PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “KIDNEY DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed2006

Potential advantages and limitations of applying the chronic kidney disease classification to kidney transplant recipients.

The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI) classification of Chronic Kidney Disease (CKD) characterizes patients by their level of kidney function and includes kidney transplant recipients (KTRs). Most KTRs have stage > or = 3 CKD (estimated glomerular filtration rate < 60 mL/min/1.73 m2) and may benefit from aggressive CKD care. Recent modifications to the K/DOQI CKD classification reflect the recognition of KTRs as a unique subset of CKD patients in whom the presentation, progression and implications of CKD may vary from those in nontransplant CKD populations. Currently, there is limited information about how adopting the CKD classification in KTRs will influence clinical management and outcomes. Appropriately designed studies are needed to develop transplant-specific CKD treatment recommendations, and to ensure patient, health provider and payer acceptance of the continued need for aggressive CKD care after transplantation. Education and implementation strategies will be required to ensure appropriate integration of the CKD classification and treatment guidelines into existing posttransplant care programs. The CKD classification thus represents an exciting potential strategy to improve clinical outcomes that should be adopted, further studied and modified to incorporate considerations unique to KTRs.

Cardiovascular Diseases↗
PubMed2004

Clinical practice guidelines for managing dyslipidemias in kidney transplant patients: a report from the Managing Dyslipidemias in Chronic Kidney Disease Work Group of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative.

The incidence of cardiovascular disease (CVD) is very high in patients with chronic kidney (CKD) disease and in kidney transplant recipients. Indeed, available evidence for these patients suggests that the 10-year cumulative risk of coronary heart disease is at least 20%, or roughly equivalent to the risk seen in patients with previous CVD. Recently, the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (K/DOQI) published guidelines for the diagnosis and treatment of dyslipidemias in patients with CKD, including transplant patients. It was the conclusion of this Work Group that the National Cholesterol Education Program Guidelines are generally applicable to patients with CKD, but that there are significant differences in the approach and treatment of dyslipidemias in patients with CKD compared with the general population. In the present document we present the guidelines generated by this workgroup as they apply to kidney transplant recipients. Evidence from the general population indicates that treatment of dyslipidemias reduces CVD, and evidence in kidney transplant patients suggests that judicious treatment can be safe and effective in improving dyslipidemias. Dyslipidemias are very common in CKD and in transplant patients. However, until recently there have been no adequately powered, randomized, controlled trials examining the effects of dyslipidemia treatment on CVD in patients with CKD. Since completion of the K/DOQI guidelines on dyslipidemia in CKD, the results of the Assessment of Lescol in Renal Transplantation (ALERT) Study have been presented and published. Based on information from randomized trials conducted in the general population and the single study conducted in kidney transplant patients, these guidelines, which are a modified version of the K/DOQI dyslipidemia guidelines, were developed to aid clinicians in the management of dyslipidemias in kidney transplant patients. These guidelines are divided into four sections. The first section (Introduction) provides the rationale for the guidelines, and describes the target population, scope, intended users, and methods. The second section presents guidelines on the assessment of dyslipidemias (guidelines 1-3), while the third section offers guidelines for the treatment of dyslipidemias (guidelines 4-5). The key guideline statements are supported mainly by data from studies in the general population, but there is an urgent need for additional studies in CKD and in transplant patients. Therefore, the last section outlines recommendations for research.

Adolescent↗
PubMed2004

[Outlines of K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease].

Recently "K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease" was published. It consists of sixteen precise guidelines which cover the wide range of this field. It is expected that these guidelines contribute ESRD treatment in Japan in spite of some differences in medical practice for dialysis therapy between Japan and the United States. This article briefly summarizes the outlines of these guidelines.

Absorptiometry, Photon↗
PubMed2003

Progression of kidney disease varies between families with defects in the polycystic kidney disease type 1 gene in eastern Finland.

