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 685 records · Page 38Linked to original sources
PubMed2005

Subclinical peripheral arterial disease in patients with chronic kidney disease: prevalence and related risk factors.

BACKGROUND: Atherosclerotic artery disease is a common condition in patients with chronic kidney disease (CKD); however, there are few published data on the prevalence of peripheral arterial disease (PAD) in nondialyzed patients with renal insufficiency. The ankle-brachial index (ABI) is a simple, noninvasive, and reliable method to assess PAD. METHODS AND RESULTS: Prevalence of PAD using ABI was investigated in 102 patients referred for the first time to a nephrology clinic with CKD in stages 3 to 5 of the K/DOQI classification, and with no previous diagnosis of PAD. Patients with ABI <0.9 were considered positive for PAD. A total of 64% of the patients were male. The mean age was 70 +/- 11 (range 58-84) years, and the estimated creatinine clearance (CrCl) was 35 +/- 12 (range 6-59) mL/min(-1). Of the total sample, 26% were diabetics, 10% active smokers, 48% ex-smokers, and 29% had a diagnosis of coronary heart disease (CHD), 15% had been previously diagnosed of stroke, and 17% had signs and symptoms compatible with intermittent claudication, which had passed unnoticed. Thirty-two percent of patients had an ABI <0.9 (mean 0.64 +/- 0.25). Of these patients with PAD, 84% were men (P < 0.005), and only 30% presented a clinical picture compatible with intermittent claudication. Absolute risk of CHD according to the Framingham 1998 score was higher in the PAD group (19.3% +/- 6 vs. 13.1% +/- 8; P= 0.01). Patients with PAD were older (75 +/- 6 vs. 66 +/- 11 years, P= 0.000), and had worse renal function (CrCl 30.8 +/- 12 vs. 37 +/- 10.7 mL.min(-1), P= 0.016) compared to patients without PAD, but no differences were found in cholesterol levels (total, HDL, LDL), calcium, phosphorus, or PTH. In the logistic regression analysis, independent indicators of PAD risk were male sex, age, and lower CrCl. Twelve percent of patients had an ABI > or =1.3, suggestive of parietal arterial calcifications. In these patients, systolic blood pressure and pulse pressure were lower (126 +/- 18 vs. 150 +/- 27, P= 0.005, and 52 +/- 13 vs. 68 +/- 25 mm Hg, P= 0.044), i-PTH levels were higher (228 +/- 267 vs. 117 +/- 63 pg/mL, P= 0.01), and a larger proportion of this group was treated with calcitriol (34% vs. 13%) compared to patients with a normal ABI. CONCLUSION: A high prevalence of PAD, considered as an ABI <0.9, was demonstrated in nondialyzed patients with CKD. This was related with age, male sex, and higher degree of renal insufficiency, while the presence of ABI > or =1.3 was associated with a greater degree of hyperparathyroidism. These data show the need to carry out routine ABI determinations in patients with CKD for early detection of peripheral arterial disease.

Aged↗
PubMed2005

Increased phagocytic nicotinamide adenine dinucleotide phosphate oxidase-dependent superoxide production in patients with early chronic kidney disease.

BACKGROUND: Oxidative stress has been implicated in the pathogenesis of atherosclerosis that develops in patients with advanced chronic kidney disease (CKD). This study was designed to investigate whether a relationship exists between phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide anion (*O2-) production and subclinical atherosclerosis in patients with early CKD. METHODS: Superoxide production was assayed by chemiluminescence under baseline and stimulated conditions on mononuclear cells obtained from asymptomatic patients with stage 1 to 2 CKD (N=22) and healthy controls (N=21). Ultrasonographic determination of carotid intima-media thickness (IMT) was used to assess the presence of atherosclerosis. RESULTS: Although there were no differences in baseline *O2- production between controls and patients, the *O2- production in phorbol myristate acetate-stimulated mononuclear cells was increased (P<0.05) in patients compared with controls. The phorbol myristate acetate-induced *O2- production was completely abolished by apocynin, a specific inhibitor of NADPH oxidase. A direct correlation (r=0.441, P<0.05) was found between plasma insulin levels and NADPH oxidase-mediated *O2- production in patients. Carotid IMT was higher (P<0.005) in patients than in controls. Carotid IMT values above the upper normal limit in controls were found in 70% and 40% of patients with increased or normal NADPH oxidase-mediated *O2- production, respectively. CONCLUSION: Generation of *O2- that is mainly dependent on NADPH oxidase is abnormally enhanced in patients with early CKD. It is suggested that this alteration could be related to the development of subclinical atherosclerosis in these patients.

