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PubMed2006

Insulin resistance, inflammatory biomarkers, and adipokines in patients with chronic kidney disease: effects of angiotensin II blockade.

Patients with chronic kidney disease (CKD) present a high prevalence of insulin resistance (IR). Some studies suggest that angiotensin II may influence some cellular pathways that contribute to the pathogenesis of IR and stimulate the release of proinflammatory cytokines. Fifty-two patients who had stages 3 and 4 CKD and no diabetes were administered an angiotensin receptor blocker (ARB), olmesartan (40 mg), for 16 wk. Before and after ARB treatment, metabolic and inflammatory parameters and adipokines were measured. IR was calculated by Homeostasis Model Assessment (HOMA) index. Baseline data were compared with data that were obtained from 25 healthy control individuals of similar age and normal renal function. Compared with control subjects, patients with CKD presented significantly higher BP and waist circumference, higher triglycerides and lower HDL levels, higher insulin levels, and higher mean HOMA index (6.0 +/- 2.7 versus 2.9 +/- 2.2 muU/ml x mmol/L; P < 0.001). In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-alpha, and IL-6. In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 +/- 16 versus 92 +/- 14 mg/dl; P < 0.05), insulin (23.1 +/- 8.8 versus 19.9 +/- 9; P < 0.05), HOMA index (6.0 +/- 2.7 versus 4.7 +/- 2.8; P < 0.05), and glycated hemoglobin (5.33 +/- 0.58 versus 4.85 +/- 0.81%; P < 0.01). At the same time, there was a significant reduction of high-sensitivity C-reactive protein levels, from 4.45 mg/L (2.45 to 9.00) to 3.55 mg/L (1.80 to 5.40; P < 0.05) and fibrinogen (412 +/- 100 versus 370 +/- 105 mg/dl; P < 0.05). There were no significant differences in adipokine levels after olmesartan treatment. These data demonstrate that patients with CKD have a high prevalence of IR, metabolic syndrome, and chronic inflammation and that the administration of the ARB olmesartan improves IR and inflammation markers in these patients. Plasma adipokine levels that are related to several metabolic risk factors in patients with CKD were not modified by ARB therapy.

Adipokines↗
PubMed2006

Survey of care provided by ambulatory care pharmacists to patients with chronic kidney disease.

PURPOSE: A survey was conducted to determine the role of ambulatory care pharmacists in the care of patients with chronic kidney disease (CKD). METHODS: Data from a survey of ambulatory care pharmacists in the treatment and management of patients with CKD were collected. A 22-item anonymous survey was sent to 1028 potential respondents in January 2004. Only pharmacists indicating routine provision of care to patients with risk factors for the development of CKD or with stages 1-4 of CKD were included in the analysis. Additional questions surveyed the timeliness and frequency of nephrology referrals and the pharmacists' familiarity with National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-K/DOQI) guidelines. RESULTS: Of 1028 surveys, 535 were completed and returned. Only respondents who provided care in an outpatient setting to geriatric patients and patients with diabetes mellitus, hypertension, or decreased creatinine clearance were included in the analysis (n = 388). Initial assessment of CKD was performed by 85% of the surveyed pharmacists. Over one third of the pharmacists made nephrology referrals. However, even pharmacists who had a high percentage of patients with a known risk for CKD infrequently screened for kidney dysfunction, and only a small portion monitored the areas recommended by NFK-K/DOQI. The respondents' familiarity with the NFK-K/DOQI guidelines indicated that 7% were very familiar, 45% were somewhat familiar, 34% were not very familiar, 13% were not at all familiar, and 1% did not respond. CONCLUSION: The ambulatory care pharmacists surveyed were not consistently involved in the routine monitoring of common complications of CKD.

Ambulatory Care↗
PubMed2006

Hematocrit, independent of chronic kidney disease, predicts adverse cardiovascular outcomes in chinese patients with type 2 diabetes.

