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Aim Cardiovascular diseases (CVD) are the leading cause of death in patients with chronic kidney disease (CKD), and the risk of CVD increases with reductions in renal function. This study aims to investigate the potential roles of B lymphocyte populations in subclinical atherosclerosis (measured by intima-media thickness, IMT) and prognosis in elderly patients with moderate-to-severe CKD. Methods In this study, a total of 219 patients (143 moderate-to-severe CKD patients with stage 3–4 and 76 non-CKD controls) were recruited. B cell subsets: CD19(+)CD5(+) and CD19(+)CD5(−) B cells were analyzed by flow cytometry. Intima-media thickness (IMT) was measured by ultrasound. Correlations between the B cell subsets with IMT and clinical outcome was analyzed. Results CKD patients showed increased IMT (P = 0.006). The level of CD19(+)CD5(+) and CD19(+)CD5(−) B cells were decreased in CKD patients. Correlation analysis showed that IMT was positively correlated with systolic blood pressure, protein/creatinine ratio and diabetes (P P P 9 /L) and CD19(+)CD5(−) B cells (≤ 0.05 × 109 /L) (P P P Conclusions Our results showed that decreased CD19(+)CD5(+) and CD19(+)CD5(−) B lymphocytes were correlated with atherosclerosis and worse survival, which indicates that B lymphocytes might involve in atherosclerosis and associated the prognosis of elderly patients with moderate-to-severe CKD.

The early detection of a kidney injury is essential to protect against the progression of kidney damage owing to the progressive nature of chronic kidney disease. A renal biopsy is the gold standard for the assessment of pathological alterations such as interstitial fibrosis and glomerulosclerosis. However, there are concerns regarding potential complications including bleeding and a reduction in renal function. Ultrasound elastography is an ideal modality for assessing the alterations in various organs and diagnosing malignant tumors. This technique has the potential to help detect early changes in renal function and pathological alterations. However, the careful application and interpretation of this technique in the kidney is required because of its complex hemodynamics and architecture. Shear wave elastography is the most widely investigated technique among ultrasound elastography. This review aims to summarize the previous investigations of the kidney using shear wave elastography, particularly for renal malignancy, kidney transplantation, and chronic kidney disease. Additionally, we have highlighted the influencing factors concerning the practical measurement of renal elasticity.

The aim of the paper is to evaluate the significance of absolute and relative renal length in the diagnoses of several chronic kidney diseases (CKDs) in which kidney size changes in different manners during the disease course. The study included 181 patients: 35 with Balkan endemic nephropathy (BEN), 31 with diabetic nephropathy (DN), 30 with primary glomerular diseases (GN), 30 with autosomal recessive polycystic kidney disease (ADPKD), and 58 healthy controls (C). Absolute renal length was the distance between two most distant points on their poles and it was measured ultrasonographically, and relative length was obtained as the ratio of renal length and body height (kidney/body ratio, KBR). In the statistical analysis, One Way ANOVA test was used to establish the differences in absolute lengths and KBR between the studied groups;  test was used to establish the differences in the number of examinees of male and female gender; correlation and linear regression analysis were used to assess the association between age of the examinees and absolute and relative parameters of kidney size. The obtained results demonstrated that the average lengths of the right and left kidney were highest in ADPKD and lowest in BEN group. The average values of KBR of the right and left kidney showed a trend similar to that of average absolute lengths in all groups, except in GN and DN groups, in which absolute parameters of kidney size differed significantly from relative parameters. The correlation analysis showed that a significant negative correlation between age and absolute i.e. relative parameters of kidney size existed only in BEN group, but even in this case the differences between correlation coefficients of absolute and relative length of both kidneys were not statistically significant. Based on the obtained results, we could not establish the advantage of absolute over relative kidney length and vice versa in the studied CKDs. Further studies of larger patient samples with better gender and age distribution are therefore warranted. Acta Medica Medianae 2015;54(2):17-23.

Backgroud. Anemia is one of the laboratory and clinical findings of chronic kidney diseases (CKD). The presence of anemia in patients with CKD has a wide range of clinically important consequences. Some of the symptoms that were previously attributed to reduced renal function are, in fact, a consequence of anemia. Anemia contributes to increased cardiac output, the development of left ventricular hypertrophy, angina, and congestive heart failure. According to current knowledge, anemia also contributes to the progression of CKD and is one of the factors that contribute to the high morbidity and mortality in patients with chronic renal failure and their reduced survival. Methods MEDLINE search was performed to collect both original and review articles addressing anemia in CKD, pathophysiology of renal anemia, erythropoiesis, erythropoietin, iron metabolism, inflammation, malnutrition, drugs, renal replacement therapy and anemia management Conclusion The present review summarized current knowledge in the field of the pathophysiology of renel anemia. Understanding the pathophysiology of anemia in CKD is crucial for the optimal treatment of anemia according to recent clinical practice guidelines and recommendation, and correct recognition of causes of resistence to treatment of erythropoietin stimulating agents (ESA).

A significant number of people in the North Central Province of Sri Lanka suffer from chronic kidney diseases (CKD), and the author revisits existing literature related to CKD to find its causative factor. There is a direct connection between high fluoride levels in drinking water and kidney disease, and there are unhealthy levels of fluoride in the groundwater in Sri Lanka's CKD-affected areas. Based on the following observations, the author believes with confidence that excess fluoride in drinking water and in the locally grown food in the affected areas are the culprits of CKD in Sri Lanka. Fluoride excretion rate is considerably lower in children than adults, leading to renal damage of children living in areas with high fluoride. Adults who had renal damage due to fluoride in childhood are vulnerable to CKD with continued consumption of water from the same source. Patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. High content of fluoride in groundwater paves the way to excess fluoride in local food crops, consequently adding more fluoride to the systems of the consumers. People who work outdoors for prolonged periods consume excess water and tea, and are subjected to additional doses of fluoride in their system. In the mid-1980s, the increase in water table levels of the affected areas due to new irrigation projects paved the way to adding more fluorides to their system through drinking water and locally grown foods.

