Validation of the equations for estimating daily sodium excretion from spot urine in patients with chronic kidney disease

Background

Measuring sodium excretion in a 24-h urine collection is the most reliable method of estimating salt intake, but it is not applicable to all patients. As an alternative, equations for estimating Na excretion from Japanese by a spot urine sample were created, but they have not been validated in patients with chronic kidney disease (CKD), which are frequently associated with nocturia and medication.

Methods

We enrolled 136 patients with CKD and collected both 24-h urine and the first morning urine. Na excretion was estimated from the first morning urine by Kawasaki’s equation, which was originally used for the second morning urine, and Tanaka’s equation, which is applied for spot urine samples taken at any time from 9?am to 7?pm. We evaluated the two equations for bias, RMSE and accuracy within 30 and 50% of the measured Na excretion.

Results

Bias, RMSE and accuracy within 30% of the estimated Na excretion were 48?±?69 and 2?±?69?mmol/day, 84 and 69?mmol/day, and 35 and 49% using Kawasaki’s equation and Tanaka’s equation, respectively. Na excretion in the first morning urine was accurately estimated by Tanaka’s equation, but it was overestimated by Kawasaki’s equation. Nocturia and medication such as diuretics and ACE inhibitor or angiotensin receptor blocker did not affect the accuracy with which Na excretion was estimated by Tanaka’s equation substantially.

Conclusion

Tanaka’s equation for estimating Na excretion from the first morning urine in patients with CKD is accurate enough for use in clinical practice.     

Eleven reasons to control the protein intake of patients with chronic kidney disease

For many years patients with chronic kidney disease have been advised to control the protein content of their diet. This advice has been given on the basis of a number of reported metabolic effects of lowering protein intake, such as lowering serum urea nitrogen levels, improving phosphocalcic metabolism and insulin resistance and, more recently, ameliorating proteinuria (independent of antiproteinuric medications). The effects on the progression of kidney disease, although spectacular in experimental studies, have been less convincing in humans. It is possible that flawed design of clinical trials is responsible for this discrepancy. In this Review, we comment on experimental findings that indicate that limiting protein intake protects the kidney and ameliorates uremic symptoms, outline how the body adapts to a reduction in protein intake, and describe the metabolic benefits to the patient. We then review the evidence from randomized controlled trials and meta-analyses that pertains to the effects of low-protein diets in adults with chronic kidney disease.     

Residual kidney function and plasma urea concentration in patients with chronic renal failure

The relationships between the plasma levels of urea (P_urea), renal clearance of urea (C_urea) and creatinine (C_cr) at an intake of 0.5 g protein/kg body weight/day were followed in 10 patients with chronic renal failure (CRF) under balance conditions. Under these conditions, P_urea attained a value of 30 mmol/l when C_urea had decreased below 3.8 ml/min. By contrast, no correlation could be demonstrated between P_urea and C_cr under these conditions. The same relationships were followed in another group of 30 outpatients with CRF. Even in patients not followed under balance conditions, C_urea determination makes it possible to establish whether the high increase in P_urea is due to the decrease in residual renal function below the critical level or whether extrarenal factors are involved. Likewise, no significant correlation between P_urea and C_cr could be demonstrated under these conditions. The findings suggest that C_urea measurement in CRF patients helps to assess residual renal function in terms of P_urea regulation and provides information that cannot be obtained by C_cr measurement.     

The correlation between urine urea nitrogen and total urine nitrogen output in perioperative patients]

Daily urine urea nitrogen (UUN) and total urine nitrogen output (TUNO) concentrations were measured in 19 patients undergoing G-I surgery during the perioperative period of 114 days. The results showed that there was a strong correlation between UUN and TUNO in statistic regression analysis. A formula is worked out TUNO = UUN + 0.7 which is of great value in estimating the nitrogen balance of TPN patients.     

Is energy intake underestimated in nondialyzed chronic kidney disease patients?

OBJECTIVE: To evaluate whether energy intake of nondialyzed chronic kidney disease (CKD) patients is underestimated. DESIGN: Cross-sectional study. SETTING: Outpatient clinic of the Federal University of Sao Paulo, Oswaldo Ramos Foundation. PATIENTS: One hundred and thirty-one nondialyzed CKD patients (86 male, 66%; body mass index [BMI] 26 +/- 4.21, mean +/- standard deviation) were included. Body weight change was evaluated after 6 to 12 months in 59 patients of the entire group. METHODS: Energy intake was evaluated using 4-day food diaries (3 weekdays and 1 weekend day), and resting energy expenditure (REE) was measured by indirect calorimetry. The ratio of energy intake to REE (EI/REE) was used to evaluate the accuracy of the recorded energy intake. An EI/REE ratio below 1.27 was used to identify patients who were underreporting their current energy intake. RESULTS: The majority of the patients reported an energy intake substantially below the recommendation (22.4 +/- 7.15 kcal/kg/d) and had an EI/REE ratio lower than 1.27. In patients with a BMI >or= 25, the mean EI/REE ratio was significantly lower than that of patients with a BMI < 25 (1.01 +/- 0.28 versus 1.27 +/- 0.42, P < .01, respectively). In addition, only in the group with higher BMI was the mean ratio indicative of underreporting. When the body weight of a subgroup of patients (n = 59) was evaluated after 7.9 +/- 2.4 months, it was observed that the subgroup of patients who maintained or gained body weight had a mean EI/REE not compatible with this condition (1.13 +/- 0.38). The low ratio, despite increasing or maintaining body weight, is highly suggestive of underreported energy intake. CONCLUSION: Energy intake of nondialyzed CKD patients seemed to be underestimated and was more pronounced in overweight and obese patients.     

