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PubMed2006

Plasma pentosidine and total homocysteine levels in relation to change in common carotid intima-media area in the first year of dialysis therapy.

BACKGROUND: Homocysteine and advanced glycation end-products (AGEs), which accumulate in chronic kidney disease (CKD), are recently proposed cardiovascular risk factors. In this study, we evaluated the association between changes in calculated intima media (cIM) area of the common carotid artery during the first year of dialysis therapy and plasma total homocysteine (tHcy) level as well as circulating AGEs such as plasma pentosidine level. METHODS: We studied 63 CKD patients (38 males) aged 52 +/- 12 years at a time-point close to start of dialysis treatment and after 12 months of dialysis treatment (41 on peritoneal and 22 on hemodialysis). The tHcy and plasma pentosidine levels were measured by HPLC. Change in cIM area was evaluated by non-invasive B mode ultrasonography. Malnutrition was assessed by subjective global assessment (SGA). RESULTS: At basal, 70% of the patients had carotid plaques, 32% had symptomatic CVD, 38% had malnutrition, 30% had inflammation (CRP > or = 1 mg/dl) and 23% had diabetes mellitus, respectively. At baseline, the mean plasma pentosidine levels were similar in the patients with and without carotid plaques (36 +/- 21 vs 36 +/- 19 pmol/mg albumin, respectively), whereas the median plasma tHcy was significantly lower in the patients with carotid plaques than in the patients without carotid plaques (32 +/- 21 vs 52 +/- 42 pmol/l, p < 0.01, respectively). The prevalence of hyperhomocysteinemia (tHcy level > 13.7 micromol/l) was 95%. In univariate analysis, the change in cIM area during the first year of dialysis was significantly correlated with basal plasma pentosidine level (p = 0.31, p = 0.01), but not with basal tHcy (p = -0.11). However, neither pentosidine nor tHcy levels were correlated with cIM area at basal or at 12 months. In a stepwise multiple regression model, age and plasma pentosidine content, but not the tHcy level, associated with changes in the cIM area. CONCLUSION: Progression of atherosclerosis, as indicated by changes in carotid intima-media area during the course of dialysis treatment, was associated with pentosidine, but not with tHcy, levels at baseline in these CKD patients. This suggests that the accumulation of AGEs in CKD patients may have a role in the pathogenesis of CVD in these patients. Since almost all CKD patients have hyperhomocysteinemia, this finding, however, does not exclude a role ofhomocysteine as a risk factor for CVD in CKD patients.

Adult↗
PubMedDate not supplied

Endothelial dysfunction and oxidative stress in chronic renal failure.

Uremic patients have an increased incidence of cardiovascular disease (CVD), endothelial dysfunction and oxidative stress that can contribute to cardiovascular (CV) events. To assess the relationship between endothelial dysfunction, oxidative stress and renal failure severity, we studied 40 patients (age 57 +/- 7 yrs, 24 males) affected by chronic kidney disease (CKD) K/DOQI stage 3-5 (serum creatinine (Cr) 5.6 +/- 2.2 mg/dL) on conservative treatment, 20 uremic patients (age 57 +/- 12 yrs, 13 males) on hemodialysis (HD) and 30 healthy controls (56 +/- 12 yrs, 20 males). Before and 2 hr after oral vitamin C (2 g) administration, we measured brachial artery endothelium-dependent vasodilation (flow mediated dilation (FMD)) to reactive hyperemia following 5 min of forearm ischemia and the response to sublingual glyceril trinitrate (GTN). Measurements were made by high-resolution ultrasound and computerized analysis. FMD was lower in CKD patients than in controls (5.3 +/- 2.2 vs. 6.9 +/- 2.8%; p<0.01) and was further reduced in HD patients (3.6 +/- 2.7; p<0.01 vs. CKD patients). Response to GTN was similar in all groups. FMD was related to Cr clearance (r=0.42; p<0.01) in CKD patients, while it related inversely to Kt/V(urea) (r=-0.52; p<0.05) in HD patients. After vitamin C administration, FMD was significantly enhanced in HD (4.7 +/- 2.4%; p<0.01 vs. baseline), but not in CKD patients. Response to GTN was unaffected. However, vitamin C load reduced oxidative stress markers, and increased plasma antioxidant capability in both groups. In conclusion, the reduced endothelium-dependent dilation in the brachial artery of CKD patients is related to renal failure severity. HD patients showed a more marked alteration, which seems to be related, at least in part, to increased oxidative stress.

