Treatment Of CKD Research Articles

1,25-Dihydroxyvitamin D3 Attenuates Angiotensin II-Induced Renal Injury by Inhibiting Mitochondrial Dysfunction and Autophagy

Background/Aims: A recent study has shown that 1,25-dihydroxyvitamin D3 (1,25-D3), the active form of vitamin D, can ameliorate renal dysfunction. In this study, we aimed to determine the role of 1,25-D3 in angiotensin (Ang II)-induced renal injury and investigate the underlying mechanisms involved. Methods: C57BL/6J mice were treated with Ang II and/or 1,25-D3 (or saline as the control) for 2 weeks. Renal injury was evaluated using transmission electron microscopy and periodic acid-Schiff reagent and Masson’s trichrome staining. The pro-fibrotic and pro-inflammatory factors were assessed using real-time PCR. The renal apoptotic pathway was evaluated with TUNEL staining and western blot. Mitochondrial dysfunction (MtD) was determined using real-time PCR and electron microscopy. The activation of autophagy was detected using western blot. Results: In the Ang II-infused mice, expanded mesangial regions, tubulointerstitial fibrosis, and foot process fusion were observed; the levels of the pro-fibrotic and pro-inflammatory cytokines and MtD were also increased when compared with the control group. However, we found that administration of 1,25-D3 significantly improved renal function and MtD and reduced the pro-fibrotic and pro-inflammatory cytokine levels. Furthermore, 1,25-D3 significantly inhibited Ang II-induced autophagy dysfunction (determined by inhibition of Beclin-1 activation and reduction of the LC3-II/LC3-I ratio). Conclusion: Our findings suggest that 1,25-D3 may attenuate Ang II-induced renal injury by improving MtD and modulating autophagy. 1,25-D3 may be a new therapeutic for the treatment of CKD.

Pooled Analysis of Multiple Crossover Trials To Optimize Individual Therapy Response to Renin-Angiotensin-Aldosterone System Intervention.

In the treatment of CKD, individual patients show a wide variation in their response to many drugs, including renin-angiotensin-aldosterone system inhibitors (RAASi). To investigate whether therapy resistance to RAASi can be overcome by uptitrating the dose of drug, changing the mode of intervention (with drugs from similar or different classes), or lowering dietary sodium intake, we meta-analyzed individual responses to different modes of interventions. Randomized crossover trials were analyzed to assess correlation of individual responses to RAASi and nonsteroidal anti-inflammatory drugs (NSAIDs; n=395 patients). Included studies compared the antialbuminuric effect of uptitrating the dose of RAASi (n=10 studies) and NSAIDs (n=1), changing within the same class of RAASi (e.g., angiotensin-converting enzyme inhibition to angiotensin receptor blockers; n=5) or NSAIDs (n=1), changing from RAASi to NSAIDs (n=2), and changing from high to low sodium intake (n=5). A two-stage meta-analysis was conducted: Deming regression was conducted in each study to assess correlations in response, and individual study results were then meta-analyzed. The albuminuria response to one dose of RAASi or NSAIDs positively correlated with the response to a higher dose of the same drug (r=0.72; 95% confidence interval [95% CI], 0.66 to 0.78), changes within the same class of RAASi or NSAIDs (r=0.54; 95% CI, 0.35 to 0.68), changes between RAASi and NSAIDs (r=0.44; 95% CI, 0.16 to 0.66), and changes from high to moderately low salt intake (r=0.36; 95% CI, 0.22 to 0.48). Results were similar when the individual systolic BP and potassium responses were analyzed, and were consistent in patients with and without diabetes. Individuals who show a poor response to one dose or type of RAASi also show a poor response to higher doses, other types of RAASi or NSAIDs, or a reduction in dietary salt intake. Whether other drugs or drug combinations targeting pathways beyond the renin-angiotensin-aldosterone system and prostaglandins would improve the individual poor response requires further study.

New Ultrasound Techniques Promise Further Advances in AKI and CKD.

