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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rising incidence of type 2 diabetes mellitus and of its complications will make it the most important health care challenge in the first quarter of the 21st Century. Diabetic nephropathy left unchecked will overwhelm the renal resources. Simple methods (proper diet and exercise, prevention of obesity) are successful in preventing type 2 diabetes in the great majority of the persons at risk. In patients with established type 2 diabetes, nephropathy can be prevented or greatly delayed by strict metabolic control, strict control of blood pressure using angiotensin-converting enzyme inhibitors and angiotensin receptor blockers as the first line of drugs, tight control of serum lipids using statins as indicated, low protein diet, avoidance of smoking and other nephrotoxic influences, prevention of abnormalities in calcium/phosphorus metabolism, and prevention of renal anemia by the early use of erythropoietin. Current research offers the promise of definitive prevention of both type 2 diabetes and diabetic nephropathy.
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PMID:Prevention of nephropathy in patients with type 2 diabetes mellitus. 1630 58

We have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreases the serum phosphate. Most recently, these observations were rediscovered in low-density lipoprotein receptor null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance). We had demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial type. We have shown that VC is worsened by CKD and ameliorated by bone morphogenetic protein -7 (BMP-7). The finding that high-fat-fed low-density lipoprotein receptor null animals without CKD have hyperphosphatemia led us to examine the skeletons of these mice. We found significant reductions in bone formation rates, associated with increased VC and superimposing CKD results in the adynamic bone disorder (ABD), while VC was worsened and hyperphosphatemia persisted. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. BMP-7 treatment corrected the ABD and corrected hyperphosphatemia, compatible with BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. Thus, in the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to ABD producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through increased bone formation and skeletal deposition of phosphate, and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury before demonstrable hyperphosphatemia, and they are preventable and treatable. Therefore, early intervention in CKD is warranted and may affect mortality of the disease.
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PMID:Connections between vascular calcification and progression of chronic kidney disease: therapeutic alternatives. 1633 68

In two independent and separate studies, we have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreased the serum phosphate. In the first study, the serum Ca PO(4), parathyroid hormone (PTH), and calcitriol were maintained normal after renal ablation in mice, and even mild renal injury equivalent to stage 3 CKD decreased bone formation rates. More recently, these observations were rediscovered in low-density lipoprotein receptor null (LDLR-/-) mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia and insulin resistance). We demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial calcification. We have also shown that VC is made worse by CKD and ameliorated by bone morphogenetic protein-7 (BMP-7). The finding that high-fat fed LDLR-/- animals with CKD had hyperphosphatemia which was prevented in BMP-7-treated animals lead us to examine the skeletons of these mice. It was found that significant reductions in bone formation rates were associated with high-fat feeding, and superimposing CKD resulted in the adynamic bone disorder (ABD), while VC was made worse. The effect of CKD to decrease skeletal anabolism (decreased bone formation rates and reduced number of bone modelling units) occurred despite secondary hyperparathyroidism. The BMP-7 treatment corrected the ABD and hyperphosphatemia, owing to BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in the metabolic syndrome with CKD, a reduction in bone forming potential of osteogenic cells leads to the ABD producing hyperphosphatemia and VC, processes ameliorated by BMP-7, in part through increased bone formation and skeletal deposition of phosphate and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury affecting the skeleton before demonstrable hyperphosphatemia and that they are preventable and treatable. Therefore, early intervention in the skeletal disorder associated with CKD is warranted and may affect mortality of the disease.
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PMID:Function and effect of bone morphogenetic protein-7 in kidney bone and the bone-vascular links in chronic kidney disease. 1688 97

For optimal management of chronic kidney disease (CKD), dietary modification should be an integral part of patient care. Dietary considerations for obese patients with CKD are numerous and complicated and involve modification of intake of calories, protein, fat, phosphorus, and electrolytes. General principles for dietary management of obese patients include (1) ensuring adequate monitoring of nutritional status through assessment of diet, nutrition-related laboratory parameters, and anthropometrics; (2) creation of an individualized diet plan that meets clinical guidelines and has favorable effects on obesity-related conditions such as blood pressure and lipids; (3) careful attention to patients' food choices, portion size, and food-preparation methods; (4) recommending adjustment of overall energy intake to promote weight loss, yet maintain good nutritional status; and (5) modification of diet as the patient's nutritional status changes and CKD progresses. The basic objectives of dietary modification are to lighten the excretory load of products of metabolism and to help the kidney maintain normal equilibrium of the body's internal environment. Dietary modifications must be individualized and appropriate to the stage of CKD. This review describes dietary factors important in optimizing nutritional status of obese patients with CKD. Additionally, current clinical practice guidelines and strategies for meeting them are discussed.
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PMID:Dietary recommendations for obese patients with chronic kidney disease. 1704 25

