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PubMed2005

Estimating kidney function in adults using formulae.

With increasing emphasis on the earlier detection and management of chronic kidney disease (CKD), estimation of the glomerular filtration rate (GFR) has assumed greater importance. It is accepted that use of serum creatinine concentration alone as a marker of kidney function is inadequate; in particular, it has a poor sensitivity for detecting CKD. International recommendations favour the reporting of creatinine-based estimates of GFR using formulae which also take into account age, gender and other variables that affect the relationship between serum creatinine and GFR: in particular, the four-variable formula derived from the Modification of Diet in Renal Disease study (4-v MDRD) is increasingly being used. We have reviewed the literature supporting the use of this formula compared with the well-established Cockcroft and Gault formula. Overall, evidence supports the use of the 4-v MDRD formula as an improved estimate of GFR in people with moderate/advanced CKD. Neither formula performs well in people with normal and mildly reduced kidney function. However, there remain significant problems with this approach and areas where further research is required. In particular, the widespread adoption of estimated GFR reporting has refocused attention on the limitations of creatinine measurement and highlighted clinical situations in which the formulae are inadequate.

Adult↗

PubMed2005

Aminoglycosides in intermittent hemodialysis: pharmacokinetics with individual dosing.

BACKGROUND: Data are limited on aminoglycoside pharmacokinetic differences between acute renal failure (ARF) and chronic kidney disease (CKD) or infection survival when maintaining peak and pre-hemodialysis serum concentrations between 7 and 10 and 3.5 and 5 mg/L, respectively. OBJECTIVE: To report aminoglycoside pharmacokinetic observations in a consecutive series of patients receiving intermittent hemodialysis (IHD), including treatment impact of patient-specific dosing regimens. METHODS: In this prospective study, all calculated pharmacokinetic parameters used concentrations drawn more than 12 hours after the initial dose and peak concentrations at least 2 hours after the dose. Analysis included pharmacokinetic parameters in stage 5 CKD, ARF, impact of the dialysis prescription, and treatment results of individualized dosing regimens lasting more than 4 days. RESULTS: Consecutive patients with IHD (N = 167) receiving 216 courses of aminoglycosides were evaluated. The mean +/- SD volume of distribution was 0.39 +/- 0.15 L/kg ideal body weight, and elimination half-life during dialysis was 4.2 +/- 2.3 hours. The elimination half-life off IHD was 30% shorter in ARF (31.9 +/- 20.8 h) versus 45.7 +/- 24.2 hours in CKD (p < 0.001). Mean extrapolated peak concentrations and pre-IHD levels were 7.7 +/- 1.6 and 3.9 +/- 1.2 mg/L, respectively. A 91% treatment success rate was observed in 117 individualized treatment courses in 100 patients receiving greater than or equal to 5 days of aminoglycoside therapy. CONCLUSIONS: A large variability in aminoglycoside pharmacokinetic parameters in IHD exists, with aminoglycoside elimination off IHD significantly faster in ARF. Individualized regimens using serum concentrations drawn in patients requiring treatment (non-synergistic) targeting peak concentrations of 7-10 mg/L and pre-hemodialysis serum concentrations of 3.5-5 mg/L appears successful for eradicating infections.

Acute Kidney Injury↗

PubMed2006

Lanthanum carbonate.

OBJECTIVE: To review the pharmacology, pharmacokinetics, clinical efficacy, and safety profile of lanthanum carbonate, a phosphate binder for chronic kidney disease (CKD). DATA SOURCES: Information was selected from PubMed (1965-October 2005). All studies presented as scientific posters and abstracts from nephrology meetings from 1999 to 2005 were also included. STUDY SELECTION AND DATA EXTRACTION: All published articles regarding lanthanum carbonate were included. In addition, abstracts and presentations from scientific meeting symposia were also considered for inclusion. DATA SYNTHESIS: Lanthanum carbonate has been recently approved as non-calcium-based therapy for phosphate reduction in patients with stage 5 CKD requiring dialysis. The recommended dose is 250-500 mg with meals, for a maximum of 1500 mg daily. Clinical studies have shown short- and long-term safety with lanthanum carbonate administration. Adverse effects were primarily gastrointestinal in nature. Clinical trials have also shown reductions in serum phosphorus to target concentrations, reductions in associated calcium-phosphorus product, and minimal effects on serum calcium and parathyroid hormone concentrations. CONCLUSIONS: Lanthanum carbonate is an effective phosphate-binding agent without significant risk of hypercalcemia or worsening metabolic acidosis. Lanthanum carbonate is a safe and effective drug for reduction of elevated serum phosphorus levels associated with stage 5 CKD. The role of lanthanum carbonate relative to other phosphate-binding drugs, such as calcium salts and sevelamer, remains to be determined.