Acetophenones↗
PubMedDate not supplied

Economic burden of patients with anemia in selected diseases.

OBJECTIVE: To examine the economic impact of patients with anemia in selected diseases. METHODS: A retrospective cohort design was used to estimate the differences in costs between anemic and nonanemic patients. The analysis used administrative claims data (1999-2001) from a US population to assess direct costs and disability and productivity data (1997-2001) to estimate indirect costs. Adult patients with a diagnosis of rheumatoid arthritis (RA), inflammatory bowel disease (IBD), chronic obstructive pulmonary disease (COPD), chronic kidney disease (CKD), cancer, or congestive heart failure (CHF) were identified. Costs were estimated using a generalized linear model, adjusting for age, sex, comorbidities, and disease severity. The adjustment variables for disease severity were based on ICD-9, HCPCS, or pharmacy codes. These costs were projected to a 1-million-member, similar population. RESULTS: The percentage of anemia patients varied among conditions (6.9-26.1%); the CKD population had the highest prevalence. CKD anemic patients incurred the greatest average annual direct costs ($78,209), followed by CHF ($72,078) and cancer ($60,447). After adjusting for baseline characteristics including severity, the difference in direct costs between anemic and nonanemic patients decreased for all diseases; CHF patients incurred the greatest adjusted cost difference between anemic and nonanemic ($29,511), followed by CKD ($20,529) and cancer ($18,418). Unmeasured severity and coding bias may account for a portion of the differences in the adjusted cost. CONCLUSION: Anemia may substantially increase health-care costs at a level that is economically very relevant, despite the fact that these patients may comprise only one tenth of the overall anemic population.

Adult↗
PubMedDate not supplied

Recent advances in understanding the malnutrition-inflammation-cachexia syndrome in chronic kidney disease patients: What is next?

Several recent clinical trials using single modalities to correct the conventional cardiovascular risk factors in patients with chronic kidney disease (CKD) or to improve dialysis dose and techniques in maintenance dialysis patients have failed despite the high rate of cardiovascular mortality in these individuals. Protein-energy malnutrition and inflammation, two relatively common and concurrent conditions in CKD patients, have been implicated as the main cause of poor short-term survival in this population. The "malnutrition-inflammation-cachexia syndrome" (MICS) appears to be the main cause of worsening atherosclerotic cardiovascular disease in the CKD population. The MICS is associated with low serum cholesterol and homocysteine levels and leads to "cachexia in slow motion." Hence a reverse epidemiology of cardiovascular risk factors is observed in dialysis patients with a paradoxical association of obesity, hypercholesterolemia, and hyperhomocysteinemia with better survival. Correction of MICS can potentially ameliorate the cardiovascular epidemic in CKD patients. Because MICS is multifactorial, its correction will require an integral approach rather than a single intervention. The ongoing obsession with conventional cardiovascular risk factors largely reflecting overnutrition in a population that suffers from the short-term consequences of undernutrition and excessive inflammation may well be fruitless. Clinical trials focusing on the causes and consequences of MICS and its modulation using nutritional interventions may be the key to improving survival in these individuals.

Cachexia↗
PubMed2006

Preoperative intravenous hydration confers renoprotection in patients with chronic kidney disease undergoing cardiac surgery.

