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PubMed2004

Balance between cytokine production by peripheral blood mononuclear cells and reactive oxygen species production by monocytes in patients with chronic kidney disease.

Hemodialysis (HD) and peritoneal dialysis are associated with inflammatory events and immunological incompetence. The purpose of this study was to evaluate the effect of both uremia and dialysis modality on the production of cytokines and reactive oxygen species (ROS) by monocytes. four groups of subjects were studied: 28 chronic kidney disease (CKD) patients, 14 chronic HD patients, 14 patients on continuous ambulatory peritoneal dialysis (CAPD) patients, and 14 healthy volunteers, peripheral blood mononuclear cells (PBMC) were isolated from blood samples and incubated for 24 hr with or without lipopolysaccharide (LPS). TNF-alpha and IL-10 production by PBMC and serum levels of these cytokines were quantified by ELISA. Aliquots of whole blood were incubated in vitro and ROS production and phagocytosis were quantified by flow cytometry. Compared to the control group, Staphylococcus aureus-stimulated ROS production by monocytes was significantly lower in the HD group. The highest levels of unstimulated TNF-alpha production in vitro were observed in the HD group. In the CKD group, as well as in the whole population, there were a negative correlation between TNF-alpha production by unstimulated PBMC and ROS production by S. aureus-stimulated monocytes and a positive correlation between PMA-stimulated ROS production by monocytes and unstimulated and LPS-stimulated IL-10 production by PBMC suggesting that the pro-inflammatory state in CKD patients is associated with decreased response to infectious challenges.

Adult↗
PubMed2005

Survival advantages of obesity in dialysis patients.

In the general population, a high body mass index (BMI; in kg/m(2)) is associated with increased cardiovascular disease and all-cause mortality. However, the effect of overweight (BMI: 25-30) or obesity (BMI: >30) in patients with chronic kidney disease (CKD) undergoing maintenance hemodialysis (MHD) is paradoxically in the opposite direction; ie, a high BMI is associated with improved survival. Although this "reverse epidemiology" of obesity or dialysis-risk-paradox is relatively consistent in MHD patients, studies in CKD patients undergoing peritoneal dialysis have yielded mixed results. Growing confusion has developed among physicians, some of whom are no longer confident about whether to treat obesity in CKD patients. A similar reverse epidemiology of obesity has been described in geriatric populations and in patients with chronic heart failure (CHF). Possible causes of the reverse epidemiology of obesity include a more stable hemodynamic status, alterations in circulating cytokines, unique neurohormonal constellations, endotoxin-lipoprotein interaction, reverse causation, survival bias, time discrepancies among competitive risk factors, and malnutrition-inflammation complex syndrome. Reverse epidemiology may have significant clinical implications in the management of dialysis, CHF, and geriatric patients, ie, populations with extraordinarily high mortality. Exploring the causes and consequences of the reverse epidemiology of obesity in dialysis patients can enhance our insights into similar paradoxes observed for other conventional risk factors, such as blood pressure and serum cholesterol and homocysteine concentrations, and in other populations such as those with CHF, advanced age, cancer, or AIDS. Weight-gaining interventional studies in dialysis patients are urgently needed to ascertain whether they can improve survival and quality of life.

Body Mass Index↗
PubMed2002

Anaemia: cardiovascular adaptations and maladaptive responses in chronic kidney disease.

Without intervention, premature cardiovascular disease is virtually certain in progressive chronic kidney disease (CKD). Whatever age the patient, the cardiovascular system in uraemia is senescent and poorly suited to dealing with supraphysiological haemodynamic demands. Anaemia and hypertension are the principal haemodynamic risk factors that can be treated. Many observational studies have shown that anaemia is a risk factor for haemodynamic overload, maladaptive left ventricular growth, left ventricular failure and death. The justification for normal target haemoglobin (Hb) in patients with CKD is still debated. Observational studies of left ventricular size, quality of life, functional status, hospital admission, and survival support higher Hb concentrations (> or =12 g/dl). Intervention trials to date suggest that a physiological approach to anaemia management benefits quality of life, and possibly left ventricular hypertrophy and dilatation. Obviously, avoiding anaemia is the only way to minimize time-averaged, anaemia-related haemodynamic load. Whether this strategy, involving efficient surveillance, early detection, early intervention, and high Hb targets that are independent of the phase of CKD, actually reduces cardiac failure or death remains to be seen.

