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PubMed2001

Patients, populations and policy: patient outcomes in chronic kidney disease.

Chronic kidney disease represents an interesting illustration for evaluating an epidemic of chronic illness, the impact of care processes and technology on health outcomes, the impact of financial incentives and cost containment on health outcomes, and the choices society must consider in responding to a chronic illness. The evidence suggests that strong economic pressures exist in the care of chronic kidney disease and that cost containment is important. The results in large part reflect the impact of economic pressures on clinical decision making in the absence of good evidence on outcomes. To improve clinical decision making we need valid evidence linking specific processes of care to patient outcomes. Specific processes amenable to study include the provision of preventive services, physician and nurse technical and interpersonal care and adherence to clinical practice guidelines. The ESRD Quality Study (EQUAL) currently underway and supported by the National Institutes of Diabetes and Digestive and Kidney Diseases, may help to guide physicians and centers in caring for their patients with chronic kidney disease. This investigation examines the relation between process of care and outcomes and expands outcomes measure to include disease-specific quality-of-life measures and patient satisfaction and accounts for case mix using the Index of Co-Existent Disease, a measure of the extent of different comorbid diseases as well as their severity (18,19,20). Better data on how processes of care are linked to health outcomes can inform decision making and allow educated cost cutting and quality maintenance.

Costs and Cost Analysis↗
PubMed2005

Treatment of hypertension in chronic kidney disease.

Chronic kidney disease (CKD) is a major public health problem in the United States. It is estimated that nearly 20 million Americans have some degree of chronic kidney disease defined as an estimated glomerular filtration rate of less than sixty milliliters per minute or evidence of kidney damage by imaging study, biopsy, biochemical testing or urine tests with an estimated glomerular filtration rate more than sixty milliliters per minute. Hypertension is present in more than 80% of patients with CKD and contributes to progression of kidney disease toward end stage (ESRD) as well as to cardiovascular events such as heart attack and stroke. In fact the risk for cardiovascular death in this patient population is greater than the risk for progression to ESRD. Proteinuria is an important co-morbidity in hypertensives with CKD and increase risk of disease progression and cardiovascular events. Treatment of hypertension is therefore imperative. The National Kidney Foundation clinical practice guidelines recommend a blood pressure goal of <130 mmHg systolic and <80 mmHg diastolic for all CKD patients. Recent post-hoc analyses of the Modification of Diet in Renal Disease study indicate that lower blood pressure may provide long-term kidney protection in patients with nondiabetic kidney disease. Specifically a mean arterial pressure <92 mmHg (e.g. 120/80 mmHg) as compared to 102-107 mmHg (e.g. 140/90 mmHg) is associated with reduced risk for ESRD. In most cases achieving this goal requires both non-pharmacologic and pharmacologic intervention. Dietary sodium restriction to no more than 2 grams daily is important. In addition, moderate alcohol intake, regular exercise, weight loss in those with a body mass index greater than 25 kg/M(2) and reduced amount of saturated fat help to reduce blood pressure. The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases. Blood pressure should be monitored closely in hypertensive patients with CKD and both clinic and home blood pressure measurements may help the clinician adjust treatment.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

National Kidney Foundation's Kidney Disease Outcomes Quality Initiative clinical practice guidelines for chronic kidney disease in children and adolescents: evaluation, classification, and stratification.

OBJECTIVES: A series of new guidelines has been developed by the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative to improve the detection and management of chronic kidney disease (CKD). In most instances of CKD, the earliest manifestations of the disorder may be identified by relatively simple tests. Unfortunately, CKD is often "underdiagnosed," in part because of the absence of a common definition of CKD and a classification of the stages in its progression. The Kidney Disease Outcomes Quality Initiative clinical practice guidelines for CKD evaluation, classification, and stratification provide a basis to remedy these deficits. The specific goals of the guidelines described in this review are to provide: 1) an overview of the clinical practice guidelines as they pertain to children and adolescents, 2) a simple classification of the stages of CKD, and 3) a practical approach to the laboratory assessment of kidney disease in children and adolescents. METHODS: The guidelines were developed as part of an evidence-based evaluation of CKD and its consequences in patients of all ages. The data that were used to generate the guidelines in this article were extracted from a structured analysis of articles that reported on children with CKD. RESULTS AND CONCLUSIONS: This review presents the definition and 5-stage classification system of CKD developed by the work group assigned to develop the guidelines, and summarizes the major recommendations regarding the early detection of CKD. Major emphasis is placed on the identification of children and adolescents with CKD by measuring the protein-to-creatinine ratio in spot urine specimens and by estimating the glomerular filtration rate from serum creatinine using prediction equations.