Animals↗

PubMed2006

25-Hydroxyvitamin D deficiency and diabetes predict reduced BMD in patients with chronic kidney disease.

UNLABELLED: In this study of 242 patients with renal failure, women, patients with diabetes, and patients on peritoneal dialysis had the highest risk of 25-hydroxyvitamin D deficiency. Levels correlated positively to BMD Z scores, and hip BMD was inversely related to prevalent fracture. Increasing 25-hydroxyvitamin D levels may benefit these patients. INTRODUCTION: 25-Hydroxyvitamin D deficiency (<37 nM) is common in patients with chronic kidney disease (CKD) stage 5 (glomerular filtration rate < 15 ml/min/1.73 m(2) or on dialysis), but it is unclear if this deficiency is associated with bone disease and if supplementation is warranted. MATERIALS AND METHODS: Blood samples were collected on 242 patients with CKD stage 5 caused by type 1 diabetes (33%), type 2 diabetes (2%), and other causes (65%), who were about to undergo kidney or kidney pancreas transplantation. Prevalent spinal fracture was assessed by X-ray and BMD by DXA. RESULTS: 25-Hydroxyvitamin D deficiency was present in 28% of patients with diabetes versus 12% without (p < 0.0001). Patients on peritoneal dialysis (PD) had lower levels of 25-hydroxyvitamin D than patients on hemodialysis (HD; 49 +/- 26 versus 77 +/- 34 nM; p < 0.0001), and women had lower levels than men (51 +/- 25 versus 77 +/- 35 pM; p < 0.0001). BMD Z scores were within 1 SD of the mean at all sites, except in patients with diabetes (femoral neck Z score, -1.07 +/- 1.2; p < 0.0001) and patients who had undergone parathyroidectomy (lumbar spine Z score, 1.03 +/- 1.34, femoral neck Z score, 1.24 +/- 1.35; p < 0.001 and p < 0.0001, respectively). In multiple stepwise linear regression analysis, levels of 25-hydroxyvitamin D correlated positively and intact PTH (iPTH) correlated negatively to Z scores at the lumbar spine and wrist. Time on dialysis correlated positively to Z scores at the femoral neck and lumbar spine. Diabetes and serum alkaline phosphatase levels correlated negatively with Z scores at the femoral neck. Lower femoral neck BMD was associated with an increased prevalence of vertebral fracture and fragility fracture at any site (p = 0.03 and p < 0.03, respectively). CONCLUSIONS: This study of patients with CKD stage 5 identifies women, patients with diabetes, and patients on PD as being at particular risk of 25-hydroxyvitamin D deficiency. We describe positive associations of 25-hydroxyvitamin D levels and BMD Z scores and an association between femoral neck BMD and fragility fracture at any site. Treatment to improve 25-hydroxyvitamin D levels may benefit these patients.

Adult↗

PubMed2006

B-type natriuretic peptide (BNP) and N-terminal pro-BNP in obese patients without heart failure: relationship to body mass index and gastric bypass surgery.