A model of chronic kidney disease (CKD)-induced vascular calcification (VC) that complicates the metabolic syndrome was produced. In this model, the metabolic syndrome is characterized by severe atherosclerotic plaque formation, hypertension, type 2 diabetes, obesity, and hypercholesterolemia, and CKD stimulates calcification of the neointima and tunica media of the aorta. The CKD in this model is associated the adynamic bone disorder form of renal osteodystrophy. The VC of the model is associated with hyperphosphatemia, and control of the serum phosphorus both in this animal model and in humans has been preventive in the development of VC. This article reports studies that demonstrate reduction of established VC by the addition of sevelamer carbonate to the diets of this murine metabolic syndrome model with CKD. Sevelamer, besides normalizing the serum phosphorus, surprisingly, reversed the CKD-induced trabecular osteopenia. Sevelamer therapy increased osteoblast surfaces in the metaphyseal trabeculae of the tibia and femur. It also increased osteoid surfaces and, importantly, bone formation rates. In addition, sevelamer was found to be effective in decreasing serum cholesterol levels. These results suggest that sevelamer may have important actions in decreasing diabetic and uremic vasculopathy and that sevelamer carbonate may be capable of increasing bone formation rates that are suppressed by diabetic nephropathy.
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PMID:Reversal of the adynamic bone disorder and decreased vascular calcification in chronic kidney disease by sevelamer carbonate therapy. 1718 86

Despite the enormous cardiovascular disease epidemic and poor survival among individuals with chronic kidney disease (CKD), traditional risk factors such as hypercholesterolemia, hypertension, and obesity appear not as relevant as was previously thought, nor would their management improve survival in patients with CKD who are undergoing dialysis. On the contrary, kidney disease wasting (KDW) (also known as the malnutrition-inflammation complex), renal anemia, and kidney bone disease (KBD) appear to be the 3 most important nontraditional risk factors associated with cardiovascular disease in CKD. KBD-associated hyperparathyroidism may contribute to worsening refractory anemia and KDW/inflammation. The main cause of secondary hyperparathyroidism is active vitamin D deficiency. Hence, treatment of patients with KBD with vitamin D analogs, especially those with lesser effects on calcium and phosphorus such as paricalcitol, may be the most promising option for improving CKD outcomes. By conducting survival analyses in a 2-year (7/2001 to 6/2003) cohort of 58,058 patients on hemodialysis, we recently found that associations between high serum parathyroid hormone and increased death risk were masked by the demographic and clinical characteristics of patients, and that alkaline phosphatase had an incremental association with mortality. Administration of paricalcitol was associated with improved survival in time-varying models. We now present additional subgroup analyses that show that administration of any dose of paricalcitol, when compared with no paricalcitol, is associated with better likelihood of survival in virtually all subgroups of patients on hemodialysis. Because these associations may be secondary to bias by indication, randomized clinical trials are necessary to verify the findings of this and similar observational studies.
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PMID:Impact of kidney bone disease and its management on survival of patients on dialysis. 1719 30

Although there are no official recommendations for specific nutrient intakes in premature infants after hospital discharge, it is agreed that the goal should be to achieve the body composition and rate of growth of that of a normal fetus of the same postmenstrual age during the entire first year of life. A general recommendation to use the special formulas designed for preterm infants after hospital discharge in place of the formulas for term infants cannot be made from the available evidence at this time. Infants fed human milk after discharge are of the greatest concern as human milk does not in theory meet the requirements for growth in these infants. Such infants should remain on supplemental vitamins and Fe while breastfeeding, and growth as well as serum levels of phosphorus and alkaline phosphatase should be carefully monitored. The increased risk of preterm infants for obesity and the metabolic syndrome secondary to the metabolic/nutritional events early in life (programming) is likely to be small compared with the contribution of other risk factors, such as parental size, weight as an adolescent, and various lifestyle factors such as physical activity.
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PMID:Post-discharge nutrition: what does the evidence support? 1746 93