OBJECTIVE: To characterize, for the first time, the phenotype and clinical course of autosomal dominant polycystic kidney disease (ADPKD) in Finnish patients. MATERIAL AND METHODS: All patients underwent an abdominal sonographic examination and most of those with ADPKD underwent magnetic resonance angiography of the head. Haplotype analysis was used to classify 20 ADPKD families into those with defects in either the polycystic kidney disease type 1 (PKD1) or polycystic kidney disease type 2 (PKD2) genes. Evaluation of the rate of progression of kidney disease in patients with ADPKD was based on creatinine values. RESULTS: Haplotype analysis showed that 16 families had defects in the PKD1 gene and one had defects in the PKD2 gene. Three families were excluded because of uninformative haplotypes. The final study population consisted of 79 unaffected family members, 109 patients with defects in the PKD1 gene and 10 with defects in the PKD2 gene. Higher prevalences of hepatic cysts (3% in healthy relatives, 60% in PKD1 patients and 90% in PKD2 patients; p < 0.001), subarachnoid hemorrhage or cerebral aneurysms (1%, 12% and 0%, respectively; p < 0.001), proteinuria (1%, 23% and 0%, respectively; p < 0.001) and hematuria (5%, 30% and 0%, respectively; p < 0.001) were found in PKD1 patients compared to the healthy relatives. PKD1 patients had a faster progression of kidney disease than PKD2 patients (p < 0.001). The progression of kidney disease varied substantially among the PKD1 families. CONCLUSION: The relative proportions of PKD1 and PKD2 patients and the phenotype of ADPKD were similar in our Finnish patients compared to previous studies in other populations. However, the progression of kidney disease differed substantially among PKD1 families, indicating a heterogeneic genetic background of PKD1 in Finnish patients.

Adolescent↗
PubMed2000

Acquired cystic kidney disease: rapid progression from small to enlarged kidneys simulating adult polycystic kidney disease.

A 57-year-old man on chronic hemodialysis presented marked bilateral renal enlargement due to acquired cystic kidney disease (ACKD). He had been on hemodialysis for less than 3 years only (14 months prior to receiving a functional renal transplant which lasted 8 years, followed by 18 additional months of dialysis), before the diagnosis of ACKD was made following an episode of flank pain with gross hematuria. The marked changes in kidney appearance during this 11-year period were documented by serial ultrasound examination showing the kidneys to be of near-normal size before the start of dialysis (> or =10 cm in 1986), then shrunken and contracted 5 years later while having a functioning renal transplant (<5 cm in 1991), and markedly enlarged reaching the size of adult polycystic kidney disease after returning to dialysis (>13 cm in 1997). Since the risk of ACKD increases with duration of dialysis, we sought additional predisposing factors in this unusual case and found that 2 years after renal transplantation, the patient was diagnosed with breast cancer for which he was treated with surgical excision and tamoxifen. Based on ultrasound evidence that the tamoxifen treatment preceeded the appearance of the renal cystic changes, we wonder whether this drug may have played a role in the rapid development of ACKD.

Antineoplastic Agents, Hormonal↗
PubMed2005

[Early diagnosis of chronic kidney diseases].

Chronic kidney diseases frequently progress to end-stage renal failure over a period of several years. Ultimately, the glomerular filtration apparatus and tubulus are destroyed to such an extent that renal replacement therapy is required. This process may last longer than 10 years. To avoid loss of renal function, chronic kidney diseases should be diagnosed as early as possible so that therapeutic measures are initiated in time. Medications which prevent or delay progression to end-stage renal failure, e.g. ACE inhibitors and AT(1) blockers, are more effective if started early in the course of renal disease. A significant number of patients with chronic kidney disease are still diagnosed too late and are without adequate therapy so that chances for prevention and/or delay of chronic kidney disease are missed.

Chronic Disease↗
PubMedDate not supplied

Aortic pulse wave velocity and arterial wave reflections predict the extent and severity of coronary artery disease in chronic kidney disease patients.

