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PubMed2005

Modulation and source of procalcitonin in reduced renal function and renal replacement therapy.

Serum procalcitonin (PCT), an accurate marker of severe infection, is moderately increased in chronic kidney disease (CKD), peritoneal dialysis (PD) and haemodialysis (HD). We studied the extent of PCT elevation and factors accounting for elevated PCT in CKD and dialysis, and whether peripheral blood mononuclear cells (PBMC) contribute to increased PCT. In 37 controls, 281 CKD, 31 PD, and 65 HD patients without infection, PCT was measured and correlated with CKD stage, PD, HD, C-reactive protein (CRP), cardiovascular disease (CVD) and other clinical parameters. PCT release by PBMC from controls, advanced CKD, PD and HD patients (12 subjects each) was measured. PCT increased in parallel to the deterioration of CKD. Oliguria, advanced CKD, PD, HD, CVD and elevated CRP were independently associated with PCT elevation. PCT release from PBMC significantly increased in advanced CKD, PD and HD. PCT release from PBMC correlated closely with the corresponding serum PCT values (r=0.76, P <0.001). In the absence of infection, PCT may increase due to reduced renal elimination and increased synthesis, as due to PBMC. Furthermore, serum PCT could serve as a marker of low-grade inflammation and CVD, which substantially increase mortality in CKD and dialysis.

C-Reactive Protein↗

PubMed2006

Failure of ICD-9-CM codes to identify patients with comorbid chronic kidney disease in diabetes.

OBJECTIVE: To determine prevalence of chronic kidney disease (CKD) in patients with diabetes, and accuracy of International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes to identify such patients. DATA SOURCES/STUDY SETTING: Secondary data from 1999 to 2000. We linked all inpatient and outpatient administrative and clinical records of U.S. veterans with diabetes dually enrolled in Medicare and the Veterans Administration (VA) health care systems. STUDY DESIGN: We used a cross-sectional, observational design to determine the sensitivity and specificity of renal-related ICD-9-CM diagnosis codes in identifying individuals with chronic kidney disease. DATA COLLECTION/EXTRACTION METHODS: We estimated glomerular filtration rate (eGFR) from serum creatinine and defined CKD as Stage 3, 4, or 5 CKD by eGFR criterion according to the Kidney Disease Outcomes Quality Initiative guidelines. Renal-related ICD-9-CM codes were grouped by algorithm. PRINCIPAL FINDINGS: Prevalence of CKD was 31.6 percent in the veteran sample with diabetes. Depending on the detail of the algorithm, only 20.2 to 42.4 percent of individuals with CKD received a renal-related diagnosis code in either VA or Medicare records over 1 year. Specificity of renal codes for CKD ranged from 93.2 to 99.4 percent. Patients hospitalized in VA facilities were slightly more likely to be correctly coded for CKD than patients hospitalized in facilities reimbursed by Medicare (OR 5.4 versus 4.1, p=.0330) CONCLUSIONS: CKD is a common comorbidity for patients with diabetes in the VA system. Diagnosis codes in administrative records from Medicare and VA systems are insensitive, but specific markers for patients with CKD.

Adult↗

PubMed2004

Managing dyslipidemia in chronic kidney disease.

OBJECTIVE: Patients with chronic kidney disease (CKD) are at higher risk for cardiovascular disease (CVD) than patients in the general population. One potentially modifiable risk factor for CVD in patients with CKD is dyslipidemia. In the current manuscript we review observational and trial data assessing dyslipidemia and its treatment in this patient population. RESULTS: Observational studies have noted a "reverse epidemiology" in patients with CKD such that low total cholesterol levels are associated with a higher mortality rate. The complex lipid profile of patients with CKD also raises questions as to whether lipid-lowering therapy will be beneficial in this patient population. Although there are only a few trials assessing the relationship between lipid-lowering therapy and CVD outcomes in CKD patients, many lipid-lowering medications are both safe and effective. In addition, there is suggestive evidence that statin therapy, in particular, also may reduce inflammation and slow the decline in glomerular filtration rate (GFR) in patients during the earlier stages of CKD. CONCLUSION: Because of the high rate of CVD in patients with CKD and the overall safety of most medical therapies for dyslipidemia in CKD, current guidelines from the National Kidney Foundation Kidney Disease Outcomes Quality Initiative recommend aggressive therapy of dyslipidemia. These guidelines do, however, acknowledge the paucity of trial data in this patient population. There are 3 ongoing randomized controlled trials that are assessing the effect of statin therapy on CVD outcomes. These studies will hopefully provide definitive answers as to the appropriate treatment of dyslipidemia in CKD.