Introduction: The introduction of direct-acting antiviral (DAA)-based therapies for hepatitis C virus (HCV) has revolutionized the approach to HCV treatment. The data of sofosubvir based regimen in HCV infected Chronic Kidney Diseases (CKD) Patients on maintenance hemodialys (MHD) is not widely available. Our study was aimed to evaluate the effect of sofosbuvir–Ledipasvircombinationregimen in HCV positive CKD patient on MHD. Materials and Methods: Patients aged more than 12 years with HCV RNA positive and on MHD were included. Patients having liver cirrhosis and already started DAAs were excluded. Before starting treatment genotype, viral load routine clinical and laboratory data (CBC, SGPT, S.Albumin, S.Fetoprotein) were collected at baseline and also at 4, 12, and 24weeks during the treatment. All patients irrespective of genotypes were started sofosbuvir 400mg plus Ledipasvir 90 mg combination alternate day for 12 weeks. HCV RNA viral load was assessed at the end of 4, 12 and 24wks.We evaluated early virological response (EVR) at end of 4th weeks, end of treatment response (ETR) at the end of 12 weeks and sustained virological response (SVR) at the end of 24 weeks after initiation of therapy. Results: We had enrolled 210 HCV RNA patients with male (n=166) predominance with mean age of 31.6±10 years. Genotype 1 in 179 (85.2%) and genotype 3 in 31(14.8%) were found. 208 patients (99.03%) had achieved complete response at 12 wks (SVR12). 2 patients (1b,3) did not respond even at 24 wks. None of patient discontinued therapy because of side effects. No significant change in hemoglobin, platelet count and bilirubin. Conclusions: Sofosbuvir-Ledipasvir therapy on alternate day for 12 weeks was found effective therapy for HCV?infected CKD patients on MHD. Keywords: Sofosbuvir, Ledipasvir, HCV treatment, Haemodialysis, Western India.

Introduction: There are few studies on comparison of iron status markers between anemia due to iron deficiency and anemia due to chronic kidney disease. Objective: To study iron status markers in iron deficiency anemia and anemia of chronic kidney diseases and compare them. Materials and Methods: A Hospital based cross sectional comparative study was carried out among 60 study subjects over a period of one year. 30 of them were having anemia due to iron deficiency and 30 of them were having anemia due to chronic kidney disease. 5 ml venous blood was collected with all universal precautions from all cases and controls. Total iron binding capacity (TIBC), serum iron, and serum ferritin were assessed among cases of IDA and healthy controls using standard methods only. Results: Hemoglobin percentage in IDA and anemia of CKD is not significant, where as serum iron, TIBC, serum ferritin and transferrin saturation percentage are significant in IDA group when compared to anemia in CKD group. But the severity of anemia as measured by hemoglobin level was more in patients with CKD. Conclusion: The severity of anemia was more in patients with chronic kidney disease compared to patients with anemia due to iron deficiency. Keywords: Iron status markers, Anemia, Comparison, Diagnosis, Severity.

Acute and chronic kidney diseases have devastating consequences on human health. Renal vascular function, glomerular filtration, and epithelial transport are required for water and electrolyte homeostasis. Nephrotoxicity and diseases such as hypertension, diabetes, and metabolic syndrome contribute significantly to acute and chronic kidney diseases (Barnett and Cummings, 2018). These pathological states impact on renal vascular and epithelial function and the ability for the kidney to maintain water and electrolyte homeostasis. Experimental and clinical studies over the past decade determined that there is a transition from acute to chronic kidney injury (Fiorentino et al., 2018). Acute kidney injury in the clinical setting can cause sustained alterations in epithelial transport and renal hemodynamics that increase the risk for developing chronic kidney disease (Sharfuddin and Molitoris, 2011). Currently, there are extremely limited options to treat acute and chronic kidney diseases. A Research Topic on acute and chronic kidney diseases is timely because this is a very fast-moving field that is focused on the tremendous need for kidney disease therapeutics. Articles in this Research Topic advance our understanding of organismal, cellular, and molecular mechanisms that contribute to acute and chronic kidney diseases. The Research Topic has broad interest since it covers acute kidney injury, chronic kidney disease, diabetic nephropathy, and hypertension mediated kidney disease. Research articles span cell signaling, animal studies, human and animal disease pathology studies, renal hemodynamics, glomerular filtration, and renal epithelial transport studies. Thirty contributions focus on novel developments defining renal vascular and epithelial mechanisms that contribute to acute and chronic kidney diseases.

We identified 1-oxa-4,9-diazaspiro[5.5]undecane-based trisubstituted ureas as highly potent soluble epoxide hydrolase (sEH) inhibitors and orally active agents for treating chronic kidney diseases. Compound 19 exhibited excellent sEH inhibitory activity and bioavailability. When administered orally at 30 mg/kg, 19 lowered serum creatinine in a rat model of anti-glomerular basement membrane glomerulonephritis but 2,8-diazaspiro[4.5]decane-based trisubstituted ureas did not. These results suggest that 19 is an orally active drug candidate for treating chronic kidney diseases.

Podocytes are essential components of the glomerular basement membrane. Epithelial-mesenchymal-transition (EMT) in podocytes results in proteinuria. Fibroblast growth factor 1 (FGF1) protects renal function against diabetic nephropathy (DN). In the present study, we showed that treatment with an FGF1 variant with decreased mitogenic potency (FGF1ΔHBS) inhibited podocyte EMT, depletion, renal fibrosis, and preserved renal function in two nephropathy models. Mechanistic studies revealed that the inhibitory effects of FGF1ΔHBS podocyte EMT were mediated by decreased expression of transforming growth factor β1 via upregulation of PPARγ. FGF1ΔHBS enhanced the interaction between PPARγ and SMAD3 and suppressed SMAD3 nuclei translocation. We found that the anti-EMT activities of FGF1ΔHBS were independent of glucose-lowering effects. These findings expand the potential uses of FGF1ΔHBS in the treatment of diseases associated with EMT.

Introduction: Cerebral small vessel diseases (SVDs) i.e. white matter lesion and cerebral microbleeds (CMBs) are related to the patients with stroke more deeply than those without. In general population, in addition to age, hypertension, diabetes chronic kidney diseases (CKD) is well known to be related to SVDs, but it remains unclear in patients with stroke. We investigated the relationship between CKD and the presence of SVDs in patients with acute ischemic stroke. Methods: We enrolled 493 patients with acute ischemic stroke patients or transient ischemic attack patients (mean age 71; 60% male) who had undergone 1.5T MR imaging within a week of the index events from April 2013 to march 2015. We evaluated kidney function by estimated glomerular filtration rate (eGFR) with the modification of diet in Renal Disease. CKD was defined as an eGFR less than 60mil/min/1.73m 2 . CMBs were defined as focal areas of very low signal intensity smaller than 10mm. White matter lesion as Periventricular hyper intensity (PVH)>grade 2 and Deep and Subcortical White Matter Hyper intensity (DSWMH)> grade 2 were defied as advanced PVH and advanced DSWMH, respectively. We investigated relationship between CKD and CMBs, advanced PVH and advanced DSWMH using a logistic regression analysis. Results: We noted CMBs in 173 patients (35%), PVH in 81 (16%), and DSWMH in 151 (31%). An univariate analysis revealed that the age, CKD, history of stroke, and antiplatelet agents were associated with presence of CMBs, advanced PVH and severe DSWMH . The multivariate analysis revealed that CMBs, advanced PVH and advanced DSWMH were associated with age (CMBs: odds ratio(OR) ; 1.32 ; 95% confidence interval(CI), 1.10-1.60, p=0.004, advanced PVH : OR ; 3.00 ; 95% CI, 2.17-4.26, p Conclusions: It seems that age and history of stroke are related to CMBs, advanced PVH and advanced DSWMH, and that CKD is associates with CMBs but not with either advanced PVH or advanced DSWMH.