AKI and CKD are important clinical problems because they affect many patients and the associated diagnostic and treatment paradigms are imperfect. Ultrasound is a cost-effective, noninvasive, and simple imaging modality that offers a multitude of means to improve the diagnosis, monitoring, and treatment of both AKI and CKD, especially considering recent advances in this technique. Ultrasound alone can attenuate AKI and prevent CKD by stimulating the splenic cholinergic anti-inflammatory pathway. Additionally, microbubble contrast agents are improving the sensitivity and specificity of ultrasound for diagnosing kidney disease, especially when these agents are conjugated to ligand-specific mAbs or peptides, which make the dynamic assessment of disease progression and response to treatment possible. More recently, drug-loaded microbubbles have been developed and the load release by ultrasound exposure has been shown to be a highly specific treatment modality, making the potential applications of ultrasound even more promising. This review focuses on the multiple strategies for using ultrasound with and without microbubble technology for enhancing our understanding of the pathophysiology of AKI and CKD.

Direct Cost for Treating Chronic Kidney Disease at an Outpatient Setting of a Tertiary Hospital: Evidence from a Cross-Sectional Study

BackgroundChronic kidney disease (CKD) has a high morbidity and mortality in developing countries. And this burden is also increasing rapidly in India. Unaffordability due to high cost of medication and hemodialysis remains one of the major barriers in the successful treatment of CKD. ObjectivesTo determine the direct cost involved in treating CKD at an outpatient department of a public tertiary care hospital. MethodsThis cross-sectional study was carried out at a public tertiary care hospital. Patients diagnosed with CKD by a physician were included in the study after obtaining a written informed consent. All the relevant data were collected on a predesigned case record form. ResultsThe results are based on data obtained from 150 patients. The average age of the patients was 55.7 ± 10.1 years. The average number of drugs per prescription was found to be 6.5 ± 1.7. The annual average costs of treatment for patients on medication only and for patients on hemodialysis plus medication were Rs 25,836 (US $386) and Rs 2,13,144 (US $3181), respectively (Rs = Indian rupee). Treatment cost was found to be statistically significantly higher in patients on hemodialysis, treatment support by employer, patients with a smoking habit, patients with comorbidities, and patients with end-stage renal disease. Calcium tablets, vitamin D sachets, iron supplements, torsemide, and amlodipine were the top five medications prescribed. ConclusionsReimbursement, patient’s dialysis status, habits, and comorbidities were found to have a significant effect on the direct cost of treatment.

Janus Kinase 2 Regulates Transcription Factor EB Expression and Autophagy Completion in Glomerular Podocytes.

The nonreceptor kinase Janus kinase 2 (JAK2) has garnered attention as a promising therapeutic target for the treatment of CKD. However, being ubiquitously expressed in the adult, JAK2 is also likely to be necessary for normal organ function. Here, we investigated the phenotypic effects of JAK2 deficiency. Mice in which JAK2 had been deleted from podocytes exhibited an elevation in urine albumin excretion that was accompanied by increased podocyte autophagosome fractional volume and p62 aggregation, which are indicative of impaired autophagy completion. In cultured podocytes, knockdown of JAK2 similarly impaired autophagy and led to downregulation in the expression of lysosomal genes and decreased activity of the lysosomal enzyme, cathepsin D. Because transcription factor EB (TFEB) has recently emerged as a master regulator of autophagosome-lysosome function, controlling the expression of several of the genes downregulated by JAK2 knockdown, we questioned whether TFEB is regulated by JAK2. In immortalized mouse podocytes, JAK2 knockdown decreased TFEB promoter activity, expression, and nuclear localization. In silico analysis and chromatin immunoprecipitation assays revealed that the downstream mediator of JAK2 signaling STAT1 binds to the TFEB promoter. Finally, overexpression of TFEB in JAK2-deficient podocytes reversed lysosomal dysfunction and restored albumin permselectivity. Collectively, these observations highlight the homeostatic actions of JAK2 in podocytes and the importance of TFEB to autophagosome-lysosome function in these cells. These results also raise the possibility that therapeutically modulating TFEB activity may improve podocyte health in glomerular disease.

Dynamin Autonomously Regulates Podocyte Focal Adhesion Maturation

Rho family GTPases, the prototypical members of which are Cdc42, Rac1, and RhoA, are molecular switches best known for regulating the actin cytoskeleton. In addition to the canonical small GTPases, the large GTPase dynamin has been implicated in regulating the actin cytoskeleton via direct dynamin-actin interactions. The physiologic role of dynamin in regulating the actin cytoskeleton has been linked to the maintenance of the kidney filtration barrier. Additionally, the small molecule Bis-T-23, which promotes actin-dependent dynamin oligomerization and thus, increases actin polymerization, improved renal health in diverse models of CKD, implicating dynamin as a potential therapeutic target for the treatment of CKD. Here, we show that treating cultured mouse podocytes with Bis-T-23 promoted stress fiber formation and focal adhesion maturation in a dynamin-dependent manner. Furthermore, Bis-T-23 induced the formation of focal adhesions and stress fibers in cells in which the RhoA signaling pathway was downregulated by multiple experimental approaches. Our study suggests that dynamin regulates focal adhesion maturation by a mechanism parallel to and synergistic with the RhoA signaling pathway. Identification of dynamin as one of the essential and autonomous regulators of focal adhesion maturation suggests a molecular mechanism that underlies the beneficial effect of Bis-T-23 on podocyte physiology.