Cardiovascular Diseases↗
PubMed2002

Is it time for a paradigm shift? Is erythropoietin deficiency still the main cause of renal anaemia?

An increasing number of reports documenting resistance to human recombinant erythropoietin (rHuEPO) therapy are challenging the concept that erythropoietin deficiency is the main cause of the anaemia of chronic kidney disease (CKD). In an attempt to establish whether other factors play a more predominant role in the anaemia of CKD, 988 patients receiving dialysis were assessed for a wide range of variables. Data were collected on haematocrit (Hct) levels, rHuEPO dose, dry weight, serum ferritin, transferrin saturation, serum albumin, serum aluminium, serum parathyroid hormone intact, eKt/V for urea, gender, dose of i.v. iron administered, time in hospital, and use of i.v. vancomycin. Hyporesponsiveness to rHuEPO was defined as patients requiring >500 IU/kg/week or failing to achieve Hct levels of >30%. Ninety-two (9.2%) of the 988 patients met the above criteria for hyporesponsiveness to rHuEPO. In 21 of these patients, Hct concentrations remained <30% at 6-month follow-up. There were known haematological causes of refractoriness to rHuEPO in nine of these patients. During extended follow-up, probable causes of hyporesponsiveness were discovered in all but two of the remaining 13 patients. Of 62 dialysis patients who received rHuEPO at doses >500 IU/kg/week, 45 (73%) had Hct concentrations of 33-42%. These patients were responding to the higher doses of rHuEPO with no obvious adverse effects. Lower values of serum ferritin, transferrin saturation, and eKt/V, or higher levels of parathyroid hormone or serum aluminium were not associated with higher rHuEPO dose requirements. These results suggest that erythropoietin deficiency is still the main cause of the anaemia of CKD. Erythropoietin replacement therapy can correct the anaemia in almost all iron replete patients providing enough hormone is given, functional iron deficiency is avoided, aluminium levels and parathyroid toxicities are controlled and that no de novo haematological condition that affects erythropoiesis or red blood cell survival develops. Consideration should be given to modifying the definition of rHuEPO hyporesponsiveness. The US Hct target of 33-36% for haemodialysis patients is narrow and the European target of Hct >33% may be significantly more practical and physiologically relevant.

Adult↗
PubMed2004

The importance of bone health in end-stage renal disease: out of the frying pan, into the fire?

In the early stages of renal failure, hyperparathyroidism develops as a compensatory mechanism to control serum levels of calcium, phosphorus and calcitriol. As kidney disease progresses, this ability to maintain mineral homeostasis is lost, leading to the development of renal osteodystrophy (ROD). Over the past decade, the pattern of ROD seen in patients with chronic kidney disease (CKD) has changed. Previously, the majority of patients had mixed uraemic osteodystrophy or aluminium-related osteomalacia. The decreased use of aluminium-based phosphate binders, coupled with improvements in the management of hyperphosphataemia, led to a reduction in the prevalence of these types of ROD. Since the mid-1990s, there has been an increase in the prevalence of adynamic bone disease as a result of increased suppression of parathyroid hormone through the use of calcium-based phosphate binders and calcitriol therapy. Adynamic bone disease is also associated with several clinical factors, such as older age, use of continuous ambulatory peritoneal dialysis and the presence of diabetes mellitus, as well as the use of calcitriol therapy. Studies of calcium metabolism in patients with CKD have shown that adynamic bone disease is a distinct clinical condition that leads to hypercalcaemia via mechanisms different from that seen in high-turnover bone disease. As high calcium x phosphorus product has been associated with soft tissue and vascular calcifications, and increased mortality, optimizing bone health may be an important way of reducing cardiovascular risk in patients with CKD. To do this, novel, effective, non-calcium, non-aluminium phosphate binders will be necessary.

Calcinosis↗
PubMed2005

Managing a fateful alliance: anaemia and cardiovascular outcomes.

