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PubMed2005

Chronic kidney disease and automatic reporting of estimated glomerular filtration rate: a position statement.

The systematic staging of chronic kidney disease (CKD) by glomerular filtration measurement and proteinuria has allowed the development of rational and appropriate management plans. One of the barriers to early detection of CKD is the lack of a precise, reliable and consistent measure of kidney function. The most common measure of kidney function is currently serum creatinine concentration. It varies with age, sex, muscle mass and diet, and interlaboratory variation between measurements is as high as 20%. The reference interval for serum creatinine concentration includes up to 25% of people (particularly thin, elderly women) who have an estimated glomerular filtration rate (eGFR) that is significantly reduced (< 60 mL/min/1.73 m). The recent publication of a validated formula (MDRD) to estimate GFR from age, sex, race and serum creatinine concentration, without any requirement for measures of body mass, allows pathology laboratories to "automatically" generate eGFR from data already acquired. Automatic laboratory reporting of eGFR calculated from serum creatinine measurements would help to identify asymptomatic kidney dysfunction at an earlier stage. eGFR correlates well with complications of CKD and an increased risk of adverse outcomes such as cardiovascular morbidity and mortality. We recommend that pathology laboratories automatically report eGFR each time a serum creatinine test is ordered in adults. As the accuracy of eGFR is suboptimal in patients with normal or near-normal renal function, we recommend that calculated eGFRs above 60 mL/min/1.73 m be reported by laboratories as "> 60 mL/min/1.73 m", rather than as a precise figure.

Journal Article↗

PubMed2005

[Serum uric acid and C-reactive protein levels in patients with chronic kidney disease].

Either inflammation or hyperuricemia has been related with increased cardiovascular risk and mortality. A hypothetical relationship between serum uric acid levels (SUA) and inflammatory markers has never been tested in chronic kidney disease (CKD) patients. The purpose of this study was to determine the prevalence of increased C-reactive protein (CRP) levels in CKD patients, and to test the hypothesis of a relationship between SUA and CRP levels. The study group consisted of 337 patients (174 males, mean age 63 +/- 16 years) with advanced chronic renal failure not yet on dialysis. None of them had overt inflammatory or infectious diseases. High sensitivity CRP levels were analyzed as a binary (above or below median value), or continuous variable (log-transformed CRP), by multiple logistic or linear regression analysis, respectively. Demographics, clinical, and biochemical characteristics, including SUA levels, were the variables tested in these analysis. In a subset of 169 patients without diabetes, the same analysis were carried out, with the inclusion of fasting insulin levels and HOMA-IR as independent variables. Median CRP level was 3.25 mg/L, and mean SUA level was 7.59 +/- 1.94 mg/dl. Patients with CRP levels above the median had significantly higher mean SUA level than that of the rest of study patients (7.93 +/- 1.79 vs 7.24 +/- 2.03 mg/dl, p = 0.001). SUA levels correlated significantly with log-transformed CRP levels (r = 0. 16, p = 0.0022). The relationship between SUA and CRP levels remained statistically significant after adjustment for age, sex, comorbid index, obesity, residual renal function, diuretic and allopurinol treatment, in the multivariate logistic and linear regression models (OR: 1.296, p = 0.0003; and beta: 0.204, p = 0.0002). The significant association between SUA and CRP levels did not change when HOMA-IR and fasting insulin levels were included as independent variables in the subset of 169 patients without diabetes. In conclusion, SUA levels are related with CRP levels in CKD patients.

C-Reactive Protein↗

PubMed2005

[Evaluation of efficacy of darbepoetin alfa administered once monthly as treatment of anemia in predialysis patients with chronic kidney disease].

BACKGROUND: Darbepoetin alfa has demonstrated its efficacy when is administered subcutaneously once-weekly and once every 2 weeks as treatment of anemia in patients with chronic kidney disease (CKD). The aim of this study is to assess the efficacy of subcutaneus darbepoetin alfa administered once monthly in patients with progressive CKD who maintained stable levels of Hb treated on once every other week dosing. METHODS: Patients included in the study maintained hemoglobin (Hb) > 11 g/dl and were receiving darbepoetin alfa once every other week during at least 4 months. We studied a frequency interval dose change: once every other week frequency was converted to once monthly at equivalent dose. The study completers were 12 patients over the third month and 7 at the end of one year evaluation period. RESULTS: A statistic significant decrease in Hb and hematocrit (Hto) was observed over the third month, although all patients maintain Hb levels higher than 11 g/dl. At the same time it was appreciated a statistic significant increased on creatinine (Cr) and parathyroid hormone levels (PTH). At the end of one year evaluation period no differences were observed in any of variables. CONCLUSION: Darbepoetin alfa administered once monthly is an efficacious option as treatment of anemia for patientes with CKD. With a dose of 1 mcg/kg/month, all patientes maintain Hb > 11 g/dl.

