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PubMed2005

Dyslipidemia and the progression of renal disease in chronic renal failure patients.

Dyslipidemia is a common complication of progressive kidney disease and contributes to the high cardiovascular morbidity and mortality of chronic kidney disease (CKD) patients. Recent evidence also suggests a role for dyslipidemia in the development and progression of renal disease. Experimental studies have demonstrated that lipids may induce glomerular and tubulointerstitial injury, and that lipid-lowering treatments ameliorate renal injury. Various lipid abnormalities have been associated with the development and progression of renal disease in diabetic and nondiabetic patients. Population-based studies and studies of diabetic patients have reported associations of various lipid abnormalities with the development of renal disease. In patients with CKD, lipid abnormalities have also been associated with renal disease progression. Post hoc analyses of some large clinical trials on patients with vascular disease, diabetes, or dyslipidemia, and a meta-analysis of small, prospective, controlled studies on patients with CKD (diabetics and nondiabetics) suggest that statins may slow the progression of kidney disease. It is unclear whether the beneficial renal effects of statins are due to the reduction of serum cholesterol levels and/or their pleiotropic effects. There is also evidence for synergistic renoprotective effects between statins and renin-angiotensin system inhibitors. According to the results of post hoc analysis of several studies, treatment with fibrates does not seem to confer renoprotection, but evidence is scarce. In summary, there is growing evidence that lipid abnormalities may be a risk factor for renal disease, and that statins appear to confer a renoprotective effect.

Anticholesteremic Agents↗
PubMedDate not supplied

The value of vaccination in chronic kidney disease.

There has been much attention directed toward the high mortality of patients with end-stage renal disease (ESRD), with much of the focus on cardiovascular disease. However, infectious disease is the second most common cause of death in late-stage chronic kidney disease (CKD) patients. Although CKD patients are immunocompromised, some vaccines such as influenza, retain their efficacy and reduce infection rates with a standard immunization schedule. Other vaccines, such as hepatitis B and pneumococcal vaccines, require more frequent and/or higher doses to produce and maintain protective antibody levels. Attention has recently been given to the efficacy of influenza vaccination in ESRD patients in reducing morbidity and mortality. Centers with vaccination protocols have demonstrated reduced infection rates and resultant decreased morbidity and mortality. It could be extrapolated from this that widespread vaccination would reduce the total cost of ESRD patient care, and potentially improve patient well-being. However, vaccination appears to be underutilized in CKD patients, and it is a readily available intervention to improve outcomes.

Chronic Disease↗
PubMedDate not supplied

Difficulties in achieving the K/DOQI practice guidelines for bone and mineral metabolism.

Hyperparathyroidism and alterations in bone and mineral metabolism are known to occur early in the course of chronic kidney disease (CKD). The etiology of these abnormalities is multifactorial. Phosphate retention and alterations in vitamin D metabolism play important roles. The recent practice guidelines from the National Kidney Foundation (NKF) have emphasized the need to approach these problems early in the course of CKD by measuring the levels of parathyroid hormone when glomerular filtration rates (GFRs) fall to less than 60 ml/min. If hyperparathyroidism is detected, then treatment must be undertaken to try to prevent its progression. Strict guidelines have been proposed for the management of these alterations in bone and mineral metabolism when kidney disease progresses to CKD stage V. Although the initial recommendations were often opinion based, evidence is accumulating to support these views. However, with our current therapeutic armamentarium, there is considerable difficulty in achieving these practice guidelines for calcium, phosphorus, calcium-phosphorus product, and parathyroid hormone on a sustained basis. New therapeutic agents are becoming available that will help with phosphorus control and control of hyperparathyroidism, and minimize the calcium load. Additional beneficial effects of vitamin D analogs are being uncovered and are being intensively investigated. It is hoped that with attention to these practice guidelines, control of the abnormalities of mineral metabolism will be improved and will lead to improved patient outcomes.

Bone Diseases, Metabolic↗
PubMedDate not supplied

Renal replacement therapy in patients with chronic liver disease.

