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PubMed2006

Reduced glomerular filtration rate in pre-dialysis non-diabetic chronic kidney disease patients is associated with impaired baroreceptor sensitivity and reduced vascular compliance.

Small uncontrolled studies of dialysis-dependent CKD (chronic kidney disease) patients have demonstrated abnormalities of cardiovascular autonomic control and vascular compliance, which may contribute to adverse cardiovascular morbidity in this population. However, there is little information utilizing newer non-invasive techniques in pre-dialysis patients with increasing degrees of uraemia. In the present study, 55 non-dialysis-dependent non-diabetic CKD patients with mean GFR (glomerular filtration rate) of 27 ml x min(-1) x m(-2) were studied. All patients underwent a 10-min period of electrocardiographic and non-invasive blood pressure monitoring. Cardiac BRS (baroreceptor sensitivity) was calculated from the combined alpha-index. PWV (pulse wave velocity) measurement and determination of arterial wave reflexion by applanation tonometry was performed in all patients. Mean (S.D.) cardiac BRS was 10.8 (7.1) ms/mmHg and mean (S.D.) PWV was 8.6 (1.7) m/s. Reduced GFR was correlated with increased PWV and decreased cardiac BRS. On logistic regression analysis with adjustment for clinical significant risk factors, severely impaired renal function (assessed by GFR < 15 ml x min(-1) x m(-2)) was associated with increased large artery stiffness [odds ratio for PWV = 3.14 (95% confidence intervals, 1.03-9.53); P = 0.04] and increased cardiovascular autonomic dysfunction [odds ratio for BRS = 0.87 (95% confidence intervals, 0.75-1.80); P = 0.06]. In conclusion, non-dialysis dependent non-diabetic CKD patients with decreasing GFR have reduced cardiac BRS and increased large artery stiffness. This may have important prognostic and therapeutic consequences for the management of vascular disease in a pre-dialysis population.

Adult↗
PubMed2002

Health care utilization among patients with chronic kidney disease.

BACKGROUND: Higher hospitalization rates among end-stage renal disease (ESRD) patients impose a substantial burden on the U.S. health care system. Early identification of patients with chronic kidney disease (CKD) and determination of factors associated with increased morbidity may lead to appropriate interventions to attenuate the complications of CKD and possibly reduce future resource utilization. METHODS: This retrospective cohort study of CKD patients in an outpatient nephrology clinic was performed to identify risk factors for hospitalization. The study population consisted of adults with elevated serum creatinine (females > or =1.5 mg/dL, males > or =2.0 mg/dL). Hospitalizations, hospital days and outpatient nephrology visits were examined. RESULTS: Among the 259 patients, 123 (47%) were hospitalized during a median follow-up of 11.4 months. The number of hospitalizations and hospital days per patient-year at risk were 0.96 and 6.6, respectively. Cardiovascular disease/hypertension accounted for the majority of hospitalizations. In a multivariate regression analysis, older age (RR 1.01, 95% CI 1.00, 1.03) and presence of cardiac disease (RR 1.91, 95% CI 1.19, 3.07) were associated with higher risk of hospitalization while higher serum albumin (RR 0.58, 95% CI 0.35, 0.95) and higher hematocrit (RR 0.92, 95% CI 0.87, 0.97) were associated with lower risk of hospitalization. Higher serum albumin (RR 0.34, 95% CI 0.21, 0.55), higher hematocrit (RR 0.87, 95% CI 0.81, 0.93) and use of ACE-inhibitors (RR 0.63, 95% CI 0.47, 0.84) were associated with lower risk of subsequent hospital days. Erythropoietin (RR 1.47, 95% CI 1.11, 1.82) use was associated with higher risk of outpatient nephrology visits. CONCLUSION: Certain potentially modifiable factors appear to be associated with increased resource utilization. It is hypothesized that attention to these factors may lead to improved outcomes in this patient population, which could result in reduced utilization.

Adult↗
PubMed2003

A double-blind randomized crossover trial of two loop diuretics in chronic kidney disease.