OBJECTIVE: Anemia and chronic kidney disease (CKD) are risk factors for cardiovascular diseases in diabetes. We examined the association between hematocrit, stratified by the presence of CKD, and cardiovascular events in a cohort of Chinese subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 3,983 patients who underwent assessment for diabetes complications were recruited. Subjects were categorized into five groups. Group I included subjects with hematocrit below the normal sex-specific range. The cutoff points for groups II-V were selected to represent the distribution of the hematocrit for each sex. CKD was defined by the estimated glomerular filtration rate <60 ml/min per 1.73 m(2). Cardiovascular events were defined as cardiovascular mortality and morbidity, including new onset of myocardial infarction, acute coronary syndrome, revascularization, heart failure, and stroke requiring hospitalization. RESULTS: A total of 294 subjects (7.4%) developed cardiovascular events during the median of 36.4 months. The rate of cardiovascular events was highest in subjects with low hematocrit (group I, 18.6%) compared with group V (3.4%, P < 0.001). The multivariate-adjusted hazard ratio for cardiovascular events diminished with increasing hematocrit (group I, 1.0; group II, 0.73 [95% CI 0.51-1.04]; group III, 0.57 [0.39-0.83]; group IV, 0.61 [0.39-0.95]; and group V, 0.36 [0.17-0.79]). After stratifying by the presence of CKD, the previously observed reduction in the risk of developing cardiovascular events with increasing hematocrit was abolished in the cohort with CKD but persisted in the non-CKD cohort. CONCLUSIONS: In Chinese subjects with type 2 diabetes, low levels of hematocrit and the presence of CKD are associated with increased risk of developing adverse cardiovascular events.

Adult↗
PubMed2004

Prevalence of proteinuria and the development of chronic kidney disease in HIV-infected patients.

AIMS: HIV-related renal diseases are increasingly prevalent and are associated with proteinuria and rapid progression to end-stage renal failure. Early treatment with highly active antiretroviral therapy (HAART) and ACE inhibition may prevent the development of chronic kidney disease (CKD), but studies evaluating the epidemiology of proteinuria and early CKD in HIV-infected patients are lacking. METHODS: All consecutive patients at Wishard Memorial Hospital (Indiana University) whose initial HIV documentation occurred from 1990 to 1998, were retrospectively studied using a computerized medical record system. Clinical data were abstracted from time of first HIV documentation through 12/31/2000. The proportions of patients who developed CKD (doubling of serum creatinine from an initial level < or = 1.5 mg/dl) and who had proteinuria (> or = 1+ protein on the first urine dipstick after HIV documentation) were calculated. Case mix and laboratory variables at the time of HIV documentation were compared between those who did and did not develop CKD and between those who had and did not have initial proteinuria. RESULTS: Of 487 subjects with initially normal renal function, 10 (2% (95% CI, 1-4%)) developed CKD. In univariable analysis, black race, a diagnosis of diabetes or hypertension and proteinuria were all significantly associated with the development of CKD; 89 (29% (95% CI, 24-35%)) of 289 evaluable subjects had > or = 1+ proteinuria on urine analysis. Multivariable regression revealed only older age (OR 1.08 per year increase; 95% CI, 1.03-1.14) to be associated with proteinuria. CONCLUSIONS: A small, but potentially clinically meaningful proportion of HIV-infected patients develop CKD, and there appears to be a high prevalence of proteinuria on the first urine analysis obtained after HIV documentation.

Adult↗
PubMed2006

Clinical characteristics of chronic kidney disease patients with and without diabetes: a subanalysis of the PAERI study.

