Progression of renal failure in patients with renal disease of diverse etiology on protein-restricted diet

The rate of progression of early renal failure was evaluated in three groups of adult patients with renal disease of diverse etiology on dietary protein and phosphorus restriction (about 0.6 g/kg of protein, 700 mg of phosphorus) and in a control group of 22 patients with the same renal disease, retrospectively studied, on a free diet. Group 1 had 33 patients with chronic glomerulonephritis (CG), initial serum creatinine (Scr) of 1.4 to 4.3 mg/dl (mean, 2.20), followed for 5 to 94 months (mean, 44). Group 2 had 17 patients with polycystic kidney disease (PKD), Scr 1.3 to 4.7 mg/dl (mean, 2.40), followed for 8 to 81 months (mean, 42). Group 3 had 28 patients with primary chronic pyelonephritis (CP), Scr of 1.5 to 4.5 mg/dl (mean, 2.57), followed for 9 to 92 months (mean, 41). The control group had 22 patients (11 with CG, five with PKD, and six with CP), with Scr 1.7 to 4.1 mg/dl, followed for 6 to 72 months (mean, 24). In the regression analysis between reciprocal creatinine and time, the slopes were -0.0017, -0.0025, and -0.00016 dl/mg/month in the three patient groups on a protein-restricted diet, respectively. The difference between both groups 1 and 2 and group 3 was statistically significant (P less than 0.05). The slopes in patients on a free diet were significantly greater than those found in patients on a protein-restricted diet. The actuarial survival probability at 72 months, assuming as "renal death" a Scr of 10 mg/dl, was 45% in patients with CG, 44% in those with PKD, and 67% in those with CP on a protein-restricted diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of protein-reduced diet on plasma lipids, apolipoproteins and lipolytic activities in patients with chronic renal failure

The effect of treatment with protein-reduced diet on plasma lipids, apolipoproteins and lipolytic activities was studied in 15 patients with chronic renal failure. Mean treatment time was 7.4 months. Before treatment serum triglycerides were elevated as were the levels of apolipoprotein C-I and especially C-III. Postheparin plasma lipolytic activities were reduced. The treatment was effective in reducing the serum urea levels but had no significant influence on either plasma lipids, apolipoprotein levels or lipolytic activities. The abnormalities of lipid transport in chronic renal failure thus seem to be more dependent on loss of renal function than the degree of uremic intoxication.     

Advanced atherosclerosis in predialysis patients with chronic renal failure

BACKGROUND: Atherosclerosis is advanced in hemodialysis patients as shown by increased intima-media thickness of carotid arteries (CA-IMT), although it is not established whether the advanced atherosclerosis results from hemodialysis treatment or from chronic renal failure. The purpose of this study was to evaluate the effects of hemodialysis and renal failure on CA-IMT in patients with chronic renal failure. METHODS: CA-IMT was measured by high-resolution B-mode ultrasonography in 110 patients with chronic renal failure before starting dialysis (CRF group), and compared with CA-IMT of 345 hemodialysis patients (HD group) and 302 healthy control subjects. They were all nondiabetic and the three groups were comparable in age and gender. RESULTS: As compared with the healthy control subjects, the CRF and HD groups had greater CA-IMTs, whereas CA-IMTs of the CRF and HD groups were not statistically different. There was no significant correlation between duration of hemodialysis and CA-IMT in the HD group. Multiple regression analysis in the total subjects indicated that presence of renal failure, but not being treated with hemodialysis, was a significant factor associated with increased CA-IMT independent of age, gender, blood pressure, smoking, high-density lipoprotein (HDL) and non-HDL cholesterol levels. CONCLUSIONS: These results demonstrate that thickening of arterial wall is present in patients with chronic renal failure before starting hemodialysis treatment, and support the concept that advanced atherosclerosis in hemodialysis patients is due not to hemodialysis treatment, but to renal failure and/or metabolic abnormalities secondary to renal failure.     