Adult↗
PubMed2005

The impact of routine vitamin supplementation on serum levels of 25 (OH) D3 among the general adult population and patients with chronic kidney disease.

BACKGROUND: Vitamin D supplementation is recommended to maintain bone health in the general population and in particular in patients with chronic kidney disease (CKD). While the nutritional status of vitamin D is assessed by circulating levels of 25 (OH) D3, it is not routinely measured to ensure the adequacy of vitamin D supplementation. Current recommendations require the maintenance of serum levels of 25 (OH) D3 > or = 70 nmol/L. The objective of this study is to assess the effect of routine vitamin supplements on the serum levels of 25 (OH) D3 in the general population and among persons with CKD. METHOD: Using data from the third National Health and Nutrition Examination Survey (NHANES III) we assessed the adequacy of routine vitamin supplementation by assessing serum levels of 25 (OH) D3 among 15,390 adult participants, both with and without CKD. RESULTS: In the general population the participants with vitamin supplements had higher serum level of 25 (OH) D3 (79.47 vs 74.38 nmol/L) and a lower prevalence of vitamin D deficiency (39% vs 48%) than participants not taking any supplements. In the CKD subgroup, the prevalence of vitamin D deficiency was lower with supplements (49%), while greater without supplements (59%). Vitamin D deficiency was higher among women, elderly, and minorities as previously reported. In an adjusted regression model the odds of severe vitamin D deficiency (<25 nmol/L) was 1.43 (P=.0032) among CKD patients, with a trend toward higher rates among patients not taking vitamin supplements (odds ratio 1.47, P=.0557). CONCLUSION: Vitamin supplementation is associated with a lower prevalence of vitamin D deficiency and higher serum levels of 25 (OH) D3. However, the current dose of vitamin D in routine vitamin supplements is still insufficient to maintain adequate serum 25 (OH) D3 levels in a substantial portion of both the general and CKD populations. We must re-asses the dose of vitamin D in routine vitamin supplements in the United States.

Adult↗
PubMed2005

The renal patient with cardiovascular disease--no longer a simple plumbing problem.

The clinical syndrome of chronic kidney disease (CKD) with coronary artery disease (CAD) is a clinical challenge. The risk of cardiovascular disease in patients with renal impairment appears to be far greater than in the general population. Despite the high prevalence of CKD related to cardiovascular disease (CVD), it remains understudied. Most of the current research comes from small community-based studies and retrospective reviews, assuming that patients with CKD will similarly benefit from treatments as patients with normal renal function. Most of the current clinical trials have excluded patients with CKD even though they represent a group of people at high risk for cardiovascular (CV) complications. CKD is associated with adverse CV outcomes and higher mortality even after adjustment for conventional risk factors. Declining renal function portends increasing CV risk and may be explained by several other factors that are being investigated, including inflammation, decreased vascular compliance, homocysteine, albuminuria and dyslipidemia. In addition, there is a lack of appropriate intervention in patients with CKD, despite established awareness of their high cardiovascular risk.

Cardiovascular Diseases↗
PubMed2006

Red blood cell and plasma glutathione peroxidase activities and selenium concentration in patients with chronic kidney disease: a review.