BACKGROUND: Torsemide has predictable absorption compared to furosemide. Thereby, torsemide results in more constant exposure to active drug. Our hypothesis was that this pharmacokinetic difference between these commonly used loop diuretics may translate into disparate antihypertensive responses in patients with chronic kidney disease (CKD). METHODS: We conducted a randomized, double-blind, two-period, crossover trial to compare the pharmacodynamics of torsemide and furosemide, in 14 subjects with stage 2 or 3 CKD. We first performed an inpatient study, where after the subjects were brought into sodium balance on a 200 mEq per day diet, a single bioequivalent dose of oral loop diuretic was administered with an intervening washout period. Measurements of urinary electrolytes were made. Subjects then participated in an outpatient study, wherein they received daily therapy for 3 weeks with the loop diuretics in random order. Twenty four-hour ambulatory blood pressure monitoring was performed before and after each drug to assess the antihypertensive response. RESULTS: In the inpatient phase, furosemide increased urinary sodium excretion from average (+/-SD) 199 +/- 49 mEq/day to 357 +/- 96 mEq/day and torsemide increased urinary sodium excretion from 213 +/- 79 mEq/day to 398 +/- 142 mEq/day. These differences between the diuretics were not significant, confirming bioequivalence. In the outpatient phase, furosemide reduced 24-hour ambulatory blood pressure from 147 +/- 17/78 +/- 11 mm Hg to 138 +/- 21/74 +/- 12 mm Hg (P = 0.021) and torsemide reduced it from 143 +/- 18/75 +/- 10 mm Hg to 133 +/- 19/71 +/- 10 mm Hg (P = 0.007). Although each diuretic was effective in reducing ambulatory blood pressure, the differences between diuretics were not statistically significant. CONCLUSION: Bioequivalent doses of torsemide and furosemide given in a randomized, double-blind design fail to demonstrate superiority of torsemide with respect to natriuresis or 24-hour ambulatory blood pressure control in subjects with stages 2 and 3 CKD.

Aged↗
PubMed2003

Role of excess volume in the pathophysiology of hypertension in chronic kidney disease.

BACKGROUND: The pathophysiology of hypertension in patients with chronic kidney disease (CKD) is largely attributed to positive sodium balance. It is unclear how loop diuretics affect fluid volume compartments, especially with respect to their antihypertensive effect. METHODS: Subjects with CKD were administered a single therapeutically equivalent dose of an oral loop diuretic (furosemide or torsemide in randomized crossover design). We measured acute volume changes over 12 hours using biophysical and hormonal biomarkers and then 24-hour ambulatory blood pressure after daily diuretic therapy for 3 weeks. RESULTS: Single-dose administration of loop diuretic decreased extracellular water (ECW) by 1.7 L [95% confidence interval (95% CI) 1.2, 2.2, P < 0.001], total body water (TBW) by 1.2 L (95% CI 0.5, 1.9, P < 0.001), and increased natural log (ln) plasma renin activity (PRA) from -1.2 +/- 1.3 ng/mL/hour to -0.5 +/- 1.5 ng/mL/hour (P < 0.001). Daily loop diuretic administration resulted in reduced ECW from 24.2 +/- 6.4 L to 22.3 +/- 5.2 L (P = 0.02) and TBW from 54.3 +/- 12.7 L to 51.6 +/- 11.9 L (P < 0.001) in 1 week. After 3 weeks of diuretic therapy, whereas ECW reduction persisted at 22.8 +/- 5.1 L (P = 0.05), TBW trended toward baseline level at 52.7 +/- 11.8 L. A concomitant increase in ln PRA from -1.0 +/- 1.3 ng/mL/hour to 0.4 +/- 1.9 ng/mL/hour (P < 0.001) and ln plasma aldosterone (PA) from 2.0 +/- 0.8 ng/dL to 2.3 +/- 0.8 ng/dL (P < 0.005) and fall in ln brain natriuretic peptide (BNP) from 4.3 +/- 0.9 pg/mL to 3.7 +/- 1.0 pg/mL (P < 0.01) were seen at 1 week. Despite a trend toward restoration of TBW, changes in hormonal biomarkers were maintained at 3 weeks. Over these 3 weeks, furosemide reduced 24-hour ambulatory blood pressure from 147 +/- 17/78 +/- 11 mm Hg to 138 +/- 21/74 +/- 12 mm Hg (P = 0.021) and torsemide reduced it from 143 +/- 18/75 +/- 10 mm Hg to 133 +/- 19/71 +/- 10 mm Hg (P = 0.007). CONCLUSION: Patients with CKD have elevated extracellular fluid volume that can be corrected acutely with loop diuretics. Persistent diuretic use results in dynamic changes in ECW and other body fluid compartments that translate into chronic blood pressure reduction.