Cardiovascular disease (CVD) is a significant complication in chronic kidney disease (CKD) and a major cause of death in dialysis patients. Clinical studies have shown that anaemia is associated with reduced survival in patients with renal disease, heart failure or both. There is also evidence that, even in otherwise healthy individuals, anaemia is independently associated with an increased risk of CVD. The body adapts to anaemia by increasing cardiac output, which may result in cardiac remodelling and progression of left ventricular (LV) growth. Indeed, low haemoglobin (Hb) has been identified as an independent risk factor for LV growth in CKD patients, suggesting that there is a direct link between anaemia and adverse cardiac outcomes. This suggests that correction of anaemia with recombinant human erythropoietin (rhEPO; epoetin) may improve prognosis. Partial correction of anaemia produces partial regression of LV hypertrophy, while complete correction of anaemia can help to prevent LV dilatation in haemodialysis patients with normal LV volumes. Moreover, in non-dialysis patients with advanced CVD, pilot studies showed that a moderate increase in Hb improved cardiac function and reduced hospitalization rates. In addition, consistent epoetin treatment before the start of dialysis was associated with a reduced risk of developing cardiac disease in CKD patients. In contrast, in dialysis patients with advanced cardiac disease, Hb normalization increased mortality risk. Therefore, early correction of anaemia appears important. The Cardiovascular risk Reduction by Early Anaemia Treatment with Epoetin beta (CREATE) study is investigating whether this approach is associated with a measurable reduction in cardiovascular risk.

Anemia↗
PubMed2005

Intravenous iron supplementation in the anaemia of renal and cardiac failure--a double-edged sword?

The anaemia of chronic kidney disease (CKD) is efficiently corrected with a combination of recombinant erythropoietin (rhEPO) and intravenous iron supplementation. Recently, patients with severe cardiac failure and anaemia have also been shown to benefit from this treatment. However, iron excess may lead to the production of free radicals and has been incriminated in the pathogenesis of atherosclerosis and increased risk of infection, the two major causes of death in end-stage renal disease. The exact risk of excess iron supplementation has not been defined and, in the absence of sensitive and specific indicators of iron overload, the risk remains difficult to quantify. There is increasing epidemiological evidence incriminating iron overload as a risk factor in CKD, but direct evidence is still hard to obtain. The precise role of iron is complicated further by the complex inter-relationships between iron metabolism and the inflammatory process characteristic of CKD. The recent discovery of the antimicrobial peptide, hepcidin, may shed light on these inter-relationships. New methods for quantifying non-transferrin-bound (or labile plasma) iron may help in the future to identify patients at risk for toxicity from excess iron supplementation.

Anemia↗
PubMed2004

Malnutrition and inflammation are associated with impaired pulmonary function in patients with chronic kidney disease.

BACKGROUND: Inflammation and malnutrition are common findings in patients with chronic kidney disease (CKD). We hypothesized that in inflamed and malnourished patients, respiratory and peripheral muscle dysfunction may have significant consequences on pulmonary function. The aim of this study was to investigate possible associations between pulmonary function and inflammation and malnutrition in patients with CKD. METHODS: We studied 109 patients (63% males; 53+/-12 years) at the initiation of dialysis treatment (GFR 7.5+/-2.5 ml/min). Pulmonary function tests [forced expiratory volume in 1 s (FEV(1)), forced vital capacity (FVC) and peak expiratory flow (PEF)] were performed and the percentages of predicted values were calculated (%FEV(1), %FVC and %PEF). Systemic inflammation, assessed by high-sensitivity C-reactive protein (hsCRP) and nutritional status assessed by subjective global assessment (SGA), lean body mass (LBM) (estimated with dual energy X-ray absorptiometry) and hand-grip strength (HGS), were evaluated at the same time. RESULTS: Significant negative correlations were found between hsCRP and the percent predicted values for all pulmonary function tests [%FEV(1) (Rho = -0.45), %FVC (Rho = -0.43) and %PEF (Rho = -0.38)], respectively. Malnourished patients defined as SGA >or=2 had lower %FEV(1) (64+/-19 vs 82+/-23%; P<0.001) and %FVC (67+/-18 vs 83+/-21%; P<0.001) than well nourished patients. Significant correlations were observed between HGS and %FVC (Rho = 0.38; P <0.001), %FEV(1) (Rho = 0.37; P<0.001) and %PEF (Rho = 0.22; P<0.05) and between LBM and %PEF (Rho = 0.20; P<0.05). Multivariate Cox analysis showed that cardiovascular disease and low %FVC were associated with poor survival. CONCLUSIONS: Impaired pulmonary function is associated with malnutrition and inflammation, and predicts mortality in CKD patients. This may reflect an impact of malnutrition and inflammation on respiratory muscle performance, leading to pulmonary dysfunction, which could influence the clinical outcome.

