phosphate in dialysis patients have been the most helpful clinically. As a consequence, there is now a growing interest to have the previous guidelines amended accordingly, which will be performed through the Kidney Disease: Improving Global Outcomes working group after a debate within the nephrology community. The new data support this call for revision in an attempt to improve survival of the dialysis patient by emphasizing the importance of intravenous vitamin D therapy and of preventing excess calcium loading. These studies also suggest avenues for future investigation into nontraditional causes and treatments of cardiovascular disease in patients with chronic kidney disease. (+info)
Impact of the preintervention rate of renal function decline on outcome of renoprotective intervention.
(62/1600)
BACKGROUND AND OBJECTIVES: Randomized clinical trials on progression of renal diseases usually include patients according to criteria for BP, renal function, and proteinuria. There are no data showing that this provides groups with similar baseline rates of renal function loss. Accordingly, the impact of preintervention rate of renal function loss (slope) on outcome of studies has not been established. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Preintervention slope was established in 60 of 89 renal patients without diabetes in whom a 4-yr prospective, randomized intervention had been performed (enalapril versus atenolol), and whether (1) preintervention slope was distributed equally over the groups; (2) treatment benefit, defined as slope improvement, corresponded to study outcome; and (3) preintervention slope was a determinant of intervention slope were analyzed. RESULTS: The preintervention slope was different in the groups: -3.7 +/- 3.2 in the group to receive enalapril versus -2.2 +/- 3.3 ml/min per yr in the group to receive atenolol. The intervention slopes were similar: -1.9 +/- 0.8 enalapril and -1.8 +/- 0.7 ml/min per yr atenolol. Accordingly, slope improved during enalapril only. When analyzed by angiotensin-converting enzyme (I/D) genotype, slope improvement was found only in DD genotype. On multivariate analysis, the preintervention slope was a main predictor of the intervention slope. CONCLUSIONS: Differences in preintervention slope are relevant to outcome of trials and can induce bias. For future studies, allocation according to preintervention slope, although time-consuming, may be useful to allow conduction of more valid studies in a smaller number of patients. (+info)
Mechanisms of vascular calcification in chronic kidney disease.
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Vascular calcification is common in chronic kidney disease and associated with increased morbidity and mortality. Its mechanism is multifactorial and incompletely understood. Patients with chronic kidney disease are at risk for vascular calcification because of multiple risk factors that induce vascular smooth muscle cells to change into a chondrocyte or osteoblast-like cell; high total body burden of calcium and phosphorus due to abnormal bone metabolism; low levels of circulating and locally produced inhibitors; impaired renal excretion; and current therapies. Together these factors increase risk and complicate the management of vascular calcification. (+info)
Creatinine-based glomerular filtration rates and microalbuminuria for detecting metabolic abnormalities in US adults: the National Health and Nutrition Examination Survey 2003-2004.
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BACKGROUND/AIMS: Guidelines suggest searching for metabolic complications of chronic kidney disease when glomerular filtration rates (GFR) or urinary albumin tests are abnormal. This study aimed to quantify diagnostic test characteristics of these measures for detecting metabolic abnormalities. METHODS: Subjects were participants aged >or=20 years (n = 7,778) in the US National Health and Nutrition Examination Survey 2003-2004. Low GFR was defined as creatinine-based estimate <60 ml/min per 1.73 m(2); abnormal urinary albumin-creatinine ratio as >or=20 mg/dl in men, >or=30 mg/dl in women; and metabolic abnormalities as abnormal potassium, hemoglobin, bicarbonate, phosphorus, or parathyroid hormone levels. RESULTS: Of adults, 5.66% had low GFR and 8.14% abnormal urinary albumin-creatinine ratio. Overall, 15.09% had >or= one metabolic abnormality, as did 34.07% with low GFR (p < 0.0001) and 24.27% with abnormal urinary albumin-creatinine ratio (p = 0.0021). Considered as a diagnostic test, the sensitivity, specificity, and positive and negative predictive values of low GFR for detecting >or=1 metabolic abnormality were 0.13, 0.96, 0.34, and 0.86, respectively. Corresponding values for abnormal urinary albumin-creatinine ratio were 0.13, 0.92, 0.24, and 0.86. CONCLUSIONS: A policy of searching for metabolic complications in every adult with low GFR or microalbuminuria has limited diagnostic yield. (+info)