Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CKD”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed2005

Risk of bleeding and restenosis among chronic kidney disease patients undergoing percutaneous coronary intervention.

BACKGROUND: Bleeding risk is increased in renal failure due to impaired platelet adhesiveness. Patients who undergo percutaneous coronary intervention (PCI) are given multiple antiplatelet agents that increase that risk. We retrospectively tested the hypothesis that chronic kidney disease (CKD) patients who undergo PCI are at higher risk of bleeding and restenosis (due to chronic inflammation) compared to patients with normal renal function. METHODS: Patients who had PCI for non-ST elevation myocardial infarction or unstable angina between July 2001 and June 2003 (1,184 patients) were included in the study. All the patients were given periprocedural clopidogrel, aspirin and glycoprotein IIb/IIIa inhibitor if indicated, and then continued on clopidogrel and aspirin daily for 12 months. The patients were classified into 5 groups according to the CKD stage and followed-up for 12 months for development of major or minor bleeding, restenosis, length of hospital stay and survival. RESULTS: The incidence of major bleeding within the first month (3.4% in normal kidney function patients (Gp 1), 4.8% for CKD Stages 1 and 2 patients (Gp2), 5.2% for CKD Stage 3 patients (Gp3), 6.1% for CKD Stage 4 patients (Gp4) and 9.3% for CKD Stage 5 patients (Gp5), p = 0.001) and for minor bleeding (5.7% in Gp1, 6.5% for Gp2, 7.4% for Gp3, 9.2% for Gp4 and 11.3% for Gp5, p = 0.001) and the incidence of restenosis at one month (4.6% in Gp1, 5.3% for Gp2, 6.8% for Gp3, 7.3% for Gp4 and 9.6% for Gp5, p = 0.001) and 6 months (11.2% in Gp1, 13.5% for Gp2, 15.7% for Gp3, 16.4% for Gp4 and 19.7% for Gp5, p = 0.001) were higher with worsening CKD. Survival at one year was worse with worsening of the kidney function. CONCLUSION: Worsening of CKD is associated with progressively increased risk of minor and major bleeding, restenosis and death during and after PCI.

Analysis of Variance↗
PubMed2004

Potential application of the National Kidney Foundation's chronic kidney disease guidelines in a managed care setting.

Chronic kidney disease (CKD) is a public health problem in the United States with rising incidence and prevalence. The disease may progress to end-stage renal disease, which is associated with significant morbidity and mortality. The National Kidney Foundation recently established clinical practice guidelines to aid in the identification and stratification of CKD. Central to these guidelines is the use of glomerular filtration rate estimation equations. Integrated healthcare systems can use the guidelines to identify patients with CKD early in its course. Early identification allows for timely nephrology referral, institution of measures to slow the progression of CKD, and treatment of CKD-specific complications. Administration of these efforts early in the course of CKD improves subsequent morbidity and mortality of affected patients. By identifying CKD early in its course, patients can be referred to a coordinated case management team that can help administer care. The team can follow up a patient from the early diagnosis of CKD to end-stage renal disease and renal replacement therapy. Finally, continuous quality improvement can be instituted to assist in improving patient care.

Early Diagnosis↗
PubMed2005

The global burden of chronic kidney disease and the way forward.

BACKGROUND: Chronic kidney disease (CKD) is increasing worldwide at an annual growth rate of 8%. Regional differences exist in the epidemiology of the condition, and non-Whites are more affected. METHODS: An English-language literature search using Medline (January 1984-October 2003) was done to assess research/review articles on burden and prevention of CKD. Particular attention was paid to epidemiology and prevention of chronic kidney diseases. RESULTS: The prevalence of CKD is higher in developing countries than in the developed world. The most common causes of CKD in the developing countries are chronic glomerulonephritis and systemic hypertension, diabetic nephropathy being the most common cause in Europe, the United States, and Japan. Factors contributing to the regional differences in the etiology and prevalence of CKD are race and ethnicity, genetic predisposition, increasing prevalence of type 2 diabetes, mortality caused by other disease, obesity, and possibly cigarette smoking. The control of hypertension, dyslipidemia, proteinuria, obesity, avoidance of low birth weight, smoking, and preventing ingesting of heavy metals such as lead are intervention strategies that retard or prevent progression of renal diseases. The magnitude of the existing burden of illness caused by renal failure, the projections for increasing incidence of CKD, and the limitations of our existing treatments for renal insufficiency all point to the need for clinical and population-based interventions aimed at prevention of CKD. CONCLUSIONS: A comprehensive health education campaign and screening of the general populace are needed in order to detect chronic kidney disease early. These measures will ensure appropriate and timely institution of proven measures to halt or reduce progression of CKD.