不同年龄慢性肾脏病患者血肌酐、血尿素氮与肾小球滤过率的相关性

临床工作中使用Scr和BUN判断肾功能时常忽略年龄对两者敏感性的影响。本研究旨在判断不同年龄慢性肾脏病（CKD）患者上述两指标与肾功能的相关性：     

Effect of simvastatin on plasma asymmetric dimethylarginine concentration in patients with chronic kidney disease

BACKGROUND: The endogenous inhibitor of nitric oxide (NO) synthase, asymmetric dimethylarginine (ADMA), is a strong cardiovascular (CV) risk marker in patients with chronic renal insufficiency. Statins have pleiotropic effects and are currently considered as potential ADMA-lowering agents. METHODS: We investigated the effect of simvastatin on plasma ADMA levels in 35 patients with chronic kidney disease (CKD) by performing a secondary analysis of a randomized double-blind placebo-controlled trial where patients were randomized to receive simvastatin or placebo for 6 months. RESULTS: Plasma ADMA was higher in CKD patients (0.84 +/- 0.14 micromol/L) than in healthy subjects (0.69 +/- 0.10 micromol/L) (p<0.001). In CKD patients, ADMA at baseline was related directly with triglycerides (r=0.42, p=0.01) and inversely with HDL cholesterol (r=-0.37, p=0.03) and creatinine clearance (p=0.03). As expected, simvastatin caused significant reductions in total cholesterol, LDL cholesterol and triglycerides, as well as in C-reactive protein (CRP; -28%, p=0.001) and IL-6 (-20%, p=0.05) but failed to decrease plasma ADMA both in crude and adjusted analyses. CONCLUSIONS: Simvastatin does not modify plasma ADMA. Because raised ADMA is known to prevent the favorable effect of statins on myocardial blood flow, cointerventions aimed at lowering or antagonizing ADMA may either prompt or potentiate the cardiovascular protective effect of simvastatin.     

Effect of salt intake on progression of chronic kidney disease

PURPOSE OF REVIEW: The attempt of this review is to bring into focus the potential role of dietary salt intake in progression of chronic kidney disease. RECENT FINDINGS: Ongoing work has elucidated a role for dietary salt intake in modulating intrarenal production of transforming growth factor-beta1. The mechanism is independent of angiotensin II and systemic blood pressure and involves activation of vascular endothelium by dietary salt intake with release of this growth factor. In this model, transforming growth factor-beta1 serves an autacoid function by stimulating nitric oxide production by the endothelium. In turn, endothelium-derived nitric oxide modulates production of this growth factor. The model further predicts that individuals who have lost the requisite endothelial cell flexibility to adapt to this environmental stress (a high salt diet) are potentially at increased risk of developing end-organ damage from excess salt intake. Animal and human studies are presented to support this working hypothesis. SUMMARY: Overproduction of transforming growth factor-beta1 permits excess biological activity of this important fibrogenic growth factor with subsequent development or acceleration of vascular and kidney damage. In patients with diseases whose pathogenesis is related to excess production of transforming growth factor-beta1, such as chronic allograft nephropathy and diabetic nephropathy, increased salt intake may hasten loss of function, particularly if nitric oxide production does not increase. The role that endothelial cell plasticity plays in altering vascular tone and renal function, especially in response to changes in dietary salt intake, should be examined further in chronic kidney disease.     

Dietary protein restriction benefits patients with chronic kidney disease

The prevalence of chronic kidney disease (CKD) is rapidly increasing so every strategy should be used to avoid the complications of CKD. Most CKD symptoms or uraemia are caused by protein intolerance; symptoms arise because the patient is unable to excrete metabolic products of dietary protein and the ions contained in protein-rich foods. Consequently, CKD patients accumulate salt, phosphates, uric acid and many nitrogen-containing metabolic products, and secondary problems of metabolic acidosis, bone disease and insulin resistance become prominent. These problems can be avoided with dietary planning. Protein-restricted diets do not produce malnutrition and with these diets even patients with advanced CKD maintain body weight, serum albumin and normal electrolyte values. Non-compliance is a problem, but this can be detected using standard techniques to provide the patient with appropriate responses. The role of dietary protein restriction in the progression of CKD has not been proven, but it can reduce albuminuria and will prevent uraemic symptoms. Until a means of preventing kidney disease or progression is found, safe methods of management such as dietary manipulation should be available for CKD patients.     