Adult↗
PubMed2004

Assessment of body composition by dual energy X-ray absorptiometry, skinfold thickness and creatinine kinetics in chronic kidney disease patients.

BACKGROUND: Finding a method that can be routinely used to assess body composition with minimum error is still a challenge for those who work with chronic kidney disease (CKD) patients. This study aimed to compare the value of two surrogate techniques, skinfold thickness (SKF) and creatinine kinetics (CK) with dual energy X-ray absorptiometry (DEXA) as the reference method for measuring body fat and fat-free mass in non-dialysed CKD patients. METHODS: The body fat and fat-free mass of 50 non-dialysed CKD patients (38 male, 12 female) were measured by DEXA and compared with measurements obtained by SKF and CK. RESULTS: The mean values of body fat and fat-free mass obtained by SKF and CK differed significantly from measurements made by DEXA. The intra-class correlation coefficient (r) for body fat between SKF and DEXA (r = 0.74) and between CK and DEXA (r = 0.47) indicated a moderate degree of reproducibility. A Bland and Altman plot analysis showed a better agreement between SKF and DEXA [5.8 +/- 3.9% (-2.0 to 13.6)] than between CK and DEXA [8.8 +/- 8.8% (-8.8 to 26.4)]. Regarding fat-free mass, the intra-class correlation coefficient (r) between SKF and DEXA (r = 0.85) indicated a good degree of reproducibility, while that between SKF and CK (r = 0.57) indicated a moderate degree of reproducibility. The Bland and Altman plot analysis for fat-free mass showed that DEXA agreed better with SKF [-3.1 +/- 3.4 kg (-9.9 to 3.7)] than with CK [-5.5 +/- 6.4 kg (-18.2 to 7.3)]. CONCLUSION: Skinfold thickness seems to be the method of choice for evaluating body fat. The limitations inherent to DEXA in evaluating fat-free mass makes it difficult to designate an alternate method of choice for assessing this body compartment.

Absorptiometry, Photon↗
PubMed2004

Adiponectin in chronic kidney disease is related more to metabolic disturbances than to decline in renal function.

BACKGROUND: Adiponectin, a newly discovered collagen-like protein of the collectin family exclusively produced by adipocytes, possesses anti-inflammatory properties. Plasma adiponectin is associated with a decreased cardiovascular risk in non-renal patients, and is reduced in obesity and insulin-resistant states. Although reports show an increase in the adiponectin level in maintenance haemodialysis, peritoneal dialysis and end-stage renal disease, there is no documentation of adiponectin levels and regulation in the early stages of chronic kidney disease (CKD). METHODS: We prospectively measured glomerular filtration rate (GFR) in 48 patients with CKD using inulin clearance. Fasting blood was drawn to determine insulin, leptin, adiponectin and C-reactive protein (CRP) levels. Body fat mass was calculated using skinfold thickness measurements. RESULTS: The patients' mean GFR was 53.5+/-24.9 (SD) ml/min/1.73 m2. Adiponectin was in the normal range in men (9.8+/-2.9 mg/l) and women (16.6+/-5.0 mg/l) with CKD, being significantly higher in women than men (P<0.001). Serum leptin was above normal (10.4+/-10.7 microg/l), whereas serum insulin and CRP were within their normal ranges (3.5+/-3.3 microU/ml and 2.6+/-5.0 mg/l, respectively). In linear regression analysis, adiponectin was negatively correlated with GFR (P = 0.02), fat mass (P = 0.03) and body mass index (P = 0.002), and strongly positively correlated with serum leptin (P = 0.003). A positive relationship was also found between plasma adiponectin and the urinary albumin/creatinine ratio (P = 0.007). No relationship was found between adiponectin and insulin or adiponectin and CRP. In multiple regression analysis, adiponectin was significantly positively correlated with leptin (P<0.0001), negatively with body mass index (P<0.0001) and only weakly with GFR (P = 0.04). CONCLUSIONS: Despite an adverse metabolic environment in chronic renal insufficiency, serum adiponectin increases in non-obese patients when renal function deteriorates. Adiponectin is only weakly affected by renal function per se, but appears influenced by proteinuria, and more significantly by body mass index and the change in serum leptin that accompanies decline in renal function.