Aged↗
PubMed2003

Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers.

BACKGROUND: Hyperphosphatemia is a risk factor for the development of several different complications of chronic kidney disease (CKD), including secondary hyperparathyroidism and cardiovascular complications, due to the formation of calcium-phosphate deposits. Fibroblast growth factor-23 (FGF-23) is a recently discovered protein that is mutated in autosomal-dominant hypophosphatemic rickets, an inherited phosphate wasting disorder, and it may represent a novel hormonal regulator of phosphate homeostasis. We therefore hypothesized that FGF-23 levels may be altered in hyperphosphatemia associated with renal failure and that its concentration changes in response to different levels of phosphate intake. METHODS: Using a two-site enzyme-linked immunosorbent assay (ELISA) detecting the C-terminal portion of FGF-23, serum concentration was measured in 20 patients with different stages of renal failure (creatinine range 155 to 724 micromol/L), in 33 patients with end-stage renal disease (ESRD) on dialysis treatment, and in 30 patients with functioning renal grafts. Furthermore, six healthy males were given oral phosphate binders in combination with low dietary phosphate intake for 2 days followed by 3 days of repletion with inorganic phosphate. FGF-23 levels were determined at multiple time points. RESULTS: FGF-23 serum levels were significantly elevated in CKD with a strong correlation between serum creatinine and FGF-23 concentration. Independent correlations were also seen between FGF-23 and phosphate, calcium, parathyroid hormone (PTH), and 1,25(OH)2D3. No changes in serum FGF-23 levels were observed in volunteers following ingestion of oral phosphate binders/low dietary phosphate intake, which led to a decline in phosphate excretion or during the subsequent repletion with inorganic phosphate through oral phosphate and a normal diet. CONCLUSION: Circulating FGF-23 was significantly elevated in patients with CKD and its concentration correlated with renal creatinine clearance. In healthy volunteers, FGF-23 levels did not change after phosphate deprivation or phosphate loading.

Adult↗
PubMed2003

Reverse epidemiology of cardiovascular risk factors in maintenance dialysis patients.

Conventional risk factors of cardiovascular disease and mortality in the general population such as body mass, serum cholesterol, and blood pressure are also found to relate to outcome in maintenance dialysis patients, but often in an opposite direction. Obesity, hypercholesterolemia, and hypertension appear to be protective features that are associated with a greater survival among dialysis patients. A similar protective role has been described for high serum creatinine and possibly homocysteine levels in end-stage renal disease (ESRD) patients. These findings are in contrast to the well-known association between over-nutrition and poor outcome in the general population. The association between under-nutrition and adverse cardiovascular outcome in dialysis patients, which stands in contrast to that seen in non-ESRD individuals, has been referred to as "reverse epidemiology." Publication bias may have handicapped or delayed additional reports with such paradoxical findings in ESRD patients. The etiology of this inverse association between conventional risk factors and clinical outcome in dialysis patients is not clear. Several possible causes are hypothesized. First, survival bias may play a role since only a small number of patients with chronic kidney disease (CKD) survive long enough to reach ESRD. Hence, the dialysis patients are probably a distinctively selected population out of CKD patients and may not represent the risk factor constellations of their CKD predecessors. Second, the time discrepancy between competitive risk factors may play a role. For example, the survival disadvantages of under-nutrition, which is frequently present in dialysis patients, may have a major impact on mortality in a shorter period of time, and this overwhelms the long-term negative effects of over-nutrition on survival. Third, the presence of the "malnutrition-inflammation complex syndrome" (MICS) in dialysis patients may also explain the existence of reverse epidemiology in dialysis patients. Both protein-energy malnutrition and inflammation or the combination of the two are much more common in dialysis patients than in the general population and many elements of MICS, such as low weight-for-height, hypocholesterolemia, or hypocreatininemia, are known risk factors of poor outcome in dialysis patients. The existence of reverse epidemiology may have a bearing on the management of dialysis patients. It is possible that new standards or goals for such traditional risk factors as body mass, serum cholesterol, and blood pressure should be considered for these individuals.

