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PubMed2001

Identification of patients and risk factors in chronic kidney disease--evaluating risk factors and therapeutic strategies.

Three strategies can help delay chronic kidney disease (CKD) progression: early identification of patients, modification of risk factors, and implementation of the best interventions. Early identification of patients requires accurate screening tools. As serum creatinine is an unreliable marker of kidney dysfunction, clinicians should focus on the glomerular filtration rate or other markers of true kidney function. Clinicians should also be aware of other indicators of abnormal kidney function, such as anaemia, acidosis, and increases in parathyroid hormone level. Additionally, both clinicians and patients should be aware of the "non-modifiable" and "modifiable" risk factors for CKD. Non-modifiable risk factors include age, gender, race, diabetes, and genetic make-up, while modifiable risk factors include elevated blood pressure and blood glucose, proteinuria, anaemia, metabolic disturbances, and dyslipidaemia. Patients should be particularly aware of the risk factors common to both cardiac and kidney disease, such as hypertension, proteinuria, anaemia, and (possibly) dyslipidaemia and diabetes. A single centre study demonstrated that inclusion in a multidisciplinary CKD clinic programme produced the greatest increases in time to renal replacement therapy, haemoglobin levels, and epoetin treatment usage at initiation of dialysis in comparison with standard nephrology care or no care. Two years after starting dialysis, the number of deaths was lowest, and the number of patients who had received a transplant or were still on dialysis was highest, in the CKD clinic-treated group. These results confirm those of previous studies, which showed that timely referral to a multidisciplinary team for management prior to dialysis decreases the risk of adverse patient outcomes. This suggests that a multidisciplinary, collaborative, proactive approach increases the likelihood of early identification of CKD patients and risk factor modification. However, further evidence-based demonstrations of success are required, showing benefit to both patients and health care systems.

Humans↗

PubMed2004

Insulin resistance and pancreatic beta-cell function in patients with hypertensive kidney disease.

BACKGROUND: Insulin resistance and hyperinsulinaemia have been reported among patients with chronic renal failure. However, little is known concerning insulin sensitivity among patients with hypertensive kidney disease (HKD), especially in those with moderate or severe renal dysfunction. METHODS: We examined and compared 30 patients with HKD, 30 normotensive patients with chronic kidney disease (CKD-NT), 30 normal controls and 30 patients with hypertension and normal renal function (HTN). Moderate and severe renal dysfunction were defined according to the K/DOQI definitions (estimated glomerular filtration rates between 15 and 59 ml/min per 1.73 m(2)). The homeostasis model assessment of insulin resistance (HOMA-R) and three surrogate indexes based on 75 g oral glucose tolerance test results were used to determine insulin sensitivity. RESULTS: A trend to higher HOMA-R values in the HTN and HKD groups than in the other groups was noted, but the difference was not statistically significant. The insulin sensitivity index (ISI) proposed by Stumvoll et al. was significantly lower in the HTN, HKD and CKD-NT groups than in controls and was significantly lower in HKD than in the HTN and CKD-NT groups. The insulin sensitivity index proposed by Gutt et al. was significantly lower in HKD than in the control and HTN groups and showed a trend to being lower in HKD than in CKD-NT. The same patterns prevailed in the oral glucose ISI. We assumed that subjects whose ISI values decreased below the mean value minus 2-SD in the control group manifest apparent insulin resistance. According to this criterion, approximately 40% of HKD subjects were in an insulin-resistant state: only <10% of HTN subjects and approximately 10-30% of CKD-NT subjects were insulin resistant. CONCLUSIONS: HKD with moderate to severe renal dysfunction is associated with insulin resistance.

Cross-Sectional Studies↗

PubMed2005

Derivation and validation of a disease-specific risk score for cardiac risk stratification in chronic kidney disease.