BACKGROUND: Further investigations are warranted to better characterize variables that may confound the clinical interpretation of plasma natriuretic peptide measurements, which are increasingly recognized to have diagnostic and predictive importance. METHODS: Blood samples (EDTA plasma) from patients (n = 206) attending clinics for the medical treatment and follow-up of obesity were analyzed for B-type natriuretic peptide (BNP; Bayer assay) and the N-terminal segment of its prohormone (NT-proBNP; Roche assay). Natriuretic peptide concentration ranges were evaluated in those without diagnosis of congestive heart failure (CHF) or chronic kidney disease (CKD). RESULTS: BNP and NT-proBNP were directly correlated (r = 0.87; P = 0.01), with NT-proBNP concentrations higher relative to BNP. Of obese patients without CHF or CKD, 21.6% (40 of 185) had NT-proBNP concentrations greater than the published assay upper reference limit. Concentrations of both natriuretic peptides were higher in patients currently exposed to beta blockers, patients with the diagnosis of hypertension or type 2 diabetes, and patients with a history of gastric bypass surgery. An inverse relationship between body mass index (BMI) and both BNP and NT-proBNP was evident. According to the National Institutes of Health, National Heart, Lung, and Blood Institute classification, more than 95% of the participants sampled in this study were either obesity class 2 (35 kg/m(2) < BMI < 39.9 kg/m(2)) or class 3 (BMI >or=40 kg/m(2)) CONCLUSIONS: A substantial proportion of obese patients without CHF or CKD have concentrations greater than the upper reference limit for NT-proBNP but not for simultaneously measured BNP. A history of gastric bypass surgery appeared to be a significant predictor of increased natriuretic peptide concentrations when assessed in a population of patients with class 2 or 3 obesity.

Adult↗

PubMed2002

Darbepoetin alfa: a new therapy for the management of anaemia associated with chronic kidney disease.

Darbepoetin alfa (Aranesp, Amgen, Inc., Thousand Oaks, California) is a new erythropoietic protein that corrects anaemia associated with chronic kidney disease (CKD) in the majority of patients. Darbepoetin alfa contains five N-linked carbohydrate chains compared with three in recombinant human erythropoietin (rHuEPO). The two additional sialic acid-containing carbohydrate chains prolong the serum half-life of darbepoetin alfa, resulting in greater biological activity and a reduced dosing frequency compared with rHuEPO. Clinical studies in patients with CKD have demonstrated that darbepoetin alfa is effective in correcting anaemia in rHuEPO-naive patients and in patients who have been converted from rHuEPO therapy. Darbepoetin alfa provides long-term maintenance of haemoglobin levels when administered once weekly or once every other week, with the possibility of once-monthly dosing in some patients. Darbepoetin alfa is well tolerated and has a safety profile similar to that of rHuEPO. Owing to its half-life being three times longer than rHuEPO, darbepoetin alfa can be administered at an extended dosing interval, without compromising efficacy. Lessfrequent dosing has potential benefits for both patients with CKD and healthcare providers. These benefits include reduced visits to the clinic, fewer injections and a reduced demand on staff and treatment facilities.

Anemia↗

PubMed2002

Darbepoetin alfa, a new therapy for the management of anemia of chronic kidney disease.

Anemia of chronic kidney disease (CKD) results primarily from a deficiency of the hormone erythropoietin. Treatment of anemia in the early stages of CKD is essential to reduce the risk of developing anemia-associated complications and to improve health-related quality of life. Treatment with recombinant human erythropoietin (r-HuEPO, epoetin alfa) can correct erythropoietin deficiency and increase red blood cell production, but the short half-life of r-HuEPO necessitates frequent injections. Reducing the frequency of administration has potential benefits for both patients and health care providers. Darbepoetin alfa is a new erythropoietic protein with greater biologic activity and a longer dosing interval than those of r-HuEPO. It has been shown to be effective when administered once/week and once every 2, 3, or 4 weeks, and is well tolerated. With the ability to simplify anemia management by allowing less frequent dosing, darbepoetin alfa offers an effective alternative to r-HuEPO for the treatment of anemia of CKD.

Anemia↗

PubMed2025

Alterations in DNA Methylation, Proteomic, and Metabolomic Profiles in African Ancestry Populations with APOL1 Risk Alleles.