BACKGROUND: Increased aortic stiffness markers - aortic pulse wave velocity (PWV) and augmentation index (AIx) - are powerful predictors of survival in ESRD patients - well-recognized for the high prevalence of coronary artery disease (CAD) and unusually high PWV and AIx. Recently, decreased aortic compliance has been shown to be predictive of primary coronary events in hypertensive patients with normal renal function. We aimed to explore relationships between arterial stiffness and CAD in cohorts of patients with chronic kidney disease (CKD). METHODS AND RESULTS: 46 patients with chronic kidney disease (33 males, aged 55.7+/- 13.2 years, 20 on dialysis, 18 post renal transplantation, and 8 with glomerular filtration rate (GFR) between 10 and 25 ml/min) underwent coronary angiography for the assessment of CAD. PWV and aortic AIx were determined from pulse waveform analysis of arterial waveforms recorded by applanation tonometry using a SphygmoCortm device. The atherosclerosis burden score was calculated by adding the percentage luminal reduction of the most severe lesion in each artery. Patients with normal angiograms had significantly less arterial stiffness (as reflected by both a lower PWV=8.42+/-1.53 m/s and a lower AIx=17.9+/-5.55 %) compared with the 35 subjects with evidence of obstructive coronary disease at angiography (PWV=9.21+/-1.15 m/s and AIx=23.4+/-5.4 %, P<0.05 for both). Moreover, as more coronary vessels were affected, PWV and AIx increased proportionally. Based on receiver operating characteristics (ROC) curve analysis mean PWV levels showed an optimal cut-off point at 8.35 m/s (sensitivity=0.77; specificity=0.60), while mean AIx levels showed an optimal cut-off point at 17% (sensitivity=0.87; specificity=0.70). There was a statistically significant linear relationship between the atherosclerosis burden and both measures of arterial stiffness: PWV (r=0.31, p=0.007) and AIx (r=0.46, p=0.003). Independent predictors for the arterial stiffness parameters in this CKD population (multiple stepwise regression analysis) were age (r=0.69 for PWV and r=0.62 for AIx), and mean arterial pressure (MAP) (for AIx, p<0.0001). CONCLUSION: This study provides the first direct evidence in a cross-sectional investigation that PWV and AIx are related to the extent of coronary obstruction in CKD patients.

Adult↗
PubMed2004

Cardiac disease in chronic kidney disease: current understandings and opportunities for change.

Cardiovascular disease (CVD) is prevalent in patients with kidney disease: in populations prior to dialysis, on dialysis and after transplantation. Publications over the last decade have focused on this, and more recently, patients with cardiac disease are now recognized as being at increased risk in the presence of even mild kidney dysfunction. The presence of both traditional and non-traditional risk factors contributes to this overwhelming burden of cardiovascular disease in patients with chronic kidney disease (CKD). Recent studies have focused on the impact of anemia and disorders of mineral metabolism on CVD outcomes, in the context of inflammation and evidence of cytokine activation. Cross-sectional and prospective observational studies have led to improved understanding, and generated novel hypotheses. To date, no clinical trial has determined the positive impact of interventions targeted at these novel risk factors. This overview describes the current state of knowledge and emphasizes the interplay between CVD and CKD as two aspects of a set of pathophysiological processes, which impact on patient outcomes.

Anemia↗
PubMed2004

Coronary revascularization in patients with coronary artery disease and chronic kidney disease.

There is a remarkable lack of randomized trial data on optimal management of coronary artery disease (CAD) in patients with chronic kidney disease (CKD). In fact, patients with CKD are often excluded from randomized trials that compare different treatment strategies for CAD. Because the most common cause of death in CKD patients is cardiovascular disease, it is crucial that studies are designed to determine the best therapy for CAD in this high-risk group. This article discusses the available data on coronary revascularization outcomes in CKD patients.

Chronic Disease↗
PubMed2005

Clinical epidemiology of cardiovascular disease in chronic kidney disease.

Cardiovascular disease (CVD) is the most common cause of death in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). The clinical epidemiology of CVD in CKD is challenging due to a prior lack of standardized definitions of CKD, inconsistent measures of renal function, and possible alternative effects of 'traditional' CVD risk factors in patients with CKD. These challenges add to the complexity of the role of renal impairment as the cause or the consequence of cardiovascular disease. The goal of this review is to summarize the current evidence on: (1) the incidence and prevalence of CVD in chronic renal insufficiency and in ESRD, (2) risk factors for CVD in CKD, (3) the outcomes of patients with renal failure with CVD, and (4) CKD as a risk factor for CVD. The epidemiological associations implicating the huge burden of CVD throughout all stages of CKD highlight the need to better understand and implement adequate screening, and diagnostic and treatment strategies.