Cardiovascular Diseases↗

PubMedDate not supplied

Management of chronic kidney disease in an academic primary care clinic.

BACKGROUND: Three million people in the United States are estimated to have chronic kidney disease (CKD). Management of these CKD patients in the outpatient primary care clinic setting has not been well studied. HYPOTHESIS: Primary care management of CKD can be assessed and opportunities for improvement can be identified. METHODS: Management of CKD based on available published literature and guidelines was assessed in a single primary care site of an academic hospital with 23,000 annual visits and 8,300 patients. Charts of patients seen between October 1, 1997 and March 25, 1999 with an elevated SCr > or = 1.7 mg/dl on two separate measurements at least 6 months apart were reviewed for predefined indicators of CKD management. RESULTS: Assessment identified several aspects of CKD management to be suboptimal: control of blood pressure, use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, assessment of proteinuria, and renal consultation. Better management was found with respect to hemoglobin A1c measurement for diabetic patients. In general, CKD care was similar for diabetic and non-diabetic patients. CKD management was also similar regardless of level of creatinine clearance (> or = 50 vs. 50-30 vs. < or = 30 ml/min). CONCLUSION: CKD care can be measured in an outpatient academic primary care clinic and opportunities to improve were identified.

Aged↗

PubMed2006

A population-based assessment of the familial component of chronic kidney disease mortality.

BACKGROUND/AIM: While the familial nature of chronic kidney disease (CKD) has been recognized, it has primarily been defined from studies of first-degree relatives of selected sets of cases. The goal of this study is an evaluation of the familial clustering of end-stage renal disease (ESRD) and CKD mortality using a population-based genealogy of Utah. This is the first population-based analysis of the familial component of ESRD and non-ESRD CKD. METHODS: We have defined two distinct patient groups for this analysis, using individuals with death certificates in the Utah Population Database indicating ESRD (n = 192) and non-ESRD CKD (n = 335) as the cause of death. Two measures of familiality were used: (1) relative risk (RR) of CKD or ESRD death in relatives of cases and (2) an average relatedness statistic, i.e., the Genealogical Index of Familiality. RESULTS: The RR for dying with ESRD among the first-degree relatives of individuals dying with ESRD is estimated to be 10.1 (p = 0.0007, 95% confidence interval CI 2.76-25.95), but is not significantly elevated among second-degree relatives. The RR for dying with non-ESRD CKD among first- and second-degree relatives of individuals dying with non-ESRD CKD was 3.89 (p = 0.0051, 95% CI 1.43-8.46) and 3.11 (p = 0.04, 95% CI 0.85-7.95), respectively. The Genealogical Index of Familiality statistic demonstrated that the individuals dying with ESRD are significantly more related than expected in this population (p = 0.013); significant excess relatedness was also observed for individuals dying with non-ESRD CKD (p = 0.006), suggesting a familial component for both, with evidence for common environmental and genetic effects. CONCLUSION: The results of this analysis of individuals dying with ESRD and non-ESRD CKD supports a significant and independent familial component to both conditions, suggesting a heritable factor playing a role.

Cause of Death↗

PubMed2007

Impact of ergocalciferol treatment of vitamin D deficiency on serum parathyroid hormone concentrations in chronic kidney disease.