As the prevalence of chronic liver disease and chronic kidney disease (CKD) increase, clinicians are likely to be increasingly faced with difficult diagnostic, treatment, and ethical challenges when facing both of these diseases in a single patient. Alterations in creatinine formation and elimination in cirrhotic patients render creatinine-based estimates of glomerular filtration rate and dialysis adequacy less accurate in this population. Furthermore, differentiating signs and symptoms of uremia from hepatic disease may be difficult and clear indications for renal replacement therapy (RRT) in these patients have not been defined. Hemodialysis is associated with a high rate of complications and has not been shown to prolong life in cirrhotic patients with acute renal failure (ARF), but has not been carefully examined in those with CKD. Peritoneal dialysis is, similarly, unhelpful in chronic liver disease complicated by ARF, but has been found to be a viable option in some cirrhotic patients with CKD. Continuous RRT is generally tolerated by patients with decompensated cirrhosis and either acute or chronic renal failure and may act to bridge patients to liver transplantation. Given the poor underlying survival of cirrhotic patients with renal failure, clinicians should carefully consider the utility of RRT in each patient.

Chronic Disease↗
PubMedDate not supplied

Anemia management in chronic kidney disease: what have we learned after 17 years?

Anemia management remains controversial in patients with chronic kidney disease (CKD). The overwhelming conclusion from retrospective data analyses show a strong correlation between higher hemoglobin values and improved outcomes, including mortality, hospitalization, left ventricular hypertrophy, and quality of life. However, the evidence available from two large prospective trials in CKD comparing hemoglobin values near the current target of 11-12 g/dl with normalization or near normalization were stopped, as there was a trend toward worsening outcomes in the higher hemoglobin groups. This disparity suggests that patients who have or achieve high hemoglobin values on low doses or no erythropoietin may be inherently different from the general CKD population. Therefore targeting to a hemoglobin value above the current recommendation with intermittent erythropoietin seems unwarranted until randomized prospective trials demonstrate both safety and efficacy.

Anemia↗
PubMedDate not supplied

Multiple myeloma in end-stage renal disease.

Multiple myeloma is a common cause of chronic kidney disease (CKD). Patients with myeloma-related kidney disease but low levels of serum monoclonal proteins can be diagnosed with symptomatic myeloma in a simplified diagnostic classification. The presence and type of renal disease in myeloma is dependent on the light chain secreted. Treatment has recently changed and now includes the use of thalidomide and bisphosphonates. Thalidomide can cause hyperkalemia and bisphosphonates can cause renal failure in patients with CKD. Their use is not contraindicated, but they should be used with caution. High-dose melphalan with an autologous stem cell transplant is now the standard of care and should not be withheld from patients with CKD, even those on dialysis. This treatment can improve the renal disease, and this is more likely if treatment is started early. In patients with persistent dialysis dependence, renal transplantation can be performed if the patient has a complete remission.

Humans↗
PubMed2006

Chronic kidney disease and functional limitation in older people: health, aging and body composition study.

OBJECTIVES: To assess whether chronic kidney disease (CKD) is independently associated with incident physical-function limitation. DESIGN: Prospective cohort study. SETTING: Two sites: Pittsburgh, Pennsylvania, and Memphis, Tennessee. PARTICIPANTS: Two thousand one hundred thirty-five men and women aged 70 to 79 without functional limitation at baseline from the Health, Aging and Body Composition Study. MEASUREMENTS: Functional limitation was defined as difficulty in walking one-quarter of a mile or climbing 10 steps on two consecutive reports 6 months apart (in the same function). Kidney function was measured using serum cystatin C. Estimated glomerular filtration rate (eGFR), using the Modification of Diet in Renal Disease formula (<60 versus > or =60 mL/min per 1.73 m(2)), was a secondary predictor. Muscle strength, lean body mass according to dual energy x-ray absorptiometry, comorbidity, medication use, and inflammatory markers were evaluated as covariates. RESULTS: Persons in the highest (> or =1.13 mg/L) quartile of cystatin C experienced a significantly higher risk of developing functional limitation than those in the lowest (<0.86 mg/L) quartile (hazard ratio (HR)=1.70, 95% confidence interval (CI)=1.40-2.07). The association between the fourth cystatin C quartile and functional limitation remained after adjustment for demographics, lean body mass, comorbidity, muscle strength, and gait speed (HR=1.41, 95% CI=1.13-1.75), although the association was attenuated after adjustment for markers of inflammation (HR=1.15, 95% CI=0.90-1.46). Similar results were found for eGFR less than 60 mL/min per 1.73 m(2), although the association with functional limitation remained after adjustment for inflammatory markers (HR=1.30, 95% CI=1.08-1.56). CONCLUSION: CKD is associated with the development of functional impairment independent of comorbidity, body composition, and tests of strength and physical performance. The mechanism may be related to a heightened inflammatory state in CKD.