Phosphate Toxicity in CKD: The Killer among Us.

Maintenance of a normal serum phosphate level depends on absorption in the gut, reabsorption and excretion by the kidney, and the flux between the extracellular and skeletal pools. Phosphate homeostasis is a coordinated, complex system of crosstalk between the bone, intestine, kidney, and parathyroid gland. Dysfunction of this system has serious clinical consequences in healthy individuals and those with conditions, such as CKD, in which hyperphosphatemia is associated with increased risks of cardiovascular morbidity and mortality. The last half-century of renal research has helped define the contribution of the parathyroid hormone, calcitriol, fibroblast growth factor 23, and Klotho in the regulation of phosphate. However, despite new discoveries and insights gained during this time, what remains unchanged is the recognition that phosphate retention is the initiating factor for the development of many of the complications observed in CKD, namely secondary hyperparathyroidism and bone and cardiovascular diseases. Controlling phosphate load remains the primary goal in the treatment of CKD. This review discusses the clinical effects of dysregulated phosphate metabolism, particularly in CKD, and its association with cardiovascular disease. The importance of early control of phosphate load in the treatment of CKD is emphasized, and the latest research in the treatment of phosphate retention is discussed.

Association between Mitochondrial DNA Copy Number in Peripheral Blood and Incident CKD in the Atherosclerosis Risk in Communities Study

Mitochondrial dysfunction in kidney cells has been implicated in the pathogenesis of CKD. Mitochondrial DNA (mtDNA) copy number is a surrogate measure of mitochondrial function, and higher mtDNA copy number in peripheral blood has been associated with lower risk of two important risk factors for CKD progression, diabetes and microalbuminuria. We evaluated whether mtDNA copy number in peripheral blood associates with incident CKD in a population-based cohort of middle-aged adults. We estimated mtDNA copy number using 25 high-quality mitochondrial single nucleotide polymorphisms from the Affymetrix 6.0 array. Among 9058 participants, those with higher mtDNA copy number had a lower rate of prevalent diabetes and lower C-reactive protein levels and white blood cell counts. Baseline eGFR did not differ significantly by mtDNA copy number. Over a median follow-up of 19.6 years, 1490 participants developed CKD. Higher mtDNA copy number associated with lower risk of incident CKD (highest versus lowest quartile: hazard ratio 0.65; 95% confidence interval, 0.56 to 0.75; P<0.001) after adjusting for age, sex, and race. After adjusting for additional risk factors of CKD, including prevalent diabetes, hypertension, C-reactive protein level, and white blood cell count, this association remained significant (highest versus lowest quartile: hazard ratio 0.75; 95% confidence interval, 0.64 to 0.87; P<0.001). In conclusion, higher mtDNA copy number associated with lower incidence of CKD independent of traditional risk factors and inflammation biomarker levels in this cohort. Further research on modifiable factors influencing mtDNA copy number may lead to improvement in the prevention and treatment of CKD.

Prevention, Diagnosis, and Treatment of Chronic Kidney Diseases in Older Adults: Current Status and Prospective

The elderly are at high risk of chronic kidney disease, who has become a major population in the newly admission to dialysis treatment. So the elderly will be the focus of CKD prevention task in future. At present, challenges still remain in the diagnosis and treatment of CKD in the elderly: there is no unified criteria for CKD diagnosis in the elderly, un-settled treatment target of CKD complications in the elderly; complicated theraputic strategies in the elderly ESRD patients. We particularly stress the importance of patient-centered, instead of disease-oriented, individualized treatment in the prevention and treatment of CKD in the elderly.