Chronic Disease↗
PubMed2006

Energy homeostasis and cachexia in chronic kidney disease.

Loss of protein stores, presenting as clinical wasting, is reported to have a prevalence of 30-60% and is an important risk factor for mortality in chronic kidney disease (CKD) patients. There is debate as to whether the clinical wasting in CKD patients represents malnutrition or cachexia. Malnutrition results from inadequate intake of nutrients, despite a good appetite, and manifests as weight loss associated with adaptive metabolic responses such as decreased basic metabolic rate and preservation of lean body mass at the expense of fat mass. Furthermore, the abnormalities in malnutrition can usually be overcome simply by supplying more food or altering the composition of the diet. In contrast, cachexia is characterized by maladaptive responses such as anorexia, elevated basic metabolic rate, wasting of lean body tissue, and underutilization of fat tissue for energy. Diet supplementation and intradialytic parenteral nutrition have not been successful in reversing cachexia in CKD. The etiology of cachexia in CKD is complex and multifactorial. Two major factors causing muscle wasting in uremia are acidosis and decreased insulin responses. Inflammation secondary to cytokines may also play a significant role. The hypoalbuminemia of CKD patients is principally associated with inflammation and not changes in food intake. There is also recent evidence that hypothalamic neuropeptides may be important in the downstream signaling of cytokines in the pathogenesis of cachexia in CKD. Elevated circulating levels of cytokines, such as leptin, may be an important cause of uremia-associated cachexia via signaling through the central melanocortin system. Further research into the molecular pathways leading to cachexia may lead to novel therapeutic therapy for this devastating and potentially fatal complication of CKD.

Animals↗
PubMed2006

Urinary liver-type fatty acid binding protein as a useful biomarker in chronic kidney disease.

BACKGROUND: We reported that urinary L-FABP reflected the progression of chronic kidney disease (CKD). This study is aimed to evaluate the clinical significance of urinary liver type fatty acid binding protein (L-FABP) as a biomarker for monitoring CKD. METHODS: Urinary L-FABP was measured using human L-FABP ELISA kit (CMIC.Co., Ltd., Tokyo, Japan). The relations between urinary L-FABP and clinical parameters were evaluated in non-diabetic CKD (n = 48) for a year. In order to evaluate the influence of serum L-FABP derived from liver upon urinary L-FABP, both serum and urinary L-FABP were simultaneously measured in patients with CKD (n = 73). RESULTS: For monitoring CKD, the cut-off value in urinary L-FABP was determined as 17.4 microg/g.cr. by using a receiver operating characteristics (ROC) curve. Renal function deteriorated significantly more in patients with 'high' urinary L-FABP (n = 36) than in those with 'low' L-FABP (n = 12). The decrease in creatinine clearance was accompanied by an increase in urinary L-FABP, but not in urinary protein. Serum L-FABP in patients with CKD was not correlated with urinary L-FABP. CONCLUSION: Urinary excretion of L-FABP increases with the deterioration of renal function. Serum L-FABP did not influence on urinary L-FABP. Urinary L-FABP may be a useful clinical biomarker for monitoring CKD.

Adult↗
PubMed2004

Cardiovascular disease and chronic kidney disease: insights and an update.