Cardiovascular Diseases↗
PubMedDate not supplied

Should hemoglobin be normalized in patients with chronic kidney disease?

In the last decade the nephrology community has learned much about the impact of anemia on patients with kidney disease. Therapy of anemia can correct many of the symptoms which seriously compromise patient function. Despite the obvious benefits, controversy continues regarding the optimal target hemoglobin concentration both in patients prior to dialysis and in dialysis populations. In this editorial we review the clinical data that contribute to this controversy and the physiologic concepts underlying the treatment of anemia. Furthermore, we discuss the need to individualize hemoglobin targets for specific patient populations and the importance of early identification and treatment of anemia in patients with kidney disease. The economic impact of normalizing hemoglobin with the use of erythropoietin and intravenous or oral iron has affected clinical practice over the last decade. Current guidelines published by Kidney Disease Outcomes and Quality Initiative (KDOQI), the European Working Group on Anemia Management, and the Canadian Society of Nephrology all recommend target hemoglobin concentrations and thresholds for initiation of therapy and also suggest the need for reevaluation of current targets in light of new evidence. This editorial supports those guidelines and challenges the reader to critically evaluate current practice in the context of the accumulating data and the physiologic principles discussed herein. The therapy of anemia in patients with chronic kidney disease (CKD) is becoming increasingly sophisticated and is an essential component of care in patients with CKD. However, the effects of therapy will be most impressive when accompanied by the optimal care of all hemodynamic and metabolic abnormalities that are associated with CKD.

Anemia↗
PubMedDate not supplied

Utilizing a disease management approach to improve ESRD patient outcomes.

In this era of processes and systems to improve quality, disease management is one methodology to improve care delivery and outcomes for patients with chronic kidney disease (CKD). In most disease management systems a senior renal nurse coordinates all aspects of the patient's care and ensures that the prescribed and necessary care is delivered for both CKD-related and comorbid conditions. The nurse also continually monitors outcomes on quality indicators and key performance measures. These outcome data are then aggregated and analyzed, are compared with local and national benchmarks, and drive the continuous quality improvement (CQI) process. Such a system attempts to centralize the currently fragmented care delivery system, continually improve patient outcomes, and conserve scarce economic resources. Early data suggest a disease management approach may improve both the morbidity and mortality of CKD patients.

Disease Management↗
PubMedDate not supplied

Is chronic kidney disease a cardiovascular disease risk factor?

Cardiovascular disease (CVD) is prevalent in patients with chronic kidney disease (CKD) and may account for 50% of all deaths. The recent Dialysis Outcomes Quality Initiative (DOQI) publication on the evaluation, classification, and stratification of CKD states that a reduced glomerular filtration rate (GFR) identifies individuals at greater risk for CVD and death. This risk is the result of traditional and nontraditional CVD risk factors. However, the relative contribution of these risk factors in the CKD population remains uncertain. Recently interest in kidney disease (reduced GFR) as an independent nontraditional risk factor for CVD has come to the forefront. Studies examining this potential link have included community-based cohort studies, studies in patients with extensive comorbidity, and reports in kidney transplant recipients. Herein, results from these studies are reviewed. The difference between an independent CVD risk factor and a causal CVD risk factor is discussed, with particular emphasis on the temporal association between exposure (GFR) and outcome (CVD and CVD death).

Cardiovascular Diseases↗
PubMed2003

Soluble Fas: a novel marker of inflammation in uremia.