CHRONIC KIDNEY DISEASE AND ITS RELATIONSHIP WITH INTAKE OF TURMERIC, CATECHINS, PROANTHOCYANIDINS AND OMEGA-3

Chronic renal disease is characterized by decreased glomerular filtration rate (GFR) < 60 ml/min/ 1.73m2 and/or the presence of kidney damage independent of the cause for a period of 3 months or more. The treatment of more advanced stages of chronic kidney disease is dialysis, and most common form of hemodialysis. This treatment is costly in our country reaching USD 900 per person. The main cause of admission to dialysis, diabetic nephropathy remains with 34% of all revenue. This alone makes any improvement in the treatment of CKD is highly desirable. There is evidence available about the fundamental role of turmeric, proanthocyanidins, catechins and omega-3 on how these compounds are related to the response to treatment of chronic kidney disease for various reasons.

CLINICAL AND ECONOMIC ANALYSIS OF USING OF LONG ACTION ERYTHROPOES STIMULATED AGENTS FOR THE TREATMENT OF ANEMIA CKD V HD PATIENTS

The article describes the ways to cost optimization of anemia treatment CKD - HD patients.&#x0D; Aims. dinical and economic analysis treatment of Anemia CKD VHD PTS with using long action Erythropoiesis Stimulating Agents (ESA).&#x0D; Methods. We calculated the true cost of anemia therapy with darbepoetin alfa compared to the methoxypolyethyleneglycol - epoetin beta.&#x0D; Results. It was established that average cost of therapy with methoxypolyethyleneglycol - epoetin beta was lower than darbepoetin alfa provided declared, wholesale or retail prices of25 - 60%.&#x0D; Conclusions. The methoxypolyethyleneglycol - epoetin beta haspharmacoeconomics advantages in comparison with the darbepoetin alfa in treatment of anemia CKD V HD patients.

Telemedicine: Development of a distance care system for pre-dialysis chronic kidney disease patients

The focus in the treatment of CKD is to prevent its progression through optimal medical control. The large number of patients with CKD has pressed nephrologists to assess more patients into ever-smaller periods of consultation. The use of light technologies as a promising form of health care. The internet offers the opportunity to manipulate the doctor in his professional contact with the user. To develop a web system to attend the patients with CKD not on dialysis and clinically stable stages at distance. Developed a system using the Java language, MySQL database and PrimeFaces framework; available on a Glassfish application server. The initial access is performed by the nephrologist, which registers the patients with their personal information and access data. After being registered, the patient (or family doctor) can enter the data of your query and these will be following, passed on to the nephrologist for evaluation. The form with the data of interest is pre-determined, but there is possibility to add free-form information. The system enables, in addition, there is exchange of messages between doctors and patients. In addition, users receive messages via e-mail alerting them of their duties. Confidentiality is guaranteed by individual passwords for doctors and patients. This tool will enable to increase the coverage area of nephrologists, reduce costs and bring the patient to the primary care physician, using the Family Health Program as an interface between the patient and the nephrology secondary care.

SREBP-1 Mediates Angiotensin II-Induced TGF-β1 Upregulation and Glomerular Fibrosis.

Angiotensin II is an important mediator of CKD of diverse etiology. A common pathologic feature of CKD is glomerular fibrosis, a central mediator of which is the profibrotic cytokine TGF-β. The mechanisms underlying the induction of TGF-β and matrix by angiotensin II are not completely understood. Recent studies showed that overexpression of the transcription factor SREBP-1 induces glomerular sclerosis and that angiotensin II can activate SREBP-1 in tubular cells. We thus studied whether SREBP-1 is activated by angiotensin II and mediates angiotensin II-induced profibrogenic responses in primary rat mesangial cells. Treatment of cells with angiotensin II induced the upregulation and activation of SREBP-1. Angiotensin II-induced activation of SREBP-1 required signaling through the angiotensin II type I receptor and activation of PI3K/Akt in addition to the chaperone SCAP and protease S1P. Notably, angiotensin II-induced endoplasmic reticulum stress was identified as a key mediator of Akt-SREBP-1 activation, and inhibition of endoplasmic reticulum stress or SREBP-1 prevented angiotensin II-induced SREBP-1 binding to the TGF-β promoter, TGF-β upregulation, and downstream fibronectin upregulation. Endoplasmic reticulum stress alone, however, did not induce TGF-β upregulation despite activating SREBP-1. Although not required for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of the SREBP-1 cotranscription factor Sp1, which provided a required second signal for TGF-β upregulation. In vivo, endoplasmic reticulum stress and SREBP-1-dependent effects were induced in glomeruli of angiotensin II-infused mice, and administration of the SREBP inhibitor fatostatin prevented angiotensin II-induced TGF-β upregulation and matrix accumulation. SREBP-1 and endoplasmic reticulum stress thus provide potential novel therapeutic targets for the treatment of CKD.