AIMS: Diabetes is the leading cause of chronic kidney disease (CKD) in the United States, and cardiac disease is the primary cause of death in patients with CKD and diabetes. The Prevalence of Anemia in Early Renal Insufficiency (PAERI) study evaluated the prevalence of anemia and associated comorbidities in a community-based sample of patients with CKD. The purpose of this post hoc analysis was to identify differences, if any, in the prevalence and severity of anemia (hemoglobin < or = 12 g/dl (120 g/l)) and other clinical characteristics between CKD patients with diabetes and patients with CKD who did not have diabetes. MATERIALS AND METHODS: The PAERI study was a prospective, cross-sectional, multicenter survey. Eligible patients were > or = 18 years old with CKD, defined as serum creatinine 1.5 - 6.0 mg/dl (132.6 - 530.4 micromol/l) in females and 2.0 - 6.0 mg/dl (176.8 530.4 micromol/l) in males within 12 months before enrollment. Study duration for each patient was a single site visit. RESULTS: Of the original 5,222 patients enrolled, 3,361 had diabetes and 1,861 did not. A family history of diabetes was present in 72.7% of diabetic patients vs. 27.2% of nondiabetic patients (p < 0.0001). Patients with diabetes had a significantly higher prevalence of anemia (52.7 vs. 39.4%, p < 0.0001) and cardiac disease (55.7 vs. 42.9%, p < 0.0001). The prevalence of hypertension was high in both groups (91.5 and 89.3%). Significantly more diabetic patients than nondiabetic patients received angiotensin-converting enzyme inhibitors (60.4 vs. 43.8%, p < 0.0001). Hyperlipidemia was more common in patients with diabetes (73.9 vs. 55.4%, p < 0.0001). Patients with diabetes were slightly younger and had a significantly higher mean body mass index and lower transferrin saturation compared with nondiabetic patients. In diabetic and nondiabetic patients, more than 97% had glomerular filtration rate < 60 ml/min/1.73 m2 and more than 70% had serum creatinine < 2.5 mg/dl (221.0 micromol/l). CONCLUSIONS: These findings underscore the extent and severity of concurrent illnesses in patients with both diabetes and CKD. In those patients, diabetes was associated with a greater prevalence of serious cardiac-related comorbidities than observed in nondiabetic patients.

Aged↗
PubMedDate not supplied

Chronic inflammation in peritoneal dialysis: the search for the holy grail?

Mortality and morbidity in chronic kidney disease (CKD) patients are unacceptably high. The annual mortality rate due to cardiovascular disease (CVD) is approximately 9%, which, for the middle-aged person, is at least 10- to 20-fold higher than for the general population. Classic risk factors for CVD are highly prevalent in CKD patients, but they cannot fully account for the excessive rate of CVD in this population. Instead, it has become increasingly clear that nontraditional risk factors, such as systemic inflammation, may play a key role in the development of atherosclerosis. It is well established that inflammatory markers are very powerful predictors of high CVD morbidity and mortality not only in the general population, but particularly in CKD patients. Signs of a sustained low-grade inflammation, such as increased levels of C-reactive protein (CRP), are present in the majority of stage 5 CKD patients, even in patients in clinically stable condition, and they are also commonly observed after the initiation of dialysis therapy. Dialysis therapy--hemodialysis as well as peritoneal dialysis (PD)--may itself contribute to systemic inflammation. Local intraperitoneal inflammation can also occur in patients treated with PD. These local effects may result in a low-grade inflammation, caused by the bioincompatibility of conventional glucose-based dialysis fluids, to intense inflammation associated with peritonitis. Given these circumstances, it is reasonable to hypothesize that strategies aiming to reduce inflammation are potentially important and novel, and could serve to reduce CVD, thereby lowering morbidity and mortality in patients with CKD. In this review we provide information supporting the hypothesis that systemic inflammation is tightly linked to the most common complications of CKD patients, in particular those on PD, and that local inflammation in PD may contribute to various related complications. The aims of this review are to discuss the reasons that make inflammation an attractive target for intervention in CKD, the particular aspects of the inflammation-CVD axis during PD treatment that are likely involved, and possible means for the detection and management of chronic inflammation in PD patients.

C-Reactive Protein↗
PubMed2004

Outcomes associated with hypogonadism in women with chronic kidney disease.