Since 2008, the Japanese government has started measures against chronic kidney disease (CKD), and steady changes have been achieved, including a decrease in the age-adjusted rate of new dialysis introduction. However, the total number of dialysis patients has not declined because of the progression of aging. Therefore, the Japanese government has started more concrete measures since 2018. It aims to prevent CKD exacerbation mainly by early referrals to nephrologists using “criteria for referral from a primary care physician to a kidney specialist/specialized medical institution”. In addition, key performance indicators are set to reduce the number of new dialysis patients from 39,000 in 2016 to ≤ 35,000 by 2028. We hope that you can refer to this measure all over the world and proceed with CKD measures. This report has been originally notified from the Ministry of Health, Labor and Welfare in Japanese. This is the English version of it.

Objective The aim of this article was to assess the association between low-carbohydrate high-protein (LCHP) diet score and the risk of incident chronic kidney disease (CKD). Design and Methods This cohort study was conducted on 1,797 Iranian participants, aged ≥20 years, followed-up for a mean of 6.1 years. Using a valid and reliable food-frequency questionnaire at baseline, LCHP diet score between 0 and 12 points were determined. Anthropometric measures and biochemical indicators were assessed. Participants were classified based on their estimated glomerular filtration rate (eGFR) levels using the National Kidney Foundation guidelines; eGFR ≥ 60 mL/minute/1.73 m2 as not having CKD and eGFR Results Mean (standard) age of participants (48% male) was 37.7 (12.2) years at baseline. The median (25-75 interquartile range) of LCHP diet for all subjects was 7 (4-8), and incidence of CKD was 14.1%. After adjusting for age, sex, smoking status, physical activity, total calorie intake, body mass index, diabetes, hypertension, and baseline eGFR, participants in the highest tertile of LCHP diet had greater risk of incident CKD (odds ratio: 1.48; 95% confidence interval: 1.03-2.15), in comparison to those in the lowest one (P for trend = .027). Conclusion Our findings demonstrate the hypothesis that higher score of LCHP diet may have adverse effects on incidence and development of CKD.

INTRODUCTION Both hepatitis C virus infection (HCV) and chronic kidney disease (CKD) have been comorbid illnesses with increasing morbidity and mortality. The present study was conducted to present real-life experiences about treatment of HCV and CKD with a fixed-dose combination of paritaprevir 150 mg/day, ritonavir 100 mg/day as a booster, ombitasvir 25 mg/day, and dasabuvir 250 mg twice/day, the PROD regimen. PATIENTS AND METHODS This was a multicenter, retrospective cohort study. Seventy-five patients with both HCV and CKD were treated with a PROD-based regimen with or without ribavirin. Fifty-three of 75 patients were on maintenance hemodialysis program. Seven patients had compensated liver cirrhosis. The patients with genotype 1a or compensated liver cirrhosis were treated with the PROD regimen and ribavirin in a dose of 200 mg every other day for 12 weeks. The patients with genotype 1b were treated with PROD for 12 weeks. The patients with genotype 4 were treated with a combination of paritaprevir, ritonavir, ombitasvir, and ribavirin 200 mg every other day. RESULTS All patients except one were HCV-RNA negative (98.6%) at the end of treatment. One patient had decompensated after the fourth day of therapy. She stopped the treatment, and she was exitus after 2 months. Two patients died of reasons not related to the drugs 2 months after negativity of HCV-RNA. Sustained viral rate 12 weeks after treatment was found in 96% of the patients. CONCLUSION The PROD regimen was very effective and safe for treatment in patients with HCV and CKD who were in stages 4 and 5.

Background: The burden of symptoms and other concerns in chronic kidney disease (CKD) is known to be high, adversely affecting the quality of life of the growing number of those with this condition in developing countries. In this paper, we describe the protocol of a longitudinal observational study among people living with CKD. The study is developed to assess the bio-psychosocial factors associated with palliative care symptoms and concerns, and pattern of health services usage among Nigerians with stages 3–5 CKD. The overall objective is to establish the evidence-base for advocacy and policy formulation, treatment guidelines, care and services, and future clinical trial studies. Methods: This is a multi-center study to investigate the longitudinal course of symptoms and other concerns among patients with stages 3–5 CKD in Nigeria. Interviewer administered and self-report measures at baseline (T0) and 3-month (T1) address socio-demographic characteristics, clinical-illness related information, palliative care-related symptoms and other concerns, pattern of formal or informal service usage, and bio psychosocial measures including estimated glomerular filtration rate (eGFR), anxiety, depression, quality of life, functioning, social support and spiritual wellbeing. Discussion: This study represents the first longitudinal investigation of palliative care symptoms and concerns among people with CKD in Nigeria. It includes early stages of CKD in compliance with best practices, and a comprehensive range of bio-psychosocial outcomes to understand how these factors are associated with symptoms. This study will provide evidence for how best to integrate palliative care into management of CKD to improve care and quality of life of people with CKD. The study team welcomes collaborations with both national and international researchers.

The relationship of metabolic syndrome (MS) and its components with incident chronic kidney disease (CKD) and rapid decline of estimated glomerular filtration rate (eGFR) was investigated. A total of 10 140 patients participating in the epidemiological study (Risk Evaluation of Cancers in Chinese Diabetic Individuals, REACTION) of risk factors of type 2 diabetes in China were followed up for 3 years, with MS being diagnosed by adult treatment panel III (ATPIII) combined with waist circumference in Asian population and renal function being evaluated by eGFR

Interest in studying the role of the gastrointestinal tract in maintaining homeostasis in chronic kidney disease is a traditional one. It served, in particular, as a starting point for the creation of enterosorbents. However, if earlier the main attention was paid to the mechanical removal of a number of potentially dangerous biologically active substances, recently an intestinal microbiota has become an object of interest. The first part of the review of the literature on this topic is devoted to questions of terminology, the normal physiology of the colon microbiota. A detailed description of dysbiosis is given. The features of the main groups of microorganisms are reflected. The hypothetical and confirmed interrelations of the intestine-kidney axis are presented. The pathogenetic mechanisms of the influence of colon dysbiosis on the processes of local and systemic inflammation are discussed. The influence of dysbiosis on the state of the kidney parenchyma and its participation in the progression of CKD are debated.