Patients with chronic kidney disease (CKD) are at risk to develop acute renal failure (ARF) after open heart surgery. This complication is associated with high morbidity, mortality, and cost. Because the ability to concentrate urine is lost early in the progression of CKD, renal patients kept on fluid restriction prior to surgery may develop severe dehydration, a situation consistently found to be one of the most critical risk factors for postoperative ARF. Our goal was to investigate whether intravenous hydration for 12 h prior to cardiac surgery could prevent acute renal injury in patients with CKD. This is a prospective study in a tertiary cardiac surgery center. Forty-five patients admitted for elective open heart surgery with moderate-to-severe CKD, as evidenced by a quantified glomerular filtration rate less than 45 mL/min, were assigned using a 2/1 randomization process, to either receive an intravenous infusion of half-isotonic saline (1 mL/kg/h) for 12 h before the operation (hydration group, n = 30, 29 men, 64 + 1.7 years old), or to be simply kept on fluid restriction (control group, n = 15, 14 men, 64.2 + 2.8 years old). Groups were not different in clinical and intraoperative variables associated with postoperative renal injury. ARF developed in 8 of 15 (53%) patients in the control group, but in only 9 of the 30 (30%) patients in the hydration group. Four patients in the control group (27%), but no one in the hydration group, required dialysis after the operation (P < 0.01). Peak creatinine and blood urea nitrogen values were two to three times higher in the control group than in the hydration group. Preoperative intravenous hydration may ameliorate renal damage in patients with moderate-to-severe renal insufficiency undergoing cardiac surgery.

Acute Kidney Injury↗
PubMed2005

Challenges in the therapy of secondary hyperparathyroidism.

Derangements in mineral metabolism are known to occur early in the course of chronic kidney disease (CKD). Recent clinical practice guidelines are designed to focus on the problem early in the course of kidney disease, when it is recommended to evaluate the levels of parathyroid hormone (PTH) and to try to intervene early if the levels are elevated. To begin early intervention for hyperparathyroidism in chronic kidney disease will require involvement of primary care physicians and other subspecialty groups to identify the patients at risk and begin to intervene with measures to control hyperparathyroidism and its consequences on mineral metabolism. It has recently been demonstrated that chronic kidney disease is a significant risk factor for vitamin D deficiency and since abnormalities in vitamin D metabolism are important in the generation of hyperparathyroidism, this is an issue that needs direct attention. Studies are needed to assess the effects of correcting this vitamin D deficiency in early CKD. As kidney disease progresses, efforts to control hyperparathyroidism will likely need to be intensified and several therapeutic options are available, such as phosphate binders, repletion of vitamin D, the use of active vitamin D sterols, or the use of vitamin D analogs. In addition, it is important to define the appropriate PTH values that need to be achieved to minimize complications on bone. Such studies are in progress at the present time to validate the current more specific PTH assays. Strict guidelines have been proposed for the management of bone and mineral metabolism in patients with CKD stage V on dialysis, and although these challenging recommendations were initially opinion-based, there is mounting evidence which provides confirmation of these targets as relevant. Treatment options for patients on dialysis involve the full spectrum of agents which include phosphate binders, active vitamin D sterols (often given parenterally), the use of calcimimetic agents, surgical parathyroidectomy, and evaluation of appropriate levels of dialysate calcium. Similar to early stages of CKD, studies are in progress to refine the PTH targets with the newer PTH assays. With increased focus on the complications of bone and mineral metabolism as part of the continuum of chronic kidney disease, and with a variety of new therapies available, it is anticipated that improved patient outcomes should be achievable in this patient group.

Bone Density↗
PubMed2006

The patient, the drug and the kidney.