BACKGROUND: Vitamin D deficiency is highly prevalent and associated with secondary hyperparathyroidism in patients with chronic kidney disease (CKD). The Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend treatment of vitamin D deficiency starting with CKD stage 3, though no data are available showing an impact on serum parathyroid hormone (PTH) concentrations. The goal of this analysis, therefore, was to determine the effect of ergocalciferol treatment on plasma PTH concentrations in vitamin D-deficient patients with stage 3 and stage 4 CKD. METHODS: A prospective, nonrandomized observational analysis was conducted in an academic community hospital CKD clinic. Fifty-two patients with stage 3 or stage 4 CKD with vitamin D deficiency and elevated PTH concentrations received ergocalciferol dosed per a modified K/DOQI guidelines protocol and adjusted every 3 months. Serum PTH, 25-vitamin D, 1,25-vitamin D, calcium, phosphorus, and albumin levels were drawn at initiation of therapy and repeated every 3 months. RESULTS: The mean 25-vitamin D levels normalized in patients with stage 3 and 4 CKD, with values of 31.6 +/- 2.2 ng/ml (78.8 +/- 5.49 nmol/l) and 35.4 +/- 1.9 ng/ml (88.4 +/- 4.74 nmol/l), respectively (p < 0.0001). A median decrease in PTH concentrations of 13.1 and 2.0% was noted in patients with stage 3 and stage 4 CKD, respectively (p = 0.041, p = nonsignificant). CONCLUSIONS: Ergocalciferol therapy is a reasonable initial therapy for vitamin D deficiency associated with elevated PTH levels in stage 3 CKD. It does not appear to have equivalent benefits in stage 4 CKD.

Adult↗

PubMed2004

Chronic kidney disease awareness, prevalence, and trends among U.S. adults, 1999 to 2000.

The incidence of kidney failure treatment in the United States increased 57% from 1991 to 2000. Chronic kidney disease (CKD) prevalence was 11% among U.S. adults surveyed in 1988 to 1994. The objective of this study was to estimate awareness of CKD in the U.S. population during 1999 to 2000 and to determine whether the prevalence of CKD in the United States increased compared with 1988 to 1994. Analysis was conducted of nationally representative samples of noninstitutionalized adults, aged 20 yr and older, in two National Health and Nutrition Examination Surveys conducted in 1988 to 1994 (n = 15,488) and 1999 to 2000 (n = 4101) for prevalence +/- SE. Awareness of CKD is self-reported. Kidney function (GFR), kidney damage (microalbuminuria or greater), and stages of CKD (GFR and albuminuria) were estimated from calibrated serum creatinine, spot urine albumin to creatinine ratio (ACR), age, gender, and race. GFR was estimated using the simplified Modification of Diet in Renal Disease Study equation. Self-reported awareness of weak or failing kidneys in 1999 to 2000 was strongly associated with decreased kidney function and albuminuria but was low even in the presence of both conditions. Only 24.3 +/- 6.4% of patients at GFR 15 to 59 ml/min per 1.73 m(2) and albuminuria were aware of CKD compared with 1.1 +/- 0.3% at GFR of 90 ml/min per 1.73 m(2) or greater and no microalbuminuria. At moderately decreased kidney function (GFR 30 to 59 ml/min per 1.73 m(2)), awareness was much lower among women than men (2.9 +/- 1.6 versus 17.9 +/- 5.9%; P = 0.008). The prevalence of moderately or severely decreased kidney function (GFR 15 to 59 ml/min per 1.73 m(2)) remained stable over the past decade (4.4 +/- 0.3% in 1988 to 1994 and 3.8 +/- 0.4% in 1999 to 2000; P = 0.23). At the same time, the prevalence of albuminuria (ACR >/= 30 mg/g) in single spot urine increased from 8.2 +/- 0.4% to 10.1 +/- 0.7% (P = 0.01). Overall CKD prevalence was similar in both surveys (9% using ACR > 30 mg/g for persistent microalbuminuria; 11% in 1988 to 1994 and 12% in 1999 to 2000 using gender-specific ACR cutoffs). Despite a high prevalence, CKD awareness in the U.S. population is low. In contrast to the dramatic increase in treated kidney failure, overall CKD prevalence in the U.S. population has been relatively stable.