Context Thyroid hormones play an important role in renal development, functioning renal mass, and early renal function. Pituitary–thyroid axis and metabolism of the peripheral thyroid hormones have been affected by chronic kidney disease (CKD). Aims The aim was to evaluate the frequency and relationship between thyroid disorders and high-sensitivity C-reactive protein (Hs-CRP) among CKD patients including hemodialysis (HD). Settings and design In Zagazig University Hospital. Participants and methods A case–control study that included 150 adult participants who were divided into: group I which included 50 patients with an estimated glomerular filtration rate (eGFR) of 41.8±23.6 ml/min/1.73 m2. Group II included 50 patients with an eGFR of 11.3±4.2 ml/min/1.73 m2.Group III included 50 participants with normal eGFR. All participants were evaluated for serum creatinine and albumin, complete blood count, estimation of GFR by modification of diet in renal disease (MDRD) equation, and serum thyroid-stimulating hormone (TSH), free T3, free T4, and Hs-CRP. Statistical analysis Using the Statistical Package for the Social Sciences under windows version 20. Qualitative variables were expressed by frequency and percentage, mean±SD, χ2-test, Student’s t-test, analysis of variance (F-test), and correlation analysis. Results The frequency of subclinical hypothyroidism (46%) and overt hypothyroid (42%) in groups I and II, respectively, has been much higher in CKD patients. There was a strong significant negative correlation of Hs-CRP with eGFR, FT3, FT4 (P

the article describes approaches to cost optimization of anemia treatment in CKD–VDst. patients by comparison of costs in phase correction and support treatment with long action ESA in patients on HD and HDF. Aims. To reveal the influence of HD and HDF to summary dozes of ESA in anemia treatment, to reveal the influence of different long action ESA to hemoglobin variability and find connection between HD, HDF and ESA type to cost of ESA using. Materials and methods. There were 14 patients on HD and 14 on HDF. All patients were treated with dialysis 3 time per week, session duration was 4,5–5 hours. eKt/У were 1,39±0,06 in HDF group and 1,29±0,07 in HD group. Mean hemoglobin was 98,3±2,46 g/l in HDF group and 92,76±2,46 g/l in HD group. In correction phase we used pegylated erythropoietin–p in both groups before achievement target hemoglobin 110 g/l, then was support phase ofanemia treatment during 6 months with hemoglobin target 100g/l to 120 g/l. Next 6 months patients were switched to darbepoetin alfa. Results. It is investigated optimization of anemia correction with long action ESP in patients on HD and HDF. It is revealed a tendency to decrease treatment cost with pegylated erythropoietin–p compared to darbepoetin alfa (1965,13±250,69 vs 2117,39±147,59 Gr/mth) and HDF group compared HD group with pegylated erythropoietin–p (1983,9±345,9 vs 1950,69±367,1 Gr/mth). Treatment with darbepoetin alfa associated with higher hemoglobin variability compared with pegylated erythropoietin–p. Conclusion. The result of our investigation lead to prove some hope to optimization of anemia treatment in patients with CKD Vst. On hemodialysis, but to have statistically reliability we need lager patients groups.

Kidney resistive index (RI) correlates with tubulointerstitial changes and predicts renal prognosis. Most patients with chronic kidney diseases (CKDs) manifest high blood pressure and atherosclerotic cardiovascular diseases. In addition, various atherosclerotic indexes relate to variations in blood pressure.Subjects were 70 CKD patients, who visited our office and agreed to measure home blood pressure and receive renal ultrasonography. Cross-sectional analyses were performed.Patient age was averaged 61 ± 15 (SD) y/o and 60% were male. Mean serum creatinine and proteinuria were 1.2 ± 0.5 mg/dl and 0.2 ± 0.5 g/gCr, respectively. Office blood pressure and kidney RI were 128 ± 17/75 ± 11 mmHg and 0.66 ± 0.08, respectively. Multivariate regression analysis revealed that age and office blood pressure independently correlated to kidney RI (p0.05 for each). Home blood pressure was averaged 122 ± 7/70 ± 6 mmHg. Both standard deviation and the maximal-minimal difference in home systolic blood pressure related to kidney RI (p0.05).The present results indicate that office blood pressure correlates to kidney RI, which predicts renal prognosis. In addition, our data implicate that kidney RI relates to variations in home systolic blood pressure, and suggest that kidney RI may be a good index for atherosclerosis in CKD patients.

Chronic kidney diseases-associated pruritus (CKD-aP) affects the patients’ mental and physical health, potentially resulting in fatigue, depression, and directly affecting quality of sleep. Hemodialysis patients were reported to experiencing moderate to extreme CKD-aP, thus exhibited higher possibilities of remaining awake at night while sleeping in the day. Therefore, CKD-aP is attributed toward nocturnal awakenings and difficulty falling asleep. This condition (CKD-aP) significantly impacts the quality of life (QOL), triggering sleep disturbance, mood changes, and uncontrollable scratching. CKD-aP patients have a compromised QOL that is generally linked to limited personal freedom and control due to lengthy treatment time. Overall, the loss of freedom has wider implications, such as altering marital, family, and social relationships.Thus, this writing highlights the vital effect of chronic kidney diseases-associated pruritus on patients’ sleep quality, social and mental well-being and providing comprehensive management and treatment options to improve patients’ qualityof life.

In medical imaging field, ultrasound imaging technique provides a tremendous service on disease recognition. It assists as non-catheterization, hazardous emission-free diagnosis at less expenses of cost. The main aim of this investigation is to detect and recognize the chronic kidney diseases CKD makes initiation and home for dysfunction of several organs of the homo sapiens. It may induce the heart disease, ischemic attack, cardiomyopathy, and cardiac disease through the hypertension. The early prediction of the kidney deformation would save the life from dreadful diseases. Renal sonography is the basic imaging technology used for kidney disease diagnosis. In this work, automatic detection and classification of kidney diseases using deep convolutional architecture have been proposed. For localizing kidney diseases, histogram-based feature along with AdaBoost algorithm is used. Deep convolutional neural network is used to recognize of kidney diseases, and TensorFlow batch prediction method is computed for recognition of diseases categories. The performance accuracy for detection of kidney disease is given as 89.79%. The performance of classification of chronic kidney diseases using CNN achieves an accuracy rate of 86.67%.