Cardiovascular Diseases↗
PubMed1997

The prevalence of proliferative kidney disease from the kidney and muscle of rainbow and brown trout in Aragón (Spain).

The prevalence and parasite density of PKX (the unknown myxosporean that causes proliferative kidney disease [PKD] of salmonids) were investigated in eight fishfarms in Aragón, Spain. Tissue sections stained with the biotynilated lectin GS-I revealed the presence of this protozoan in only one of the farms. In rainbow trout, the renal prevalence and parasite density peaked in July, but in brown trout the maximum renal prevalence and maximum renal parasite density were reached in May and in July, respectively. In rainbow trout, after the acute phase of the disease, the number of PKX decreases in the kidney but increases in the muscle. In this species of fish, the prevalence and parasite density are much higher in the muscles than in the kidney in October.

Acute Disease↗
PubMed2005

Cilia and centrosomes: a unifying pathogenic concept for cystic kidney disease?

Cystic kidney diseases are among the most frequent lethal genetic diseases. Positional cloning of novel cystic kidney disease genes revealed that their products (cystoproteins) are expressed in sensory organelles called primary cilia, in basal bodies or in centrosomes. Primary cilia link mechanosensory, visual, osmotic, gustatory and other stimuli to mechanisms of cell-cycle control and epithelial cell polarity. The ciliary expression of cystoproteins explains why many other organs might be also affected in patients with cystic kidney disease. Protein-protein interactions among cystoproteins, and their strong evolutionary conservation, provide a basis for a multidisciplinary approach to unravelling the novel signalling mechanisms that are involved in this disease group.

Centrosome↗
PubMedDate not supplied

Chronic kidney disease and cardiovascular disease--using the ANNA Standards and Practice Guidelines to improve care. Part 1: the epidemiology of chronic kidney disease: the risk factors and complications that contribute to cardiovascular disease.

Recent National Kidney Foundation Kidney Disease Outcome Quality Initiative Guidelines for cardiovascular disease recommend that patients with chronic kidney disease be considered at highest risk for development of cardiovascular disease and that cardiac risk factor reduction begin with diagnosis of chronic kidney disease. Risk factors for cardiovascular disease in patients with chronic kidney disease include both traditional and nontraditional renal-related cardiac risk factors. The ANNA Nephrology Nursing Standards of Practice and Guidelines for Care can provide the foundation for planning care to patients with CKD and not only slow the progression of CKD but reduce exposure to cardiac risk factors. This article, on the epidemiology of chronic kidney disease and the risk factors and complications that contribute to cardiovascular disease, is the first in a series of three articles on the risk factors and complications related to chronic kidney disease and its impact on cardiovascular disease.

Adult↗
PubMed2025

Using Large Genomic Biobanks to Generate Insights into Genetic Kidney Disease.

Chronic kidney disease (CKD) affects approximately 9% of the global population, leading to increased risks of end-stage kidney disease (ESKD), cardiovascular disease (CVD), and mortality. Patients with CKD are a huge burden on health care resources globally. CKD is a complex condition influenced by a combination of genetic, environmental, and traditional risk factors. Family studies have suggested heritability rates for CKD ranging from 30% to 75%, and large genomic biobank studies have proven essential in identifying genes with substantial effects on CKD risk and in capturing cumulative genetic risk through polygenic risk scores. These biobanks are crucial for discovering new genes associated with kidney health and disease, and their growing size enhances the power to detect novel genetic associations. Integrating multi-omics technologies such as transcriptomics, metabolomics, and proteomics further enriches our understanding of CKD, while advanced computational tools continue to expand our insights into genetic data. Polygenic risk scores, derived from hundreds of genetic variants with small effect sizes, can help identify individuals at high risk of CKD. Genomic biobanks offer valuable opportunities for early identification and personalized treatment of monogenic kidney disorders, such as autosomal dominant polycystic kidney disease and Alport syndrome. These biobanks help fill knowledge gaps, particularly in individuals with milder or asymptomatic presentations who are often underrepresented in traditional studies. Expanding genomic biobank efforts globally, especially in diverse populations, is vital to enhancing our understanding of the genetic underpinnings of kidney disease. This review highlights the significant contributions of genomic biobanks to advancing our comprehension of the genetics of CKD.

Humans↗