This paper reports findings of a cross-sectional study of the growth and nutrition of children living in rural Ontario, Canada. The objectives of the research were threefold: (1) to obtain data on obesity prevalence and nutrient intake in a sample of rural Canadian schoolchildren, (2) to compare findings with rural and national-level data on obesity prevalence and nutrient intake, and (3) to provide data to school board and public health agencies planning and implementing nutrition policy and programs to this population. Measures of height and weight were obtained for 504 children ages 7-13 years. Height for age and body mass index scores were calculated and compared with 2000 data from the Centers for Disease Control (Kuczmarski et al. [2002]: Vital Health Stat 246:1-190). Weekday 24-h dietary recall was conducted on a subsample of 352 children and the results compared with Canada's Food Guide (Health Canada,1997) and dietary reference data from the US Institute of Medicine (2000). Prevalence of overweight and obesity were high in this sample, with 17.7% of children classified as overweight and 10.9% of children classified as obese. Fifteen percent of boys were classified as obese, compared to 6.8% of girls. Boys consumed significantly more servings from the grain and meat food groups than girls. While mean daily intake of fiber and micronutrients was significantly low for both boys and girls, there were significant gender differences in nutrient intake, with boys consuming greater energy, protein, carbohydrate, calcium, iron, phosphorus, and sodium than girls. A number of limitations are discussed, in particular issues arising from the use of Dietary Reference Intakes.
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PMID:Gender differences in growth and nutrition in a sample of rural Ontario schoolchildren. 1767 11

Well-balanced diet is one of the determinants of the health and wellbeing. Inadequate nutrients' intake can promote disease development. The purpose of this study was to assess the intake of calcium, phosphorus and protein and relation between calcium intake and lipids and glucose serum concentration in patients with obesity. The studied group consisted of 57 subjects, aged 21-63 years. Dietary assessment was based on 3-d dietary record. Serum lipids concentrations were assessed by enzymatic methods, serum calcium concentrations were assessed by Vitros 250. The mean calcium intake in men was 588.8 mg/d, in women 549.3 mg/d. Calcium intake was statistically significant correlated with glucose concentration in women and men, but not with lipids concentrations. Dietary calcium intake in studied group was below the RDA. Calcium intake could be one of determinants of glucose concentration in obese persons.
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PMID:[Calcium intake and glucose and lipids concetrations in overweight and obese patients]. 1771 Nov 28

Orlistat, an anti-obesity drug, is a potent and specific inhibitor of intestinal lipases. In light of the recent US FDA approval of the over-the-counter sale of orlistat (60 mg three times daily), clinicians need to be aware that its use may be associated with less well known, but sometimes clinically relevant, adverse effects. More specifically, the use of orlistat has been associated with several mild-to-moderate gastrointestinal adverse effects, such as oily stools, diarrhoea, abdominal pain and faecal spotting. A few cases of serious hepatic adverse effects (cholelithiasis, cholostatic hepatitis and subacute liver failure) have been reported. However, the effects of orlistat on non-alcoholic fatty liver disease are beneficial. Orlistat-induced weight loss seems to have beneficial effects on blood pressure. No effect has been observed on calcium, phosphorus, magnesium, iron, copper or zinc balance or on bone biomarkers. Interestingly, the use of orlistat has been associated with rare cases of acute kidney injury, possibly due to the increased fat malabsorption resulting from the inhibition of pancreatic and gastric lipase by orlistat, leading to the formation of soaps with calcium and resulting in increased free oxalate absorption and enteric hyperoxaluria. Orlistat has a beneficial effect on carbohydrate metabolism. No significant effect on cancer risk has been reported with orlistat.Orlistat interferes with the absorption of many drugs (such as warfarin, amiodarone, ciclosporin and thyroxine as well as fat-soluble vitamins), affecting their bioavailability and effectiveness. This review considers orlistat-related adverse effects and drug interactions. The clinical relevance and pathogenesis of these effects is also discussed.
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PMID:Orlistat-associated adverse effects and drug interactions: a critical review. 1809 46


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