Background: secondary hyperparathyroidism (SHPT) is an early complication of chronic kidney disease (CKD). Maintaining the level of 25(OH)D and parathyroid hormone concentrations in the target range reduce its associated complications (fractures and cardiovascular calcification). Aims: to examine the effectiveness of vitamin D supplementation and selective vitamin D receptor agonists treatment on SHPT in CKD. Material and methods: prospective observational study to evaluate the efficacy and safety of vitamin D therapy SHPT in 54 in patients with CKD. The first phase (24 weeks) – treatment of suboptimal 25-hydroxycalciferol (25(OH)D) levels. The second (16 weeks) – treatment colecalciferol-resistant SHPT by combination of cholecalciferol with paricalcitol. Blood samples were taken to assess parathyroid hormone (PTH), 25(OH)D, creatinine, calcium, phosphorus levels and calcium excretion. Results: After 8 weeks of cholecalciferol treatment all patients achieved 25(OH)D levels above 20 ng/ml, however 78% of patients still had SHPT. After 16 weeks, the decrease of PTH was achieved in all patients, but significantly only in patients with CKD 2 (19.2%, p< 0.01) and 3 (31%, p 0.05). After 24 weeks of therapy, PTH normalized in all patients with CKD 2, in 15 (79%) with CKD 3 and in 9 (50%) patients with CKD 4. Cholecalciferol treatment resulted in a substantial increase in 25(OH)D levels with minimal or no impact on calcium, phosphorus levels and kidney function. After 24 weeks we initiated combination therapy (cholecalciferol and paricalcitol) for patients with colecalciferol-resistant SHPT (n=13). PTH levels decreased from 149.1±13.4 to 118.2±14.1 pg/ml at 8 weeks, and to 93.1±9.7 pg/ml (p

Background Urinary mitochondrial DNA (mtDNA) fragment level has been proposed as a biomarker of chronic kidney disease (CKD). In this study, we determine the relation between urinary mtDNA level and rate of renal function deterioration in non-diabetic CKD. Methods We recruited 102 non-diabetic CKD patients (43 with kidney biopsy that showed non-specific nephrosclerosis). Urinary mtDNA level was measured and compared to baseline clinical and pathological parameters. The patients were followed 48.3 ± 31.8 months for renal events (need of dialysis or over 30% reduction in estimated glomerular filtration rate [eGFR]). Results The median urinary mtDNA level was 1519.42 (inter-quartile range 511.81–3073.03) million copy/mmol creatinine. There were significant correlations between urinary mtDNA level and baseline eGFR (r = 0.429, p

Chronic kidney disease is the most common form of kidney disease and high blood pressure is the most common cause the pressure on the glomeruli increases due to high blood pressure which can prove to be very dangerous. Lack in VITAMIN D isn't restricted to the dynamic chemical, calcitriol (25-hydroxycholecalciferol) is likewise insufficient in many patients with constant kidney sickness (CKD), free of their fundamental renal capacity. Diminishes in calcitriol happen generally right off the bat in the movement of kidney illness and may originate before the increment in PTH. These progressions in calcitriol and PTH add to the upkeep of moderately ordinary serum and calcium fixations until the glomerular filtration rate (GFR) diminishes to

Diabetes induces glomerular hyperfiltration, affects kidney function, and may lead to chronic kidney diseases. A novel therapeutic treatment for diabetic patients targets the sodium–glucose cotransporter isoform 2 (SGLT2) in the kidney. SGLT2 inhibitors enhance urinary glucose, $$\hbox {Na}^+$$ and fluid excretion and lower hyperglycemia in diabetes by inhibiting $$\hbox {Na}^+$$ and glucose reabsorption along the proximal convoluted tubule. A goal of this study is to predict the effects of SGLT2 inhibitors in diabetic patients with and without chronic kidney diseases. To that end, we applied computational rat kidney models to assess how SGLT2 inhibition affects renal solute transport and metabolism when nephron population are normal or reduced (the latter simulates chronic kidney disease). The model predicts that SGLT2 inhibition induces glucosuria and natriuresis, with those effects enhanced in a remnant kidney. The model also predicts that the $$\hbox {Na}^+$$ transport load and thus oxygen consumption of the S3 segment are increased under SGLT2 inhibition, a consequence that may increase the risk of hypoxia for that segment. To protect the vulnerable S3 segment, we explore dual SGLT2/SGLT1 inhibition and seek to determine the optimal combination that would yield sufficient urinary glucose excretion while limiting the metabolic load on the S3 segment. The model predicts that the optimal combination of SGLT2/SGLT1 inhibition lowers the oxygen requirements of key tubular segments, but decreases urine flow and $$\hbox {Na}^+$$ excretion; the latter effect may limit the cardiovascular protection of the treatment.

Poor long-term adherence and persistence to drug therapy is universally recognized as one of the major clinical issues in the management of chronic diseases, and patients with renal diseases are also concerned by this important phenomenon. Chronic kidney disease (CKD) patients belong to the group of subjects with one of the highest burdens of daily pill intake with up to >20 pills per day depending on the severity of their disease. The purpose of the present review is to discuss the difficulties encountered by nephrologists in diagnosing and managing poor adherence and persistence in CKD patients including in patients receiving maintenance dialysis. Our review will also attempt to provide some clues and new perspectives on how drug adherence could actually be addressed and possibly improved. Working on drug adherence may look like a long and tedious path, but physicians and healthcare providers should always be aware that drug adherence is in general much lower than what they may think and that there are many ways to improve and support drug adherence and persistence so that renal patients obtain the full benefits of their treatments.

The incident of Kidney Disease increased year by years. Hemodialysis treatment is one of supportive therapies that can be maintained in health conditions of the chronocal kidney disease patient. This therapy can not replace the fuction of the kidney, however it could manage the quality of life of the kidney disease patients. The research descriptive qualitative approach was used in this study. The research results found 5 themes about chronic kidney disease patients with hemodyalisis. Those five themes were the knowledge of hemodynamic therapy, the impact of hemodynamic therapy, patients coping during the treatment process, family support and chronic kidney disease with hemodynamic therapy.

BACKGROUND: Hypertension is common among children with chronic kidney disease (CKD), and dihydropyridine calcium channel blockers (dhCCBs) are frequently used as treatment. The impact of dhCCBs on proteinuria in children with CKD is unclear. METHODS: Data from 722 participants in the Chronic Kidney Disease in Children (CKiD) longitudinal cohort with a median age of 12 years were used to assess the association between dhCCBs and log transformed urine protein/creatinine levels as well as blood pressure control measured at annual visits. Angiotensin-converting enzyme inhibitor (ACEi) and angiotensin receptor blocker (ARB) use was evaluated as an effect measure modifier. RESULTS: Individuals using dhCCBs had 18.8% higher urine protein/creatinine levels compared to those with no history of dhCCB or ACEi and ARB use. Among individuals using ACEi and ARB therapy concomitantly, dhCCB use was not associated with an increase in proteinuria. Those using dhCCBs had higher systolic and diastolic blood pressures. CONCLUSIONS: Use of dhCCBs in children with CKD and hypertension is associated with higher levels of proteinuria and was not found to be associated with improved blood pressure control.

Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, imposing a great burden on the healthcare system. Regrettably, effective CKD therapeutic strategies are yet available due to their elusive pathogenic mechanisms. CKD is featured by progressive inflammation and fibrosis associated with immune cell dysfunction, leading to the formation of an inflammatory microenvironment, which ultimately exacerbating renal fibrosis. Transforming growth factor β1 (TGF-β1) is an indispensable immunoregulator promoting CKD progression by controlling the activation, proliferation, and apoptosis of immunocytes via both canonical and non-canonical pathways. More importantly, recent studies have uncovered a new mechanism of TGF-β1 for de novo generation of myofibroblast via macrophage-myofibroblast transition (MMT). This review will update the versatile roles of TGF-β signaling in the dynamics of renal immunity, a better understanding may facilitate the discovery of novel therapeutic strategies against CKD.

Background As chronic kidney disease (CKD) is amongst the current global health challenges, this study is aiming to evaluate the long-term intake of total polyphenol and its subclasses in association with CKD incidence. Methods For the purpose of this study, a sample of 3021 Iranian adults (47 % men, aged 20–79 years) with no CKD diagnosis at baseline, were selected from the Tehran Lipid and Glucose Study population. The total intake of polyphenol and its major subclasses were assessed by a validated food frequency questionnaire and categorized as flavonoids, phenolic acids, stilbenes, and lignans. Although the morphological abnormalities of the kidneys or 3-month persistent urinalysis can distinctively define CKD, the glomerular filtration rate (eGFR) reduction is accepted as a more precise index of renal function. Therefore, eGFR 2 was the exclusive index of CKD diagnosis in the current study. The eGFR was calculated by the Modification of Diet in Renal Disease Study equation. Cox-regression analysis was used to assess the hazard ratio and 95 % confidence intervals of CKD in quartiles of the total polyphenols. Results In this study, 355 CKD cases over 11,058.464 person-years was reported. The median (IQR) age of participants was 36 years (27–46) at baseline. Moderate intake of lignans (≤ 6.8 mg) was negatively associated with the incidence of CKD in the adjusted model. No significant associations were detected between higher amounts of lignin and total polyphenols (HR: 0.97, 95 % CI 0.67–1.40) and CKD incidence. Conclusions Based on the current findings, moderate intake of lignin possess CKD-protective properties by approximately 32 %. No independent associations were observed between higher amounts of lignins and CKD incidence.

Objectives The mortality of patients with chronic kidney diseases (CKD) increases with the decrease in glomerular filtration rate (eGFR). In the progress of CKD that is closely linked to non-communicable diseases (NCDs), the role of coenzyme Q10 (CoQ10) is not fully evaluated. We aimed to evaluate the importance of CoQ10, CoQ10/cholesterol ratio, and oxidative stress in the progress of CKD. Patients and methods The control group was constituted of 19 healthy subjects who volunteered to enrol in the study, CKD group consisted of 58 patients with CKD, of whom 54 had CKD combined with hypertension, 22 had CKD combined with hypertension and diabetes type 2 , and 18 had CKD combined with hypertension and statin therapy. We observed age, BMI, creatinine, uric acid, eGFR, hemoglobin, CRP, glucose, lipids fraction, and liver enzymes. Coenzyme Q10-TOTAL (ubiquinol+ubiquinone) in platelets and plasma were determined using HPLC method with UV detection. Indexed of CoQ10/lipid fractions were evaluated. Oxidative stress was determined as thiobarbituric acid‑reactive substances (TBARS). Results With increased stages of CKD, eGFR and CoQ10 as well as its ratio to lipids were significantly reduced while TBARS increased. Conclusion We assume that lower endogenous CoQ10 level may be one of the reasons of kidney dysfunction. CoQ10/lipids ratio and increase in oxidative stress can predict the progression of CKD in patients with arterial hypertension, diabetes mellitus and dyslipidemia (Tab. 2, Fig. 4, Ref. 49).

Diabetic nephropathy, hypertension, and glomerulonephritis are the most common causes of chronic kidney diseases (CKD). Since CKD of various origins may not become apparent until kidney function is significantly impaired, a differential diagnosis and an appropriate treatment are needed at the very early stages. Conventional biomarkers may not have sufficient separation capabilities, while a full-proteomic approach may be used for these purposes. In the current study, several machine learning algorithms were examined for the differential diagnosis of CKD of three origins. The tested dataset was based on whole proteomic data obtained after the mass spectrometric analysis of plasma and urine samples of 34 CKD patients and the use of label-free quantification approach. The k-nearest-neighbors algorithm showed the possibility of separation of a healthy group from renal patients in general by proteomics data of plasma with high confidence (97.8%). This algorithm has also be proven to be the best of the three tested for distinguishing the groups of patients with diabetic nephropathy and glomerulonephritis according to proteomics data of plasma (96.3% of correct decisions). The group of hypertensive nephropathy could not be reliably separated according to plasma data, whereas analysis of entire proteomics data of urine did not allow differentiating the three diseases. Nevertheless, the group of hypertensive nephropathy was reliably separated from all other renal patients using the k-nearest-neighbors classifier &ldquo, one against all&rdquo, with 100% of accuracy by urine proteome data. The tested algorithms show good abilities to differentiate the various groups across proteomic data sets, which may help to avoid invasive intervention for the verification of the glomerulonephritis subtypes, as well as to differentiate hypertensive and diabetic nephropathy in the early stages based not on individual biomarkers, but on the whole proteomic composition of urine and blood.

Almost 50–90% of chronic kidney disease patients undergoing haemodialysis have been reported to have Chronic kidney disease-associated pruritus (CKD-aP). The intensity of CKD-aP may vary from a mild itch to an unbearable pruritic sensation which interferes with the patient’s quality of life. CKD-aP has become one of the upmost distressing cutaneous and most common symptom of chronic kidney disease which is often overlooked by nephrologists, primary care physicians, and other health-care professionals. Typically sleep disorders, mental and social well-being have been correlated with chronic kidney disease patients. With that this article presents vital comprehensive review which includes epidemiology of chronic kidney disease in Malaysia and Pakistan, CKD-associated pruritus and other dermatological disorders associated with chronic kidney diseases, pathophysiology of CKD-associated pruritus, clinical features of chronic kidney disease-associated pruritus, diagnosis of CKD-associated uremic pruritus, differential diagnosis of CKD-associated uremic pruritus, assessment and quantification of pruritus severity.