Adult↗

PubMed2006

Early changes in bioelectrical estimates of body composition in chronic kidney disease.

The aim of this study was to detect the potential occurrence of early abnormalities of body composition in patients with chronic kidney disease (CKD) at first referral to an outpatient nephrology clinic. Eighty-four patients with CKD (49 men and 35 women) were compared with 604 healthy control subjects (298 men and 306 women). Anthropometry and bioelectrical impedance analysis (BIA) were performed in all participants, whereas renal function, laboratory tests for nutritional status, and nutrient intake were assessed in the CKD group only. Creatinine clearance was 27.8 +/- 13.8 and 27.4 +/- 13.0 ml/min per 1.73 m(2) in male and female patients with CKD, respectively. No patient showed peripheral edema; frank malnutrition, defined by presence of serum albumin <3.5 g/dl plus body mass index <20 kg/m(2); or protein intake <0.6 g/kg per d. At the BIA, patients with CKD showed lower resistance (R) and abnormal mean impedance vectors for the bivariate normal distribution of R/height and reactance/height. Phase angle also was reduced (-22%), especially in patients with diabetes. When BIA-derived data were considered, total body water was slightly higher (+4.3% in men; +3.5% in women) and body cell mass was lower (-6.7% in men; -7.7% in women) in patients with CKD. No difference in either BIA parameters or nutritional indexes was observed among various CKD stages. Despite the absence of overt malnutrition, patients with CKD exhibit altered BIA variables from the early phases of renal disease. These alterations are related to the renal dysfunction, are more marked in the presence of diabetes, and mainly indicate the presence of overhydration in the absence of edema. Therefore, BIA represents an attractive clinical tool to detect impairment of body composition from the early stages of CKD.

Aged↗

PubMed2006

The chronic kidney disease epidemic: stepping back and looking forward.

Estimating the prevalence of chronic kidney disease (CKD) is no simple task. The overall prevalence is relatively low but may be higher in select populations that are not accessible to surveys (e.g., certain ethnic groups, the sick or elderly). Moreover, the tests that define CKD lack precision and transportability to healthy populations. During the past decade, it is not clear that CKD has grown substantially. Some epidemiologic factors that are associated with CKD (obesity and diabetes) are increasing, whereas others (uncontrolled hypertension and smoking) are decreasing. Reasons for the discrepancy between a stable CKD population and ongoing ESRD growth remain speculative. There is evidence that ESRD rates may be stabilizing and that efforts to reduce progression in high-risk groups may be starting to show benefit. Expanding the definition of CKD and increasing detection may be required to reduce overall ESRD prevalence. One concern is that many of the well-defined high-risk patient groups (diabetes and black) are still undertreated. Increasing the investigation and treatment of low-risk patients may not be the answer. Clinical inertia (failure to initiate or change therapy) may be a more significant and modifiable barrier toward reducing ESRD, and this deserves increased attention. Furthermore, reducing CKD prevalence will require controlling the precipitating causes. The incremental benefit of detecting CKD in low-risk patients, use of expensive therapies in CKD, or new strategies such as the treatment of prehypertension require solid evidence, not only of the variety that shows benefit (hard end points) but also to whom, when, and at what cost.

Chronic Disease↗

PubMed2001

Opportunities for improving the care of patients with chronic renal insufficiency: current practice patterns.