Despite the high prevalence and significant morbidity and mortality rates of chronic kidney disease (CKD) related to cardiovascular disease, it remains vastly understudied. Most of the current practice recommendations come from small under-powered prospective studies, retrospective reviews, and assuming patients with CKD will similarly benefit from medications and treatments as patients with normal renal function. In addition, because of the previous lack of a consistent definition of CKD and how to measure renal function, definitions of the degree of renal dysfunction have varied widely and compounded the confusion of these data. Remarkably, despite patients with CKD representing the group at highest risk from cardiovascular complications, even greater than patients with diabetes mellitus, there has been a systematic exclusion of patients with CKD from therapeutic trials. This review outlines our current understanding of CKD as a cardiovascular risk factor, treatment options, and the future directions that are needed to treat cardiovascular disease in patients with CKD.

Cardiovascular Diseases↗
PubMed2005

Prevalence of chronic kidney disease in a middle and old-aged population of Beijing.

BACKGROUND: Chronic kidney disease (CKD) was epidemic worldwide. The prevalence of CKD indicators, including proteinuria, hematuria/uninfectious leukocyturia and reduced GFR, was investigated in the middle and old-aged population of Beijing Shijingshan district. METHODS: Subjects of 2310 aged > or =40 y were enrolled. Their health conditions were taken by questionnaires and physical check-ups. Spot urine albumin to creatinine ratio, spot urine dipstick and microscopy for urine red cell and leukocyte, and serum creatinine was determined. Using simplified Modification of Diet in Renal Disease Study equation estimated GFR assessed renal function. The associations between age, gender, diabetes mellitus, and hypertension, and indicators of kidney damage were examined. RESULTS: Through the questionnaires, the history of diabetes mellitus, hypertension and CKD were found in 28%, 47.1% and 3.6% of subjects, respectively. Albuminuria was detected in 8.4% of subjects, hematuria and uninfectious leukocyturia in 0.7%, and reduced GFR in 4.9%. Approximately 12.9% had at least 1 indicator of CKD. The known rate of CKD in the studied population was 7.1%. Age, diabetes mellitus, hyper fasting blood glucose and hypertension were independently associated with albuminuria; age, gender, hyper uric acid and albuminuria with reduced GFR. When proteinuria and reduced GFR were determined using spot urine dipstick protein > or =25 mg/dl and serum creatinine > or =133 micromol/l, the prevalence of proteinuria and reduced GFR were 4.7% and 0.8%, respectively. CONCLUSION: The prevalence of CKD is common in middle and old-aged population of Beijing, especially in the elderly, but the known rate was relatively low. These findings highlight the clinical and public health importance of CKD.

Aged↗
PubMed2006

Renal osteodystrophy in children: a systemic disease associated with cardiovascular manifestations.

The increasing prevalence of chronic kidney disease (CKD) in the United States demands a closer evaluation of and attention to associated morbidities, and, particularly, the rising mortality related to cardiovascular disease in all age groups. Patients with CKD demonstrate an increased risk of coronary artery disease due to calcium deposition and subsequent arterial stiffening, in addition to left ventricular dysfunction with associated heart failure and arrhythmias. While clearly impacted by the traditional risk factors for development of cardiovascular disease (CVD), patients with CKD are also affected by non-traditional risk factors, including calcium overloading related to aggressive management of secondary hyperparathyroidism. Recent data have shown that a substantial number of patients with CKD are deficient in vitamin D on a nutritional basis, in addition to the known decrease in the kidney-produced active metabolite during progressive CKD. Historically, vitamin D has been described as an endocrine hormone that regulates blood calcium and parathyroid hormone levels. It has become increasingly clear, through the recognition of a vitamin D receptor in most tissues, that vitamin D possesses functions well beyond calcium homeostasis, such that a deficiency may contribute to the development of CVD. In this brief review, the role of vitamin D activation through its vitamin D receptor will serve as an introduction to the magnitude of the nutritional deficits in children, adults, and those with CKD. As therapeutic entities in the management of renal osteodystrophy, vitamin D analogues play an important role in cardiovascular health that continues to evolve. Preliminary studies indicate that vitamin D therapy for control of secondary hyperparathyroidism may confer cardioprotection and reduce mortality. Attention to care of osteodystrophy in CKD must take into account heart health as well.