Recent policy changes have focused attention on the prevalence of chronic kidney disease (CKD) in the UK. In particular, automatic reporting of estimated glomerular filtration rate (e-GFR) is a requirement of the National Service Framework (NSF) for Renal Services in England. Also, the Quality and Outcomes Framework (QOF) of the UK General Medical Services (GMS) Contract (revised in April 2006) requires GPs to keep a renal register of patients with CKD with e-GFRs below 60 mL/min/1.73 m2. Prescribers managing such patients are faced with difficult decisions about starting or continuing treatment with drugs that are handled by, or potentially toxic to, the kidney. Here we review methods of identifying and classifying CKD in adults and the implications of CKD for patients' health. We also offer advice on prescribing for these patients while minimising the risks of drug-related renal toxicity. We do not aim to give detailed guidance on every drug, but rather to highlight general principles of drug therapy and key sources of information and advice.

Chronic Disease↗
PubMed2007

Kidney disease and cardiovascular risk.

Kidney failure and chronic kidney disease (CKD) are associated with accelerated cardiovascular disease, apparently because of a high burden of traditional vascular risk factors and possibly nontraditional risk factors such as inflammation, chronic volume overload, and abnormal calcium-phosphate metabolism. Although the burden of cardiovascular disease in CKD patients is well documented, potentially beneficial therapies appear to be underused in mild to moderate CKD and are relatively understudied in those with kidney failure. This review describes the epidemiology and pathophysiology of cardiovascular disease in CKD. We also discuss the clinical and public health implications of current knowledge and outline opportunities for further research.

Cardiovascular Diseases↗
PubMed2006

DOCA/NaCl-induced chronic kidney disease: a comparison of renal nitric oxide production in resistant and susceptible rat strains.

Recent studies show nitric oxide (NO) deficiency is both a cause and consequence of chronic kidney disease (CKD). Reduced renal neuronal NO synthase (nNOS) abundance and activity parallel development of CKD with different models in the Sprague-Dawley (SD) rats, whereas Wistar Furth (WF) rats are protected against CKD and show preserved renal NO production. In this study, we compared renal NO in response to DOCA/salt-induced injury between the WF and SD. Studies were conducted on sham WF (n = 6) and SD (n = 6) and uninephrectized (UNX)+75 mg DOCA+1% NaCl (WF n = 9; SD n = 10) rats followed for 5 wk. Kidneys were harvested for Western blot, NOS activity, and histology. Other measurements included creatinine clearance and 24-h total NO production and urinary protein excretion. Absolute values of kidney weight were lower in WF than SD rats that showed similar percent increases with UNX+DOCA/NaCl. Proteinuria and decreased creatinine clearance were present in the SD but not the WF rats following UNX+DOCA/NaCl. Glomerular injury was mild in the WF compared with SD rats that showed many globally damaged glomeruli. Although renal nNOS abundance was decreased in both strains (higher baseline in WF), soluble NOS activity was maintained in the WF but significantly reduced in the SD rats. Renal endothelial NOS abundance and membrane NOS activity were unaffected by treatment. In summary, WF rats showed resistance to UNX+DOCA/NaCl-induced CKD with maintained renal NO production despite mild reduction in nNOS abundance. Further studies are needed to evaluate how WF rats maintain renal NO production despite similar changes in abundance as the vulnerable SD strain.

Animals↗
PubMed2002

Proinflammatory effects of oxidative stress in chronic kidney disease: role of additional angiotensin II blockade.