Adiponectin↗
PubMed2005

Prevalence of chronic kidney disease based on estimated glomerular filtration rate and proteinuria in Icelandic adults.

BACKGROUND: The purpose of this study was to compare three different equations to calculate estimated glomerular filtration rate (eGFR) based on serum creatinine (SCr) and to estimate the prevalence of chronic kidney disease (CKD) in the Icelandic population. METHODS: This was a cross-sectional study using data from the Reykjavik Heart Study. GFR was estimated with three equations: Equation I was based on 1/SCr; Equation II based on the Cockcroft-Gault equation; and Equation III was the modified MDRD equation. The eGFR calculated with Equation III and proteinuria were used to estimate the prevalence of CKD. The prevalence was age-standardized to the truncated world population. We used chi-square and ANCOVA to compare the group with low eGFR to age-matched controls. RESULTS: The subjects consisted of 9229 males and 10,027 females, aged 33-85 years. The equations performed very differently. Equation I showed women with higher eGFR than men and little change with age. Equation II showed men with higher eGFR than women and marked decline in eGFR with age. Equation III was similar to Equation II but the decline in eGFR with age was not as great. Regardless of the equation used, most subjects (63.7-80.7%) had an eGFR in the range of 60-89 ml/min/1.73 m2. Using Equation III, age-standardized prevalence of low eGFR for the population aged 35-80+ years was estimated to be 4.7 and 11.6% for men and women, respectively. The proportion of subjects with eGFR <60 ml/min/1.73 m2 increased with advancing age. An additional 2.39% of men and 0.89% of women had proteinuria. The prevalence of renal and cardiovascular risk factors including proteinuria, hypertension, lipid abnormalities and markers of inflammation was higher among those with low eGFR than age-matched controls. CONCLUSIONS: GFR estimates and the prevalence of CKD are dependent on the equation used to calculate eGFR. Unexpectedly, a low proportion of the Icelandic population had normal kidney function according to the eGFR regardless of the equation used. These equations may not be useful in epidemiological research.

Adult↗
PubMed2005

Pulse pressure and inhibition of renin-angiotensin system in chronic kidney disease.

BACKGROUND: Elevated pulse pressure (PP) is an indicator of poor outcome in hypertensives in the general population and on haemodialysis. The prognostic value of PP in pre-dialysis patients with chronic kidney disease (CKD) stages 4/5 and its interaction with renin-angiotensin system (RAS) inhibitors is unknown. METHODS: This retrospective study of 349 patients from the pre-dialysis clinic analysed the effect association of PP and RAS inhibition on adverse outcomes in CKD stages 4/5. Primary endpoints were a composite of death or dialysis. RESULTS: At baseline, 349 patients (63% males, 34% diabetics) were aged 60+/-0.8 years (mean+/-SEM) with systolic blood pressure (SBP) 149+/-1.3 mmHg, diastolic BP (DBP) 83+/-0.7 mmHg, PP 66+/- 1.0 mmHg, creatinine 442+/-16 micromol/l and haemoglobin 10.7+/-0.1 g/dl. Patients were followed up for 297+/-19 days and 93% took one to seven (2.45+/-0.07) antihypertensives. At presentation, the adverse outcome group had higher SBP (151+/-1.5 vs 145+/-2.4 mmHg; P<0.05), proportion of diabetes (39% vs 23%; P<0.05) and creatinine (478+/-22 vs 354+/-11 micromol/l; P<0.05), but lower haemoglobin (10.6+/-0.1 vs 11.2+/-0.2 g/dl; P<0.05). PP increased with age (r(2): 0.4; P<0.0001). PP >80 mmHg was associated with adverse outcome (Kaplan-Meier survival analysis, log-rank test P<0.05). In a model of proportional hazards regression, adjusted for age, baseline creatinine, diabetes and haemoglobin, elevated PP was associated with poorer outcome (hazards ratio: 1.09; 95% confidence interval: 1.01-1.18; P<0.05) and angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker use was beneficial (hazards ratio: 0.73; 95% confidence interval: 0.53-0.99; P<0.05). CONCLUSIONS: The study demonstrates that elevated PP indicates high risk of death or dialysis and the benefit of blockade of the RAS is independent of the baseline PP in patients with CKD stages 4/5.