Modification of serum and membrane lipid composition induced by diet in patients with chronic renal failure

Disorders of lipid metabolism during chronic renal failure (CRF) play a crucial role in the pathogenesis of early cardiovascular complication of this syndrome. In addition, some experimental evidence suggests that hyperlipidemia may accelerate progression of renal disease. We have studied 65 patients with CRF (S-creatinine 1.5-9.0 mg/dl), 52.3% of whom were hypertensive. Patients were divided in 2 groups matched for age, sex and degree of renal failure: group 1 was kept for 36 +/- 8 months on a free diet; group 2 was kept for 39 +/- 6 months on a low-protein diet with an elevated polyunsaturated/saturated fatty acid (PUFA/SFA) ratio. We found significantly higher levels of triglycerides (TG) and lower levels of esterified cholesterol in high density lipoprotein (HDL-C) in group 1 than in group 2. Patients on the diet had a lower percentage of membrane SFA and a higher percentage of PUFA than patients on free diet. Only in group 1 a direct correlation between cholesterol/phospholipid (Chol/P) ratio and age was observed; in group 2, a negative correlation between levels of PUFA and TG and between linoleic/oleic (Lin/Ol) ratio and serum Chol was shown. S-creatinine levels were directly correlated with Chol/P ratio in group 1 and indirectly with Lin/Ol ratio and PUFA in group 2. These data show that a low-protein diet, containing an elevated PUFA/SFA ratio, is able to counteract lipid abnormalities in patients with CRF and the normalization of this pattern is associated with significant improvement of membrane lipid composition and, presumably, of "functional" activity of cell membranes with a better control of supposed "renal lipoprotein toxicity".     

Effect of a soy protein diet on serum lipids of renal transplant patients.

OBJECTIVE: The aim of the present study was to evaluate the effect of a soy-protein diet on plasma lipid levels of renal transplant recipients with moderate hypercholesterolemia. DESIGN: Dietary intervention case-control observational study. SETTING: Renal transplantation outpatient clinic. PATIENTS: Fifteen stable patients who had renal transplantation (serum creatinine < 2 mg/dL) with moderate hypercholesterolemia (low-density lipoprotein [LDL] cholesterol > 140 mg/dL). INTERVENTION: After a baseline dietary interview, dietary counseling was given individually with the goal of substituting 25 g of animal protein with 25 g of soy protein for a 5-week period, using commercially available soy foods, according to each patient's own preference.Main outcome measures Before and after the soy-diet period, plasma lipid profiles including total, LDL, and high-density lipoprotein (HDL) cholesterol, triglycerides, apolipoprotein A1 and B were determined. Protein catabolic rate was assumed as a measure of dietary protein intake. RESULTS: Two patients dropped out. After the soy diet, total cholesterol (254 +/- 22 to 231 +/- 31 mg/dL, P <.05) and LDL cholesterol (165 +/- 20 versus 143 +/- 20 mg/dL, P <.01) decreased significantly. No significant changes were observed regarding HDL cholesterol and triglycerides. Dietary protein intake did not differ at baseline (73.2 +/- 22.9 g/day) and during the soy diet (72.6 +/- 15.6 g/day), when the reported actual soy protein intake resulted 26 +/- 8 g/day. CONCLUSIONS: This study shows that soy proteins given as part of the daily protein intake have beneficial effects on serum LDL cholesterol levels of renal transplant recipients with moderate hypercholesterolemia. Soy proteins could be of use in the nutritional management of renal transplant recipients.     

The effect of a low-protein diet on serum levels of ceruloplasmin and transferrin in patients with chronic renal failure

In patients with chronic renal failure the administration of a diet providing 20 g protein per day for five weeks caused a significant rise in the serum ceruloplasmin level. A low dietary copper content (0.8 mg/day) may have been the limiting factor for any further rise of the ceruloplasmin level. The rise of ceruloplasmin was associated with a continuous decline of total iron binding capacity. The temporarily raised serum iron levels and the continuous decline of unsaturated iron binding capacity suggested enhanced iron mobilization caused by the raised ceruloplasmin level. The rise of ceruloplasmin correlated with the decline of UIBC.     