Aged↗
PubMed2006

Effect of improvement in anemia on electroneurophysiological markers (P300) of cognitive dysfunction in chronic kidney disease.

Our aim is to study the effect of improvement in anemia on event-related potentials (ERPs; P300) as markers of cognitive dysfunction in predialysis and dialysis patients of chronic kidney disease (CKD). Thirty anemic patients of CKD (hemoglobin [Hb] < 9 g%), 15 in the predialysis group (Group A), and 15 patients on biweekly hemodialysis (Group B) were recruited for the study. Patients of uremic encephalopathy, dyselectrolytemia, and those with hearing problems were excluded. Both groups were given recombinant human erythropoietin (rhuEPO) 100 IU/kg biweekly for 6 weeks by the subcutaneous route. No intervention was performed in the third control group (Group C), which consisted of 30 normal healthy volunteers. The improvement in Hb was assessed every 2 weeks, and the amplitude and latency of the P300 component of the ERPs were studied before initiating treatment and after 6 weeks of rhuEPO administration. There was a significant increase in Hb in both the study groups without any significant alteration in kidney functions. A significant reduction in P300 latency was noted in both the study groups after intervention. Similarly, the amplitude of P300 also increased in both study groups, but attained statistical significance for the dialysis group only. No significant changes were observed in the control group. Administration of EPO in patients of anemia with CKD resulted in a significant improvement in the electrophysiological markers of cognitive function in the form of increased amplitudes and decreased latencies of P300 in both predialysis and dialysis patients.

Anemia↗
PubMed2006

Continuous Erythropoietin Receptor Activator (C.E.R.A.) administered at extended administration intervals corrects anaemia in patients with chronic kidney disease on dialysis: a randomised, multicentre, multiple-dose, phase II study.

This dose-finding, open-label study examined the potential of subcutaneous Continuous Erythropoietin Receptor Activator (C.E.R.A.) to correct anaemia at extended administration intervals in 61 erythropoiesis-stimulating agent-naïve patients with chronic kidney disease (CKD) on dialysis. After a 4-week run-in, patients were randomised to C.E.R.A. 0.15, 0.30 and 0.45 microg/kg/week. Within these dose groups, patients were further randomised to once weekly, once every 2 weeks or once every 3 weeks treatment. Mean changes in haemoglobin (Hb) increased with increasing C.E.R.A. dose during a period of 6 weeks where no dose adjustments were permitted. The effect was independent of administration schedule. Erythropoietic responses were sustained until the end of the study (12 weeks) in all groups. In total, 90% of patients in the 0.30 microg/kg/week group and 79% in the 0.45 microg/kg/week group responded to treatment (Hb increase > or =1.0 g/dl), compared with 72% in the 0.15 microg/kg/week group. Faster median response time was associated with increasing dose (51, 38 and 31 days, respectively) and response was unrelated to administration frequency. C.E.R.A. was generally well tolerated. Our results suggest that 0.60 microg/kg twice monthly would be a suitable starting dose of C.E.R.A. for the initiation of anaemia correction in patients with CKD on dialysis. Phase III studies will confirm the feasibility of using C.E.R.A. at extended administration intervals in patients with CKD and anaemia.

Adult↗
PubMed2006

Effect of aggressive risk factor modification on cardiac events and myocardial ischaemia in patients with chronic kidney disease.