OBJECTIVE: Cardiac events (CE; cardiac death, non-fatal myocardial infarction and acute coronary syndrome) are the principal causes of death in patients with chronic kidney disease (CKD). We sought to devise and validate a cardiac risk score to risk-stratify patients with CKD. METHODS: Clinical history and biochemical data were obtained in 167 CKD patients. CE were recorded over a median follow-up of 22 months. The hazard ratio (HR) of each independent variable using Cox regression analysis was used to derive a cardiac risk score for the prediction of events. The cardiac risk score was then applied to a validation population of 99 CKD patients to confirm its validity in predicting CE. RESULTS: CE occurred in 20 patients in the derivation group. The independent predictors of CE were cardiac history (HR 9.83, P = 0.001), body mass index (BMI; HR 1.15, P = 0.002), dialysis duration (HR 1.24, P = 0.004) and serum phosphate (HR 4.29, P = 0.001). The resulting cardiac risk score (range 26-67) gave an area under the receiver operating characteristic curve of 0.86. CE occurred in 25 patients in the validation group; the ROC curve area was similar (0.84, P = 0.11). An optimal cardiac risk score cut-off of 50 assigned high risk to 29% of the derivation and 35% of the validation group (P = 0.26). CE occurred in 35 and 57% of the high-risk derivation and validation groups, respectively (P = 0.09), and in 2 and 8% of the low-risk groups (P = 0.15). CONCLUSION: Application of a cardiac risk score using cardiac history, dialysis duration, BMI and phosphate identifies CKD patients at risk of future CE.

Adult↗

PubMed2005

Haemoglobin at time of referral prior to dialysis predicts survival: an association of haemoglobin with long-term outcomes.

Haemoglobin (Hgb) levels are known to be associated with numerous adverse outcomes in both chronic kidney disease (CKD) and non-CKD patients. This analysis evaluates the association of baseline haemoglobin levels on survival in CKD patients, who are followed by nephrologists, irrespective of glomerular filtration rate (GFR), prior to initiation of renal replacement therapy (RRT) and erythropoietin hormone replacement therapy. Analysis of data from the provincial database (PROMIS, Patient Registration and Outcome Management Information System) in British Columbia, Canada, was undertaken. Records used for the analysis included all CKD patients at first registration: GFR <60 ml/min/1.73 m(2), not yet on dialysis, starting from May 1998 to October 2002, and who had complete data (defined as age and gender, diabetic status, eGFR and Hgb levels). The primary objective of this study was to determine the association of Hgb and survival controlling for eGFR at first registration value, age, gender and diabetic status. Multivariate Cox proportional hazards analysis with time to death as outcome variable was performed. The cohort included 3028 patients: the mean age was 65 years, 28% were diabetic, and the mean eGFR in the cohort was 21 ml/min/1.73 m(2). The cohort is representative of the BC CKD and dialysis population regarding ethnicity: 64% Caucasian, 32% Asian. Median follow-up was 27 months, 1 year survival was 0.92, 2 year survival was 0.85. Hgb at initial registration is a statistically independent predictor of survival (RR = 0.875 for every 10 g/l, 95% CI: 0.835-0.917, P = 0.0001), after adjusting for age, gender, diabetic status and baseline eGFR. Further analysis, controlling for RRT, demonstrated a similar association between Hgb and survival (RR = 0.853 for every 10 g/l, 95% CI: 0.799-0.910, P = 0.0001), after adjusting for above variables. Substantial variation in Hgb values exists at all GFR levels. These findings underscore the importance of evaluating Hgb at all GFR levels, and the need to study the impact of modification of Hgb at different GFR levels on survival.

Aged↗

PubMed2005

In vivo and in vitro effects of simvastatin on inflammatory markers in pre-dialysis patients.