Oxidative stress plays an important role in causing progressive chronic kidney disease (CKD). We examined the influence of add-on ANG II receptor blockade administered as losartan (50 mg/day for 1 mo) on oxidative stress and proinflammatory state of the kidney in patients with CKD. All subjects were taking an angiotensin-converting enzyme inhibitor plus other antihypertensive agents. Oxidative stress to lipids and proteins was measured by an HPLC assay for malondialdehyde (MDA) and carbonyl concentration, respectively. Urinary inflammation was measured by monocyte chemotactic protein-1 (MCP-1) excretion rate. The etiology of CKD was type 2 diabetes mellitus in 12 and glomerulonephritis in 4 patients. There was no change in proteinuria or 24-h ambulatory blood pressure (BP) with add-on ANG II receptor blockade with losartan therapy. Before losartan therapy, urinary protein and albumin oxidation were 99 and 71% higher, respectively, compared with in plasma (P < 0.05). There was a 35% reduction in urinary oxidized albumin with add-on losartan therapy (P = 0.036). Urinary and plasma MDA were elevated compared with age-matched controls. Urinary MDA was significantly reduced from 4.75 +/- 3.23 to 3.39 +/- 2.17 micromol/g creatinine with add-on losartan therapy. However, plasma MDA or oxidized proteins did not change in response to additional ANG II blockade. A good correlation was seen between the change in urinary oxidized albumin and MCP-1 levels (r = 0.61, P = 0.012). These data demonstrate that oxidative damage to urinary protein and lipids can be reduced with additional ANG II receptor blockade, independently of reductions in proteinuria or BP. Urinary measurements of markers of oxidative damage to lipids and proteins appear to be more sensitive than plasma measurements in patients with CKD. The significant association of the change in urinary MCP-1 with a reduction in oxidative stress supports the role of the redox state in the kidney with renal fibrosis and progressive kidney damage.

Angiotensin Receptor Antagonists↗
PubMed2003

Chronic kidney disease and the transplant recipient.

The recent Kidney Disease Outcomes Quality Initiative (K/DOQI) classification of chronic kidney disease (CKD) includes transplant recipients. Although there are important differences between kidney transplant recipients (KTRs) and patients with native kidney disease, the inclusion of KTRs along with other CKD patients is an important step to improve long-term outcomes among transplant recipients. In this article we discuss the applicability of the K/DOQI classification of CKD to transplant recipients and the importance of premature patient death with graft function as a cause of graft loss. The implementation of a comprehensive program of CKD care beginning prior to transplantation and continuing after graft failure is discussed as a strategy to improve patient outcomes and specific areas of concern for KTRs are highlighted.

Humans↗
PubMed2004

International care models for chronic kidney disease: methods and economics--United States.

In the United States, there is a major chronic kidney disease (CKD) problem with over 8 million adults having stage 3 or 4 CKD. There is good medical evidence that many of these patients can benefit from focused interventions. And while there are strong theoretical reasons to believe these interventions are cost-effective, there are little published data to back up this assertion. However, despite the lack of financial data proving cost-effectiveness and against the background of a disorganized health care system in the US, some models of CKD care are being employed. At the present time, the most comprehensive models of care in the US are emerging in vertically integrated health care programs. Other models of care are developing in the setting of managed care health plans that employ CKD disease management programs, either developed internally or in partnership with renal disease management companies.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Angiotensin receptor blockade and arterial compliance in chronic kidney disease: a pilot study.

BACKGROUND: Almost 20 million people in the US have chronic kidney disease (CKD). Cardiovascular disease and arterial wall abnormalities are common in this population. Because angiotensin II may have adverse effects on the arterial wall, we hypothesized that an angiotensin receptor blocker (ARB) would improve arterial compliance as compared with placebo in subjects with CKD. METHODS: We performed a double-blinded, placebo-controlled pilot study in which 25 subjects with stages 2 or 3 CKD and proteinuria <1 g were randomized to either the ARB, eprosartan, or placebo and titrated to achieve a goal blood pressure (BP) <130/85 mm Hg. Arterial compliance was measured at baseline and at 8 weeks. RESULTS: Baseline characteristics were similar between the groups and included mean estimated glomerular filtration rate 63 +/- 14 ml/min/1.73 m(2), heart rate 76 +/- 10 beats/min, BP 142 +/- 12/81 +/- 8 mm Hg, 64% diabetic, 44% male, and 40% white, though subjects in the eprosartan group were younger (60 +/- 12 vs. 70 +/- 6 years, p = 0.01). There were no significant differences between the groups in large or small artery compliance measurements either at baseline or at 8 weeks, but there was a statistically significant improvement from baseline in small artery compliance in the eprosartan group (from median 2.5 ml/mm Hg x 100 [90% CI (1.1, 4.7)] to 4.0 ml/mm Hg x 100 [90% CI (1.9, 6.7)] (p = 0.01)) not seen in the placebo group. CONCLUSION: Use of an ARB to achieve recommended BP is associated with improved small artery compliance in people with CKD, though larger studies are needed to confirm these findings.