The metabolism of oxygen in aerobic organisms leads to generation of reactive oxygen species (ROS). These entities are able to oxidize almost all classes of macromolecules, including proteins, lipids and nucleic acids. The physiological level of ROS is usually regulated by antioxidant defense mechanisms. There are at least three groups of antioxidant enzymes: superoxide dismutases, catalases and glutathione peroxidases (GSH-Pxs) which neutralize ROS. The trace elements (copper, zinc and selenium) bound to the active sites of the above listed enzymes play an important role in the antioxidant defense system. In mammals, a major function of selenium (Se) and Se-dependent GSH-Pxs is to protect cells from oxidative stress. Selenium concentrations and GSH-Px activities are altered in blood components of chronic kidney disease (CKD) patients. The Se level is frequently lower than in healthy subjects and the concentration very often decreases gradually with advancing stage of the disease. Studies on red cell GSH-Px activity in CKD patients reported its values significantly lower, significantly higher and lower or higher, but not significantly as compared with healthy subjects. On the other hand, all authors who studied plasma GSH-Px activity have shown significantly lower values than in healthy subjects. The degree of the reduction decreases gradually with the progression of the disease. High inverse correlations were seen between plasma GSH-Px activity and creatinine level. A gradual decrease in plasma GSH-Px activity in CKD patients is due to the fact that this enzyme is synthesized predominantly in the kidney and thus the impairment of this organ is the cause of the enzyme's lower activity. Se supplementation to CKD patients has a slightly positive effect in the incipient stage of the disease, but usually no effect was observed in end-stage CKD. Presently, kidney transplantation is the only treatment that may restore plasma Se level and GSH-Px activity in patients suffering from end-stage CKD. A few studies have shown that in kidney recipients, plasma Se concentration and GSH-Px activity are restored to normal values within a period of 2 weeks to 3 months following surgery and thus it can be acknowledged that Se supplementation to those patients has a positive effect on plasma GSH-Px activity.

Erythrocytes↗
PubMedDate not supplied

[Left ventricular hypertrophy in chronic kidney disease].

Chronic kidney disease (CKD) is associated with increased cardiovascular (CV) risk. Left ventricular (LV) hypertrophy (LVH), together with coronary artery disease, has been considered the main target of intervention. LVH is highly prevalent in CKD even in early stages, as compared to general non-selected population. This is mainly due to the multifactorial pathogenesis of LVH in renal patients where both haemodynamic and non-haemodynamic stimuli synergically act inducing either an increase in left ventricular mass or an LV dilation. Anaemia and arterial hypertension seem to be the most important factors. Interventional studies have shown that partial correction of anaemia through epoetin, together with an arterial hypertension successful therapy through renin-angiotensin system acting drugs, such as ACE-inhibitors, were able to induce a LVH regression in CKD. Indeed, the unfavourable outcome in patients with both CKD and LVH, whose survival is reduced and incidence of fatal and non-fatal CV events increased, can be reversed if LVH is regressed by therapy. The most promising strategy in CKD seems to be LVH early diagnosis through echocardiography, the correct screening of risk factors, a LVM longitudinal monitoring through echo, as well as starting treatment in the early stages of CKD, with the aim of improving general and CV prognosis for these patients.

Anemia↗
PubMed2006

[Regression of cardiac hypertrophy using angiotensin II receptor blocker in patients with chronic kidney diseases].

OBJECTIVE: Cardiovascular complications proportionally increase as chronic kidney diseases (CKD) progress into chronic renal insufficiency or failure. The present study addressed whether the long-term use of angiotensin II receptor blocker (ARB) exerts a cardio-protective effect in CKD patients with mild to moderate renal damage. MATERIAL AND METHODS: Fifteen patients with CKD above stage 3 were enrolled in the study. While their previous antihypertensive therapy remained unchanged, the ARB candesartan, was newly added to the concurrent therapy and the patients were followed for 12-24 months thereafter. RESULTS: The main results were as follows: 1) The use of ARB improved the status of BP control classifications, shifting them to the better control categories where there was less morning hypertension. 2) ARB significantly reduced the left ventricular (LV) mass index(LVMI), the relative wall thickness (RWT), the LV intra-dimension in diastole(LVIDd), and as a result, the LV ejection fraction(LVEF) improved. In parallel, the LV mass category shifted to lower categories, indicating a significant improvement. 3) The levels of BNP decreased significantly from 135.2 +/- 136.0 to 85.0 +/- 80.3 pg/mL. 4) ARB reduced urinary protein excretion in all cases. Regardless of an inevitable increase in the serum creatinine(Cr) concentration, the slope of reciprocal serum Cr concentration (l/Cr) in the treatment period with ARB was significantly less steep compared to that in the run-in period. 5) Throughout the observation period, no serious side effects were found in any of the patients. CONCLUSION: The present study indicated that the long-term use of ARB exerts both cardio-, and renoprotective effects in patients with advanced CKD. This agent could be especially indicative and useful not only for patients with CKD, but also for patients of CKD with cardiac hypertrophy.