Cardiovascular Diseases↗
PubMed2006

Cardiovascular disease in children with chronic renal failure.

Cardiovascular disease (CVD), including atherosclerosis, hypertension, myocardial infarction, and cerebrovascular accidents, constitutes an important cause of morbidity and mortality in adults with chronic kidney disease (CKD). However, evidence has been accumulating over the past several years that children and young adults with CKD also experience significant cardiovascular complications. Studies in the United States and Europe have shown that CVD is a leading cause of death in young adults diagnosed with CKD in childhood. Risk factors include hypertension, dyslipidemia, anemia, and abnormal calcium-phosphorus metabolism, all of which are present in many children with CKD. Although improved control of uremia and treatment of traditional and nontraditional cardiovascular risk factors have proved to be beneficial in adults with CKD, no such data exist for children. The NIH is currently conducting a large-scale, prospective observational study of children with CKD that should help to elucidate the role of CVD in the progression of CKD in children and what interventions might reduce the risk of cardiovascular complications in these young patients.

Cardiovascular Diseases↗
PubMed2005

Clinical evaluation of urinary excretion of liver-type fatty acid-binding protein as a marker for the monitoring of chronic kidney disease: a multicenter trial.

To confirm the clinical usefulness of the measurement of urinary liver-type fatty acid-binding protein (L-FABP) in chronic kidney disease (CKD), we carried out a multicenter trial. Clinical markers were measured in patients with nondiabetic CKD (n = 48) every 1 to 2 months for a year. We divided patients retrospectively into progression (n = 32) and nonprogression (n = 16) groups on the basis of the rate of disease progression, then assessed several clinical markers. Initially creatinine clearance (Ccr) was similar in the 2 groups; however, the urinary L-FABP level was significantly higher in the former group than in the latter (111.5 vs 53 microg/g creatinine, P < .001). For the monitoring CKD, we set the cutoff values for urinary L-FABP and urinary protein at 17.4 microg/g creatinine and 1.0 g/g creatinine, respectively. Urinary L-FABP was more sensitive than urinary protein in predicting the progression of CKD (93.8% and 68.8%, respectively). However, urinary protein showed greater specificity than did urinary L-FABP (93.8% and 62.5%, respectively). Over time, the progression of CKD tended to correlate with changes in urinary L-FABP (r = - .32, P < .05), but not in urinary protein (r = .18, not significant). The dynamics of urinary protein differed from that of urinary L-FABP, which increased as Ccr declined. Urinary L-FABP is more sensitive than urinary protein in predicting the progression of CKD. Urinary excretion of L-FABP increases with the deterioration of kidney function. Urinary L-FABP is therefore a useful clinical marker in the monitoring of CKD.

Adult↗
PubMed2005

Executing change in the management of chronic kidney disease: perspectives on guidelines and practice.