There are between 2 and 13 million Americans with chronic kidney disease (CKD). Recent reports suggest that their treatment is currently suboptimal. To further investigate this issue, patterns of practice for the treatment of patients with CKD who were enrolled in a large health maintenance organization in New Mexico were analyzed. Among the >200,000 patients who were enrolled in the health maintenance organization between 1994 and 1997, a cohort of 1658 patients who exhibited at least two gender-specific, elevated creatinine concentrations (Cr), separated by at least 90 d, were identified. The proportions of patients with Cr values of <2.0, 2.0 to 2.9, 3.0 to 3.9, and > or =4.0 mg/dl were 73, 17, 3, and 7%, respectively. The majority of patients were treated by a primary care physician until Cr values reached 3.0 mg/dl, at which time a nephrologist was consulted. Care tended to be transferred to the nephrologist when the Cr reached 4.0 mg/dl. Only 7.4% of patients received erythropoietin (EPO). Use of EPO increased as Cr increased. EPO was unlikely to be prescribed unless the patient had visited a nephrologist. Fewer than one half of all patients with CKD and fewer than 20% of patients with CKD with Cr values of > or =4.0 mg/dl received an angiotensin-converting enzyme inhibitor (ACEI). Nephrologists were not more likely to prescribe ACEI than were primary care physicians. Diabetic patients were more likely to receive ACEI than were nondiabetic patients, but ACEI use was quite low even among diabetic patients with CKD. The average number of hospitalizations per patient-year increased as Cr increased and was more than twice as high for patients with Cr values of > or =4.0 mg/dl, compared with those with Cr values of <2.0 mg/dl. The reasons for hospitalization were more likely to be related to comorbidities than to CKD itself, however. There are many opportunities to improve the care of patients with CKD. Better adherence to practices known to be of clinical benefit for patients with CKD not only will improve patient outcomes but also may reduce the costs of care. Providers, policy-makers, and payers should view CKD as a major public health problem and initiate innovative programs to address this growing patient population.

Adult↗

PubMed1982

Bone lesions in growing swine fed 3% cement kiln dust as a source of calcium.

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.

Animals↗

PubMed2006

The utility of non-HDL in managing dyslipidemia of stage 5 chronic kidney disease.

BACKGROUND: The Kidney Disease Outcomes Quality Initiative (K/DOQI) treatment guidelines for managing dyslipidemia in patients with chronic kidney disease (CKD) designate CKD as a high-risk category for coronary heart disease and, in Stage 5 CKD patients, recommend maintaining low-density lipoprotein (LDL) < 100 mg/dl and, for patients with hypertriglyceridemia (> or = 200 mg/ dl), non-high-density lipoprotein (non-HDL) < 130 mg/dl, the latter to achieve very low-density lipoprotein (VLDL) < 30 mg/dl. More recently, the National Cholesterol Education Program has recommended an LDL target of < 70 mg/dl for high-risk patients. AIMS: The purposes of this study were: to document the point prevalence of dyslipidemia in CKD patients at hemodialysis inception, prior to potential impact of dialysis treatments; to assess the hypothesis that non-HDL serves as a reliable surrogate marker for elevated VLDL; to examine the performance of K/DOQI guidelines in treating dyslipidemia; and to evaluate the utility of non-HDL as an alternative primary trigger/target of lipid-lowering therapy in Stage 5 CKD patients. METHODS: Consistent with K/DOQI guidelines, lipid levels drawn immediately prior to hemodialysis sessions, thus possibly non-fasting, were analyzed in 21,893 incident dialysis patients by laboratory measurements of triglycerides, total cholesterol, and HDL and from calculated values of non-HDL, LDL, VLDL and intermediate-density lipoprotein. RESULTS: Prevalence of dyslipidemia, by guideline definitions, was 82%, predominantly manifested by elevated triglycerides (52%) and VLDL (52%) and decreased HDL (51%), with less frequent elevations of LDL (40%) and total cholesterol (24%). Non-HDL > or = 130 mg/dl was neither a sensitive (61%) nor specific (75%) marker for elevated VLDL. There was a striking disparity between the high prevalence of dyslipidemia and the percentage of dyslipidemic patients qualified by K/DOQI guidelines for therapy. Non-HDL > or = 130 mg/dl was as effective in qualifying dyslipidemic patients for lipid-lowering therapy (54%) as the entire K/DOQI treatment algorithm (57%). Lowering the trigger of non-HDL to > or = 100 mg/dl would qualify 81% of dyslipidemic patients for treatment while offering the important advantage of being uninfluenced by the non-fasting state. CONCLUSIONS: In Stage 5 CKD patients at hemodialysis inception, dyslipidemia is highly prevalent with predominance of the atherogenic triad (hypertriglyceridemia, elevated VLDL and reduced HDL). Non-HDL is a poor surrogate marker for VLDL. As a valid non-fasting lipid parameter, non-HDL alone at the level of > or = 130 mg/dl qualifies dyslipidemic Stage 5 CKD patients for therapy as effectively as the K/DOQI guidelines. Setting the non-HDL trigger/target cut-off at 100 mg/dl overcomes the insensitivity of non-HDL as a marker for atherogenic lipoproteins represented by the VLDL designation while ensuring more aggressive lipid-lowering therapy for Stage 5 CKD patients at high risk for cardiovascular events. Accordingly, non-HDL of 100 mg/dl is proposed as the all-encompassing primary trigger/target of lipid-lowering therapy in high-risk Stage 5 CKD patients, particularly those patients on dialysis in whom lipid samples obtained before dialysis cannot be guaranteed to be fasting.