The successful use of renal replacement therapy has resulted in longer survival and a population of older patients with chronic kidney disease (CKD) that includes patients with other significant preexisting illnesses. In this review, we analyze the short-term and long-term outcomes associated to persisting hypogonadism in CKD patients. The short-term manifestations, commonly observed in normal postmenopausal women, are either a rare complaint of women with CKD or are frequently attributed to the uremic state. These symptoms include hot flashes, sleep disturbances and depression, sexual dysfunction, vaginal dryness and atrophy, urinary incontinence, and skin aging and wrinkling. The long-term outcomes of hypogonadism have potentially devastating effects on bone, cardiovascular system, and cognitive function, which could significantly alter the quality of life and survival of women with stage 5 CKD (CKD-5). Postmenopausal osteoporosis has been recognized as an important entity associated with renal osteodystrophy, and efforts have begun to tackle the reduced bone-mineral density (BMD) and increased fracture rate seen in this population. Similarly, cardiovascular disease represents the major cause of death in the CKD-5 population, with a 10 to 20 times greater mortality than in the general population. The accumulating evidence for a possible link between osteoporosis and atherosclerosis is discussed, as well as new directions in the understanding of postmenopausal osteoporosis in the context of renal bone disease, under the guidance of the Global Bone and Mineral Initiative endorsed by the Kidney Disease: Improving Global Outcomes initiative. Nephrologists must face gynecological issues with their women patients and design interdisciplinary clinical studies that include strategies that utilize well-tested and newer drug regimens in the management of osteoporosis, cardiovascular disease, and other postmenopausal manifestations in CKD-5 patients.

Arteriosclerosis↗
PubMed2005

Chronic kidney disease--management update.

BACKGROUND: Chronic kidney disease (CKD), defined as a glomerular filtration rate less than 60 mL/min/1.73 m2 and/or evidence of kidney damage for a period of at least 3 months, is an increasingly common, serious and under-recognised condition. A recent population study demonstrated that one in every 6 Australian adults has CKD (of which the vast majority are unaware). OBJECTIVE: This article aims to provide timely information to health professionals about how to classify and manage CKD. DISCUSSION: Management of CKD involves regular monitoring of cardiovascular and renal risk factors, identifying and treating common CKD complications, and avoiding medications that may worsen CKD. Early detection and timely appropriate management of CKD (especially with respect to blood pressure control) will substantially reduce kidney failure progression and cardiovascular risk by up to 50%.

Adult↗
PubMed2006

[Early diagnosis of chronic kidney disease. New insights into creatinine and proteinuria].

The progression of chronic kidney disease (CKD) is more than just a simple, creeping loss of kidney function finally resulting in end-stage renal disease (ESRD). First, the growing incidence of CKD implies an exploding socioeconomic burden. Second, clear evidence indicates that CKD is associated with an independent massive increase in the patient's cardiovascular risk. Concerning screening and early diagnosis of CKD serum creatinine alone is an inadequate parameter for the evaluation of renal function. Proteinuria is both an indicator of renal damage as well as a progression factor for ongoing loss of renal function. Optimized treatment of arterial hypertension is of outstanding importance in the management of CKD patients, since high blood pressure is directly as well indirectly, via proteinuria, related to progression of CKD. Agents interfering with the renin-angiotensin system have been proven to be especially effective in antiproteinuric treatment and in slowing the progression of CKD. Our current understanding of optimized antihypertensive and antiproteinuric therapy favors a multimodal treatment regimen. Reduction of proteinuria toward levels < 0.5 g per day would be ideal. By this intervention the risk for both ongoing renal function loss as well as the risk of cardiovascular disease can be markedly reduced.

Cardiovascular Diseases↗
PubMedDate not supplied

Statins for treatment of dyslipidemia in chronic kidney disease.