Acrylates↗
PubMed2006

Vascular calcification in patients with chronic kidney disease.

Chronic kidney disease (CKD) represents an extremely common condition, and cardiovascular diseases are frequently reported in this patient population. Traditional risk factors are not accurate prognostic predictors in CKD patients, and new potential markers to predict the cardiovascular involvement in uremic patients need to be identified. Vascular calcification (VC) represents a hallmark of the atherosclerotic process in CKD. This review summarizes the processes responsible for VC (particularly focusing on the mechanisms operative in the presence of renal dysfunction), discusses the utility of computer tomography modalities in the detection of VC in patients with CKD, and reports the potential role of VC as pathophysiological link between kidney disease and cardiovascular events.

Atherosclerosis↗
PubMed2006

Anemia management in chronic heart failure: lessons learnt from chronic kidney disease.

The importance of anemia in chronic kidney disease (CKD) has become increasingly well recognized over recent years, as have the benefits of treating anemic CKD patients with recombinant human erythropoietin (rHuEPO, epoetin). As well as reducing the need for blood transfusions and the complications associated with renal failure in CKD patients, rHuEPO treatment decreases patient morbidity and mortality, particularly as a result of cardiovascular disease. The strong correlation between anemia, renal failure and cardiac failure is one that has received much attention recently, with each factor recognized to cause the other to worsen in a 'vicious cycle'. Recent studies have concentrated on the possible benefits of anemia treatment in patients with CHF. Currently available data suggest improvements in CHF symptoms, left ventricular ejection fraction (LVEF) and a reduction of hospitalizations associated with anemia correction through epoetin treatment. Available data from CKD patients suggest that anemia management should begin as early as possible, although the optimal target level for individual patients is as yet unclear. In addition to the currently available evidence, additional large, randomized, controlled studies are required to further define the morbidity/mortality benefits of epoetin treatment in CHF patients with anemia.

Anemia↗
PubMed2006

Prediction of coronary artery disease by transesophageal echocardiographic detection of thoracic aortic plaque in patients with chronic kidney disease.

BACKGROUND/AIMS: Our aim was to examine the significance of thoracic aortic plaque detected by transesophageal echocardiography (TEE) in the prediction of coronary artery disease (CAD) in patients with chronic kidney disease (CKD). METHODS: We examined 118 patients (mean age 52 +/- 12 years) with CKD and followed them for a mean of 3.4 +/- 0.8 years. The study group included 52 predialysis patients with moderate to severe CKD (plasma creatinine > or = 200 micromol/l), 32 patients on dialysis treatment, and 34 renal transplant recipients. At baseline, TEE was performed to evaluate thoracic aortic atherosclerosis. CAD was defined by a history of a documented myocardial infarction, a coronary angiogram or a post-mortem autopsy finding showing significant occlusive CAD by the end of the follow-up period. RESULTS: CAD was documented in 31 (26%) of the 118 study patients. The presence of thoracic aortic plaque had a sensitivity of 100% and a specificity of 37% for CAD and the positive and negative predictive values were 36 and 100%, respectively. In the subset of 36 patients with morphological findings of coronary arteries by angiogram or autopsy, the presence of large thoracic aortic plaques (> or = 3 mm in diameter) had a 73% sensitivity and 90% specificity for significant coronary artery stenosis. The positive and negative predictive values were 95 and 56%, respectively. CONCLUSION: TEE may be used for detecting high-risk patients with CKD; the absence of thoracic aortic plaque predicted the absence of CAD, and the presence of large aortic plaques predicted significant coronary artery stenosis.