KEY POINTS: We aimed to elucidate potential methylation, proteomic, and metabolomic mechanisms by which APOL1 variants may be linked to kidney disease. We report distinct methylation profiling between APOL1 risk allele carriers and noncarriers, many near APOL gene family. We report higher APOL1 protein and lower C18:1 cholesteryl ester in two risk allele carriers. BACKGROUND: The APOL1 high-risk haplotype has been associated with CKD and the deterioration of kidney function, particularly in populations with West African ancestry. However, the mechanisms by which APOL1 risk variants increase the risk for kidney disease and its progression have not been fully elucidated. METHODS: We compared methylation (N=3191; 715 [22%] carriers), proteomic (N=1240; 169 [14%] carriers), and metabolomic (N=6309; 674 [11%] carriers) profiles in African and Hispanic/Latino carriers of two APOL1 high-risk alleles (G1/G1, G2/G2, G1/G2) and noncarriers (G0/G0), excluding heterozygotes (G0/G1, G0/G2), from the Population Architecture using Genomics and Epidemiology Consortium and UK Biobank. In each study, the associations between the APOL1 high-risk haplotype and up to 722,719 cytosine-phosphate-guanine (CpG) sites, 2923 proteins, or 836 metabolites were estimated using covariate-adjusted linear regression models, followed by fixed-effects sample size–weighted meta-analyses. RESULTS: Significant associations were observed between APOL1 high-risk haplotype and methylation at 52 CpG sites, with 48 located on chromosome 22 and 18 in the vicinity of APOL1–4 and MYH9. All significant CpG sites near APOL2 were hypomethylated, whereas those near APOL3 and APOL4 were hypermethylated. APOL1-associated CpG sites were also identified in genes involved in ion transport and mitochondrial stress pathways. Sensitivity analyses indicated consistent yet attenuated effects among heterozygotes, supporting an additive effect of APOL1 risk alleles. Further analyses of the 52 CpG sites identified two near APOL4 exhibiting G1-specific effects, eight associated with CKD but none with eGFR, and three showing heterogeneity by CKD status. In addition, carrying two APOL1 risk alleles was associated with higher plasma APOL1 protein (β=1.12, PFDR = 2.26e-70) and lower C18:1 cholesteryl ester metabolite (Z=−4.50, PFDR = 4.83e-3). CONCLUSIONS: Our results demonstrate differential methylation, proteomic, and metabolomic profiles associated with APOL1 high-risk haplotypes.

APOL1↗

PubMed2005

Primed peripheral polymorphonuclear leukocyte: a culprit underlying chronic low-grade inflammation and systemic oxidative stress in chronic kidney disease.

This study characterizes the causal relationship between peripheral polymorphonuclear leukocyte (PMNL) priming, systemic oxidative stress (OS), and inflammation in patients with varying degrees of renal insufficiency (chronic kidney disease [CKD] not on renal replacement therapy [RRT]: continuous ambulatory peritoneal dialysis or hemodialysis [HD]) and healthy control subjects. Rate of superoxide release was measured after stimulation of PMNL with phorbol 12-myristate 13-acetate or zymosan. Priming was estimated by the rate of superoxide release after phorbol 12-myristate 13-acetate stimulation. Systemic OS was related to PMNL priming and intracellular myeloperoxidase activity. Inflammation was linked to peripheral white blood cells and PMNL counts, PMNL apoptosis, and PMNL ex vivo survival in autologous and heterologous sera. PMNL priming and counts were related to the severity of renal failure in CKD not on RRT. Compared with control subjects, PMNL from all CKD patients showed increased priming, highest in HD, with a significant decrease in their response to zymosan. PMNL myeloperoxidase activity and apoptosis were increased in all renal failure patients. Decreased ex vivo cell survival and elevated leukocyte counts were found in all patients, highest in HD. Both PMNL priming and counts correlated negatively with the GFR. A positive significant correlation was shown between PMNL counts and their priming in all groups, suggesting that the increased PMNL count in peripheral blood is an adaptive response to PMNL priming. Hence, PMNL priming is a key mediator of low-grade inflammation and OS associated with renal failure, occurring before the onset of RRT and further augmented in chronic HD.

Adult↗

PubMed2005

Calcium channel blockers and renal protection: insights from the latest clinical trials.