Aged↗

PubMed2006

Prevalence of chronic kidney disease in Thai adult population.

OBJECTIVE: Chronic kidney disease (CKD) is a major public health problem worldwide. Until now, no large-scale data about the prevalence of pre-dialysis CKD has been reported in Thailand. MATERIAL AND METHOD: The clinical and laboratory data from the ground air force personnel who were routinely checked up during 2002-2003 were collected and descriptively analyzed. The pilots and air crews were excluded. All personnel were working in Bangkok. RESULTS: 15,612 RTAF personnel completed the annual check up. Eighty-two percent were male. The average age was 45.7 +/- 8 (19-65) years. According to the classification of stages of CKD by Kidney Disease Outcome Quality Initiative (K/DOQI), the prevalence of CKD is 9.1% by Cockcroft Gault formula and 4.6% by Modification of Diet in Renal Disease. Patients with diabetes mellitus, hypertension, hypercholesterolemia and proteinuria were found in 8.2%, 45.8 %, 28.2 % and 1.8% respectively. CKD patients were older had higher body weight, Body Mass Index (BMI), blood pressure and blood sugar than non CKD personnel. CONCLUSION: CKD were not uncommon among RTAF personnel. The Cockcroft-Gault and MDRD equations were different in detecting CKD in the present study. The appropriate equation to determine GFR in Thai population should be evaluated. Low sensitivity of dipstick proteinuria may cause the low prevalence of stage 1 and 2 CKD.

Adult↗

PubMed2006

Cardiovascular disease risk factors in chronic kidney disease: overall burden and rates of treatment and control.

BACKGROUND: Mild to moderate chronic kidney disease (CKD) is associated with increased risk for cardiovascular disease. The burden of cardiovascular disease risk factors in this setting is not well described. METHODS: We compared the age- and sex-adjusted prevalence of cardiovascular disease risk factors and their treatment and control among persons with and without CKD in 3258 Framingham offspring cohort members who attended the seventh examination cycle (1998-2001). Glomerular filtration rate (GFR) was estimated using the simplified Modification of Diet in Renal Disease Study equation. We defined CKD as a GFR of less than 59 mL/min per 1.73 m(2) in women and less than 64 mL/min per 1.73 m(2) in men. RESULTS: Those with CKD were older, more likely to be obese (33.5% vs 29.3%; P=.02), and more likely to have low levels of high-density lipoprotein cholesterol (45.2% vs 29.4%; P<.001) and high triglyceride levels (39.9% vs 29.8%; P<.001). Those with CKD had a higher prevalence of hypertension (71.2% vs 42.7%; P<.001) and hypertension treatment (86.0% vs 72.5%; P<.001), but were less likely to achieve optimal blood pressure control (27.0% vs 45.5%; P<.001). Participants with CKD had a higher prevalence of elevated low-density lipoprotein cholesterol levels (60.5% vs 44.7%; P=.06) and lipid-lowering therapy (57.1% vs 42.6%; P=.09), although this was not statistically significant. A greater proportion of individuals with CKD than those without had diabetes (23.5% vs 11.9%; P=.02) and were receiving diabetes treatment (63.6% vs 46.9%; P=.05), but were less likely to achieve a hemoglobin A(1c) level of less than 7% (43.8% vs 59.4%; P=.03). CONCLUSIONS: Chronic kidney disease is associated with a significant burden of cardiovascular disease risk factors in the community. The diagnosis of CKD should alert the practitioner to look for potentially modifiable cardiovascular risk factors.