The final dilution of urine is regulated via aquaporin-2 water channels in the distal part of the nephron. It is unclear whether urine dilution ability in autosomal dominant polycystic kidney disease patients (ADPKD patients) differs from other patients with similar degree of impaired renal function (non-ADPKD patients). The purpose of this case control study was to measure urine dilution ability in ADPKD patients compared to non-ADPKD patients and healthy controls. Methods. Eighteen ADPKD, 16 non-ADPKD patients (both with chronic kidney disease, stage I-IV), and 18 healthy controls received an oral water load of 20 ml/kg body weight. Urine was collected in 7 consecutive periods. We measured free water clearance (CH2O), urine osmolality, urine output, fractional excretion of sodium, urine aquaporin2 (u-AQP2), and urine epithelial sodium channel (u-ENaC). Blood samples were drawn four times (at baseline, 2 h, 4 h, and 6 hours after the water load) for analyses of plasma osmolality, vasopressin, renin, angiotensin II, and aldosterone. Brachial and central blood pressure was measured regularly during the test. Results. The three groups were age and gender matched, and the patient groups had similar renal function. One hour after water load, the ADPKD patients had an increased CH2O compared to non-ADPKD patients (2.97 ± 2.42 ml/min in ADPKD patients vs. 1.31 ± 1.50 ml/min in non-ADPKD patients, p 0.029 ). The reduction in u-AQP2 and u-ENaC occurred earlier in ADPKD than in non-ADPKD patients. Plasma concentrations of vasopressin, renin, angiotensin II, and aldosterone and blood pressure measurements did not show any differences that could explain the deviation in urine dilution capacity between the patient groups. Conclusions. ADPKD patients had a higher CH2O than non-ADPKD patients after an oral water load, and u-AQP2 and u-ENaC were more rapidly reduced than in non-ADPKD patients. Thus, urine-diluting capacity may be better preserved in ADPKD patients than in non-ADPKD patients.

In the clinic, the pathological types of chronic kidney diseases (CKD) are considered references for choosing treatment protocols. From a statistical viewpoint, a non-invasive method to predict pathological types of CKD is a focus of our work. In the current study, following a frequency analysis of the clinical indices of 588 CKD patients in the department of nephrology, a third-grade class-A hospital, a novel theory is proposed: “bi-directional cumulative probability dichotomy”. Further, two models for the prediction and differential diagnosis of CKD pathological type are established. The former indicates an occurrence probability of the pathological types, and the latter indicates an occurrence of CKD pathological type according to logistic binary regression. To verify the models, data were collected from 135 patients, and the results showed that the highest accuracy rate on membranous nephropathy (MN-100%), followed by IgA nephropathy (IgAN-83.33%) and mild lesion type (MLN-73.53%), whereas lower prediction accuracy was observed for mesangial proliferative glomerulonephritis (0%) and focal segmental sclerosis type (21.74%). The models of bi-directional probability prediction and differential diagnosis indicate a good prediction value in MN, IgAN and MLN and may be considered alternative methods for the pathological discrimination of CKD patients who are unable to undergo renal biopsy.

Anti-endothelial cell antibodies (AECA) have been reported to cause endothelial dysfunction, but their clinical importance for tissue-specific endothelial cells is not clear. We hypothesized that AECA reactive with human kidney endothelial cells (HKEC) may cause renal endothelial dysfunction in patients with chronic kidney diseases. We report that a higher fraction (56%) of end-stage renal disease (ESRD) patients than healthy controls (5%) have AECA reactive against kidney endothelial cells ( P 2+and rearrangement of actin filaments in HKEC compared with controls. This was followed by an enhancement in protein flux and phosphorylation of VE-cadherin, events associated with augmented endothelial cell permeability. Additionally, kidney biopsies from ESRD patients with AECA but not controls demonstrated a marked decrease in adherens and tight junctions in glomerular endothelium, confirming our in vitro data. In summary, our data demonstrate a causal link between AECA and their capacity to induce alterations in glomerular vascular permeability.

Introduction:chronic kidney disease is an important risk factor for cardiovascular-related morbidity and death. In Ghana, relatively little is known about the prevalence of chronic kidney disease (CKD) in homeless and slum dwellers in the major cities of the country. This study aimed at determining the prevalence of CKD among homeless people in Nima and Agbogbloshie, Accra, Ghana, and to evaluate the association between socio demographic characteristics and CKD. Methods:we recorded information on individuals' socio-demographic characteristics and anthropometric indices, and took blood samples from a total of 512 homeless participants for serum creatinine measurement. Renal function was estimated according to the 4-variable Modification of Diet in Renal Disease (MDRD) and Cockcroft–Gault (C-G) equations. Results:participants with normal serum creatinine (SCr), made up of 232 males and 280 females totaling 512 took part in the study. Those with normal glomerular filtration rate (GFR) were 86% and 84.6% by means of the C-G and MDRD equations respectively. According to the C-G formula, kidney damage and mild to severe renal insufficiency was found in 13.2% of the participants and 4 participants (0.8%) had renal failure. On the other hand, 15.4% of the participants were found to have some kidney damage and mild to severe renal insufficiency according to the MDRD formula with no participant suffering from kidney failure. Conclusion:the prevalence of CKD among the homeless Ghanaians was significant, especially among those with hypertension, diabetes and human immunodeficiency syndrome virus (HIV) infection.

Acute and chronic renal failure have long been described and now renamed as acute kidney injury (AKI) and chronic kidney disease (CKD). New concepts are emerging in the pathophysiology of kidney diseases. AKI is often caused by triggering factors (e.g., toxic, ischemic, immunologic) either individually or combined such as in sepsis (inflammation and hypoxia), and it is initiated at a defined time. Several experimental models of AKI have provided deep insight and have convincingly shown important proof-of-concepts of therapeutic relevance over the years. CKD is now considered a slowly developing disease with often an insidious course, lasting many years whereby co-morbidities (e.g., diabetes, hypertension, dysmetabolic syndrome) may act as worsening factors. It has become increasingly evident that even a single event of AKI may lead to a higher predisposition to develop a progressive CKD. In the present review, we will report studies on the renal protection by adult stem cells in different experimental models and clinical trials. The emerging role of extracellular vesicles (EVs) in cell-to-cell communication and their predominant effect in the paracrine mechanisms of stem cell-dependent actions have prompted several studies on their ability to attenuate both AKI and fibrosis occurring in CKD. We discuss several critical issues that need to be addressed before EVs may have a therapeutic application in humans.