Management of End Stage Renal Disease-Bangladesh Perspective

End stage renal disease (ESRD) is an important cause of morbidity and mortality throughout the world. The treatment of renal replacement therapy (RRT) for patients with ESRD is expensive. There is a direct relationship between per capita income and treatment of ESRD. Eighty five per cent of the world’s population lives in low income or middle-income countries, where the mortality is highest in patients with chronic kidney disease.The future perspective is not satisfactory for Bangladesh where treatment of ESRD is out of reach for majority of people. Effort should made for prevention and treatment of CKD at an initial stage of disease.

Management of hypertension in CKD

Abstract Hypertension is a leading cause of morbidity and mortality in clinical practice. It may be either a consequence or a cause of CKD. It is a major factor contributing to the kidney disease and to faster decline in GFR. Management of hypertension is a key component in the treatment of CKD, in preventing the progression of CKD and other target organ damage in the schema of hypertension spectrum.

Syndecan-4 knockout leads to reduced extracellular transglutaminase-2 and protects against tubulointerstitial fibrosis.

Transglutaminase type 2 (TG2) is an extracellular matrix crosslinking enzyme with a pivotal role in kidney fibrosis. The interaction of TG2 with the heparan sulfate proteoglycan syndecan-4 (Sdc4) regulates the cell surface trafficking, localization, and activity of TG2 in vitro but remains unstudied in vivo. We tested the hypothesis that Sdc4 is required for cell surface targeting of TG2 and the development of kidney fibrosis in CKD. Wild-type and Sdc4-null mice were subjected to unilateral ureteric obstruction and aristolochic acid nephropathy (AAN) as experimental models of kidney fibrosis. Analysis of renal scarring by Masson trichrome staining, kidney hydroxyproline levels, and collagen immunofluorescence demonstrated progressive fibrosis associated with increases in extracellular TG2 and TG activity in the tubulointerstitium in both models. Knockout of Sdc-4 reduced these effects and prevented AAN-induced increases in total and active TGF-β1. In wild-type mice subjected to AAN, extracellular TG2 colocalized with Sdc4 in the tubular interstitium and basement membrane, where TG2 also colocalized with heparan sulfate chains. Heparitinase I, which selectively cleaves heparan sulfate, completely abolished extracellular TG2 in normal and diseased kidney sections. In conclusion, the lack of Sdc4 heparan sulfate chains in the kidneys of Sdc4-null mice abrogates injury-induced externalization of TG2, thereby preventing profibrotic crosslinking of extracellular matrix and recruitment of large latent TGF-β1. This finding suggests that targeting the TG2-Sdc4 interaction may provide a specific interventional strategy for the treatment of CKD.

Cysteamine Modulates Oxidative Stress and Blocks Myofibroblast Activity in CKD

Therapy to slow the relentless expansion of interstitial extracellular matrix that leads to renal functional decline in patients with CKD is currently lacking. Because chronic kidney injury increases tissue oxidative stress, we evaluated the antifibrotic efficacy of cysteamine bitartrate, an antioxidant therapy for patients with nephropathic cystinosis, in a mouse model of unilateral ureteral obstruction. Fresh cysteamine (600 mg/kg) was added to drinking water daily beginning on the day of surgery, and outcomes were assessed on days 7, 14, and 21 after surgery. Plasma cysteamine levels showed diurnal variation, with peak levels similar to those observed in patients with cystinosis. In cysteamine-treated mice, fibrosis severity decreased significantly at 14 and 21 days after unilateral ureteral obstruction, and renal oxidized protein levels decreased at each time point, suggesting reduced oxidative stress. Consistent with these results, treatment of cultured macrophages with cysteamine reduced cellular generation of reactive oxygen species. Furthermore, treatment with cysteamine reduced α-smooth muscle actin-positive interstitial myofibroblast proliferation and mRNA levels of extracellular matrix proteins in mice and attenuated myofibroblast differentiation and proliferation in vitro, but did not augment TGF-β signaling. In a study of renal ischemia reperfusion, cysteamine therapy initiated 10 days after injury and continued for 14 days decreased renal fibrosis by 40%. Taken together, these data suggest previously unrecognized antifibrotic actions of cysteamine via TGF-β-independent mechanisms that include oxidative stress reduction and attenuation of the myofibroblast response to kidney injury and support further investigation into the potential benefit of cysteamine therapy in the treatment of CKD.