Aged↗

PubMed2025

Multiomics Analysis Reveals Therapeutic Targets for Chronic Kidney Disease With Sarcopenia.

BACKGROUND: The presence of sarcopenia in patients with chronic kidney disease (CKD) is associated with poor prognosis. The mechanism underlying CKD-induced muscle wasting has not yet been fully explored. This study investigates the influence of renal secretions on muscles using multiomics sequencing. METHODS: The kidney transcriptome analysis by RNA-seq and protein profiling by tandem mass tag (TMT), serum TMT and muscle TMT were performed in CKD established using 0.2% adenine and control mice. Spp1 recombinant protein was used to study its effect on myotube atrophy in vitro. In animal experiments on CKD, pharmacological inhibition of Spp1 was used to explore the role of Spp1 in skeletal muscle wasting. Transcriptome analysis was performed to identify differentially expressed genes (DEGs) in the gastrocnemius muscle following Spp1 pharmacological inhibition. RESULTS: In the renal transcriptome and TMT, 503 and 377 proteins/genes respectively were co-upregulated and co-downregulated. In the serum TMT of CKD and normal control (NC) mice, 22 upregulated and 7 downregulated differentially expressed proteins (DEPs) showed the same expression patterns as those in the kidney transcriptome and TMT analysis. Based on bioinformatics analysis and reported studies, we selected Spp1 for further validation. Spp1 recombinant protein was added to C2C12 myotubes in vitro, and the results indicated that Spp1 significantly increased the protein levels of the muscle atrophy marker (Murf-1) and promoted the smaller myotubes (all p < 0.05). Compared with NC mice, Spp1 mRNA and protein levels were significantly upregulated in the kidneys of CKD mice, and the serum concentration of Spp1 was also markedly increased (all p < 0.05). In animal experiments, pharmacological inhibition of Spp1 increased the weights of gastrocnemius and tibialis anterior muscles (p < 0.05) and improved muscle atrophy phenotype. Transcriptome analysis showed that DEGs in the gastrocnemius muscle following Spp1 pharmacological inhibition were enriched in protein digestion and absorption, glucagon signalling pathway, apelin signalling pathway and ECM-receptor interaction pathway. CONCLUSIONS: Our study is the first to establish a regulatory network of kidney-muscle crosstalk to explore the potential mechanism of CKD-related sarcopenia. Employing multiomics analysis, cellular assessment and animal experiments, we have identified that Spp1 could potentialy serve as a promising therapeutic target for CKD patients with sarcopenia.

Sarcopenia↗

PubMed2005

Orexigenic and anorexigenic mechanisms in the control of nutrition in chronic kidney disease.