BACKGROUND: Inflammation has been associated with atherosclerotic cardiovascular disease (CVD) and anemia in patients with end-stage renal disease (ESRD). Recent studies have shown that serum levels of soluble Fas (sFas), an antiapoptotic and proinflammatory molecule, are elevated in patients with cardiac disease and patients with ESRD. We therefore sought to investigate serum levels of sFas in uremic patients and its correlation with known markers of inflammation, anemia and CVD. METHODS: The study included 25 ESRD patients (14 on hemodialysis, 11 on CAPD), 27 patients with chronic kidney disease (CKD; creatinine clearance <50 ml/min/1.73 m2), and 14 normal control subjects. We measured serum levels of sFas, C-reactive protein (CRP), and albumin. We also investigated the association of serum sFas levels with the presence of CVD and with erythropoietin (EPO) dosage. RESULTS: Levels of sFas were elevated in CKD and ESRD patients compared to controls. sFas levels correlated negatively with creatinine clearance. In the dialysis patients, we observed that sFas levels were higher among those with CVD. Serum levels of sFas correlated with serum levels of CRP (r=0.31; P=0.03), serum levels of albumin (r=-0.35, P=0.02), and EPO dosage (r=0.51; P=0.009). CONCLUSION: These results suggest that sFas may be a marker of inflammation in CKD and ESRD patients.

Adult↗
PubMed2005

The influence of obesity on the development and survival outcomes of chronic kidney disease.

The prevalence of obesity, defined as a body mass index (BMI) greater than 30 kg/m2 , has more than doubled in many Western countries over the past 2 decades and has become a major public health challenge. This epidemic of obesity in developed countries has been matched closely by alarming increases in the incidence of diabetes mellitus, hypertension, chronic kidney disease (CKD), and cardiovascular disease. However, the exact role that increased body size plays in the development of nephropathy and its subsequent contribution to cardiovascular morbidity and mortality remain unclear. For example, whether obesity per se is a risk factor for CKD independent of diabetes mellitus and hypertension is uncertain. Moreover, in patients with end-stage kidney disease, strong evidence suggests that obesity may paradoxically enhance patient survival. This review will focus on the evidence for obesity as an independent risk factor for the development and progression of CKD and as a paradoxical survival factor in patients with end-stage kidney failure. Possible mechanisms underlying these observed associations will be discussed.

Animals↗
PubMed2006

Diagnosis and management of kidney involvement in Fabry disease.

Interest in the diagnosis and treatment of Fabry disease has been greatly stimulated by the availability of Food and Drug Administration-approved, effective enzyme replacement therapy. This review will update the progress in this area since enzyme replacement therapy has become available. Fabry disease is often associated with proteinuric chronic kidney disease (CKD), and it appears that the treatment paradigms that have proven to be so effective in diabetes mellitus and other forms of proteinuric kidney disease are also effective in conjunction with enzyme replacement therapy for treating the kidney manifestations of Fabry disease. As such, Fabry disease represents an interesting example of progressive proteinuric kidney disease in which the usual blood pressure is lower than in other forms of CKD. This makes the use of effective antiproteinuric therapy challenging, especially considering the autonomic dysfunction that appears to be part of the disease. Comprehensive therapy for Fabry disease includes enzyme replacement therapy and all of the adjunctive therapies that are currently used to treat all forms of proteinuric CKD. It is anticipated that this approach will preserve kidney function and also benefit the cardiac and cerebrovascular systems in patients with Fabry disease.

Diagnosis, Differential↗
PubMed2006

Infections and cardiovascular disease in patients with chronic kidney disease.

Although interest in the nexus of cardiovascular disease and chronic kidney disease (CKD) has mushroomed, especially in the in past 5 years, activity in the arena of CKD-related infection has been much more modest. This development is surprising when one considers the increasing evidence that links inflammation, kidney disease, and cardiovascular disease. Also, major infections, such as pneumonia and septicemia, are paradigmatic inflammatory states, and accumulating evidence indicates that they are a common antecedent of new cardiovascular events in dialysis patients. Major infections are associated with higher rates of cardiovascular events and death in dialysis patients, and similar associations have been observed in community settings. Although recent studies suggest that hospitalization for major infections is much more common in nondialysis CKD than in the general population, the prognostic implications remain unexplored.