Adult↗
PubMed2006

A randomized controlled trial of oral versus intravenous iron in chronic kidney disease.

BACKGROUND: It is unknown whether intravenous iron or oral iron repletion alone can correct anemia associated with chronic kidney disease (CKD). We conducted a randomized multicenter controlled trial in adult anemic, iron-deficient non-dialysis CKD (ND-CKD) patients (>or=stage 3) not receiving erythropoiesis-stimulating agents (ESAs). METHODS: The participants were randomized to receive either a sodium ferric gluconate complex (intravenous iron) 250 mg i.v. weekly x 4 or ferrous sulfate (oral iron) 325 mg t.i.d. x 42 days. Hemoglobin (Hgb), ferritin and transferrin saturation (TSAT) were measured serially, and the Kidney Disease Quality of Life (KDQoL) questionnaire was administered on days 1 and 43. The primary outcome variable was change from baseline (CFB) to endpoint in Hgb values. RESULTS: Seventy-five patients were analyzed (intravenous iron n = 36, oral iron n = 39). CFB in Hgb was similar in the two groups (intravenous iron 0.4 g/dl vs. oral iron 0.2 g/dl, p = n.s.). However, the increase in Hgb was only significant with intravenous iron (p < 0.01). In comparison to oral iron, intravenous iron achieved greater improvements in ferritin (232.0 +/- 160.8 vs. 55.9 +/- 236.2 ng/ml, p < 0.001) and TSAT (8.3 +/- 7.5 vs. 2.9 +/- 8.8%, p = 0.007). Intravenous iron caused greater improvements in KDQoL scores than oral iron (p < 0.05). The most common side effect reported with intravenous iron was hypotension, while constipation was more common with oral iron. CONCLUSIONS: Oral and intravenous iron similarly increase Hgb in anemic iron-depleted ND-CKD patients not receiving ESAs. Although in comparison to oral iron, intravenous iron may result in a more rapid repletion of iron stores and greater improvement in quality of life, it exposes the patients to a greater risk of adverse effects and increases inconvenience and cost.

Administration, Oral↗
PubMed2006

Seroprevalence of hepatitis B and C viruses in patients with chronic kidney disease in the predialysis stage at a university hospital in Turkey.

BACKGROUND: Hepatitis B (HBV) and C (HCV) viruses are the most common viruses that cause viral infections among the hemodialysis patients. OBJECTIVES: To assess the prevalence of HBV and HCV in predialytic chronic kidney disease (CKD) patients. DESIGN: A cross-sectional study. SUBJECTS: 171 consecutive predialytic CKD patients. MEASUREMENTS: Third-generation micro-ELISA assay was used for hepatitis B surface antigen (HBsAg), antibody to hepatitis B core (anti-HBc) and surface antibody (anti-HBs), secretory form of hepatitis B envelop antigen (HBeAg), antibody to secretory form of hepatitis B envelop antigen (anti-HBe), and ELISA for antibody to hepatitis C virus (anti-HCV). RESULTS: The main causes of CKD were 29.8% diabetic nephropathy, 19.9% chronic glomerulonephritis, 16.3% hypertensive nephrosclerosis, 14.0% unknown, 5.3% amyloidosis, 4.7% autosomal-dominant polycystic kidney disease, 4.1% chronic tubuluointerstitial nephritis, 3.5% malignancies, 1.7% benign prostatic hypertrophy, 0.6% Alport syndrome. The seroprevalence of hepatitis was: HBsAg 10.5%, anti-HBc 36.8%, anti-HBs 28.7%, HBeAg 5.3%, anti-HBe 32.7%, anti-HCV 7% and HBsAg+anti-HCV 0.6%. CONCLUSIONS: The seroprevalence of HBsAg and anti-HCV among predialytic CKD patients was similar to our patients in hemodialysis program.

Adolescent↗