Elevated levels of serum sulfite in patients with chronic renal failure

Sulfite, a well known air pollutant, is toxic for humans, especially those with sulfite hypersensitivity. Sulfite is also generated endogenously, during normal metabolism of sulfur-containing amino acids. Mammalian tissues contain the enzyme sulfite oxidase, which detoxifies both endogenous and exogenous sulfite by oxidation to sulfate. Deficiency of sulfite oxidase in humans is fatal, demonstrating its physiologic importance. Nevertheless, information about serum and tissue levels of sulfite in normal and pathologic conditions is limited. Using a sensitive HPLC assay, it is shown here that sera from patients with chronic renal failure (CRF) contain significantly higher amounts of sulfite than those from healthy subjects. Mean +/- SD of serum sulfite in healthy subjects (n = 20) was 1.55 +/- 0.54 microM, whereas those in patients under maintenance hemodialysis (HD patients; n = 44) and CRF patients before introducing dialysis therapy (pre-HD patients; n = 33) were 3. 23 +/- 1.02 microM (P < 0.01) and 3.80 +/- 3.32 microM (P < 0.01), respectively. Among pre-HD patients, serum sulfite was positively correlated with serum creatinine (r = 0.714, P < 0.0001), and negatively with serum albumin (r = -0.407, P = 0.0188), hematocrit (r = -0.524, P = 0.0017), and total cholesterol (r = -0.375, P = 0. 0318). There was no significant association between sulfite and patient age, gender, or leukocyte counts. Multiple regression analysis revealed serum creatinine as the sole independent predictor of serum sulfite levels. Each HD treatment was associated with approximately 27% reduction in serum sulfite levels, suggesting the presence of a dialyzable form in serum. Thus, these results indicate that reduced glomerular filtration is a factor that determines serum sulfite levels. Chronic elevation in serum sulfite levels might contribute to tissue or organ dysfunction in patients with CRF.     

Mortality risk factors in chronic renal failure patients after coronary artery bypass grafting

Perioperative risk during coronary artery bypass grafting (CABG) is high in patients with chronic renal disease. We aimed to determine postoperative two-year mortality and identify the preoperative risk factors of mortality during CABG surgery in hemodialysis (HD)-dependent and HD-non-dependent CRF patients. We included 102 CRF patients who underwent CABG in Baskent University Hospital between 2000 and 2005. There were 47 patients with CRF undergoing HD (Group I) and 55 CRF patients without dialysis requirement (Group II). We retrospectively retrieved demographic variables; clinical, operative, and echocardiographic data; and biochemical parameters at the time of the operation and six months postoperation. Postoperative HD requirement in Group II patients and infectious complications were recorded. In the second postoperative year, mortality rate was 27.7% in group I and 16.4% in group II (p > .05). When preoperative risk factors evaluated by univariate Cox analysis, only age (RR = 1.06, p = .04) was a significant determinant of survival in Group I patients. Among the operative and postoperative risk factors of mortality such as duration of operation, numbers of coronary vessel bypass, HD requirement, and infection were investigated in Group I and II patients. Rate of infectious complication (including mediastinitis) was found to be a major determinant of mortality by multivariate Cox analyses in both group I (RR = 4.42, p 相似文献   

Autoantibodies against oxidized LDL in chronic renal failure: role of renal function, diet, and lipids