Dyslipidemia is a potent cardiovascular (CV) risk factor in the general population. Elevated low-density lipoprotein cholesterol (LDL-C) and/or low high-density lipoprotein (HDL-C) are well-established CV risk factors, but more precise determinants of risk include increased apoprotein B (ApoB), lipoprotein(a) [Lp(a)], intermediate and very low-density lipoprotein (IDL-C, VLDL-C; "remnant particles"), and small dense LDL particles. Lipoprotein metabolism is altered in association with declining glomerular filtration rate such that patients with non dialysis-dependent chronic kidney disease (CKD) have lower levels of HDL-C, higher triglyceride, ApoB, remnant IDL-C, remnant VLDL-C, and Lp(a), and a greater proportion of oxidized LDL-C. Similar abnormalities are prevalent in hemodialysis (HD) patients, who often manifest proatherogenic changes in LDL-C in the absence of increased levels. Patients treated with peritoneal dialysis (PD) have a similar but more severe dyslipidemia compared to HD patients due to stimulation of hepatic lipoprotein synthesis by glucose absorption from dialysate, increased insulin levels, and selective protein loss in the dialysate analogous to the nephrotic syndrome. In the dialysis-dependent CKD population, total cholesterol is directly associated with increased mortality after controlling for the presence of malnutrition-inflammation. Treatment with statins reduces CV mortality in the general population by approximately one third, irrespective of baseline LDL-C or prior CV events. Statins have similar, if not greater, efficacy in altering the lipid profile in patients with dialysis-dependent CKD (HD and PD) compared to those with normal renal function, and are well tolerated in CKD patients at moderate doses (<or=20 mg/day atorvastatin or simvastatin). Statins reduce C-reactive protein as well as lipid moieties such as ApoB, remnants IDL and VLDL-C, and oxidized and small dense LDL-C fraction. Large observational studies demonstrate that statin treatment is independently associated with a 30%-50% mortality reduction in patients with dialysis-dependent CKD (similar between HD- and PD-treated patients). One recent randomized controlled trial evaluated the ability of statin treatment to reduce mortality in type II diabetics treated with HD ("4D"); the primary end point of death from cardiac cause, myocardial infarction, and stroke was not significantly reduced. However, results of this trial may not apply to other end-stage renal disease populations. Two ongoing randomized controlled trials (SHARP and AURORA) are underway evaluating the effect of statins on CV events and death in patients with CKD (including patients treated with HD and PD). Recruitment to future trials should be given a high priority by nephrologists and, until more data are available, consideration should be given to following published guidelines for the treatment of dyslipidemia in CKD. Additional consideration could be given to treating all dialysis patients felt to be at risk of CV disease (irrespective of cholesterol level), given the safety and potential efficacy of statins. This is especially relevant in patients treated with PD, given their more atherogenic lipid profile and the lack of randomized controlled trials in this population.

Dyslipidemias↗
PubMed2006

Estimating glomerular filtration rate in Asian patients with chronic kidney diseases from bioelectrical impedance analysis.

BACKGROUND: Estimation of glomerular filtration rate (GFR) is usually determined from 24-hour urine collection, but it is time-consuming, and difficult in clinical practice. The authors attempted to select an accurate and safe, but more convenient test to obtain an estimated GFR. OBJECTIVE: To compare estimation of GFR by Bioelectrical impedance analysis (BIA) with GFR calculated by 24-hour urine averaged creatinine clearance and urea clearance (Ccr-Cu-GFR). MATERIAL AND METHOD: The authors examined 79 non-diabetic chronic kidney disease (CKD) patients that had estimated GFR between 15 and 89 ml/min/1. 73 m(2). Subjects were categorized into three subgroups according to K/DOQI-CKD classification: GFR of 60-89 m/min/1. 73m(2) (stage 2, 5 subjects), 30-59 ml/min/ 1.73m(2) (stage 3, 31 subjects), and 15-29 ml/min/1.73m(2) (stage 4, 43 subjects). RESULTS: The mean value of Ccr-Cu-GFR was 33.79+/-14.78 ml/min/1. 73 m(2) and GFR by BIA (BIA-GFR), 34.63 +/- 14.86 ml/min/1. 73 m(2) with no overall statistical differences (p = 0.838). In stage 3 CKD patients, the mean BIA-GFR and Ccr-Cu-GFR were similar (38.84+/-12.47 vs 41.16+/-9.17, p = 0. 399) while in stage 2 CKD, BIA-GFR tended to underestimate (63.50+/- 19.35 vs 70.94+/-7.82, p = 0.407) and in stage 4 CKD, BIA-GFR significantly overestimated Ccr-Cu-GFR (27.31+/-9.11 vs 23.76+/-5.68, p = 0.040). CONCLUSION: The findings suggest that BIA-GFR in non-diabetic CKD patients closely resembled with Ccr-Cu-GFR especially in stage 3 CKD patients. BIA-GFR may be considered as a more convenient test for an assessment of GFR in non-diabetic CKD patients.

Adult↗
PubMed2004

Achievement of target blood pressure levels in chronic kidney disease: a salty question?