Bacterial Infections↗
PubMed2006

Obesity, cardiometabolic syndrome, and chronic kidney disease: the weight of the evidence.

The epidemic of obesity experienced in both industrialized and nonindustrialized countries largely accounts for the increase in the prevalence of the cardiometabolic syndrome (CMS). Obesity and the CMS significantly increase the risk for cardiovascular disease (CVD) and chronic kidney disease (CKD). Multiple abnormalities that can lead to kidney injury have been identified in overweight and obese people, including insulin resistance, compensatory hyperinsulinemia, inappropriate activation of the renin-angiotensin-aldosterone system and increased oxidative stress, endoplasmic reticulum stress, coagulability, and impaired fibrinolysis. The combined effects of these conditions induce in the kidneys impaired pressure natriuresis, glomerular hypertension, endothelial dysfunction, and vasoconstriction, as well as matrix proliferation and expansion. Among the consequences are microalbuminuria, now known to be a surrogate of diffuse endothelial dysfunction as well as a predictor of CVD, and CKD. Diet and regular physical activity are the cornerstones of weight management, and they add to currently available pharmacologic agents and bariatric surgery. The understanding of the pathophysiology of obesity/CMS helps to explain the benefits of agents that improve insulin sensitivity, control inflammation, and block the renin-angiotensin-aldosterone system. The increasing prevalence of obesity and CMS contribute to the growing frequency of CKD and demands the development of multifactorial strategies directed at identifying people at risk, as well as preventing excessive weight gain and its deleterious consequences.

Albuminuria↗
PubMed2004

Early renal insufficiency and late venous thromboembolism after renal transplantation in the United States.

BACKGROUND: Pulmonary embolism (PE) is the most common preventable cause of death in hospitalized patients. Patients with severe chronic kidney disease (CKD) may be at increased risk for PE in comparison to the general population. Whether severe CKD is associated with increased risk for late venous thromboembolism (VTE) in a population of renal transplant recipients has not been determined. METHODS: Using the US Renal Data System database, we studied 28,924 patients receiving a kidney transplant from January 1, 1996, to July 31, 2000, with Medicare as primary payer, followed up until December 31, 2000. Cox proportional hazards regression models were used to calculate the association of transplant recipient estimated glomerular filtration rate (eGFR; by the Modification of Diet in Renal Disease formula) less than 30 mL/min/1.73 m2 (versus >30 mL/min/1.73 m2) 1 year after renal transplantation with Medicare claims for VTE (either deep-venous thrombosis or PE/infarction) 1.5 to 3 years after renal transplantation. RESULTS: The rate of VTE occurring 1.5 to 3 years after transplantation was 2.9 episodes/1,000 person-years. eGFR less than 30 mL/min/1.73 m2 versus higher at the end of the first year after renal transplantation was associated with significantly increased risk for later VTE (adjusted hazard ratio, 2.05; 95% confidence interval, 1.08 to 3.89). CONCLUSION: Patients with severe CKD after renal transplantation should be regarded as high risk for late VTE, which is a potentially preventable cause of death in this population.

Glomerular Filtration Rate↗
PubMed2004

Prevention of radiocontrast nephropathy with N-acetylcysteine in patients with chronic kidney disease: a meta-analysis of randomized, controlled trials.

BACKGROUND: Radiocontrast nephropathy (RCN) is a common cause of hospital-acquired acute renal failure. Results of several studies using N-acetylcysteine (NAC) for the prevention of RCN have yielded conflicting results. We performed a meta-analysis of group data extracted from previously published studies to assess the effect of NAC on the prevention of RCN in patients with pre-existing chronic kidney disease (CKD). METHODS: Ovid's multidatabase search for MEDLINE, Cochrane Central Registry of Controlled Trials, Cochrane Database of Systematic Reviews, and HealthSTAR were used to identify candidate articles. Abstracts from proceedings of scientific meetings also were screened. We selected blinded and unblinded randomized controlled trials (RCTs) performed in humans 18 years and older with pre-existing CKD, defined by a mean baseline serum creatinine level of 1.2 mg/dL or greater (> or =106.1 micromol/L) or creatinine clearance less than 70 mL/min (<1.17 mL/s). The overall risk ratio (RR) for the development of RCN was computed using a random-effects model. RESULTS: Eight RCTs (n = 885 patients) published in full-text articles were included in the primary analysis. In the control group, the overall rate of RCN was 18.5% (95% confidence interval [CI], 15 to 22). In the primary analysis, overall RR for RCN associated with the use of NAC was 0.41 (95% CI, 0.22 to 0.79; P = 0.007). In a sensitivity analysis that included 4 additional RCTs published in abstract form, RR remained significant at 0.55 (95% CI, 0.34 to 0.91; P = 0.020). CONCLUSION: NAC reduces the risk for RCN in patients with CKD.