Angiotensin Receptor Antagonists↗
PubMed2006

Association of low blood pressure with increased mortality in patients with moderate to severe chronic kidney disease.

BACKGROUND: Blood pressure shows an inverse association with mortality in patients with chronic kidney disease (CKD) on dialysis. It is unclear if the same phenomenon exists in patients with CKD not yet on dialysis. METHODS: We examined the association of systolic (SBP) and diastolic (DBP) blood pressure with all-cause mortality in a historical prospective cohort of 860 patients (age 68.1+/-10.1 years, 99.1% male, 24.4% black) with estimated glomerular filtration rate (GFR) < 60 ml/min/1.73 m2. We used Cox models to adjust for the effects of age, race, diabetes mellitus, atherosclerotic cardiovascular disease (ASCVD), congestive heart failure, smoking, antihypertensive medications, body mass index, GFR, albumin, cholesterol, haemoglobin and proteinuria. To examine the role of comorbidities, we performed subgroup analyses based on prevalent ASCVD status and level of estimated GFR. RESULTS: Higher SBP and higher DBP were both associated with lower mortality [adjusted hazard ratio (95% confidence interval) for SBP 133-154, 155-170 and > 170 mmHg, compared with < 133 mmHg, respectively: 0.61 (0.44-0.85), 0.62 (0.45-0.87) and 0.68 (0.49-0.96); and for DBP 65-75, 76-86 and > 86 mmHg, compared with < 65 mmHg: 0.85 (0.62-1.18), 0.72 (0.52-1.00) and 0.60 (0.41-0.86)]. The same association was present for both SBP and DBP only in subgroups with GFR < or = 30 ml/min/1.73 m2 and for DBP only in the subgroup with ASCVD. CONCLUSIONS: Lower blood pressure is associated with higher mortality in patients with moderate to severe CKD, but interactions with kidney function and with ASCVD suggest that blood pressure may play a surrogate rather than a causative role in this association.

Age Distribution↗
PubMed2006

Do inflammatory markers add predictive information of death beyond that provided by age and comorbidity in chronic renal failure patients?

BACKGROUND: Elevated levels of inflammatory markers have been shown to be associated with increased mortality in chronic kidney disease (CKD) patients. Comorbid indexes are also helpful clinical instruments for predicting mortality. At present, it is unknown whether inflammatory markers add predictive information of death beyond that provided by comorbid indexes. METHODS: This observational single-centre study included 404 patients (mean age 63+/-16 years) with CKD stage 4 and 5 predialysis who were prospectively followed-up. Data obtained at baseline: demographics, grade of comorbidity by Davies index, serum albumin, creatinine clearance, total white blood cell (WBC), polymorphonuclear leukocyte (PMN) counts, and high-sensitivity C-reactive protein (CRP) were analysed as potential determinants of the subsequent all-cause mortality. Receiver-operating characteristic (ROC) curves were used to determine the values of CRP, WBC and PMN most closely related to mortality. These cut-off values were used to define subgroups with high or low inflammatory markers. Uni- and multivariate Cox regression models were performed. RESULTS: Median follow-up time was 583 days, with a mortality of 26%, and overall survival rate of 47%. In unadjusted Cox models, inflammatory markers (CRP, WBC and PMN) were all significantly associated with all-cause mortality. Age (HR 1.05; 95% CI 1.03-1.07, P<0.0001) and comorbid index (HR 2.15; 95% CI 1.54-3.00, P<0.0001) were strongly associated with mortality. The introduction of inflammatory markers into the multivariate Cox regression model did not add significant predictive power. In a stepwise Cox model, the age, comorbid index, serum albumin levels and creatinine clearance were the best predictive variables of mortality. CONCLUSIONS: Although elevated inflammatory markers are associated with a worse outcome in CKD patients, they did not add predictive information of all-cause mortality beyond that provided by age and the comorbid index.