A large body of evidence supports the validity of lowering blood pressure (BP) to prevent cardiovascular (CV) disease in the general population. This issue becomes even more critical in renal patients because they carry a greater CV risk across the entire spectrum of chronic kidney disease (CKD). In these patients, achievement of lower BP levels also is fundamental to limit the progression of renal damage, especially in the presence of significant proteinuria. Although expert panels have strongly recommended to intensively decrease BP in patients with CKD, management of hypertension in these patients remains inadequate. Armed with the knowledge of the extreme salt-sensitivity of BP in patients with CKD, it is reasonable to hypothesize that more aggressive treatment of volume expansion can be helpful. Nevertheless, although abundant literature has evidenced that dietary sodium restriction decreases BP levels in patients with essential hypertension, no large and prospective study has been conducted to date on this issue in patients with CKD. A potential reason is the low compliance of patients with CKD to dietary prescriptions; however, this problem can be overcome by specific counseling. Alternatively, loop diuretics administered at a high dose should represent the cornerstone of therapy, but, again, well-designed studies verifying the effectiveness of these agents in a large CKD population are still awaited. Nephrologists seem to be reluctant to adequately administer diuretics because of the fear of adverse events. Conversely, the major detrimental effect, that is, excessive hypovolemia, can be prevented if daily body weight loss is limited to 0.3 to 0.5 kg during the initial period of treatment.

Antihypertensive Agents↗
PubMed2006

Growth hormone for children with chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) is an uncommon but important condition. Growth retardation, one of the complications of CKD, is of concern to families. Recombinant human growth hormone (rhGH) treatment has been used to help short children with CKD attain a height more in keeping with their age group. However, there are concerns that rhGH may have an adverse effect on the preservation of native kidney function, predispose to acute rejection in kidney transplant recipients, and cause benign intracranial hypertension and slipped capital femoral epiphysis. OBJECTIVES: To evaluate the benefits and harms of rhGH treatment in children with CKD. SEARCH STRATEGY: Randomised controlled trials (RCTs) were identified from the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, article reference lists and through contact with local and international experts in the field. Date of most recent search: July 2005 SELECTION CRITERIA: RCTs were included if they were carried out in children aged 0-18 years, diagnosed with CKD, who were pre-dialysis, on dialysis or post-transplant; if they compared rhGH treatment with placebo/no treatment or two doses of rhGH treatments; and if they included height outcomes. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed studies for methodological quality and extracted data from eligible trials. Data was pooled using a random effects model with calculation of weighted mean difference (MD) for continuous outcomes and relative risk (RR) for categorical outcomes with 95% confidence intervals (CI). MAIN RESULTS: Fifteen RCTs (629 children) were identified. Treatment with rhGH (28 IU/m(2)/wk) resulted in a significant increase in height standard deviation score (SDS) at one year (MD 0.78 SDS, 95% CI 0.52 to 1.04), and a significant increase in height velocity at six months (MD 2.85 cm/6 mo, 95%CI 2.22 to 3.48) and one year (MD 3.80 cm/y, 95%CI 3.20 to 4.39). Compared to the 14 IU/m(2)/wk group, there was a 1.34 cm/y (0.55 to 2.13) increase in height velocity in the 28 IU/m(2)/wk group. The frequency of reported side effects of rhGH were similar to that of the control group. AUTHORS' CONCLUSIONS: One year of 28 IU/m(2)/wk rhGH in children with CKD resulted in a 3.80 cm/y increase in height velocity above that of untreated patients. Trials were too short to determine if continuing treatment resulted in an increase in final adult height.

Adolescent↗
PubMed2006

Neurocognitive outcomes in children with chronic kidney disease: Current findings and contemporary endeavors.