Adolescent↗
PubMed1995

Animal models of polycystic kidney disease.

Polycystic kidney disease (PKD) is one of the most prevalent causes of heritable renal failure. The disease is characterized by the occurrence of numerous fluid-filled cysts within the parenchyma of kidney. The cysts are epithelial in origin and expand in size, leading to crowding of normal kidney tissue. Ultimately, there is gross enlargement of the kidneys with loss of normal functions, and death usually occurs because of complications related to renal failure. Animal models of polycystic kidney disease are proving to be extremely useful for studying the molecular basis of renal cyst formation and for the isolation of genes carrying the mutations. This article describes the various animal models of polycystic kidney disease, spontaneously and experimentally derived, that have recently been identified.

Animals↗
PubMed2005

Polycystic kidney disease.

Polycystic kidney disease, an inherited systemic disorder, is characterized by the development of multiple cysts in the kidneys and other organs. Patients can present at any age, but more often come to clinical attention (unless there is a family history) after age 30. Patients who are diagnosed before age 30 have a worse renal survival. Although palpation of the abdomen occasionally provides a clue to the presence of polycystic kidney disease, radiographic procedures most often suggest the diagnosis. Mutations in the PKD1 or PKD2 genes give rise to cyst formation. Flank pain, hematuria, polyuria, nephrolithiasis, urinary tract infections, and hypertension may be part of the syndrome of polycystic kidney disease. It is the fourth most common cause of end-stage renal disease. Blood pressure treatment goals are less than 130/80 mm Hg. Treatment should include the use of angiotensin-converting enzyme inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Integrating clinical nutrition practice guidelines in chronic kidney disease.

Chronic kidney disease (CKD) is a permanent, progressive loss of kidney function characterized by a decline in glomerular filtration rate (GFR). Early identification of CKD risk factors provides an opportunity to prevent or delay the progression of kidney disease and decrease morbidity and mortality. There is increasing evidence to suggest that the adverse outcomes of CKD can be delayed or prevented by early detection and treatment. Current literature suggests that a low-protein, low-phosphorus diet may retard the progression of kidney disease. Other modifiable risk factors affecting CKD include proteinuria, hypertension, hyperglycemia, dyslipidemia, bone disease, anemia, and obesity. This discussion will review the current clinical nutrition guidelines for managing adult patients with CKD.

Humans↗
PubMed2007

Mineral metabolism and mortality in patients with chronic kidney disease.

Chronic kidney disease is associated with profound alterations in mineral metabolism. A growing body of evidence, based largely on observational studies, indicates that patient mortality is associated with altered mineral metabolism. Evidence is reviewed concerning the association between mortality and high concentrations of serum phosphorus, calcium, calcium-phosphate product, and parathyroid hormone. In addition, mortality may be independently associated with dialysate calcium concentration, type of phosphate binder therapy, and use of vitamin D analogs. Practices related to management of altered mineral metabolism may prove to be a promising means of improving outcomes for patients with chronic kidney disease.

Calcium↗
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

Genetics of progressive renal failure in diabetic kidney disease.