Aged↗

PubMed2005

[Epidemiology of chronic renal failure in the elderly].

The prevalence of chronic renal failure (CRF) increases, particularly in the elderly. According to countries, 7% to 55% of the population over the age of 60 is presenting with CRF. In France, the incidence per year of end stage renal disease (ESRD) is 400 pmp over the age of 65 years, with regional fluctuations. The incidence rate of ESRD in patients with chronic kidney disease (CKD) decreases with age and is 2 to 3 folds higher in the 20-60 year age group than in the 61-74 year age group. Among patients presenting with CKD, the counts of patients developing ESRD diminishes with age; it is 2 to 3 fold lower in 61-74 years old patients than in 20-60 years old. This is due to an increased cardiac and vascular morbidity and to increasing mortality associated to CRF. For the elderly it is estimated that 18 to 20% patients-year presenting with CKD die before entering ESRD. In 30 to 50% patients-year a cardiovascular disease occurs. Diabetic and hypertensive nephropathies are responsible for 48% to 73% of ESRD cases in patients older than 65, according to countries and regions; on the other hand, glomerular diseases account for only 10% of cases. Moreover, in Europe, between 1990 and 1999, the incidence of ESRD due to diabetic, hypertensive and vascular diseases increased for more than 10% per year in the elderly. CRF is a serious condition in the elderly particularly owing to the fact that cardiac and vascular morbidity is high as well as mortality. The risk of evolution towards ESRD is also increased in the elderly.

Aged↗

PubMed2006

[Vitamin D metabolism and chronic kidney disease].

Vitamin D is finally converted into the active form in the kidney, which is regulated and affected by several factors such as calcium . phosphate balance, parathyroid hormone (PTH), calcitonin and fibroblast growth factor 23 (FGF23). Activated vitamin D works as hormone and engages in calcium . bone metabolism. In chronic kidney disease, the active form can be decreased and therefore, renal osteodystrophy can be lead as consequences of mineral metabolism abnormality and unregulated PTH production/secretion as increased activity of the parathyroid glands (2HPT). Moreover, because chronic kidney disease (CKD)-associated abnormal states in above are detrimental to CKD patients not only in terms of renal osteodystrophy, but progress of cardiovascular disease and mortality. Therefore new concept is proposed as chronic kidney disease-mineral bone disorder (CKD-MBD).

Bone Diseases, Metabolic↗

PubMedDate not supplied

Endothelial dysfunction in chronic kidney disease: determinant of susceptibility to end-organ damage and therapeutic response.

Endothelial dysfunction (ED) seems to be a crucial mediator of increased cardiovascular risk observed among patients with chronic kidney disease (CKD). Importantly, systemic ED does not only occur in patients with severe renal failure, but also in individuals with earlier stages of CKD. Close association between microalbuminuria and systemic ED renders renal vascular function an important marker for the severity of cardiovascular damage. Furthermore, changes in renal endothelium might be actively involved in the progression of renal end-organ damage. Recently, experimental evidence showed that interindividual variability in endothelial function of healthy rats predicts susceptibility to renal damage and the efficacy of renoprotective treatment. Therefore, a specific manipulation of renal and systemic ED might provide benefits in various stages of CKD. ED thus may represent an ideal therapeutic target not only for treatment, but also for primary prevention of renal disease.

Cardiovascular Diseases↗

PubMedDate not supplied

KDOQI clinical practice guidelines and clinical practice recommendations--2006 updates.

In scanning through the KDOQI guidelines for this article, I applaud the Work Group members as there is an emphasis placed on timely education of the patient, their family members, close friends, and/or primary care providers for both HD and PD. We have all seen in our practice setting, how critical education is for our patients. Studies have shown that timely patient education as CKD advances can both improve outcomes and reduce cost. These guidelines certainly emphasize the importance of advocating for education of patients with CKD. We know that we as nephrology nurses are crucial for educating the patient with CKD, the patient with ESRD, family members, and caregivers and for re-enforcing their education.