BACKGROUND: The beneficial effects of statins in reducing cardiovascular events have been attributed predominantly to their lipid-lowering effects, recent studies suggest that these effects might be due to their anti-inflammatory properties. We here investigate the in vivo and in vitro effects of simvastatin on cytokine production in pre-dialysis chronic renal failure patients. METHODS: Our clinical study has been designed as a randomized double-blind placebo controlled study. A total of 55 chronic kidney disease (CKD) patients at stages 3 and 4 (mean creatinine clearance 45 ml/min, range 15-60) were randomly assigned to receive simvastatin 40 mg/day or placebo, added to their ongoing treatment, for 6 months. Blood samples were obtained at baseline, and after 3 and 6 months of observation for the determination of lipids, inflammatory markers and renal function. For the in vitro studies, the effect of increasing doses of simvastatin on cytokine production [namely interleukin (IL)-6 and IL-8] in human cultured monocytes from 10 healthy subjects (HS) and 15 CKD patients stimulated by lipopolysaccharide (LPS) was investigated. RESULTS: A significant reduction in total cholesterol from 221+/-44 mg/dl to 184+/-41 mg/dl (3 months) and to 186+/-39 mg/dl (6 months) (P<0.02) and low-density lipoprotein cholesterol from 139+/-40 mg/dl to 104+/-29 mg/dl (3 months) and to 100+/-31 mg/dl (6 months) (P<0.001) was observed in the 28 patients treated with simvastatin. In this group, C-reactive protein (CRP) levels significantly decreased from 2.6 mg/l [interquartile range (IQR 4.9)] to 2.0 mg/l (IQR 1.9) (P = 0.03) at 6 months (P<0.05). A parallel reduction of IL-6 levels from 5.1 pg/ml (IQR 3.8) to 3.5 pg/ml (IQR 3.1) (P = 0.001) at 6 months was also observed. No significant reduction in inflammatory markers [CRP from 5.1 mg/l (IQR 1.9) to 5.4 mg/l (IQR 1.3) (P = NS) at 6 months] or plasma lipids [LDL-cholesterol from 127+/-32 mg/dl to 131+/-21 mg/dl (6 months)] was observed in the 27 patients of the placebo group. In the in vitro studies, the average value for cell-associated IL-6 and IL-8 was higher in CKD (155+/-95 pg/ml monocytes for IL-6 and 722+/-921 pg/ml monocytes for IL-8) vs HS (137+/-87 pg/ml monocytes and 186+/-125 pg/ml monocytes) (P<0.01) and was not affected by simvastatin alone. LPS resulted in a significant increase in cytokine production (IL-6: 1954+/-321 pg/ml monocytes for CKD and 1451+/-237 pg/ml monocytes for HS; P<0.001); the simultaneous addition of increasing doses of simvastatin to these cultures induced a dose-dependent inhibition of IL-6 and IL-8 production in stimulated peripheral blood mononuclear cells in all groups. CONCLUSIONS: These results indicate that simvastatin in commonly used doses has an in vitro and in vivo anti-inflammatory effect in CKD patients, and may play an important role in counteracting the mechanisms involved on the pathogenesis of cardiovascular disease.

Biomarkers↗

PubMed2006

Patients receiving maintenance dialysis have more severe functionally significant skeletal muscle wasting than patients with dialysis-independent chronic kidney disease.

BACKGROUND: Chronic renal replacement therapy patients exhibit reduction in skeletal muscle function as a result of a combination of metabolic effects and muscle fibre size reduction. The aim of this study was to compare muscle mass with function in patients with chronic kidney disease (CKD) at stages 4 and 5 on haemodialysis (HD) and peritoneal dialysis (PD), and investigate the associations of muscle wasting in a cross-sectional cohort. METHODS: We studied 134 patients (60 HD, 28 PD and 46 CKD 4). The three groups were well matched for age, sex, diabetes and dialysis vintage. Cross-sectional area (CSA) of muscle and fat was measured from a standardized multi-slice CT scan of a 6 cm long section of thigh. CSA of soft tissue was taken from appropriate fat and muscle densities. Functional assessment was by the sit-to-stand 60 test, assessing both the number of sit-to-stands possible under controlled conditions in 60 s (STS 60), and the time taken to perform five sit-to-stand movements (STS 5). Data were collected on a wide range of potential determinants of muscle CSA. RESULTS: There were no significant differences in haemoglobin between males or females or between any of the groups studied. Serum phosphate and calcium-phosphate product were higher in HD patients as compared to CKD4 patients, but there were no differences in these variables when comparing PD patients with either CKD4 or HD patients. Muscle CSA correlated well with objective functional assessments in males (STS 60 R = 0.52, P<0.0001) and females (R = 0.41, P = 0.004), and STS performance was reduced in dialysed patients as compared with CKD 4. Univariate analysis demonstrated that muscle CSA was associated with serum albumin concentration (R = 0.49, P<0.0001), age (R = -0.35, P = 0.005) and C-reactive protein (R = -0.34, P = 0.004). Creatinine clearance, dialysis adequacy, dialysis vintage and time-averaged serum bicarbonate, calcium and phosphate concentrations were not correlated with muscle CSA. CONCLUSION: In conclusion, patients with dialysis-treated CKD 5 exhibited more functionally significant muscle wasting than patients with CKD 4. This may be amenable to modification with targeted exercise or amelioration of factors associated with observed differences in muscle mass.