Calcium channel blockers have been widely used in clinical practice because of their antihypertensive capacity. Prevention of renal damage is a very important aim of antihypertensive therapy. This is particularly so taking into account the high prevalence of chronic kidney disease (CKD) in the general population. Recent data have shown that CKD is related to the absence of adequate BP control and also to the clustering of other cardiovascular risk factors seen in the metabolic syndrome. The knowledge of the capacities of the different antihypertensive drugs or their combinations to simultaneously control BP while protecting the kidney and avoiding the facilitation of metabolic alterations is warranted. Recent data from the Intervention as a Goal in Hypertension Treatment trial, Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, and African American Study of Kidney Disease and Hypertension (AASK) allow the conclusion that in hypertensive patients with preserved renal function or with CKD, calcium channel blockers are effective antihypertensive drugs to be considered alone or in combination with an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.

Calcium Channel Blockers↗

PubMed2005

Control of hyperphosphatemia among patients with ESRD.

Derangements of mineral metabolism occur during the early stages of chronic kidney disease (CKD). Hyperphosphatemia develops in the majority of patients with ESRD and has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy. More recent observational data have associated hyperphosphatemia with increased cardiovascular mortality among dialysis patients. Adequate control of serum phosphorus remains a cornerstone in the clinical management of patients with CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduce the risk for vascular calcification and cardiovascular mortality. These measures include dietary phosphorus restriction, dialysis, and oral phosphate binders. Dietary restriction is limited in advanced stages of CKD. Phosphate binders are necessary to limit dietary absorption of phosphorus. Aluminum hydroxide is an efficient binder; however, its use has been nearly eliminated because of concerns of toxicity. Calcium salts are inexpensive and have been used effectively worldwide as an alternative to aluminum. Concerns of calcium overload have led to the investigation of alternatives. Currently, only two Food and Drug Administration-approved noncalcium, nonaluminum binders are available. Sevelamer hydrochloride is an exchange resin and was not as effective as calcium acetate in meeting new guideline recommendations in one double-blind clinical trial. Lanthanum carbonate is a rare earth element and has been studied less extensively. Concerns of long-term administration and toxicity exist. Furthermore, these agents are significantly more expensive than calcium salts, which may contribute to patient noncompliance.

Humans↗

PubMed2005

Reducing the burden of cardiovascular calcification in patients with chronic kidney disease.

Patients with chronic kidney disease (CKD) have a higher burden of atherosclerotic coronary artery disease compared with age- and gender-matched individuals with normal renal function. Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalent in these patients and is associated with serious clinical consequences. The pathogenesis of CVC is complex and includes factors that promote calcification and others that inhibit calcification. Thus, multiple therapeutic interventions should be used simultaneously to reduce the burden of calcification in patients with CKD. Thus far, interventional attempts have focused on curtailing the effects of factors that promote calcification such as management of known traditional factors for atherosclerotic coronary artery disease and on adopting specific approaches to normalize mineral metabolism, deliver adequate dialysis, and control serum cholesterol level. By contrast, interventions that may bolster the effects of inhibitors of calcification have not yet been studied well but are beginning to attract attention. Ideally, the goal of interventions is not only to slow or halt progression of calcification but also to reverse pre-existing calcification. Whether this goal is achievable is not currently known. This review examines the potential of various therapeutic interventions in reducing the CVC burden in patients with CKD. Moreover, the review is intended to stimulate more research in this area because the efficacy of these interventions has not been examined in controlled clinical trials.

Calcinosis↗

PubMed2006

Update on erythropoietin treatment: should hemoglobin be normalized in patients with chronic kidney disease?