Aged↗
PubMed2006

Global approach to cardiovascular risk in chronic kidney disease: reality and opportunities for intervention.

The current implementation into nephrology clinical practice of guidelines on treatment of cardiovascular (CV) risk factors in chronic kidney disease (CKD) is unknown. We designed a cross-sectional analysis to evaluate the prevalence and treatment of eight modifiable CV risk factors in 1058 predialysis CKD patients (stage 3: n=486; stage 4: n=430, stage 5: n=142) followed for at least 1 year in 26 Italian renal clinics. The median nephrology follow-up was 37 months (range: 12-391 months). From stages 3 to 5, hypertension was the main complication (89, 87, and 87%), whereas smoking, high calcium-phosphate product and malnutrition were uncommon. The prevalence of proteinuria (25, 38, and 58%), anemia (16, 32, and 51%) and left ventricular hypertrophy (51, 55, and 64%) significantly increased, while hypercholesterolemia was less frequent in stage 5 (49%) than in stages 4 and 3 (59%). The vast majority of patients received multidrug antihypertensive therapy including inhibitors of renin-angiotensin system; conversely, diuretic treatment was consistently inadequate for both frequency and dose despite scarce implementation of low salt diet (19%). Statins were not prescribed in most hypercholesterolemics (78%), and epoietin treatment was largely overlooked in anemics (78%). The adjusted risk for having a higher number of uncontrolled risk factors rose in the presence of diabetes (odds ratio 1.29, 95% confidence interval 1.00-1.66), history of CV disease (odds ratio 1.48, 95% confidence interval 1.15-1.90) and CKD stages 4 and 5 (odds ratio 1.75, 95% confidence interval 1.37-2.22 and odds ratio 2.85, 95% confidence interval 2.01-4.04, respectively). In the tertiary care of CKD, treatment of hypertension is largely inadequate, whereas therapy of anemia and dyslipidemia is frequently omitted. The risk of not achieving therapeutic targets is higher in patients with diabetes, CV disease and more advanced CKD.

Aged↗
PubMed2004

Detection of chronic kidney disease with laboratory reporting of estimated glomerular filtration rate and an educational program.

BACKGROUND: Serum creatinine concentration is an inadequate screening test for chronic kidney disease, especially in elderly patients. We hypothesized that laboratory reporting of estimated glomerular filtration rate (GFR) accompanied with an educational intervention would improve recognition of chronic kidney disease (CKD). METHODS: We conducted a before-and-after study at an outpatient family medicine practice. Patients 65 years or older for whom a Cockcroft-Gault GFR could be calculated from their medical record were included. The intervention consisted of automatic reporting of estimated GFR by the hospital laboratory along with an educational intervention directed toward the primary care physicians. The primary outcome was the recognition of CKD (defined as a Cockroft-Gault GFR <60 mL/min [<1.0 mL/s]) by the primary care physician. Factors associated with the recognition of CKD were also determined. RESULTS: The study population comprised 324 patients. Prior to the study intervention, 22.4% of patients with CKD were recognized, which increased to 85.1% after the intervention. Before the intervention, recognition was more likely in male subjects (odds ratio, 4.3; 95% confidence interval, 1.9-9.8) and patients with diabetes (odds ratio, 3.4; 95% confidence interval, 1.6-7.6). These associations were no longer statistically significant after the intervention. CONCLUSION: Laboratory reporting of estimated GFR coupled with an educational program markedly improves the recognition of CKD in the primary care setting.

Aged↗
PubMed2007

Statin therapy in renal disease: harmful or protective?