In this era of escalating information, costly technology, and an increasing prevalence of chronic complex diseases in an aging population, a systematic approach to execute changes in the care of patients with kidney disease must be developed. Specifically, there is a need to facilitate the translation of research and clinical guidelines into the delivery of quality clinical care. At present in nephrology, there is some knowledge of disease processes, accumulating knowledge about risk factors for progression, and knowledge about how to best deliver care to those with a chronic disease. The current health care environment is not suited to either the care of chronic conditions or to prevention. Information technology should facilitate shared models of care delivery for chronic conditions and allow opportunities to add new knowledge and deliver good care to complex patient groups. To execute change in the management of patients with CKD, medical students, healthcare professionals, and established physicians need to be educated about the prevalence and consequences of CKD. These educational initiatives should be done in the context of cases or specific patients especially for established practitioners, and should be simplified to make analogies to familiar concepts. The concept that CKD is a risk factor for cardiovascular disease, and needs to be managed (as does diabetes and dyslipidemia), should be more clearly articulated. Basic and clinical research in kidney disease has been enhanced by discoveries in vascular biology, diabetes, and cardiology. Much of the clinical research has been limited, however, by lack of clear definition of CKD. The development of the new K/DOQI staging system that defines and classifies the severity of kidney disease may improve the execution of ongoing robust clinical trials. Incorporating this classification system into the clinical practice of all physicians by automatic laboratory reporting of estimates of GFR raises awareness and improves communication between all medical professionals. Collaborative management of CKD patients between different physicians and multidisciplinary teams, in conjunction with the ongoing investigation of treatments and treatment strategies by both clinician and researchers, may well lead to improved outcomes for patients with CKD. Executing change in the management of CKD requires an increased awareness on the part of all clinicians, including nephrologists, regarding the prevalence and importance of the problem of earlier stages of kidney disease. The systematic evaluation of all patients and incorporation of simplified definitions and classification systems should enhance the ability to improve the outcomes of patients with kidney disease irrespective of time of identification.

Guideline Adherence↗
PubMed2003

Leukocytosis, hypoalbuminemia, and the risk for chronic kidney disease in US adults.

BACKGROUND: Atherosclerosis and chronic kidney disease (CKD) share several common antecedents. However, the association between inflammatory markers and incident CKD is unknown. METHODS: We determined risk for incident CKD, defined by treatment for kidney failure or death related to kidney disease, in 9,250 US adults aged 30 to 74 years who participated in the Second National Health and Nutrition Examination Survey (NHANES II), a nationally representative prospective cohort study with 17 years of follow-up. RESULTS: After adjusting for age, race, sex, blood pressure, smoking, and body mass index, there was a graded positive association with increasing total white blood cell (WBC) count and risk for CKD (P for trend < 0.001; relative hazard (RH) highest versus lowest quartile, 2.34; 95% confidence interval [CI], 1.30 to 4.19). This association remained statistically significant after adjusting further for the presence of diabetes and cardiovascular disease at baseline (RH, 2.01; 95% CI, 1.11 to 3.65). A similarly strong and graded association with incident CKD was observed for hypoalbuminemia after adjusting for age, race, sex, blood pressure, smoking, and body mass index (P for trend = 0.02; RH lowest versus highest quartile, 1.91; 95% CI, 0.89 to 4.07) and additionally adjusting for the presence of diabetes and cardiovascular disease at baseline (P for trend = 0.02; RH lowest versus highest, 2.05; 95% CI, 0.96 to 4.39). CONCLUSION: In a nationally representative sample of US adults, elevated WBC count and hypoalbuminemia were associated with future risk for CKD. These results support the hypothesis that systemic inflammation is an independent risk factor for CKD.

Adult↗
PubMed2006

[Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant].

BACKGROUND: Chronic kidney disease (CKD) is extremely common in adults, although often undiagnosed and thus untreated. Cardiovascular disease is the leading cause of death among patients with CKD and reducing its risk in this population is an important priority. Dyslipidemia is almost always present when proteinuria is above 3 gr/24 hours. Roughly two thirds of all patients with end-stage renal failure and kidney transplants suffer from dyslipidemia and should receive lipid-lowering therapy, as suggested by recent Afssaps (French drug agency) and NKF-K/DOQI (National Kidney Foundation-Kidney Disease Outcomes Quality Initiative) guidelines. We reviewed recent studies on efficacy, tolerability and prescription recommendations of statins in CKD and renal transplant patients. METHODS: We searched Medline, the international medical database, to conduct a systematic review of the literature on the efficacy and tolerability of statins in CKD and renal transplant patients and on specific recommendations for dosage adjustments in this population. RESULTS: The efficacy of statins in decreasing total cholesterol and LDL-cholesterol levels in dialysis and renal transplant patients is similar to that in the general population. On the other hand, large-scale randomized clinical trials among CKD (4D) and renal transplant (ALERT) patients do not demonstrate that statins significantly decrease rates of cardiovascular disease. They have a beneficial effect on proteinuria and lower the rate of kidney function deterioration in patients with dyslipidemia. Early introduction of a statin in transplant patients did not lead to improved kidney function or prevent loss of the graft. Although most statins are not excreted by the kidneys, the dosage of some must be adapted in CKD patients because of pharmacokinetic modifications induced by renal impairment. CONCLUSION: Statins at appropriately adapted doses have the same efficacy in CKD patients as in subjects with normal kidney function, and tolerance is not a problem. Their effectiveness in cardiovascular prevention in this population has not been demonstrated to date. Results about statin-induced kidney protection are encouraging but further and more specific studies are needed.