The partial correction of ESRD anemia by recombinant human erythropoietin (EPO) has resulted both in generalized improvement in quality of life and physical activity and in reduced mortality and hospitalization rate. The question remains as to whether normalizing hemoglobin (Hgb) is desirable in patients with chronic kidney disease (CKD). This review provides an analysis and commentary on the available reports and, for the most part, randomized, controlled trials on the topic. In dialysis patients, normalization of Hgb is associated with improved quality of life and exercise capacity but not with reduced mortality and hospitalization rate. Moreover, no significant changes in the degree of left ventricular hypertrophy have been demonstrated. By contrast, an increased mortality rate has been reported for hemodialysis patients with overt cardiovascular disease (CVD) when randomly assigned to normal hematocrit by EPO. Data regarding patients who have CKD but are not yet on renal replacement therapy are scarce, and the effects of EPO on renal disease progression require further elucidation through controlled trials. The conclusion that can be drawn from the available studies is that Hgb >11 g/dl is the minimum required to achieve improved quality of life in patients with CKD, whereas values >12 g/dl are not recommended for patients with overt CVD. Finally, Hgb normalization might reasonably be restricted to a selected population of younger, employed, and active individuals, provided that they do not have CVD.

Chronic Disease↗

PubMed2006

Renal manifestations in the metabolic syndrome.

The metabolic syndrome, which is characterized by obesity, serum lipid profile alterations, hypertension, and fasting hyperglycemia, is very common in developed countries, and its prevalence is likely to increase. Chronic kidney disease (CKD) also has become a significant public health problem because it affects a considerable proportion of the adult population and is a major risk factor for cardiovascular disease and premature death. Although it is widely known that the metabolic syndrome is a major risk factor for the development of type 2 diabetes and cardiovascular disease, its precise relationship with the risk for renal impairment only recently has been clarified: Patients with the metabolic syndrome are at significantly higher risk for microalbuminuria and/or CKD, and the level of risk is related to the number of components of the syndrome itself. Although it is difficult to discriminate the detrimental renal effects of the metabolic syndrome from those of hypertension and impaired glucose metabolism, its other aspects (particularly obesity) may favor independently the development of renal abnormalities and may be considered new modifiable risk factors for CKD. These observations provide a rationale for intervention studies that aim to verify whether treating the many components of the metabolic syndrome can effectively prevent the development and progression of renal damage.

Albuminuria↗

PubMed2006

Inverse association between lipid levels and mortality in men with chronic kidney disease who are not yet on dialysis: effects of case mix and the malnutrition-inflammation-cachexia syndrome.

High total cholesterol is associated with lower mortality in dialysis patients, but the relationship between lipid levels and mortality in patients who have chronic kidney disease (CKD) and are not yet on dialysis is poorly described. This study examined the association between lipid levels and all-cause and cardiovascular mortality in 986 male patients (age 67.4 +/- 10.9 yr; race 23.7% black) who had CKD and were not yet on dialysis. Associations were determined in fixed-covariate and time-dependent Cox models, before and after adjustment for components of case mix and surrogates for malnutrition-inflammation-cachexia syndrome (MICS). Lower total cholesterol quartiles were associated with higher all-cause mortality in a fixed-covariate model that was adjusted for age, race, and body mass index (hazard ratio [95% confidence interval] for cholesterol <153, 153 to 182, and 183 to 215 versus >215 mg/dl: 1.91 [1.35 to 2.69], 1.36 [0.96 to 1.92], 1.10 [0.78 to 1.57]; P < 0.001 for trend), but this association was attenuated after adjustment for case mix (P = 0.023 for trend) and abolished after additional adjustment for MICS (P = 0.14 for trend), with time-dependent Cox models showing similar results. Similar tendencies also were detected in the association between levels of LDL cholesterol with total and cardiovascular mortality and triglycerides with all-cause mortality in both fixed-covariate and time-dependent analyses. Lower lipid levels are associated with higher mortality in patients who have moderate and advanced CKD and are not yet on dialysis. This inverse association is explained in part by case-mix characteristics and the presence of surrogates for MICS.

Aged↗

PubMed2006

Lipid changes and statins in chronic renal insufficiency.