Adipose Tissue↗

PubMed2006

Decline in kidney function before and after nephrology referral and the effect on survival in moderate to advanced chronic kidney disease.

BACKGROUND: The burden of chronic kidney disease (CKD) is high, but its natural history and the benefit of routine nephrology care is unclear. This study investigated the decline in kidney function prior to and following nephrology referral and its association with mortality. METHODS: This study provides a retrospective review of the individual rates of glomerular filtration rate (GFR) decline (millilitre per minute per 1.73 m(2)/year) for the 5 years before and after referral in 726 new referrals with stages 3-5 CKD to one renal unit between 1997 and 2003. Blood pressures are averages at referral, 1 and 3 years post referral. Logistic regression and Cox's models tested factors predicting post-referral GFR decline and the impact on mortality. RESULTS: Mean (SD) age was 72 (14), and 389 (54%) patients had stages 4-5 CKD. GFR decline slowed significantly from -5.4 ml/min/1.73 m(2)/year (-13. to -2) before to -0.35 ml/min/1.73 m(2)/year (-3 to +3) after referral (P < 0.001). Blood pressure also reduced significantly (155/84 to 149/80, P < 0.05) with most changes occurring within 1 year of referral. Factors predicting a non-progressive post-referral decline included a lower systolic blood pressure at referral and 1 year after referral, a CKD diagnosis other than diabetic nephropathy, less baseline proteinuria and a non-progressive pre-referral GFR decline. A non-progressive post-referral GFR decline was independently associated with significantly better survival (hazard ratio 0.55, 95% CI 0.40-0.75, P <or = 0.001) after adjustment for known risk factors. CONCLUSIONS: Following nephrology referral, GFR decline slowed significantly and was associated with better survival. Earlier detection of patients with progressive CKD and interventions to slow progression may have benefits on both kidney and patient survival.

Aged↗

PubMed2006

Do ultrasound renal resistance indices reflect systemic rather than renal vascular damage in chronic kidney disease?

BACKGROUND: In patients suffering from chronic kidney disease (CKD), ultrasound renal resistance indices predict progression of kidney disease and death. Although ultrasound resistance indices were initially considered to directly reflect intrarenal vascular resistance, they are complex composite parameters that are influenced by various vascular factors. We hypothesized that renal resistance indices reflect systemic vascular disease rather than local renal damage in patients with CKD. METHODS: In 140 patients suffering from CKD not receiving renal replacement therapy, intrarenal resistance indices were measured in interlobar arteries. For assessment of systemic atherosclerotic disease, common carotid intima-media thickness (IMT) and ankle-brachial blood pressure index were determined. Categories of risk for coronary heart diseases were defined by Framingham risk scoring. RESULTS: Increased renal resistance indices were associated with high Framingham risk scores and with the presence of atherosclerotic disease. In addition, ultrasound renal resistance indices progressively increased with the stage of renal function impairment, and patients suffering from diabetic nephropathy had higher resistance indices than patients suffering from other renal diseases. In a multivariate linear regression analysis, IMT, Framingham risk score, renal function, presence of diabetic nephropathy and pulse pressure independently predicted resistance indices. However, when additionally adjusting for age, IMT and Framingham risk score were no longer independent predictors of resistance indices. CONCLUSIONS: In patients suffering from CKD, intrarenal resistance indices are independently associated with cardiovascular risk score and systemic vascular disease as well as with aetiology and stage of CKD. This may explain their strong association with both impaired renal outcome and death.

Aged↗

PubMed2003

Prevention of hypertension and its complications: theoretical basis and guidelines for treatment.