Hemodialysis duration impairs food intake and nutritional parameters in chronic kidney disease patients

Introduction  

The aim of this study was to evaluate the effect of hemodialysis (HD) duration on food intake and nutritional markers in patients with chronic kidney disease (CKD).     

血浆维生素D与慢性肾脏病患者心血管疾病的相关性研究

目的了解慢性肾脏病(chronic kidney disease,CKD)患者维生素D状态及缺乏原因,并探讨血浆维生素D缺乏是否独立影响CKD患者心血管疾病(cardiovasculardisease,CVD)的发生。方法选取北京医院肾脏内科住院的CKD 1~5期非透析患者80例为研究对象,门诊健康查体人群10例为对照组,测定其血浆25-OH-D_3、1,25(OH)_2D_3水平并进行相关实验室检查。根据血浆25-OH-D_3水平将患者分为维生素D缺乏组和非维生素D缺乏组,比较组间临床和实验室检查资料以及心脏超声检查相关参数差异;根据超声心动图结果,将患者分为左室肥厚(1eft ventricular hypertrophy,LVH)组和非LVH组,比较组间患者相关临床资料差异,并采用多因素分析CKD患者LVH的独立危险因素。结果 CKD组及对照组25-OH-D3分别为(15.09±2.44)μg/L和(18.60±1.88)μg/L;2组维生素D水平均较低,但CKD组较对照组更低,组间有统计学差异(P0.05)。CKD患者维生素D水平普遍偏低,血浆25-OH-D_3波动于10.29~20.51μg/L,1,25(OH)2 D3波动于16.23~54.32 ng/L,两者之间存在线性相关,两者与CKD患者肾功能分期均无线性相关。CKD患者维生素D缺乏组(≤15μg/L)和非维生素D缺乏组(15μg/L)组间比较,发现2组血磷、左心室质量指数存在统计学差异(P0.05)。维生素D水平与左心室质量指数无线性相关;比较LVH组及非LVH组相关临床资料,单因素分析发现血肌酐、尿素氮、估算肾小球滤过率、脑钠肽、肌钙蛋白、血红蛋白、红细胞比容、24h尿蛋白定量、高密度脂蛋白均存在统计学差异(P0.05);多元逐步Logistic回归发现BNP升高(≥1 000 ng/L),24h尿蛋白定量(≥3.5 g),LDL升高(≥2.59 mmol/L)可进入方程(P0.05)。结论 CKD患者25-OH-D_3水平低于普通人群,但与CKD患者肾功能水平无线性相关;BNP升高、24h尿蛋白定量、高低密度脂蛋白血症是CKD患者左室肥厚的独立危险因素,目前尚不认为25-OH-D_3水平下降影响CKD患者左室肥厚的发生。     

Estimation of oxidative stress markers in chronic kidney disease

Changes mediated by oxidative stress are thought to be involved with atherosclerosis in patients with chronic kidney disease (CKD). The purpose of this study was to analyze the markers of oxidative damage and the activity of antioxidative enzymes as well as the total antioxidant capability in patients with different stages of CKD, both conventionally treated and dialyzed. We evaluated the oxidative modification of lipids (by oxidized low-density lipoprotein and malonodialdehyde levels) and proteins (by advanced oxidation protein products level). We also assessed the activity of paraoxonase-1 and glutathione peroxidases and total antioxidant status. Compared with the control group, the uremic patients, both dialyzed and nondialyzed, had higher levels of all studied plasma oxidative stress markers and decreased activity of antioxidative enzymes. Our results lead us to conclude that oxidative stress seems to be related rather to the uremic state than to the dialysis treatment. We also showed that estimating total antioxidant status in a simple test is unreliable for assessing the antioxidant ability of patients with CKD.     

Cardiovascular disease in patients with chronic kidney disease

Cardiovascular disease (CVD) is the major cause of morbidity and mortality in patients with renal failure. Patients with chronic kidney disease have significant CVD, and carry a high cardiovascular burden by the time they commence renal replacement therapy (RRT). The severity of CVD that has been observed in dialysis patients lead to a growing body of research examining the pathogenesis and progression of CVD during the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD) (ie, predialysis phase). Multiple factors are involved in the development of CVD in CKD. More importantly, critical and key factors seem to develop early in the course of CKD, and result in preventable worsening of CVD in this patient population. Anemia is common in patients with CKD, and has been shown to have an independent role in the genesis of left ventricular hypertrophy (LVH) and subsequent CVD. Unfortunately, it is underdiagnosed and undertreated in patients with CKD. Early intervention, and better correction of anemia, seems to gain a great momentum in the prevention and management of CVD in CKD. Hypertension is another risk factor that has been targeted by the National Kidney Foundation Task Force on CVD in chronic kidney disease. This article reviews the different factors involved in the pathogenesis of CVD in CKD and the evidence supporting early and aggressive intervention.