Malnutrition is defined as abnormalities caused by an inadequate diet, but this term is often used inappropriately to describe the syndrome of loss of body weight with muscle mass being replaced by fatty tissue and declining serum proteins present in adults and children with chronic kidney disease (CKD). This syndrome is more accurately described as cachexia, and manifests as growth failure in children with CKD. Cachexia is common and is an important risk factor for poor quality of life and increased mortality and morbidity in both adults and children with CKD. Anorexia, acidosis and inflammation are important causes of cachexia, but the underlying molecular mechanism is not well understood. Dietary intake is often poor and resting metabolic rate is increased in CKD. The energy cost of growth is increased in experimental CKD. Circulating concentrations of cytokines, such as leptin, tumor necrosis factor-alpha and interleukins 1 and 6 are increased in patients with CKD and correlate with the degree of cachexia in these individuals. We hypothesize that cytokines signal through orexigenic neuropetides such as agouti-related peptide and neuropeptide Y (NPY), and anorexigenic neuropetides such as proopiomelanocortin and alpha-melanocyte-stimulating hormone in the arcuate nucleus in the hypothalamus. This signaling system also involves the NPY receptor and the melanocortin receptors and controls appetite and metabolic rate in health and disease. Furthermore, the first order neurons of this system are located outside the blood-brain barrier and can therefore sense the circulating levels of cytokines, as well as long-term satiety hormones such as leptin and insulin and short-term satiety hormones such as ghrelin and peptide (P) YY. There is experimental evidence that this hypothalamic neuropeptide signaling system may have an important role in the pathogenesis of cachexia in CKD. Understanding the molecular mechanism of cachexia in CKD may lead to novel therapeutic strategies.

Cachexia↗

PubMed2005

Chronic kidney disease and inflammation in pediatric patients: from bench to playground.

Signs of an activated immune system can be observed already in the early stages of chronic kidney disease (CKD). Markers of a chronically activated immune system are closely linked to several complications of CKD, such as accelerated atherosclerosis, vascular calcification, insulin resistance, increased muscle catabolism, loss of appetite, bone remodeling, and increased peritoneal permeability. Interestingly, all the aforementioned pathological states resemble a state of accelerated ageing and are strongly associated with increased morbidity and mortality in CKD patients. In recent studies, signs of inflammation have been shown as predictors for mortality in dialysis patients, and the role of inflammation as a risk factor for complications of CKD in children has emerged. Although preliminary findings suggest that inflammation is highly prevalent in the pediatric population with CKD, information related pathogenic links and to clinical outcomes is lacking. For the future, it is crucial for investigations to address the mechanisms and complications of inflammation that are manifested in pediatric patients with CKD in all stages. Since early identification and intervention may generate the most efficient strategies for prevention and treatment of cardiovascular disease in CKD patients, the pediatric population deserves special attention in future studies. In this review, we discuss the mechanisms involved in the inflammatory activation and the main causes and consequences of the inflammatory state observed in the CKD patient, with special emphasis on the pediatric population.

Aging↗

PubMed2006

Predictive factors of chronic kidney disease in primary focal segmental glomerulosclerosis.

Renal histological features of focal segmental glomerulosclerosis (FSGS) are found in 75% of pediatric patients with steroid-resistant nephrotic syndrome. In order to evaluate the predictive factors of chronic kidney disease (CKD), we retrospectively reviewed the records of 110 children with biopsy-proven FSGS admitted between 1972 and 2004. Renal survival was analyzed by the Kaplan-Meier method and Cox's regression model. Two multivariate models were developed: (1) from the onset of symptoms to the occurrence of CKD and (2) from the time of renal biopsy to CKD. Mean follow-up time was 10 years [standard deviation ((SD) 5.5], and 24 patients (21.8%) progressed to CKD. At baseline, after adjustment three variables remained as independent predictors of CKD: age >6.5 years (RR=3.3, 95% CI=1.3-7.8), creatinine >1 mg/dl (RR=2.5, 95% CI=0.97-6.5), and non-response to steroids (RR=7.3, 95% CI=2.7-19.7). In a model with continuous variables only age and non-response to steroids were associated with CKD. At the time of renal biopsy, after adjustment two variables remained as independent predictors of CKD: hematuria (RR=3.0, 95% CI=1.2-7.3) and creatinine >0.8 mg/dl (RR=4.3, 95% CI=1.7-10.6). In a model with continuous variables four factors predicted CKD: age, creatinine, hematuria, and percentage of global sclerosis.

Adolescent↗