Chronic kidney disease (CKD) creates one of the highest-risk atherosclerotic states that can occur in human beings. The use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) has gained widespread acceptance in the general population for the purposes of lowering low-density lipoprotein cholesterol (LDL-C) and reducing the future risks of myocardial infarction, stroke, and cardiac death. In patients with CKD, these benefits are believed to be enjoyed to the same or greater degrees. Reductions in LDL-C with statins may be associated with a reduced progression of CKD. Importantly, recent studies suggest statins are associated with a reduction in rates of acute renal failure after cardiopulmonary bypass surgery and exposure to iodinated contrast. In patients with end-stage renal disease (ESRD), recent data suggest that the annual rate of coronary artery calcification can be attenuated or reduced with LDL-C reduction. However, two large trials demonstrating LDL-C reduction with statins and with these drugs have failed to demonstrate a reduction in cardiovascular events in ESRD. Thus, the potential benefits of statins and LDL-C reduction in CKD have to be considered in light of evidence suggesting a reduced benefit if any, in patients with ESRD. In addition, studies suggest that there are higher adverse drug effects with statins in CKD.

Acute Kidney Injury↗
PubMed2003

The midnight-to-morning urinary cortisol increment method is not reliable for the assessment of hypothalamic-pituitary-adrenal insufficiency in patients with end-stage kidney disease.

A previous study reported that the midnight-to-morning urinary cortisol increment method could be used to reliably assess the insufficiency of the hypothalamic-pituitary-adrenal (HPA) axis. The principal aim of the present study is to verify whether the midnight-to-morning urinary cortisol increment is a reliable method for the assessment of the HPA axis in patients with various degrees of impaired kidney function. Fifty-six clinically stable patients with chronic kidney disease (CKD) and 14 healthy subjects were enrolled in the present study. Patients with CKD were divided on the basis of glomerular filtration rate (GFR) into the following arbitrary groups: mild (GFR: 60-89 ml/min/1.73 m2, no.=15), moderate (GFR: 30-59 ml/min/1.73 m2, no.=12) and severe kidney insufficiency (GFR: 15-29 ml/min/1.73 m2, no.=13), and hemodialysis patients. Plasma cortisol and ACTH levels were measured. The HPA axis was assessed by short Synacthen test and overnight dexamethasone suppression test. Double voided urine samples were collected at midnight and waking in the patients and the controls. Urinary free cortisol (UFC) and creatinine levels were measured and the UFC/creatinine ratio (Cort/Cr) was calculated. Then, the Cort/Cr increment was calculated as the morning Cort/Cr minus the midnight Cort/Cr. Baseline plasma cortisol levels were not significantly different between two groups. However, we found that CKD patients had significantly greater plasma ACTH levels than controls. The patients with CKD had also significantly lower morning UFC levels than controls and there was a progressive fall in morning UFC levels with decreasing GFR. The assessment of the HPA axis in patients with GFR lower than 29 ml/min was hampered by falsely abnormal responses to the midnight-to-morning urinary cortisol increment method. Plasma cortisol responded normally to exogenously administered ACTH, while plasma cortisol was suppressed by overnight dexamethasone administration in all patients with CKD. In conclusion, this method is not a reliable test for assessment of the HPA insufficiency in patients with GFR lower than 29 ml/min.

Adrenocorticotropic Hormone↗
PubMed2006

Predictive factors of chronic kidney disease in severe vesicoureteral reflux.

The aim of this retrospective cohort study was to evaluate independent predictive factors of chronic kidney disease (CKD) in children with severe bilateral primary vesicoureteral reflux (VUR). Between 1970 and 2004, 184 patients were diagnosed with VUR (grades III-V) and were systematically followed up at a single tertiary renal unit. CKD was defined as estimated glomerular filtration rate <75 ml/min per 1.73 m2 body surface area in two consecutive examinations. Risk of CKD was analyzed by the Kaplan-Meier method and Cox's regression model. The probability of CKD for patients with bilateral severe reflux was estimated at 15% by 10 years after VUR diagnosis. After adjustment, four variables remained independently associated with CKD during follow-up: age at diagnosis >24 months [relative risk (RR)=4.8, 95% confidence interval (95%CI), 1.8-12.7, P<0.001], VUR grade V (RR=3.5, 95%CI, 1.5-7.9, P=0.002), bilateral renal damage (RR=2.86, 95%CI, 1.3-6.1, P=0.007), and decade of admission after 1990 as a protective factor (RR=0.16, 95%CI 0.06-0.43, P<0.001). A delay in the diagnosis of VUR more than 12 months after urinary tract infection (UTI) was also a predictive factor in an alternative model (RR=2.2, 95%CI, 1.1-6.6, P=0.03). Prognosis regarding renal function was relatively poor after a long-term follow-up of patients with bilateral severe reflux.