Adult↗
PubMed2024

A methylation risk score for chronic kidney disease: a HyperGEN study.

Chronic kidney disease (CKD) impacts about 1 in 7 adults in the United States, but African Americans (AAs) carry a disproportionately higher burden of disease. Epigenetic modifications, such as DNA methylation at cytosine-phosphate-guanine (CpG) sites, have been linked to kidney function and may have clinical utility in predicting the risk of CKD. Given the dynamic relationship between the epigenome, environment, and disease, AAs may be especially sensitive to environment-driven methylation alterations. Moreover, risk models incorporating CpG methylation have been shown to predict disease across multiple racial groups. In this study, we developed a methylation risk score (MRS) for CKD in cohorts of AAs. We selected nine CpG sites that were previously reported to be associated with estimated glomerular filtration rate (eGFR) in epigenome-wide association studies to construct a MRS in the Hypertension Genetic Epidemiology Network (HyperGEN). In logistic mixed models, the MRS was significantly associated with prevalent CKD and was robust to multiple sensitivity analyses, including CKD risk factors. There was modest replication in validation cohorts. In summary, we demonstrated that an eGFR-based CpG score is an independent predictor of prevalent CKD, suggesting that MRS should be further investigated for clinical utility in evaluating CKD risk and progression.

Humans↗
PubMed2006

Metabolic syndrome and chronic kidney disease in Okinawa, Japan.

We assessed the prevalence of chronic kidney disease (CKD) in a hospital-based screening program in Okinawa, Japan. The significance of metabolic syndrome as a determinant of CKD was examined using multivariate logistic regression analysis. A total of 6980 participants, aged 30-79 years, participated in a screening program in Tomishiro Chuo Hospital. Metabolic syndrome was defined according to the criteria of the Adult Treatment Panel III (ATP III). Data were also analyzed according to the modified criteria of the National Cholesterol Education Program (NCEP) that defines abdominal obesity as a waist circumference of > oe =85 cm in men and > or =90 cm in women. CKD was defined as dipstick proteinuria (> or =1+) or a reduced glomerular filtration rate (GFR). GFR was estimated using the abbreviated Modification of Diet in Renal Disease (MDRD) formula. The prevalence of metabolic syndrome and CKD was 12.8 and 13.7%, respectively. Metabolic syndrome was a significant determinant of CKD (adjusted odds ratio (OR) 1.537 and 95% confidence interval (CI) 1.277-1.850, P<0.0001). The adjusted OR (95% CI) was 1.770 (1.215-2.579, P=0.0029) for those with four metabolic syndrome risk factors compared to those with no metabolic syndrome risk factors. Metabolic syndrome was a significant determinant for younger participants (<60 years; OR 1.686, 95% CI 1.348-2.107, P<0.0001), but not for older participants (> or =60 years; OR 1.254, 95% CI 0.906-1.735, NS). The relationship between the number of metabolic syndrome risk factors and the prevalence of CKD was linear using the modified criteria. The results suggest that metabolic syndrome is a significant determinant of CKD in men under 60 years of age, in Okinawa, Japan.

Adult↗
PubMed2006

Predicting initiation and progression of chronic kidney disease: Developing renal risk scores.