OBJECTIVE: To examine whether aggressive risk factor modification in chronic kidney disease (CKD) can limit the development of new ischaemia or reduce cardiac events. METHODS: Patients with CKD were randomly assigned to either an aggressive risk factor modification strategy (targeted treatment of hypertension, dyslipidaemia, homocysteine, haemoglobin and phosphate) or standard care. An intention to treat analysis was performed on 152 patients who had baseline dobutamine stress echocardiography (DSE), including 107 who had follow-up DSE. Biochemical parameters, cardiac risk factors and investigations (ECG, two-dimensional echocardiography) were recorded at baseline. New ischaemia was classed as new or worsening stress wall motion abnormality between follow-up and baseline DSE. Patients were followed up for the development of new ischaemia or cardiac death, acute coronary syndrome and non-fatal myocardial infarction over 1.8 years. RESULTS: The development of new ischaemia was common but not different between the standard and aggressively treated groups (15 (21%) v 18 (23%), p = 0.8). Independent predictors of new ischaemia were older age, abnormal ECG, higher systolic blood pressure and lower serum high density lipoprotein cholesterol, but not treatment arm. The standard and aggressively treated groups did not differ in cardiac event rate (10% v 13%, p = 0.6) or all-cause mortality (10% v 19%, p = 0.2). In patients with an abnormal baseline DSE (non-diagnostic, scar or ischaemia), the event rate was similar (22% v 20%, p = 0.9). CONCLUSION: Aggressive risk factor modification in CKD does not limit the development of new ischaemia or reduce cardiac events in patients with an abnormal DSE.

Coronary Disease↗
PubMed2006

Resistance to renal damage by chronic nitric oxide synthase inhibition in the Wistar-Furth rat.

Chronic nitric oxide synthase inhibition (NOSI) causes chronic kidney disease (CKD) in the Sprague Dawley (SD) rat. We previously showed that the Wistar-Furth (WF) rats are resistant to several models of CKD and maintain renal nitric oxide (NO) production compared with SD rats, whereas low-dose NOSI caused progression of CKD in WF rats. Here, we evaluate the impact of high-dose chronic NOSI in WF and SD rats, as well as intrarenal responses to an acute pressor dose of NOSI in the normal WF. Rats were given N(G)-nitro-l-arginine methyl ester (l-NAME) (150 and 300 mg/l for 6-10 wk) in the drinking water after an initial bolus tail vein injection. Both strains showed significant reductions in total NO production with chronic l-NAME. SD given 150 mg/l l-NAME for 6 wk developed proteinuria and renal injury, whereas WF rats receiving 150 mg/l l-NAME for 6-10 wk or 300 mg/l for 6 wk developed no proteinuria and minimal renal injury. Blood pressure was significantly elevated with chronic NOSI in both strains but was higher in the SD rat. There was little impact on renal nitric oxide synthase expression with l-NAME, except that cortical endothelial nitric oxide synthase abundance increased in WF after 6 wk (150 mg/l). Micropuncture experiments with acute pressor NOSI resulted in similar increases in systemic blood pressure in SD and WF rats, whereas WF rats showed a much smaller increment in glomerular blood pressure compared with SD rats. In conclusion, WF rats do not develop renal injury after chronic NOSI at, or above, a dose that causes significant injury in the SD rat. This protection may be associated with protection from glomerular hypertension.

Animals↗
PubMed2006

Sex difference in urine concentration across differing ages, sodium intake, and level of kidney disease.

Men are known to be at greater risk of urolithiasis and cardiovascular and renal diseases than women. Previous studies suggest that greater urine concentration is associated with acceleration of progression of chronic kidney disease (CKD), increased urinary albumin excretion, and delayed renal sodium excretion. The present review addresses possible sex-related differences in urine volume and osmolality (U(osm)) that could participate in this male risk predominance. Because of the scarcity of information, we reanalyzed 24-h urine data collected previously by different investigators for other purposes. In nine studies concerning healthy subjects (6 studies) or patients with CKD or diabetes mellitus, U(osm) (or another index of urine concentration based on the urine/plasma creatinine concentration ratio) was 21-39% higher (i.e., about a 150 mosm/kgH2O difference) in men than in women. Urine volume was not statistically different. Thus, the larger osmolar load of men (related to their higher food intake) is excreted in a more concentrated urine with no difference in urine volume. This sex difference was not influenced by the level of sodium excretion and was still present in CKD patients. Sex differences in thirst threshold, AVP level, and other regulatory mediators may all contribute to the higher male U(osm). Because of the previously demonstrated adverse effects of vasopressin and/or high urine concentrating activity, the greater tendency of men to concentrate urine could participate in their greater susceptibility to urolithiasis and hypertension and to the faster progression towards end-stage renal failure.