Child, Preschool↗
PubMed2006

The kidney and bone metabolism: Nephrologists' point of view.

The kidney plays an important role in the regulatory system for bone and mineral metabolism. In chronic kidney disease (CKD), various abnormalities, recently named CKD-mineral and bone disorder (CKD-MBD), may develop in this system. The optimal management of CKD-MBD should be achieved without increasing the risk of metastatic calcification, including that of blood vessels. Thus, it is quite important to identify severe cases of hyperparathyroidism refractory to medical therapy. The size of the parathyroid glands, serum levels of fibroblast growth factor (FGF)23, and, possibly, the overproduction of a novel form of parathyroid hormone (PTH), serve as useful markers for this purpose. Adynamic bone disease with low buffering capacity for calcium is another major cause of hypercalcemia in dialysis patients. Our recent studies suggest that indoxyl sulfate accumulated in uremic serum is responsible for the suppression of osteoblastic function. In order to maintain the bone quality in patients with CKD, bone changes due to aging, menopause, and malnutrition need to be considered by nephrolgists and non-nephrologists in collaboration.

Animals↗
PubMed2004

Hypertension management: special considerations in chronic kidney disease patients.

It has been estimated that approximately 11% of the US adult population has chronic kidney disease (CKD), and it has been demonstrated that the prevalence of hypertension rises significantly as renal function declines. Even mild CKD significantly increases mortality risk, and cardiovascular disease remains the main cause of death among these patients. Although CKD patients have generally been excluded from trials testing the effect of lowering blood pressure on cardiovascular outcomes, guidelines suggest lowering blood pressure in hopes of reducing cardiovascular mortality and slowing the progression of renal disease. The preferred antihypertensive agents among these patients are drugs that block the renin-angiotensin system. In most hypertensive CKD patients, however, multiple agents are necessary to reach blood pressure targets. In general, diuretics and calcium channel blockers are added subsequently as adjunctive therapy. Hopefully, with increased recognition of the unique aspects of treating hypertension in this population, end-stage renal disease and cardiovascular morbidity and mortality will be delayed or avoided in the millions of patients with CKD.

Antihypertensive Agents↗
PubMed2005

Treatment of metabolic bone disease in patients with chronic renal disease: a perspective for rheumatologists.

As glomerular filtration rate (GFR) declines from age-related bone loss or disease that specifically induces a decline in GFR, there are a number of metabolic bone conditions that may accompany the decline in GFR. These metabolic bone conditions span a spectrum from mild-to-severe secondary hyperparathyroidism in early stages of chronic kidney disease (CKD) to the development of additional heterogeneous forms of bone diseases each with distinctly quantitative bone histomorphometric characteristics. Osteoporosis can also develop in patients with CKD and end-stage renal disease (ESRD) for many reasons beyond age-related bone loss and postmenopausal (PMO) bone loss. Diagnosing osteoporosis in patients with severe CKD or ESRD is not as easy to do as it is in patients with PMO. The diagnosis of osteoporosis in patients with CKD/ESRD must be done by first excluding other forms of renal osteodystrophy, through biochemical profiling or by double tetracycline-labeled bone biopsy and the finding of low trabecular bone volume. In such patients oral bisphosphonates seem to be safe and effective down to GFR levels of 15 mL/min. In patients with stage 5 CKD, who are fracturing because of osteoporosis or who are on chronic glucocorticoids, reducing the oral bisphosphonate dosage to half of its usual prescribed dosing for PMO seems reasonable from known bisphosphonate pharmacokinetics. However, we need better scientific data to fully understand bisphosphonate usage in this population. This paper deals with the evidence available to understand management of patients with CKD and opinions on what might be a reasonable clinical approach where evidence is currently lacking.

Bone Diseases, Metabolic↗
PubMed2005

Chinese herbal medicine in the treatment of chronic kidney disease.