Evidence-Based Medicine↗

PubMedDate not supplied

Vitamin D retains an important role in the pathogenesis and management of secondary hyperparathyroidism in chronic renal failure.

Chronic kidney disease (CKD) causes alterations in mineral metabolism inducing the development of secondary hyperparathyroidism (HPT) and renal osteodystrophy. Recently, it has been suggested that these alterations play an important role in determining extraskeletal calcification and thus cardiovascular morbidity and mortality among CKD patients. An impaired 1 alfa -hydroxylation of 25-hydroxycholecalciferol (25(OH)D3) to 1,25-dihydroxycholecalciferol (1,25(OH)2 D3) with decreased circulating 1,25(OH)2 D3 levels is commonly observed in patients with creatinine clearance below 70 ml/min. The reduction in 1,25(OH)2 D3 production triggers the up-regulation of parathyroid hormone (PTH) synthesis, through a decreased suppression on PTH gene transcription and a decreased intestinal calcium absorption. A reduced expression of vitamin D receptor (VDR) and a less efficient binding of the complex 1,25(OH)2 D3 -VDR to specific DNA segments account for the resistance to 1,25(OH)2 D3 in target cells. Thus, absolute and relative 1,25(OH)2 D3 deficiency is one of the causes of secondary HPT in patients with CKD, together with phosphate retention and skeletal resistance to PTH. Consistently with these pathophysiological mechanisms, the therapeutic use of 1,25(OH)2 D3 still represents a milestone for the treatment of secondary HPT and renal osteodystrophy, even though hypercalcemia and hyperphosphatemia are common adverse events and may increase the risk of cardiovascular calcifications. To reduce the impact of such adverse effects while retaining anti-PTH activity, 1,25(OH)2 D3 analogues with lower calcemic effects have been synthesized and are now available for clinical use.

Calcinosis↗

PubMedDate not supplied

Effect of antitubercular medications on blood pressure control in chronic kidney disease patients with tuberculosis: a prospective cohort study.

BACKGROUND: Previous anecdotal reports suggested a decrease in antihypertensive medication potency after starting antitubercular medications. This interaction could be unpredictable in presence of renal failure due to increased half-lives of most commonly used antihypertensive medications. METHODS: In a cohort study involving 135 patients with chronic kidney disease (CKD), 62 patients with tuberculosis star-ted on antitubercular medications (TB group) were prospectively compared with 73 CKD controls (with no TB and not on antitubercular medications) for a change in antihypertensive medications. Antihypertensive dose was converted to unit score. RESULTS: The TB group had a greater increase in antihypertensive medication dose as compared with controls (89% vs. 54%, p<0.0001). In absolute terms an overall increase in antihypertensive medications was observed in 60% of pa-tients in the TB group, with a 2-fold dose increase from the baseline (p<0.0001). Four patients from the TB group de-veloped a hypertensive emergency. In multivariate linear regression, the association between TB group and increase in antihypertensives remained significant ( beta =0.38; p<0.0001). CONCLUSIONS: In CKD patients, antihypertensive medication potency is reduced in TB patients on antitubercular the-rapy in a significant number of patients, to a clinically significant degree with a potential risk for hypertensive emergency.

Adult↗

PubMed2006

Hepatitis B virus infection: implications in chronic kidney disease, dialysis and transplantation.

Hepatitis B virus (HBV) infection occurs worldwide but is most prevalent in Southeast Asia and sub-Saharan Africa with reported prevalence rates varying from 3 - 26 %. The higher prevalence of infection has been reported in patients with HBV and human immunodeficiency virus (HIV) co-infection. Hepatitis B virus not only affects the liver but has also been implicated in the pathogenesis of membranous, membranoproliferative and mesangial proliferative glomerulonephritides. Though controlling the spread of HBV infection in renal dialysis units has been one of the major triumphs in the management of end-stage renal disease, transmission of HBV can still occur through contamination of equipments and environmental surfaces and the use of multiple dose vials of drugs. Some reports have indicated that prior HBV infections have negative impact on graft and host survival following transplantation. Interferon can be used in the treatment of HBV-associated glomerulonephritides (HBV- GN) but is contraindicated in transplantation because of its immuno-modulatory effects. Despite the fact that patients with chronic kidney disease (CKD) have suboptimal response to HBV immunization, immunization is still beneficial to these patients. However, reports indicate that most patients with CKD were either not immunized or were given suboptimal doses. Control of HBV in the population by immunization can lead to a reduction in the prevalence of HBV- GN. In addition, immunization of patients with CKD will help in controlling HBV infection in dialysis settings and can lead to improved graft and host survival following transplantation.