Given the rise in chronic kidney disease (CKD) in both children and adults, CKD has recently been targeted as a public health priority. Childhood onset kidney disease is generally a noncurable and progressive condition that leads to kidney failure by early adulthood. Fortunately, improved identification of kidney problems allows for early intervention, which is thought to slow progression toward end-stage renal disease. In addition, medical interventions for pediatric end-stage renal disease have also improved, allowing children to take advantage of lifesaving renal replacement treatments such as dialysis and kidney transplantation. In spite of improvements in identification and treatment, CKD causes both direct and indirect insults to a variety of organ systems. This paper reviews recently published studies pertaining to the neurocognitive and psychosocial impact of CKD on children of various ages and at various stages of kidney failure. Specific attention is focused on summarizing peer reviewed research that describes associations between kidney functioning and cognitive functioning, language acquisition, visual spatial abilities, memory, and executive functioning. In addition, peer reviewed research describing psychosocial outcomes associated with CKD related to academic achievement, social-behavioral functioning, and quality of life are summarized. The authors also identified disease-specific factors that likely mediate neurocognitive outcomes (e.g., anemia, hypertension, cardiovascular) and endorse the importance of continued interdisciplinary research collaborations that will provide a better understanding of the mechanisms responsible for improved neurocognitive functioning after transplantation. The authors conclude this review by describing a multicenter, prospective, longitudinal, National Institutes of Health funded study that is currently examining the developmental outcomes of children with mild to moderate CKD. The authors speculate that the Chronic Kidney Disease in Children Prospective Cohort Study (CKiD) findings will provide additional evidence-based guidance for clinicians and researchers working with children and adolescents with deteriorating kidney function to improve medical and developmental outcomes.

Adolescent↗
PubMed2005

Blood pressure and total peripheral resistance in children with chronic kidney disease.

We performed a study to assess cardiac output (CO) and total peripheral resistance (TPR) at rest and during peak exercise with the goal to better define the role of these parameters in the development of hypertension in children with chronic kidney disease (CKD) stage 2-4. Fifty-two pediatric patients with CKD (mean age 12.7+/-3.7 years) and 28 healthy individuals of comparable age and sex participated in the study. At rest, children with CKD had a significantly higher systolic and diastolic blood pressure (BP) and calculated mean arterial pressure (MAP) than healthy controls. Total peripheral resistance was significantly higher in children with CKD than in controls (1627.7+/-534.6 vs 1354.6+/-338.9 dynexsxcm(-5), p =0.02). There was no significant difference in heart rate or CO between the two groups. Children taking antihypertensive medications had lower TPR than children without BP medications (1514.6+/-439.6 vs 1788.2+/-505.4 dynexsxcm(-5), respectively, p =0.06). At peak exercise, children with CKD had a significant increase in MAP, heart rate and CO and had a significant decrease in TPR (difference between rest and peak exercise: -782.4+/-375.9 dynexsxcm(-5), p <0.001). Children taking BP medications had blunted MAP and CO responses when compared to controls (Delta CO: 6.2+/-2.8 l/min vs 9.8+/-4.5 l/min, respectively, p =0.01; MAP: 13.9+/-10.2 mmHg vs 21.5+/-11.7 mmHg, respectively, p =0.01). Children without BP medications had a similar to controls response to exercise in respect to CO, MAP and TPR. We conclude that increased TPR is a major contributor to elevated blood pressure in children with CKD and suggest that BP medications decreasing vascular resistance should be used as a first line of antihypertensive therapy in these patients.

Adolescent↗
PubMed2006

Growth impairment shows an age-dependent pattern in boys with chronic kidney disease.

The impact of chronological age on longitudinal body growth from early childhood through adolescence using detailed anthropometric methods has not yet been studied in children with chronic kidney disease (CKD). We have evaluated growth failure by measuring four components of linear growth: body height (HT), sitting height (SHT), arm length (AL) and leg length (LL). Data were prospectively collected for up to 7 years on 190 boys (3-21 years old) with congenital or hereditary CKD (all had developed at least stage 2 CKD by the age of 10 years). Patients showed the most severe growth failure in early childhood, followed by an acceleration in growth in pre-puberty, a slowing-down of growth at puberty, as expected, and thereafter a late speeding-up of growth until early adulthood. This pattern was observed irrespective of the degree of CKD and different treatment modalities, such as conservative treatment, recombinant human growth hormone (rhGH) therapy or transplantation. LL showed the most dynamic growth changes of all the parameters evaluated and emerged as the best indicator of statural growth in children with CKD. A specific age-dependent pattern of physical growth was identified in pediatric male CKD patients. This growth pattern should be considered in the evaluation of individual growth and the assessment of treatment efficacy such as rhGH therapy.