Lipid peroxidation (LP) has recently been suggested to trigger the atherosclerotic process as well as to worsen the progression of renal disease. Autoantibodies against oxidized low-density lipoproteins (Ox-LDLAb) were considered to provide a sensitive marker to detect LDL oxidation in vivo. To date few studies have been reported on Ox-LDLAb levels in patients with different degrees of renal failure. The aim of this study was to evaluate the influences of renal function, dietary manipulation, and lipids on Ox-LDLAb concentrations in uremic patients either on conservative or replacement therapy. Seventy-one patients (42 males, 29 females) aged 60 +/- 19 years with chronic renal failure (CRF) of different etiology and degree were divided into four groups according to serum creatinine levels [sCr(mg/dl)] and diet: CRF I > or = 1.5-3.0, CRF II > 3.0-5.5, and CRF III > 5.5 were all patients on a conventional low-protein diet, while a fourth group included patients on a vegetarian diet supplemented with keto analogues and amino acids (CRF SD >3.0). A further group was represented by patients on dialysis therapy. All patients were examined for Ox-LDLAb, triglycerides (TG), total cholesterol, HDL and LDL cholesterol, and apolipoproteins Apo A1, Apo B, and Lp(a). The results were compared with those of 20 controls (9 males and 11 females) aged 52 +/- 11 years with sCr <1.5 mg/dl. Ox-LDLAb increased, although not significantly, with TG and Lp(a) from the early stages of CRF along with the deterioration of renal function. However, TG and Lp(a) levels were significantly higher in all groups of patients except those on vegetarian diet (CRF SD). This group also showed the lowest Ox-LDLAb levels. No relationship was observed between lipids or apolipoproteins and Ox-LDLAb. Hyperlipidemic patients did not show higher Ox-LDLAb levels than normolipidemics. Our results show a progressive increase of LP as the renal function declines, which may account for the increased risk of cardiovascular disease reported in uremia. Dialysis does not correct significantly the oxidative state observed in patients with end-stage renal disease. Vegan diet, by reducing LP, TG, and Lp(a), is supposed to decrease the risk of cardiovascular disease and worth being reconsidered as an alternative effective therapeutic tool in patients with advanced CRF.     

Measurement of serum leptin in patients with chronic renal failure on hemodialysis.

BACKGROUND: Leptin, the product of the obese gene, is produced exclusively in fat cells. SUBJECTS, MATERIALS AND METHODS: To evaluate the clinical significance of measuring serum leptin in 56 patients with chronic renal failure on hemodialysis (HD), we measured leptin levels using radioimmunoassay in 34 normal volunteers and in 56 patients on HD. RESULTS: Normal serum leptin averaged 5.7 +/- 0.7 (mean +/- SEM) ng/ml, which correlated significantly (p < 0.001) with the body fat percentage as measured by bioelectrical impedance analysis. Serum leptin in HD patients ranged from 1.3 to 142 ng/ml. The mean serum leptin analyzed after the logarithmic conversion was 5.6 ng/ml, which was not significantly different from the normal control value, although the body fat percentage was significantly lower than normal volunteers. There was a significant (p < 0.01) positive correlation between body fat percentage and serum leptin in both normal controls and HD patients. The slope of the regression curve was steeper in HD patients than in normal controls. CONCLUSION: (1) serum leptin levels to body fat mass are significantly higher in HD patients than controls; (2) the variability is much wider in HD patients; and (3) a significant relation exists between percent body fat and log serum leptin, the relation being steeper in HD patients than in controls.     

慢性肾功能衰竭患者血清粒系集落刺激因子水平观察

为了解血清粒系集落刺激因子（Ｇ－ＣＳＦ）的代谢途径，用自行建立ＥＬＩＳＡ法检测了６１例慢性肾功能衰竭（ＣＲＦ）患者及６０例健康对照者Ｇ－ＣＳＦ水平。结果表明８６．９ＣＲＦ患者血清Ｇ－ＣＳＦ水平明显升高，其原因可能是由于Ｇ－ＣＳＦ的排泄障碍，在体内堆积之敌。     

Cardiovascular risk factors in chronic renal failure and hemodialysis populations.

Cardiovascular disease is the leading cause of death in patients with end-stage renal disease (ESRD). Risk factors for cardiovascular disease, including hypertension, lipid abnormalities, left ventricular hypertrophy (LVH), and glucose intolerance, are present more frequently in patients with chronic renal failure than in the general population, even before the onset of replacement therapy. The prevalence, pathogenesis, and significance of these factors in the uremic population are examined, and the potential roles of intervention are reviewed. Evidence suggests, but is not conclusive, that these factors are of predictive value for cardiovascular complications in patients with chronic renal failure. The effect of modification of these factors on cardiovascular morbidity and mortality in this population, especially in the early stages of renal failure, is an important area for further study.     