Hypertension is a nutritional-hygienic disease. Long-term caloric intake in excess of energy expenditures, chronic supraphysiological intake of dietary sodium, excessive alcohol consumption, and psychosocial stressors all contribute to the development of hypertension throughout the world. Elevated BP, particularly systolic BP, has been linked to multiple adverse clinical outcomes including stroke, heart failure, myocardial infarction, renal insufficiency/failure, peripheral vascular disease, retinopathy, dementia, and premature mortality. These undesirable clinical outcomes are typically, although not invariably, preceded by pressure-related target-organ injury such as left ventricular hypertrophy, renal insufficiency and proteinuria. The relation of BP and CKD and, in turn, the prevention of CKD or forestalling its progression by hypertension treatment, will be the focus of this manuscript. In hypertensive persons with reduced kidney function and/or proteinuria, lowering BP with multidrug therapy that is inclusive of pharmacologic modulators of the renin-angiotensin-aldosterone-kinin system is an effective strategy to forestall the progressive loss of kidney function. The totality of data support low therapeutic BP targets for persons with proteinuria >1 g/d. Nevertheless, in persons with CKD, even those with proteinuria below the dipstick positive level (approximately 300 mg/d or urine protein to creatinine ratio of 0.22), aggressive BP control also may be warranted because of the high risk of nonrenal cardiovascular disease. Multiple antihypertensive drugs will be required in the vast majority of patients with diabetes and/or reduced kidney function to attain BP goal. Renin-angiotensin system (RAS) modulator therapy is indicated among persons with diabetes mellitus and CKD. Available data support the use of angiotensin receptor blockers in persons with type 2 diabetes and overt nephropathy for preservation of kidney function. Among persons with type I diabetes with or without overt nephropathy, type 2 diabetes without overt nephropathy and in nondiabetic CKD, the available clinical data support the use of angiotensin-converting enzyme inhibitors as the RAS modulator of choice. Low therapeutic target BP levels <130/80 mmHg in persons with type 2 diabetes mellitus also appear warranted based on available data mostly for reducing the risk of nonrenal cardiovascular disease and overall mortality.

Diabetes Mellitus, Type 1↗

PubMed2003

Screening for chronic kidney disease: unresolved issues.

End-stage renal disease is epidemic in the United States. As a measure to control this epidemic, it has been recommended that individuals who are at risk for CKD be tested for undetected kidney disease during routine health care encounters. There are generally accepted criteria against which screening recommendations for CKD control and prevention programs should be judged. If detection strategies are to be adopted for the screening of kidney disease, then CKD must represent a significant public health problem, be characterized by a clear natural history with a detectable asymptomatic period, outcomes should be improved by early treatment, and acceptable screening tests should be available. Health systems must provide adequate and appropriate follow-up medical care for individuals with newly detected CKD. Finally, the cost-effectiveness of screening needs to be demonstrated and the effectiveness of screening as a means of achieving reductions in CKD should be proven in randomized trials.

Chronic Disease↗

PubMed2024

Racial and regional disparities in the risk of noncommunicable disease between sub-Saharan black and European white patients.

OBJECTIVES: Greater vulnerability of Black vs. White individuals to cardiovascular disease (CVD) and chronic kidney disease (CKD) is well charted in the United States, but studies involving sub-Saharan blacks are scarce. METHODS: Baseline data (2021-2024) were collected in 168 sub-Saharan Blacks and 93 European Whites in an ongoing clinical trial (NCT04299529), using standardized patient selection criteria. Data included clinical and biochemical risk factors, ECG and echocardiographic traits, Framingham CVD risk, CKD grades (KDIGO 2024), self-assessed symptoms (WHO questionnaire), and urinary proteomic profiles predictive of left ventricular dysfunction (LVD) and CKD, HF1, and CKD273, respectively. Racial comparisons rested on unadjusted and multivariable-adjusted analyses. RESULTS: Despite being younger (60.4 vs. 68.3 years), blacks had a worse risk profile, as evidenced by higher diabetes prevalence, higher BMI, faster heart rate, unfavourable serum cholesterol fractions, lower estimated glomerular filtration rate, microalbuminuria, and sedentary lifestyle. This resulted in blacks having higher 10-year CVD risk, higher heart age (index of vascular ageing with chronological age as reference), and a worse CKD grades. In both races, CKD273 increased with CKD grade, but CKD273 and HF1 were not different by race. These observations were robust in subgroup and adjusted analyses. CONCLUSION: This study did not differentiate host (genetic, molecular, and pathogenic) from environmental drivers of disease. Nonetheless, the findings call for a multipronged and comprehensive implementation of innovative health policies in sub-Saharan countries. Education, research, empowerment of stakeholders, and international learned societies connecting experts from a wide array of disciplines should vigorously sustain this effort.

Humans↗

PubMed2025

Genetic risk factors in rheumatoid arthritis: A Mendelian randomization study of chronic kidney disease in European populations.