Age Factors↗
PubMed2006

Polynocturia in chronic kidney disease is related to natriuresis rather than to water diuresis.

BACKGROUND: Nocturnal polyuria has been well known in renal insufficiency. Recently, we found that as renal function deteriorated in chronic kidney disease (CKD), natriuresis was enhanced during the night with nocturnal blood pressure elevation. In the present study, we investigated whether nocturnal polyuria in CKD was due to the inability to concentrate urine, as previously proposed, or based on osmotic diuresis mainly by natriuresis. METHODS: In 27 CKD patients, circadian rhythms of urinary sodium, potassium, urea and osmolar excretion rates (U(Na)V, U(K)V, U(urea)V, U(osm)V) as well as of urinary volume (V) and free-water clearance (C(H(2)O)) were estimated during both daytime (6:00 to 21:00) and nighttime (21:00 to 6:00). Then, the night/day ratios of these parameters were analysed in relation to creatinine clearance (C(cr)) as a marker of glomerular filtration rate. RESULTS: C(cr) had significantly negative relationships with night/day ratios of V (R = -0.69; P < 0.0001), U(osm)V (R = -0.54; P = 0.004) and U(Na)V (R = -0.63; P = 0.0005), but no correlation with night/day ratios of C(H(2)O) (R = -0.33; P = 0.1), U(K)V (R = -0.29; P = 0.1) or U(urea)V (R = -0.31; P = 0.1). Linear and multiple regression analysis identified nocturnal natriuresis rather than urea excretion as an independent determinant of nocturia. CONCLUSION: As renal function deteriorated, nocturnal polyuria was seen, being consistent with classical recognition. Furthermore, this increase in nocturnal urine volume seemed related to osmotic diuresis mainly by natriuresis rather than to water diuresis or urea excretion.

Blood Pressure↗
PubMed2006

Fetuin-A and kidney function in persons with coronary artery disease--data from the Heart and Soul Study.

BACKGROUND: Fetuin-A is a serum protein that inhibits ectopic vascular calcification and is present in lower concentrations in end-stage renal disease than in healthy controls. Whether fetuin-A concentrations are also lower in the setting of mild-to-moderate chronic kidney disease (CKD) is unknown. METHODS: We evaluated the associations of several parameters of kidney function including measured 24 h urinary creatinine clearance (CrCl), estimated glomerular filtration rate (GFR) by the Mayo Clinic quadratic GFR equation (qGFR), serum cystatin-C concentrations, and urinary albumin-to-creatinine ratio with serum fetuin-A concentrations in 970 outpatients with coronary artery disease. We used general linear models to determine the adjusted mean fetuin-A concentrations within each kidney function category. RESULTS: The mean age of the study sample was 67 years, 82% were male, 71% had hypertension and 26% had diabetes mellitus. In adjusted analysis, we observed no significant differences in mean fetuin-A concentrations across groups defined by CrCl, qGFR, or albumin-to-creatinine ratio groups. For example, adjusted mean fetuin-A concentrations were 0.66 g/l in participants with CrCl > 90, 60-90 and 45-60 ml/min/1.73 m(2), and 0.65 g/l in participants with CrCl < 45 ml/min/1.73 m(2). Higher serum cystatin-C (indicating worse kidney function) was associated with higher adjusted mean serum fetuin-A concentrations (lowest quartile 0.62 g/l, highest quartile 0.68 g/l; P for trend <0.001). CONCLUSIONS: Among ambulatory patients with coronary artery disease, there is no evidence that mild-to-moderate CKD is associated with lower concentrations of serum fetuin-A compared with persons with normal renal function. The mechanisms explaining the association between CKD and vascular calcification remain elusive.