Special characteristics of atherosclerosis in chronic renal failure

Cardiovascular complications are a major clinical problem in patients with chronic kidney disease and end stage renal failure. Death from cardiac causes accounts for 40%-50% of all deaths in these patients and is thus up to 20 times more common in uremic patients than in the general population. Cardiovascular pathology in patients with renal failure is complex, but accelerated atherosclerosis has repeatedly been discussed as one major cause. The prevalence of coronary atheroma in uremic patients is approximately 30% by autopsy and coronary angiography studies. Not only is the prevalence of atherosclerotic lesions very high, but also the case fatality rate of myocardial infarction. Recently, excess mortality in uremic patients having had a myocardial infarct was noted; the one year mortality was 55.4% and 62.3% in uremic patients with and without diabetes, respectively, compared to about 10-15% in non-uremic patients. This study goes beyond the well-known notion that urea is associated with more severe atherosclerosis and shows that, in addition, the adaptation to coronary perfusion deficits is inappropriate. Recent clinical and autoptical studies in pre-dialysis and dialysis cohorts have documented increased intima and media thickness which appear early in the course of renal disease; Vascular wall thickening in renal failure seems to be modified at least in part by parathyroidhormone (PTH) and endothelin-1 (ET-1) which are both elevated in patients with renal failure. In experimental renal failure a direct effect of high phosphorus diet in arterial wall thickening was also documented. In addition to thickening of the vascular wall marked structural alterations were noted in renal failure i.e. a decrease in elastic fibre content and an increase in extracellular matrix. Furthermore, increased calcification of coronary atherosclerotic plaques and of the media of the aorta and some peripheral arteries has been documented in patients with renal failure. Factors contributing to this increased calcification process may be deposition of abundant circulating calcium, microinflammation, oxidative stress, de novo expression of bone morphogenous proteins and lack of inhibitors of calcifcation. These changes in vascular wall composition may alter vessel elasticity and thus contribute to impaired vessel function in renal failure. It is obvious from the above mentioned facts that cardiovascular disease in the renal patient is certainly multifaetorial in origin. There are, however, important issues to adress in the future, like (I) the characterization of vascular morphology in the different vascular beds, (II) the pathomechanisms of vascular and plaque calcification as well as the potential beneficial effect of rigorous control of non-classical risk factors (i.e. high P or Ca x P, inflammation, oxidative stress, etc.), (III) an additive or supraadditive effect of various classical and non-classical risk factors and (IV) the role of diabetes mellitus in modifying these vascular alterations.     

The risk of acute renal failure in patients with chronic kidney disease

Few studies have defined how the risk of hospital-acquired acute renal failure varies with the level of estimated glomerular filtration rate (GFR). It is also not clear whether common factors such as diabetes mellitus, hypertension and proteinuria increase the risk of nosocomial acute renal failure independent of GFR. To determine this we compared 1,746 hospitalized adult members of Kaiser Permanente Northern California who developed dialysis-requiring acute renal failure with 600,820 hospitalized members who did not. Patient GFR was estimated from the most recent outpatient serum creatinine measurement prior to admission. The adjusted odds ratios were significantly and progressively elevated from 1.95 to 40.07 for stage 3 through stage 5 patients (not yet on maintenance dialysis) compared to patients with estimated GFR in the stage 1 and 2 range. Similar associations were seen after controlling for inpatient risk factors. Pre-admission baseline diabetes mellitus, diagnosed hypertension and known proteinuria were also independent risk factors for acute kidney failure. Our study shows that the propensity to develop in-hospital acute kidney failure is another complication of chronic kidney disease whose risk markedly increases even in the upper half of stage 3 estimated GFR. Several common risk factors for chronic kidney disease also increase the peril of nosocomial acute kidney failure.     

The assessment of risk factors in 462 patients with acute renal failure

Risk factors associated with the mortality of patients with acute renal failure (ARF) were investigated. This was accomplished by a review of 462 patients with ARF and the utilization of a logistic regression analysis to develop a model that can be used to predict the mortality odds for an ARF patient. The significant risk factors were age, oliguria, pulmonary and cardiovascular complications, jaundice, and hypercatabolism. Based on these factors, our model was able to account for 77% of the mortality associated with ARF.