It has been known for a long time that chronic kidney disease (CKD) is associated with dyslipidemia, but the full extent of abnormalities has been appreciated only recently, because routine laboratory tests fail to disclose the entire spectrum of lipid abnormalities. Lipids, particularly HDL cholesterol, are predictive of cardiovascular events, but a paradoxic inverse relation between cholesterol concentration and cardiovascular death has been noted in uremic patients. This currently is thought to be explained by the confounding effect of microinflammation and possibly calcification, but this is not definitely proved. Several retrospective analyses that included patients with mild or moderate CKD documented benefit from lowering of cholesterol by statins. In contrast, the Die Deutsche Diabetes Dialyse (4D) study and a small Scandinavian study failed to show a benefit from lowering of cholesterol by statins in ESRD. Pathomechanistically, it is possible that nonclassical pathomechanisms override statin-sensitive mechanisms as also suggested by the observation that statins fail to reduce carotid intima-media thickening. Although, experimentally, exposure to lipids (particularly oxidized lipids) aggravates progression, data on the effect of statins on progression in patients with CKD are not definite. The most likely explanation is that the impact of numerous confounders obscures their effect on progression. The increase in urinary protein excretion of patients who are treated with statins had been a cause of concern, but the underlying mechanism (i.e. interference with proximal tubular reabsorption of protein) meanwhile has been well documented.

Atherosclerosis↗

PubMed2006

Vascular calcifications: pathogenesis, management, and impact on clinical outcomes.

The predisposition to vascular calcifications in patients with chronic kidney disease (CKD) has gained great interest in recent years as many studies have described its likely impact on morbidity and mortality. The mechanism by which the process of vascular calcification is produced is complex, and it does not consist in a simple precipitation of calcium and phosphate but is instead an active and modifiable process. Several "modifiable and nonmodifiable" factors that are able to promote vascular calcification are extremely frequent in patients with CKD. Most of the present strategies to decrease vascular calcifications are based in the control of the more prevalent modifiable risk factors. Unfortunately, the extremely important nonmodifiable risk factors, which are highly prevalent, such as older age, time on dialysis, and diabetes, are not under one's control. Recent studies also have shown that vascular calcifications in some localizations were associated with increased osteoporotic fractures not only in dialysis patients but also in the general population, and interestingly, mortality also was associated significantly and positively with vascular calcifications and nontraumatic bone fractures. Despite that new strategies may improve the management of vascular diseases and specifically have a positive impact on the high prevalence of vascular calcifications, still the best possible control of the bone metabolic and inflammatory parameters are in the primary line. The horizon of the coming decade looks promising, but solid clinical and epidemiologic data are needed to manage better the bone- and cardiovascular-related disorders in patients with CKD.

Bone Density↗

PubMedDate not supplied

Tolerability and efficacy of benazepril in cats with chronic kidney disease.

The objective of the study was to test the effect of the angiotensin-converting enzyme inhibitor (ACEI) benazepril in cats with chronic kidney disease (CKD). A total of 192 cats with CKD with an initial plasma creatinine concentration > or = 2 mg/dL (> or = 177 micromol/L) and urine specific gravity < or = 1.025 were recruited into a double-blind, parallel-group, prospective, randomized clinical trial. Cats received daily (q24h) PO placebo (n = 96) or benazepril x HCl at a dosage of 0.5-1.0 mg/kg (n = 96) for up to 1,119 days. Most cats were fed exclusively a diet containing low amounts of phosphate, protein, and sodium. Benazepril produced a significant reduction in proteinuria, assessed by the urine protein-to-creatinine ratio (UPC, P = .005). This effect of benazepril was present in all subgroups tested, including cats with UPC <0.2, although the effect was largest in cats with higher UPCs. Plasma protein was maintained at higher concentrations with benazepril as compared with placebo during treatment in cats with initial UPC <1 (P = .038 versus P = .079 for all cats). There was no difference in renal survival time between the 2 groups when all 192 cats were compared. Mean +/- SD renal survival times were 637 +/- 480 days with benazepril and 520 +/- 323 days with placebo (P = .47). Mean +/- SD renal survival times in the 13 cats with initial UPC > or = 1 were 402 +/- 202 days with benazepril and 149 +/- 90 days with placebo (P = .27). Cats with initial UPC > or = 1 treated with benazepril had better appetite (P = .017) as compared with those treated with placebo. Benazepril was well tolerated. In conclusion, benazepril decreased proteinuria in cats with CKD.

Angiotensin-Converting Enzyme Inhibitors↗