Africa South of the Sahara↗

PubMed2006

Impact of chronic kidney disease and diabetes on percutaneous coronary intervention outcomes.

Abnormalities of glucose metabolism and chronic kidney disease (CKD) complicate treatment and outcomes for patients undergoing percutaneous coronary intervention (PCI). Likely causes of the complicating effects of diabetes include hyperglycemia, abnormalities of microvascular perfusion, and a prothrombotic and proinflammatory state. CKD predisposes to atherosclerosis, adds to the mortality and morbidity risk of cardiovascular disease (CVD), and increases risks for patients undergoing PCI. The complexity of the renal dysmetabolic syndrome and its close association with CVD must be taken into account when developing a therapeutic plan for these patients. Clinical data support the use of abciximab for patients with disturbances of glucose metabolism or with CKD who are undergoing PCI. The use of drug-eluting stents reduces the rate of target vessel revascularization and restenosis.

Abciximab↗

PubMed2007

Effect of omeprazole on the pharmacokinetics of paricalcitol in healthy subjects.

Paricalcitol capsules are indicated for the prevention and treatment of secondary hyperparathyroidism in chronic kidney disease (CKD). Proton pump inhibitors are prescribed to CKD patients to treat gastroesophageal reflux. This was a single dose, crossover study evaluating the effect of omeprazole, change in gastric pH as a result thereof, on the pharmacokinetics (PK) of paricalcitol. Twenty-six healthy subjects were administered paricalcitol capsules (16 microg) alone (regimen A), and following a single dose of OMP (40 mg) (regimen B), with a washout of at least 7 days. Plasma samples for paricalcitol concentrations were collected for 48 h post-paricalcitol dose. The plasma paricalcitol concentrations were measured using an LC-MS/MS assay (LOQ=0.02 ng/ml) and paricalcitol pharmacokinetic parameters were estimated using non-compartmental methods. The point estimates and the corresponding 90% confidence intervals for Cmax and AUC0-infinity to evaluate paricalcitol-omeprazole interaction were 1.032 [0.920-1.158] and 1.041 [0.951-1.139], respectively. No significant differences in Tmax (regimen A: 2.9 h vs regimen B: 2.6 h) or t1/2 (6.83 h vs 6.6 h) between the regimens were observed. Hence, the co-administration of omeprazole does not affect the PK of paricalcitol. Both regimens were well tolerated and no apparent differences among the regimens with respect to safety were observed.

Adolescent↗

PubMed1997

Time-frequency analysis of the first heart sound. Part 2: An appropriate time-frequency representation technique.

A simulated first heart sound (S1) signal is used to determine the best technique for analysing physiological S1 from the following five time-frequency representations (TFR): the spectrogram, time-varying autoregressive modelling, binomial reduced interference distribution, Bessel distribution and cone-kernel distribution (CKD). To provide information on the time and frequency resolutions of each TFR technique, the instantaneous frequency and the -3 dB bandwidth as functions of time were computed for each simulated component of the S1. The performance index for selecting the best technique was based on the relative error and the correlation coefficient of the instantaneous frequency function between the theoretical distribution and the computed TFR. This index served to select the best technique. The sensitivity of each technique to noise and to small variations of the signal parameters was also evaluated. The results of the comparative study show that, although important limitations were found for all five TFRs tested, the CKD appears to be the best technique for the time-frequency analysis of multicomponent signals such as the simulated S1.

Heart↗

PubMed2006

[Pathophysiology of hypertension: what's new?].

The pathophysiology of primary hypertension is still unresolved and appears more complex than ever. It is beyond the scope of this article to review all new scientific developments in this field. On clinical grounds, hypertension is divided into primary and secondary forms. Here, the authors discuss the pathophysiology of hypertension associated with three common disease entities showing a large overlap with primary hypertension: chronic kidney disease (CKD), obstructive sleep apnea (OSA), and hyperaldosteronism. Especially in CKD and OSA, the activation of the sympathetic nervous system plays a crucial role. It is the authors' belief that hypertension due to these three diseases is more common than previously appreciated and may account for about 20% of the hypertensive population. The knowledge of the underlying pathophysiology allows early diagnosis and guides optimal treatment of these hypertensive patients.