Adolescent↗
PubMed2002

Epidemiology of vascular disease in renal failure.

Cardiovascular disease (CVD) is the leading cause of death in the general population and a major cause of morbidity and mortality chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients. The high prevalence of CVD in incident dialysis populations suggests that CVD begins during or before the stage of chronic renal insufficiency. While traditional risk factors observed in the general population may play a role in the progression of CVD in CKD and ESRD patients, the presence of several nontraditional factors related to the extent of uremia seems to be the more significant feature of CVD in this patient population. Recently, there have been significant advances in our understanding of how inflammation contributes to the pathogenesis of atherosclerosis and myocardial infarction. The fact that chronic inflammation and CVD are highly prevalent in ESRD patients, it is probable that chronic inflammation may be a causative factor for accelerated atherosclerosis observed in CKD and ESRD patients. Given the extent of the problem, efforts to lower the mortality rate among ESRD patients will require new approaches to reduce and/or prevent cardiovascular morbidity and mortality.

Cardiovascular Diseases↗
PubMedDate not supplied

Treatment of anemia with darbepoetin alfa administered de novo once every other week in chronic kidney disease.

BACKGROUND/AIMS: Darbepoetin alfa is an erythropoiesis-stimulating protein that works via the same mechanism and has a threefold longer serum half-life than recombinant human erythropoietin (rHuEPO). The objective of this study was to evaluate extending the dosing interval of darbepoetin alfa to once every other week administration for the treatment of anemia in patients with chronic kidney disease (CKD) not requiring dialysis who were naive to rHuEPO therapy. METHODS: This was a multi-center, open-label study. Seventy-six rHuEPO-naive patients were enrolled to receive darbepoetin alfa (0.75 microg/kg) once every other week for up to 24 weeks. Doses were titrated to achieve and maintain a hemoglobin target of 11.0 to 13.0 g/dl. RESULTS: Ninety-seven percent (95% CI: 0.92, 1.00) of patients completing 24 weeks of treatment achieved a hemoglobin response. The median time to response was 5 weeks (range 1-25 weeks). The median darbepoetin alfa dose at the time of response was 60 microg(range 30-130 microg). Darbepoetin alfa was safe and well tolerated, and no antibodies to darbepoetin alfa were detected. CONCLUSION: These results demonstrate the utility of darbepoetin alfa administered once every other week in rHuEPO-naive CKD patients. This new treatment paradigm may allow for more widespread management of anemia in patients with CKD.

Anemia↗
PubMed2003

Cardiovascular risk in peritoneal dialysis.

All patients with CKD have multiple risk factors for CVD and CAD in particular. Some of these risk factors such as age and gender cannot be modified. Others such as diabetes and hypertension are not only CVD risk factors but are also the cause of the patient's CKD. Finally there are a group of risk factors such as disturbances of mineral metabolism and oxidative stress which are present either uniquely in or are exaggerated by renal failure. PD gives patients a more atherogenic lipid and lipoprotein profile, puts them at greater risk for AGE formation and usually causes hyperinsulinemia. All of these contribute to CVD risk. However, they can also achieve excellent blood pressure control, usually easily reach targets for anemia management and have continuous ultrafiltration allowing for the maintenance of good volume status, all of which will reduce risk for CVD. All treatable risk factors should be treated early in the development of CKD and should continue through their time on dialysis and after transplantation.

Cardiovascular Diseases↗
PubMed2003

Management of secondary hyperparathyroidism: the importance and the challenge of controlling parathyroid hormone levels without elevating calcium, phosphorus, and calcium-phosphorus product.