Rheumatoid arthritis (RA) is a heritable autoimmune disease linked to chronic kidney disease (CKD) in observational studies. However, whether this association is causal and driven by shared genetic risk remains unclear, warranting genetic investigation. To investigate possible causal relationships between RA and different CKD subtypes, we used Mendelian randomization (MR) analyses with data from genome-wide association studies. The inverse variance weighted (IVW) methodology was the main method, and sensitivity analyses were added to improve the validity of the causal estimations. Our analysis predicted that RA significantly increases the risk of IgA nephropathy (IVW odds ratio [OR] = 1.041, 95% confidence interval [CI] = 1.018-1.065, P = 4.286e-04), diabetic nephropathy (IVW OR = 1.078, 95% CI = 1.009-1.152, P = .027), nephrotic syndrome (IVW OR = 1.164, 95% CI = 1.078-1.257, P = 1.012e-04), and chronic renal failure (IVW OR = 1.046, 95% CI = 1.018-1.075, P = 1.000e-03). MR analyses confirmed RA's positive causal effect on these CKD subtypes (all P < .05). While heterogeneity was observed for IgA nephropathy and chronic renal failure, sensitivity analyses (MR-Egger intercept, all P > .05) revealed no evidence of horizontal pleiotropy, supporting the robustness of our findings. Our findings suggest that in European-ancestry populations, a genetic predisposition to RA is causally associated with a higher risk of specific types of CKD. While these results require validation in diverse ethnic groups, they highlight the potential importance of renal monitoring for genetically susceptible RA patients, which may help mitigate the public health burden of CKD.

Humans↗

PubMedDate not supplied

The consequences of uncontrolled secondary hyperparathyroidism and its treatment in chronic kidney disease.

Secondary hyperparathyroidism (HPT) is a common complication of chronic kidney disease (CKD) and a frequent cause of clinically significant bone disease. Soft-tissue and vascular calcification, cardiovascular disease, and calcific uremic arteriolopathy (CUA) are additional serious consequences of the disorder that may contribute directly to cardiovascular morbidity and mortality in patients with CKD. Less widely appreciated manifestations include neurological disturbances, hematological abnormalities, and endocrine dysfunction. Secondary HPT arises from alterations in calcium, phosphorus, and vitamin D metabolism that develop early in the course of CKD and become more pronounced as kidney function declines. Treatment is often delayed, however, until the disease is well established. Current therapeutic strategies rely largely on the use of vitamin D sterols to diminish excess parathyroid hormone (PTH) synthesis and to lower serum or plasma PTH levels, but their use is often confounded by increases in serum calcium and phosphorus concentrations, changes that can aggravate soft-tissue and vascular calcification. As such, there is a need for new therapeutic interventions that can effectively lower serum or plasma PTH levels without producing untoward side effects. The current review summarizes the diverse manifestations of secondary HPT in patients with CKD. The consequences of inadequately controlled secondary HPT and the adverse effects of selected therapeutic interventions for the disorder on vascular calcification and cardiovascular disease in those with CKD are discussed.

Calcinosis↗

PubMed2005

The epidemiology and control of anaemia among pre-ESRD patients with chronic kidney disease.

Anaemia is a common condition among pre-end-stage renal disease (pre-ESRD) patients with chronic kidney disease (CKD). Indeed, data from clinical studies indicate that anaemia may be present in as many as two-thirds of such patients. Use of recombinant human erythropoietin (EPO) provides an effective means of correcting anaemia in CKD patients and helps to reduce the risk of renal disease progression and related problems. Unfortunately, EPO therapy is underutilized in these persons. Consequently, anaemia remains a major problem in the pre-ESRD CKD population. Evidence suggests that anaemia in the presence of CKD can lead to an increased risk of a number of adverse outcomes, including mortality, progression of kidney disease, coronary heart disease, stroke, hospitalization, and decreases in quality of life. Anaemia's association with these adverse outcomes suggests that effective treatment of anaemia in pre-ESRD CKD patients is of great importance and that substantial efforts should be made to ensure that these patients receive appropriate therapy to correct anaemia.

Anemia↗

PubMed2006

Vascular calcification and renal osteodystrophy relationship in chronic kidney disease.