Aged↗
PubMed2006

Are prediction equations for glomerular filtration rate useful for the long-term monitoring of type 2 diabetic patients?

BACKGROUND: The aim of this study was to compare the accuracy of prediction equations [modification of diet in renal disease (MDRD), simplified MDRD, Cockcroft-Gault (CG), reciprocal of creatinine and creatinine clearance] in a cohort of patients with type 2 diabetes. METHODS: A total of 525 glomerular filtration rates (GFRs) using (125)I-iothalamate were carried out over 10 years in 87 type 2 diabetic patients. Accuracy was evaluated at three levels of renal function according to the baseline values obtained with the isotopic method: hyperfiltration (GFR: >140 ml/min/1.73 m(2); 140 isotopic determinations in 27 patients), normal renal function (GFR: 140-90 ml/min/1.73 m(2); 294 isotopic determinations in 47 patients) and chronic kidney disease (CKD) stages 2-3 (GFR: 30-89 ml/min/1.73 m(2); 87 isotopic determinations in 13 patients). The annual slope for GFR (change in GFR expressed as ml/min/year) was considered to ascertain the variability in the equations compared with the isotopic method during follow-up. Student's t-test was used to determine the existence of significant differences between prediction equations and the isotopic method (P < 0.05 with Bonferroni adjusted for five contrast tests). RESULTS: In the subgroup of patients with hyperfiltration, a GFR slope calculated with (125)I-iothalamate -4.8 +/- 4.7 ml/min/year was obtained. GFR slope in patients with normal renal function was -3.0 +/- 2.3 ml/min/year. In both situations, all equations presented a significant underestimation compared with the isotopic GFR (P < 0.01; P < 0.05). In the subgroup of CKD stages 2-3, the slope for GFR with (125)I-iothalamate was -1.4 +/- 1.8 ml/min/year. The best prediction equation compared with the isotopic method proved to be MDRD with a slope for GFR of -1.4 +/- 1.3 ml/min/year (P: NS) compared with the CG formula -1.0 +/- 0.9 ml/min/year (P: NS). Creatinine clearance presented the greatest variability in estimation (P < 0.001). CONCLUSIONS: In the normal renal function and hyperfiltration groups, none of the prediction equations demonstrated acceptable accuracy owing to excessive underestimation of renal function. In CKD stages 2-3, with mean serum creatinine > or =133 micromol/l (1.5 mg/dl), the MDRD equation can be used to estimate GFR during the monitoring and follow-up of patients with type 2 diabetes receiving insulin, anti-diabetic drugs or both.

Adult↗
PubMed2006

Functional impairment of monocyte-derived dendritic cells in patients with severe chronic kidney disease.

BACKGROUND: Dendritic cells (DCs) are antigen-presenting cells that are pivotal for the initiation of the primary immune response. Patients with chronic kidney disease (CKD) with or without chronic intermittent haemodialysis (CIHD) show an impaired immune response. Dysfunction of DCs may underlie this phenomenon. METHODS: In this study, several different functions of monocyte-derived DCs (moDC) of patients with CKD class IV-V (glomerular filtration rate <30 ml/min) and patients on CIHD were studied in vitro and compared with age- and sex-matched healthy volunteers. RESULTS: We demonstrate that, independent of the maturation stimulus used, mature moDC from both groups of patients did not acquire the same level of terminal differentiation as moDC from controls, as shown by analysis of cell surface markers and the relative high macropinocytosis activity of moDC. The stimulation of allogeneic T-cells by immature moDC and mature moDC did not differ between patients and controls. However, in the presence of immature moDC or antigen-loaded maturated moDC from patients, less proliferation of autologous T-cells was observed in response to recall antigens. There was no difference between moDC from controls and patients in their ability to activate naive T-cells and to differentiate them into Th1 and Th2 cells. CONCLUSIONS: These results show that the terminal differentiation of moDC in patients with severe CKD is impaired. This impairment is not restricted to one maturation stimulus and is independent of treatment with haemodialysis.

Adult↗