Adolescent↗
PubMed2006

Vascular calcification in chronic kidney disease.

Vascular calcification is often encountered in advanced atherosclerotic lesions and is a common consequence of aging. Calcification of the coronary arteries has been positively correlated with coronary atherosclerotic plaque burden, increased risk of myocardial infarction, and plaque instability. Chronic kidney disease (CKD) patients have two to five times more coronary artery calcification than healthy age-matched individuals. Vascular calcification is a strong prognostic marker of cardiovascular disease mortality in CKD patients. Vascular calcification has long been considered to be a passive, degenerative, and end-stage process of atherosclerosis and inflammation. However, recent evidence indicates that bone matrix proteins such as osteopontin, matrix Gla protein (MGP), and osteocalcin are expressed in calcified atherosclerotic lesions, and that calcium-regulating hormones such as vitamin D3 and parathyroid hormone-related protein regulate vascular calcification in in vitro vascular calcification models based on cultured aortic smooth muscle cells. These findings suggest that vascular calcification is an actively regulated process similar to osteogenesis, and that bone-associated proteins may be involved in the development of vascular calcification. The pathogenesis of vascular calcification in CKD is not well understood and is almost multifactorial. In CKD patients, several studies have found associations of both traditional risk factors, such as hypertension, hyperlipidemia, and diabetes, and uremic-specific risk factors with vascular calcification. Most patients with progressive CKD develop hyperphosphatemia. An elevated phosphate level is an important risk factor for the development of calcification and cardiovascular mortality in CKD patients. Thus, it is hypothesized that an important regulator of vascular calcification is the level of inorganic phosphate. In order to test this hypothesis, we characterized the response of human smooth muscle cell (HSMC) cultures to inorganic phosphate levels. Our findings indicate that inorganic phosphate directly regulates HSMC calcification through a sodium-dependent phosphate transporter mechanism. After treatment with elevated phosphate, there is a loss of smooth muscle lineage markers, such as alpha-actin and SM-22alpha, and a simultaneous gain of osteogenic markers such as cbfa-1 and osteocalcin. Elevated phosphate may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification, and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. Furthermore, putative calcification inhibitory molecules have been identified using mouse mutational analyses, including MGP, beta-glucosidase, fetuin-A, and osteoprotegerin. Mutant mice deficient in these molecules present with enhanced cardiovascular calcification, demonstrating that specific molecules are normally important in suppressing vascular calcification. These findings suggest that the balance of inducers, such as phosphate, and inhibitors, such as MGP, fetuin-A, and others, are likely to control whether or not calcification occurs under pathological conditions.

Alkaline Phosphatase↗
PubMed2006

Care of elderly patients with chronic kidney disease.

BACKGROUND: Providing optimal care to the growing number of chronic kidney disease (CKD) patients remains a significant problem in the United States. There is little known about the care of elderly CKD patients by primary care physicians as well as nephrologists. METHODS: We performed a retrospective study of 377 elderly male CKD (serum creatinine >1.4 mg/dl on 2 separate occasions 3 months apart) patients referred to the Nephrology Clinic at the Buffalo Veterans Administration Medical Center between 1999 and 2002 to see if the pattern of care changed during this time. RESULTS: The mean age of the patients was 75.9 years. Eighty-four percent were Caucasian, 15% were African-American, and 1% were of other race. Etiology of CKD included hypertensive nephrosclerosis (49%), diabetic nephropathy (23%), renovascular disease (18%), and others (10%). Sixty-five percent of patients had estimated glomerular filtration rate (eGFR) >30 ml/min. Overall angiotensin converting enzyme inhibitor (ACEI) was used in 51% of patients with CKD, and in 63% of patients with diabetic nephropathy. Twenty percent of patients had a hemoglobin <11 g/dl, darbepoietin/epogen was used in 31% of these patients. Screening for kidney related tests were done infrequently while lipid profile and hemoglobin A1C were done in the majority of patients because of clinical reminders in the VA computerized patient record system (CPRS). CONCLUSION: These results emphasize the need for increased education of primary care physicians and nephrologists to improve the care of elderly CKD patients. Although there was a trend towards earlier referral, care did not change significantly between years 1999 and 2002.

Aged↗