Secondary hyperparathyroidism (HPT) is a common complication of chronic kidney disease (CKD) that can lead to clinically significant bone disease. Additional consequences of secondary HPT, such as soft-tissue and vascular calcification, cardiovascular disease, and calcific uremic arteriolopathy, may contribute to the increased risk of cardiovascular morbidity and mortality among CKD patients. Secondary HPT arises from disturbances in calcium, phosphorus, vitamin D and parathyroid hormone metabolism, which develop early in the course of CKD and become more prominent as kidney function declines. The standard therapies currently recommended to correct mineral metabolism and bone disease in these patients include calcium supplementation, dietary phosphorus restriction, phosphate-binding agents, and treatment with vitamin D sterols. However, such medications often have significant effects on the serum levels of calcium and phosphorus, which result in exacerbation of the disease and significant extraskeletal morbidity and mortality. Thus, there is a need to identify more effective treatment approaches. This review discusses the pathophysiology of secondary HPT, the challenges faced in the management of this disorder, and the impact of current treatment options on patients' risks of morbidity and mortality. In addition, the development of new, more physiologically relevant therapies, which may lead to successful management of secondary HPT, is reviewed.

Calcitriol↗
PubMed2005

Calcium loading, calcium accumulation, and associated cardiovascular risks in dialysis patients.

Calcium and phosphate imbalances are important mutable risk factors for cardiovascular disease in chronic kidney disease (CKD). Nearly all dialysis patients require phosphate binders. These include traditional calcium-based compounds and, more recently, the calcium-free, metal-free, non-absorbed agent, sevelamer hydrochloride. Both binder types reduce serum phosphorus, but differ with respect to calcium load and metabolism. Absorption from calcium-based agents very likely promotes positive total calcium balance in many patients. Positive calcium balance is inappropriate in adults and may promote or accelerate soft-tissue and vascular calcification even in the absence of hypercalcemia. Calcium accumulation in heart and vascular tissues contributes to rapidly progressive cardiovascular calcification - a strong predictor of cardiovascular and all-cause mortality in stage 5 CKD. More than two-thirds of stage 5 CKD patients have calcification scores above the 75th percentile for matched controls -- scores associated with extremely high risk of cardiovascular events and death.

Calcium↗
PubMed2005

Comparison of intravenous iron sucrose to oral iron in the treatment of anemic patients with chronic kidney disease not on dialysis.

BACKGROUND: Few studies compare oral to intravenous (IV) iron for managing anemia in patients with chronic kidney disease (CKD) not on dialysis. METHODS: We enrolled 96 CKD anemic patients on erythropoietin in a randomized, open-label, multicenter, controlled study. Patients received 29 days of oral FeSO4 (325 mg t.i.d.) or intravenous (IV) iron sucrose (5 doses of 200 mg weekly). Assessments were made up to 14 days after the last dose. Primary endpoints were changes in hemoglobin and ferritin, and clinical success was evaluated from the percent of patients with combined endpoints of rises in hemoglobin/ferritin, hemoglobin/ferritin/TSAT, and hemoglobin/TSAT. RESULTS: There was no significant difference in hemoglobin values between IV and oral therapy. IV iron patients had greater increases in mean serum ferritin (288 ng/ml, p < 0.0001) compared to oral iron patients (-5.1 ng/ml, p = NS). IV iron patients with baseline ferritin < 100 ng/ml had a greater increase in hemoglobin (1.4 g/dl) compared to oral iron patients (0.9 g/dl) (p < 0.05). More IV iron patients (54.2%) attained hemoglobin values > 11.0 g/dl compared to oral iron patients (31.3%, p = 0.028), and met hemoglobin/ferritin (62.5%), hemoglobin/TSAT (47.9%), hemoglobin/ferritin/TSAT (43.8%), and ferritin/TSAT criteria (54.2%) than oral iron patients (0, 22.9, 0, and 0%, respectively). There were no serious side effects. CONCLUSIONS: These CKD patients had increases in both hemoglobin and ferritin following IV iron therapy, whereas those treated with oral iron had increases in hemoglobin without increases in iron stores. Iron sucrose, given weekly as 200 mg IV push over 5 min is an effective and safe anemia treatment in this population.

Administration, Oral↗