Diabetic kidney disease is a microvascular complication that is observed in a minority of patients with long-standing hyperglycemia. Diabetic nephropathy (DN) is associated with shortened patient survival, severe morbidity, and increased health care costs. Unfortunately, the incidence rates of DN continue to increase in Western societies, and DN is now the most common reported cause of end-stage renal disease in developed nations. DN results from a complex interplay between inherited and environmental factors. This article reviews the data that support an inherited basis for susceptibility to DN by summarizing familial aggregation studies, genome-wide linkage, and population-based association analyses in diabetic and nondiabetic kidney disease. Recent evidence linking genes involved in the regulation of endothelial function with genetic predisposition to albuminuria is presented. The integration of carefully designed genetic linkage and association studies with gene expression experiments in human and animal models of diabetic kidney disease appear to offer great promise for detecting the molecular mechanisms underlying susceptibility to DN.

Albuminuria↗
PubMed2006

Oxidants in chronic kidney disease.

Chronic kidney disease is a worldwide public health problem that affects approximately 10% of the US adult population and is associated with a high prevalence of cardiovascular disease and high economic cost. Chronic renal insufficiency, once established, tends to progress to end-stage kidney disease, suggesting some common mechanisms for ultimately causing scarring and further nephron loss. This review defines the term reactive oxygen metabolites (ROM), or oxidants, and presents the available experimental evidence in support of the role of oxidants in diabetic and nondiabetic glomerular disease and their role in tubulointerstitial damage that accompanies progression. It concludes by reviewing the limited human data that provide some proof of concept that the observations in experimental models may be relevant to human disease.

Animals↗
PubMed2003

Sexual dysfunction in men and women with chronic kidney disease and end-stage kidney disease.

Sexual dysfunction is a common finding in both men and women with chronic kidney failure. Common disturbances include erectile dysfunction in men, menstrual abnormalities in women, and decreased libido and fertility in both sexes. These abnormalities are primarily organic in nature and are related to uremia as well as the other comorbid conditions that frequently occur in the chronic kidney failure patient. Fatigue and psychosocial factors related to the presence of a chronic disease are also contributory factors. Disturbances in the hypothalamic-pituitary-gonadal axis can be detected before the need for dialysis but continue to worsen once dialytic therapy is initiated. Impaired gonadal function is prominent in uremic men, whereas the disturbances in the hypothalamic-pituitary axis are more subtle. By contrast, central disturbances are more prominent in uremic women. Therapy is initially directed toward optimizing the delivery of dialysis, correcting anemia with recombinant erythropoietin, and controlling the degree of secondary hyperparathyroidism with vitamin D. For many practicing nephrologists, sildenafil has become the first line therapy in the treatment of impotence. In the hypogonadal man whose only complaint is decreased libido, testosterone may be of benefit. Regular gynecologic follow-up is required in uremic women to guard against potential complications of unopposed estrogen effect. Uremic women should be advised against pregnancy while on dialysis. Successful transplantation is the most effective means of restoring normal sexual function in both men and women with chronic kidney failure.

Female↗
PubMed1999

New insights into the molecular pathophysiology of polycystic kidney disease.

Polycystic kidney diseases are characterized by the progressive expansion of multiple cystic lesions, which compromise the function of normal parenchyma. Throughout the course of these diseases, renal tubular function and structure are altered, changing the tubular microenvironment and ultimately causing the formation and progressive expansion of cystic lesions. Renal tubules are predisposed to cystogenesis when a germ line mutation is inherited in either the human PKD1 or PKD2 genes in autosomal dominant polycystic kidney disease (ADPKD) or when a homozygous mutation in Tg737 is inherited in the orpk mouse model of autosomal recessive polycystic kidney disease (ARPKD). Recent information strongly suggests that the protein products of these disease genes may form a macromolecular signaling structure, the polycystin complex, which regulates fundamental aspects of renal epithelial development and cell biology. Here, we re-examine the cellular pathophysiology of renal cyst formation and enlargement in the context of our current understanding of the molecular genetics of ADPKD and ARPKD.

Animals↗
PubMedDate not supplied

K/DOQI guidelines for bone metabolism and disease in chronic kidney disease patients: some therapeutic implications.