Acetylcysteine↗
PubMed2004

Doxercalciferol safely suppresses PTH levels in patients with secondary hyperparathyroidism associated with chronic kidney disease stages 3 and 4.

BACKGROUND: Calcitriol lowers parathyroid hormone (PTH) levels in patients with chronic kidney disease (CKD) stages 3 and 4, but its use is limited by a low therapeutic index and concerns regarding hypercalcemia and acceleration of kidney disease. We evaluated doxercalciferol (1alpha-hydroxyvitamin D2) as an alternative therapy in a randomized, double-blinded, placebo-controlled, multicenter trial. METHODS: Fifty-five adults with stage 3 or 4 CKD and an intact PTH (iPTH) level greater than 85 pg/mL (ng/L) completed 8 baseline weeks, followed by 24 weeks of oral therapy with doxercalciferol or placebo. Pretreatment demographics and biochemical features did not differ between groups. Dosages were increased gradually if iPTH level was not decreased by 30% or greater and serum calcium and phosphorus levels were stable. Regular monitoring included plasma iPTH, serum calcium and phosphorus, urinary calcium, bone-specific serum markers, and serum lalpha,25-dihydroxyvitamin D levels. Glomerular filtration rate (GFR) was measured before and after treatment. RESULTS: Mean plasma iPTH level decreased by 46% from baseline after 24 weeks of doxercalciferol treatment (P <0.001), but was unchanged with placebo. After 6 weeks, iPTH level reductions with doxercalciferol treatment exceeded those with placebo at all subsequent intervals (P <0.001). No clinically significant differences in mean serum calcium or phosphorus or urinary calcium levels or incidence of hypercalcemia, hyperphosphatemia, or hypercalciuria were noted between groups. Serum C- and N-telopeptide and bone-specific alkaline phosphatase levels decreased with doxercalciferol treatment relative to both baseline and placebo (P <0.01). Adverse-event rates and changes in GFR did not differ between groups. CONCLUSION: Doxercalciferol is safe and effective in controlling secondary hyperparathyroidism of patients with CKD stages 3 and 4.

Aged↗
PubMed2004

High-protein diets: potential effects on the kidney in renal health and disease.

High-protein (HP) weight-loss diets have existed in the United States for decades, although their popularity has recently surged as obesity has become more common. Despite their widespread use, valid concerns exist that HP diets may induce clinically important alterations in renal function and health. HP consumption has been found, under various conditions, to lead to glomerular hyperfiltration and hyperemia; acceleration of chronic kidney disease (CKD); increased proteinuria; diuresis, natriuresis, and kaliuresis with associated blood pressure changes; increased risk for nephrolithiasis; and various metabolic alterations. Unfortunately, a comprehensive understanding of the implications of HP diets is limited by the lack of a universally accepted definition for HP intake, a paucity of rigorous long-term human interventional studies that necessitate relying on short-term or fairly circumstantial evidence, and sparse data on the effects of HP consumption in obese individuals. In addition, matters are further complicated because the renal impact HP diets for limited periods is most likely different than that for more chronic consumption. Nevertheless, although there are no clear renal-related contraindications to HP diets in individuals with healthy kidney function, the theoretical risks should be reviewed carefully with the patient. In contrast, HP diets have the potential for significant harm in individuals with CKD and should be avoided if possible. Because CKD is often a silent disease, all individuals should undergo a screening serum creatinine measurement and urinary dipstick test for proteinuria before the initiation of such a diet.

Animals↗