Tripterygium Preparations for the Treatment of CKD: A Systematic Review and Meta-analysis

Preparations of the herb Tripterygium wilfordii Hook F are used widely for the treatment of chronic kidney disease in China. The efficacy and safety of Tripterygium preparations still have not been fully identified. Systematic review and meta-analysis. Patients with chronic kidney disease. Randomized controlled trials. Tripterygium preparations (Tripterygium glycoside tablets, Tripterygium hypoglaucum Hutch tablets, and Tripterygium granules or extracts) versus placebo, standard care, or other immunosuppressive treatment. Weighted mean difference and summary estimates of relative risk (RR) reductions with 95% CIs were calculated with a random-effects model. Outcomes analyzed included change in proteinuria, serum creatinine level, and creatinine clearance rate, as well as remission and relapse rate and drug-related adverse events. We identified 75 trials that included 4,386 participants. Overall, Tripterygium therapy reduced proteinuria by protein excretion of 628 (95% CI, -736 to -521) mg/d and reduced serum creatinine level by 0.12 (95% CI, -0.17 to -0.06) mg/dL compared with controls (both P < 0.001) in a range of kidney conditions. Tripterygium preparations also increased the rate of complete remission by 56% (95% CI, 32%-85%; P < 0.001) and of complete or partial remission by 24% (95% CI, 17%-31%; P < 0.001) while reducing relapse by 58% (95% CI, 42%-69%; P < 0.001). Tripterygium preparations increased the rate of liver function test result abnormalities (RR, 4.03; 95% CI, 2.24-7.25; P < 0.001) and altered menstruation (RR, 5.29; 95% CI, 2.09-13.38; P < 0.001). Suboptimal study quality, significant heterogeneity in the primary outcome. Tripterygium preparations may have nephroprotective effects, but high-quality trials are required to reliably determine the balance of benefits and harms.

Mechanisms and Treatment of CKD

As CKD continues to increase worldwide, along with the demand for related life-saving therapies, the financial burden of CKD will place an increasing drain on health care systems. Experimental studies showed that glomerular capillary hypertension and impaired sieving function with consequent protein overload play a pathogenic role in the progression of CKD. Consistently, human studies show that proteinuria is an independent predictor of progression and that its reduction is renoprotective. At comparable BP control, inhibitors of the renin-angiotensin system (RAS), including angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), more effectively than non-RAS inhibitor therapy reduce proteinuria, slow progression to ESRD, and even improve the kidney function achieving disease regression in some cases. In participants with diabetes, RAS inhibitors delay the onset of microalbuminuria and its progression to macroalbuminuria, and ACE inhibitors may reduce the excess cardiovascular mortality associated with diabetic renal disease. In addition to RAS inhibitors, however, multimodal approaches including lifestyle modifications and multidrug therapy will be required in most cases to optimize control of the several risk factors for CKD and related cardiovascular morbidity. Whether novel medications may help further improve the cost-effectiveness of renoprotective interventions is a matter of investigation.

Impact of Dietary Protein Exchange 0n Patient’s Compliance, Applicability and Efficiency in Chronic Kidney Disease

The application of Low Protein Diet (LPD) in the treatment of CKD has been more accepted by all medical stuffs nowadays. However, the diversity and complexity of therapeutic diet as well as being difficult to obtain more detailed consultation have caused poor long-term maintenance and compliance in most patients.To investigate patient’s compliance to dietary therapy as well as the impact of Dietary Protein Exchange (DPE) on patient’s compliance in CKD patients.To investigate patient’s self understanding and prehension to educational resources on DPE in CKD patients.CKD patients are diagnosed in clinics from 6 hospitals according to the random digits table. 200 enrolled patients are randomly divided into test groups and control groups after signing the concent forms.Test groups:Face to face education of the utilization of new DPE as well as attentions in follow-up is conducted by dietitians.Control groups:Regular face to face counseling as well as attentions in follow-up is conducted by dietitians.Time arrangement for follow-up,3 times within 24 weeks (week 4, 12 and 24 respectively).180 cases completed the trail. Compared with control group, the test group patients’s compliance with DPI was better, 58.5±6.8 gvs45.6±8.9 g p