The National Kidney Foundation (NKF) has recently published clinical practice guidelines for bone metabolism and disease in chronic kidney disease (CKD) patients (the Kidney Disease Outcomes Quality Initiative [K/DOQI]). Data from the literature show that the majority of dialysis patients treated with traditional calcium-containing phosphorus binders and vitamin D or vitamin D analogue preparations have serum parathyroid hormone (PTH), calcium, and phosphorus levels outside these strict K/DOQI target ranges. In fact, it appears that achieving and maintaining the targets values set by these guidelines is virtually impossible without the simultaneous use of the new calcimimetic agents and non-calcium-containing binders, agents that have significant cost barriers to their use in many patients. These guidelines are welcome, but they may be impractical for the majority of dialysis patients. The impact of these guidelines in improving the parameters of bone metabolism and disease among dialysis patients remains to be determined.

Bone Diseases, Metabolic↗
PubMed2004

Epidemiology, pathophysiology and therapeutic implications of lipoprotein(a) in kidney disease.

Chronic kidney disease is associated with a tremendously increased risk for cardiovascular disease. Traditional risk factors for cardiovascular disease, however, show a diminished predictive power in these patients compared with the general population. This review provides an overview of lipoprotein(a), which is considered a nontraditional risk factor. The characteristic genetic and nongenetic changes of lipoprotein(a) in kidney disease are discussed and set into the context of risk prediction. In particular, genetically determined apolipoprotein(a) polymorphism is a powerful risk predictor for cardiovascular disease and total mortality in these patients. Finally, the limited interventional strategies available to lower lipoprotein(a) are considered.

Biomarkers↗
PubMed2005

Laparoscopic hand-assisted nephrectomy for crossed fused ectopia with polycystic kidney disease.

Polycystic kidney disease occurring in individuals with crossed fused renal ectopia is an extremely rare occurrence. The treatment of individuals with this condition is a unique surgical challenge for the operating physician. Today's advances in laparoscopic techniques provide us with new and innovative ways of performing complex procedures while subjecting patients to relatively minimal surgical trauma. We describe the laparoscopic removal of a severely diseased polycystic crossed fused kidney.

Choristoma↗
PubMed1993

Downregulation of Ke 6, a novel gene encoded within the major histocompatibility complex, in murine polycystic kidney disease.

Polycystic kidney disease (PKD) is characterized by progressive enlargement of the kidneys due to numerous expanding cysts ultimately leading to renal failure. We have identified a gene, Ke 6, located within the H-2K/tw5 region on mouse chromosome 17, which is downregulated in two distinct murine models of heritable PKD. Ke 6 is a member of the short-chain alcohol dehydrogenase family and possess remarkable amino acid sequence conservation with several bacterial proteins with oxidoreductase function. The Ke 6 gene gives rise to two transcripts--a 1-kb Ke 6a mRNA which is abundant in kidney and liver tissue and a 1.4-kb Ke 6b mRNA which is found at a moderate level in spleen tissue. We report here the complete nucleotide sequence of Ke 6a cDNA and the expression of the Ke 6 gene in murine models of PKD. The Ke 6 gene may be intimately involved in the manifestation of these cystic kidney diseases.

Alcohol Dehydrogenase↗
PubMed2004

Coronary artery disease in chronic kidney disease patients: assessing the evidence for diagnosis, screening and revascularization.

The prevalence of chronic kidney disease (CKD) is increasing in North America, with an attendant increase in cardiovascular complications. The bulk of the mortality and morbidity in CKD patients can be attributed to coronary artery disease (CAD), especially in the presence of diabetes mellitus. Thus, screening and diagnosis of CAD is particularly important in the management of these patients, especially during evaluation for renal transplantation. However, numerous limitations exist with noninvasive tests that cloud the ideal strategy for diagnosis. In addition, the optimal revascularization strategy (surgery versus percutaneous intervention) for CAD is controversial for these patients. Randomized trials are clearly needed; unfortunately, major cardiovascular trials usually exclude patients with significant renal dysfunction. The current diagnostic and revascularization strategy for CAD in CKD patients is discussed, highlighting current controversies that warrant further investigation.

Clinical Trials as Topic↗