Cardiovascular disease and stroke account for 60-70% of all deaths in patients with end-stage renal disease (ESRD), at a risk that is 10-20-fold the age- and sex-matched general population. There is also increased coronary artery calcification and increased cardiovascular mortality in chronic kidney disease (CKD) and dialysis patients compared with the general population. Bone is similarly abnormal in CKD. There is an increased incidence of low bone mass and fractures in dialysis patients compared with the general population. Furthermore, a hip fracture in a dialysis patient is associated with a doubling of the mortality observed in nondialysis patients with a hip fracture. These two problems may be linked, as cross-sectional studies have demonstrated an inverse relationship between osteoporosis and coronary artery calcification in the general population and in ESRD patients. In vitro and ex vivo, there is clear evidence that vascular calcification is an active cell-mediated process, made worse by disorders of mineral metabolism. Many factors known to be associated with cardiovascular disease in CKD patients can directly increase calcification in vitro. In addition, in CKD, there are many mechanisms by which bone may adversely affect vascular calcification including disorders of bone remodelling, altered secretion of parathyroid hormone (PTH), hyperphosphatemia, hypercalcaemia, use of calcium based binders, and excessive vitamin D therapy. The coexistence of vascular risk factors and abnormal bone represent a double threat to the well being of patients with CKD.

Bone Remodeling↗

PubMed2006

Statin therapy in patients with chronic kidney disease: to use or not to use.

Dyslipdemia is a common complication of chronic kidney disease (CKD) and contributes to high cardiovascular morbidity and mortality of CKD patients. Experimental studies have demonstrated that lipids induce glomerular and tubulointerstitial injury and that lipid-lowering treatments ameliorate renal injury. Therapy with statins not only has the potential to lower cardiovascular morbidity and mortality in patients with CKD but also to slow progression of renal disease. Whereas the guidelines for treatment of hyperlipidaemia in nonrenal patients are based on prospective, randomized, placebo-controlled mega-trials, such data are not available for CKD patients. This review outlines the limited information currently available on the effect of statins among patients with CKD and summarizes the ongoing randomized trials designed to address this question.

Cholesterol↗

PubMed2004

Increased prevalence of oxidant stress and inflammation in patients with moderate to severe chronic kidney disease.

BACKGROUND: The prevalence of increased oxidative stress and acute-phase inflammation in patients with chronic kidney disease (CKD) has not been thoroughly investigated. METHODS: Biomarkers of oxidative stress and acute-phase inflammation were measured in a cohort of 60 patients with stage 3-5 CKD compared to a healthy subject cohort. Levels of oxidative stress and inflammation were also compared to estimated glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula. RESULTS: All biomarkers of oxidative stress (plasma protein carbonyl group content, plasma free F2-isoprostane content, plasma protein reduced thiol content) and all markers of inflammation [C-reactive protein (CRP), interleukin-6 (IL-6)] differed significantly between CKD patients and healthy subjects. There was no significant relationship between estimated GFR and any oxidative stress or inflammation biomarker. CRP levels were higher in patients with known coronary vascular disease (CVD) and in patients not taking angiotensin II inhibitors. Plasma IL-6 levels were significantly higher in patients with known coronary vascular disease and lower in patients taking statins. Biomarkers of oxidative stress were significantly higher in patients with diabetes and hypercholesterolemia. CONCLUSION: There is evidence of increased oxidative stress and acute-phase inflammation in patients with stage 3-5 chronic kidney disease compared to healthy subjects that does not closely correlate with estimates of GFR. Among CKD patients, inflammatory biomarkers correlate with known CVD and inversely correlate with the use of angiotensin II inhibitors and statins. A further increase in oxidative stress was noted in diabetic and hypercholesterolemic patients. Inflammation and oxidative stress may contribute to cardiovascular risk in CKD patients.

Acute-Phase Reaction↗

PubMed2004

Detecting and managing patients with type 2 diabetic kidney disease: proteinuria and cardiovascular disease.

BACKGROUND: The increasing prevalence of type 2 diabetes (T2DM) places more patients at risk for developing chronic kidney disease (CKD) or cardiovascular (CV) events. Effective therapy for CKD or CV disease (CVD) requires a method of identifying affected patients and monitoring the effectiveness of therapy. METHODS: We tested the predictive value of proteinuria for identifying patients at risk for progressive CDK and CVD, and monitoring treatment was determined using RENAAL study results. RESULTS: Baseline proteinuria identified patients at risk for progressive CKD and CVD. Suppression of proteinuria was associated with decreased likelihood of CKD or CVD. CONCLUSION: Proteinuria identifies the risk of CKD and CVD, and can be used to monitor the effectiveness of therapy.

Cardiovascular Diseases↗