Adipocytes↗

PubMed2006

Impact of diabetes on haemoglobin levels in renal disease.

AIMS/HYPOTHESIS: Anaemia is a common complication of renal impairment. It has been suggested that renal failure secondary to diabetes is associated with more severe anaemia, but this has not been clearly substantiated in the published literature. To clarify this, we undertook a single centre, retrospective study to identify the impact of diabetes on anaemia associated with renal impairment. MATERIALS AND METHODS: Information on clinical, biochemical and haematological parameters of 2,052 stable ambulatory patients attending a single tertiary referral renal unit was collected. The impact of diabetic kidney disease on haemoglobin levels at all degrees of renal impairment was studied by comparison with patients with non-diabetic kidney disease after correcting for other commonly associated variables that influence anaemia in patients with renal impairment. RESULTS: Linear regression analysis showed lower haemoglobin in patients with diabetic kidney disease (p < 0.01). At chronic kidney disease (CKD) stages 3, 4 and 5, mean haemoglobin levels in patients with diabetic kidney disease compared with those in patients with non-diabetic kidney disease were 129.5 vs 136.9 g/l (p < 0.001), 120.5 vs 126.9 g/l (p < 0.001) and 107.1 vs 115.9 g/l (p < 0.01), respectively. At CKD stage 4 and 5 the two groups were comparable for ferritin, plasma intact parathyroid hormone levels, ACE inhibitor use and length of follow-up by a nephrologist. CONCLUSIONS/INTERPRETATION: Diabetic kidney disease is associated with lower haemoglobin in comparison with non-diabetic kidney disease, especially at GFR <60 ml/min.

Anemia↗

PubMed2006

Gene expression analysis in a canine model of X-linked Alport syndrome.

Chronic kidney disease (CKD) often culminates in renal failure as a consequence of progressive interstitial fibrosis and is an important cause of illness and death in dogs. Identification of disease biomarkers and gene expression changes will yield valuable information regarding the specific biological pathways involved in disease progression. Toward these goals, gene expression changes in the renal cortex of dogs with X-linked Alport syndrome (XLAS) were examined using microarray technology. Extensive changes in inflammatory, metabolic, immune, and extracellular matrix biology were revealed in affected dogs. Statistical analysis showed 133 genes that were robustly induced or repressed in affected animals relative to age-matched littermates. Altered expression of numerous major histocompatibility complex (MHC) molecules suggests that the immune system plays a significant role in XLAS. Increased expression of COL4A1 and TIMP-1 at the end stage of disease supports the suggestion that expression increases in association with progression of fibrosis and confirms an observation of increased COL4A1 protein expression. Clusterin may function as one of the primary defenses of the renal cortex against progressive injury in dogs with XLAS, as demonstrated here by increased CLU gene expression. Cellular mechanisms that function during excess oxidative stress might also act to deter renal damage, as evidenced by alterations in gene expression of SOD1, ACO1, FDXR, and GPX1. This investigation provides a better understanding of interstitial fibrosis pathogenesis, and potential biomarkers for early detection, factors that are essential to discovering more effective treatments thereby reducing clinical illness and death due to CKD.

Animals↗

PubMed2004

The nervous system and chronic kidney disease in children.

This paper provides a review of the literature on the nervous system involvement incurred by children and adolescents with chronic kidney disease (CKD), with a particular focus on neuropsychological functioning. In addition to an historical overview of earlier literature, published studies from the past 14 years that address both central and peripheral nervous system function in children with CKD are reviewed (1990-2003). These studies span work in neuroimaging, electrophysiology, and neuropsychology. A key focus for this review is on variables that might affect neurodevelopmental status in these children. The paper concludes with suggestions for achieving progress in the understanding of this complication of kidney disease in children.

Adolescent↗

PubMed2004

Impact of inflammation and oxidative stress on vascular calcifications in chronic kidney disease.

Vascular and/or valvular calcifications in patients with chronic kidney disease (CKD) appear to indicate a poor prognosis in terms of overall survival and cardiovascular morbidity and mortality. Inflammation and oxidative stress represent new features of the arterial and/or valvular calcification process. However, only limited observational and epidemiological data are available in these areas. Therefore, the link between inflammation, oxidation and vascular and/or valvular calcifications deserves careful consideration in CKD patients, since they may become targets for the development of new therapeutic strategies.

Calcinosis↗