Chronic kidney disease (CKD) is a worldwide public health issue with poor outcomes and high cost. There is growing evidence that some of the adverse outcomes of CKD can be prevented or delayed by early treatment using angiotensin II-converting enzyme inhibitors and angiotensin II-receptor blockers. A great amount of the world's population has been using traditional Chinese herbal medicine (TCHM) for treatment of CKD and has accumulated their experience for years. In this article, the knowledge and the therapeutic principles of traditional Chinese medicine in the treatment of CKD are briefly reviewed. The efficacy of several TCHMs, supported by either clinical evidence or experimental studies, is presented. The future direction for the study of Chinese herbal medicines in CKD is discussed.

Angelica↗
PubMed2006

Increased targeting of cardiovascular risk factors in patients with chronic kidney disease does not improve atheroma burden or cardiovascular function.

BACKGROUND: Although multiple risk factor intervention (MRFI) is recommended to reduce the increased morbidity and mortality of cardiovascular disease (CVD) in chronic kidney disease (CKD), its efficacy is unknown. We studied the efficacy of a MRFI program in CKD. METHODS: This randomized controlled study of 200 patients with stage 4 or 5 CKD compared a physician-supervised, nurse-driven MRFI clinic (focused on dyslipidemia, hyperhomocysteinemia, blood pressure [BP], anemia, and hyperphosphatemia) with conventional care in CKD. One hundred eleven subjects completed 2 years of follow-up (median follow-up 674 days [interquartile range {IQR} 348-719 days]). Outcome measures were atheroma burden (carotid intimamedia thickness [IMT]) and endothelial function (brachial artery reactivity [BAR]). RESULTS: The MRFI group showed significant improvements, compared with usual care, in serum low-density lipoprotein cholesterol (-30.9 mg/dL vs -12.7 mg/dL, P = .001), homocysteine (-6.95 vs -0.67 micromol/L, P < .001), systolic BP (-6.9 vs -0.2 mm Hg, P = .049), and diastolic BP (-4.8 vs -1.0 mm of Hg, P = .043). No significant changes were seen in serum phosphate or hemoglobin level. Despite observed improvements in risk factors, no differences from baseline were demonstrated for IMT (-0.00 vs -0.01 mm, P = .533) or BAR (0.09% vs 0.22%, P = .834). Forty-two patients reached a composite end point of CVD death, acute coronary syndrome, revascularization, nonfatal stroke, and amputation and this was similar between groups (23 vs 19 events, P = .475). CONCLUSIONS: A MRFI program was not associated with improvement in vascular structure or function in stage 4 or 5 patients with CKD.

Adult↗
PubMed2005

Increased sodium intake correlates with greater use of antihypertensive agents by subjects with chronic kidney disease.

BACKGROUND: Hypertension is a common disease in patients with chronic kidney disease (CKD) and predisposes to heart disease, stroke, and progression of renal failure. In the general population, sodium restriction has been shown to improve blood pressure (BP) control, but this is not widely recommended in CKD patients. The aim of this study was to assess the sodium balance in a CKD clinic and its effect on BP management. METHODS: We retrospectively reviewed charts from June 1998 through to June 2003 and included all patients with an estimated glomerular filtration rate (GFR) of <30 mL/min who completed a 24-h urine collection for sodium. Patients were divided into tertiles based upon their 24-h sodium excretion and analyzed by ANOVA. RESULTS: We included 141 CKD patients who had a mean (+/- SE) sodium excretion of 145.7 +/- 4.7 mmol/day. There were a significantly greater number of antihypertensive agents used with increasing sodium excretion (2.00 +/- 0.16, 2.61 +/- 0.20, and 2.77 +/- 0.19 medications, respectively for each tertile; P = .01). This difference was even more prominent when only those patients with a GFR <or=15 mL/min (n = 77) were examined (1.69 +/- 0.19, 2.52 +/- 0.27, and 3.08 +/- 0.26 medications, respectively; P = .001). Control of BP was equivalent in all groups. Multivariable analysis revealed sodium excretion (P = .00005) and age (P = .007) to be significantly associated with use of antihypertensive medication. CONCLUSIONS: We have demonstrated that increased sodium intake is associated with an increased number of antihypertensive medications to achieve comparable BP control in a population with CKD.

Adult↗