Epidemiological studies have raised awareness of the problem of undiagnosed chronic kidney disease (CKD) and suggest that early identification and treatment will reduce the global burden of patients requiring dialysis. This has highlighted the twin problems of how to identify subjects for screening and target intervention to those with CKD most likely to progress to end-stage renal disease. Prospective studies have identified risk factors for CKD in the general population as well as risk factors for progression in patients with established CKD. Risk factors may thus be divided into initiating factors and perpetuating factors, with some overlap between the groups. In this paper, we review current data regarding CKD risk factors and illustrate how each may impact upon the mechanisms underlying CKD progression to accelerate loss of renal function. We propose that these risk factors should be used as a basis for developing a renal risk score, analogous to the Framingham risk score for ischemic heart disease, which will allow accurate determination of renal risk in the general population and among CKD patients.

Biomarkers↗
PubMed2002

Treatment of a murine model of high-turnover renal osteodystrophy by exogenous BMP-7.

BACKGROUND: The secondary hyperparathyroidism of chronic kidney disease (CKD) produces a high turnover osteodystrophy that is associated with peritrabecular fibrosis. The nature of the cells involved in the development of peritrabecular fibrosis may represent osteoprogenitors expressing a fibroblastic phenotype that are retarded from progressing through osteoblast differentiation. METHODS: To test the hypothesis that osteoblast differentiation is retarded in secondary hyperparathyroidism due to CKD producing bone marrow fibrosis, we administered bone morphogenetic protein 7 (BMP-7), a physiologic regulator of osteoblast regulation, to C57BL6 mice that had CKD produced by electrocautery of one kidney followed by contralateral nephrectomy two weeks later. Following the second surgical procedure, a subgroup of mice received daily intraperitoneal injections of BMP-7 (10 microg/kg). Three to six weeks later, the animals were sacrificed, blood was obtained for measurements of blood urea nitrogen (BUN) and parathyroid hormone (PTH) levels, and the femora and tibiae were processed for histomorphometric analysis. RESULTS: The animals had significant renal insufficiency with BUN values of 77.79 +/- 22.68 mg/dL, and the level of renal impairment between the CKD untreated mice and the CKD mice treated with BMP-7 was the same in the two groups. PTH levels averaged 81.13 +/- 51.36 and 75.4 +/- 43.61 pg/mL in the CKD and BMP-7 treated groups, respectively. The animals with CKD developed significant peritrabecular fibrosis. In addition, there was an increase in osteoblast surface and osteoid accumulation as well as increased activation frequency and increased osteoclast surface consistent with high turnover renal osteodystrophy. Treatment with BMP-7 eliminated peritrabecular fibrosis, increased osteoblast number, osteoblast surface, mineralizing surface and single labeled surface. There was also a significant decrease in the eroded surface induced by treatment with BMP-7. CONCLUSIONS: These findings indicate that BMP-7 treatment in the setting of high turnover renal osteodystrophy prevents the development of peritrabecular fibrosis, affects the osteoblast phenotype and mineralizing surfaces, and decreases bone resorption. This is compatible with a role of osteoblast differentiation in the pathophysiology of osteitis fibrosa.

Animals↗
PubMedDate not supplied

The Study of Treatment for Renal Insufficiency: Data and Evaluation (STRIDE), a national registry of chronic kidney disease.

Optimization of care in patients with chronic kidney disease (CKD) could be the key to improved clinical and economic outcomes, both during the phase of CKD as well as in patients with end-stage renal disease (ESRD). CKD is a major public health problem that has been insufficiently studied. There is little published information on outcomes among CKD patients, specifically, data on mortality, morbidity, and quality of life. Indeed, recent efforts by the National Kidney Foundation (NKF) have served to define the classification, evaluation, and approach to management of CKD in practice. The Study of Treatment for Renal Insufficiency: Data and Evaluation (STRIDE) registry is an initiative to study CKD patients in nephrology practices across the country. It is a prospective observational study whose objective is to profile demographic and clinical variables, practice patterns, comorbid conditions, quality of life, and outcomes in a nationally based sample of CKD patients. This article details the design, methodology, and process of enrollment into the registry.

Data Interpretation, Statistical↗