Background and Aims We have recently demonstrated that small molecule inhibitors of CCR2 rapidly reduced proteinuria and preserved renal structure in animal models of diabetic nephropathy (DN) and focal segmental glomerular sclerosis (FSGS). Similar beneficial effects of CCR2 inhibition were also observed in DN patients in a large diabetic nephropathy Phase 2 clinical trial. Despite its rapid and robust effects in these kidney diseases, the mechanism by which CCR2 inhibition affords such renal protection remains unclear. CCR2 is well-known to be expressed on cells of the immune system, where it mediates inflammation and immunological functions by controlling the trafficking of monocytes and T cells. However, immune cell expression of CCR2 may not adequately explain the rapid pharmacologic benefits of CCR2 inhibitors in DN and FSGS because these diseases do not exhibit appreciable kidney inflammation. To better understand the protective mechanism(s) of CCR2 inhibition in renal diseases, we have used a variety of in vivo nephropathy models to determine if CCR2 is expressed on kidney parenchymal cells. Our results suggest that a subset of CD45 negative, renal parietal epithelial cells express CCR2. Method To characterize CCR2 expression in the kidney we used CCR2 RFP heterozygous mice (CCR2RFP/+) in which one copy of CCR2 was replaced by red fluorescent protein (RFP), whose expression is under the control of the endogenous CCR2 promoter. This approach provided a highly sensitive method for CCR2 detection by both flow cytometry and immunofluorescence, and compensated for the lack of validated, commercially available anti-CCR2 antibodies. Enriched glomerular cells were obtained by a non-enzymatic disruption of kidneys, followed by centrifugation at low speed (80gs), and sieving through 300µm and 150µm meshes. The Adriamycin (ADR)-nephropathy model with CCR2 RFP heterozygous mice was used to determine CCR2 expression on renal cells. 5/6 nephrectomy models of FSGS, as well as the db/db diabetic nephropathy model were used to access the change of activated parietal epithelial cells and proteinuria, both in the presence and absence of a CCR2 inhibitor in the setting of kidney injury. Results We observed dramatic increases in the number of activated parietal epithelial cells (PECs, identified as CD133+CD24+CD44hi cells by flow cytometry) in all three renal disease models. In the ADR nephropathy model, we found that in 30-40% of activated PEC cells within an enriched population of glomerular cells expressed CCR2/RFP. CD44hi RFP+ increased much more dramatically than CD44hi RFP- cells in response to ADR, and this was highly correlated with proteinuria, suggesting that CCR2 plays an important role in PEC cell activation and kidney pathology in ADR induced kidney injury. Furthermore, we found that blocking CCR2 with the CCR2-specific antagonist CCX872 significantly reduced both proteinuria and the number of activated PECs in the 5/6 nephropathy and db/db diabetic nephropathy models. Conclusion This is the first report that CCR2 is present on a subset of activated renal PECs. This population is markedly upregulated during kidney injury in a variety of murine models of nephropathy. Changes in the abundance CCR2+ activated PECs in the glomerular enriched preparations in response to CCR2 inhibition suggests that CCR2 antagonism may represent a novel approach for the treatment of chronic kidney disease.

Aim: Loss of renal function is associated with immune deficiency; however, few studies have addressed the role of B lymphocytes in elderly patients with chronic kidney disease (CKD). In this study, we examined the distribution and the relationship of the B lymphocyte subpopulation with clinical outcomes in elderly CKD patients.Methods: In this study, a total of 380 patients (312 CKD patients and 68 non-CKD controls) were recruited. Venous blood samples were analyzed by flow cytometry to determine the following B cell subsets: total B cells (CD19+), innate B1 cells (CD19+CD5+), and conventional B2 cells (CD19+CD5–). Correlations between the B cell subsets with clinical features and patient prognosis were analyzed.Results: A total of 380 patients (mean age 82.29 ± 6.22 years, 76.3% male) were included. The median follow-up time was 37.0 months (range, 1–109 months); 109 (28.7%) patients died. The main causes of death were infections (59.6%) and cardiovascular diseases (22.9%). Correlation analysis showed that levels of serum creatinine (SCr), blood urea nitrogen (BUN), and CKD were negatively associated with B1 cells. However, lymphocytes, T lymphocytes, and estimated glomerular filtration rate (eGFR) were positively correlated with B1 cells (all P < 0.05). B2 cells were negatively associated with age, SCr, cystatin C, BUN, and CKD, and were positively correlated with hemoglobin, lymphocytes, T lymphocytes, NK cells, and eGFR (all P < 0.05). Patient survival was significantly better in patients with B cells > 0.05 × 109/L, B1 cells > 0.02 × 109/L, and B2 cells > 0.04 × 109/L. Multivariate Cox regression analysis showed that B1 cells > 0.02 × 109/L [hazard ratio (HR) = 0.502, 95% confidence interval (CI): 0.297–0.851, P = 0.010] and B2 cells > 0.04 × 109/L (HR = 0.536, 95% CI: 0.319–0.901, P = 0.019) were independent protective factors for all-cause mortality.Conclusions: Our results showed that B1 and B2 cells exhibited a significantly negative correlation with the progression of CKD in elderly patients. Moreover, B1 and B2 cells were independent prognostic factors for survival, which indicates that the decrease in B cells may be associated with the progression of kidney diseases.

Pathologic changes such as renal tubular atrophy and interstitial fibrosis are common in chronic kidney disease (CKD), which in turn, leads to loss of renal function. The aims of present study were to screen critical genes with tubulointerstitial lesion in CKD by weighted gene correlation network analysis (WGCNA). Gene expression data including 169 tubulointerstitial samples of CKD and 21 controls downloaded from Gene Expression Omnibus (GEO) database. Totally 294 differentially expressed genes (DEGs) were screened, including 180 upregulated and 114 downregulated genes. Meanwhile, 90 expression data of tubulointerstitial samples combined with clinic information were applied to explore the potential mechanisms of tubulointerstitial lesion. As a consequence, the blue, brown and yellow modules which included the most DEGs compared to the other modules and exhibited strongly association with eGFR, were significantly enriched in several signalling pathways that have been reported involved in pathogenesis of CKD. Furthermore, it was found that the four genes (PLG, ITGB2, CTSS and CCL5) was one of the DEGs which also be identified as hub genes according to Kwithin. Finally, the Nephroseq online tool showed that the tubulointerstitial expression levels of PLG significantly positively correlated with the estimated glomerular filtration rate (eGFR), while ITGB2, CTSS and CCL5 connected negatively to the eGFR of CKD patients. Taken together, WGCNA is an efficient approach to system biology. By this procedure, the present study enhanced the understanding of the transcriptome status of CKD and might shed a light on the further investigation on the mechanisms of renal tubulointerstitial injury in CKD. SIGNIFICANCE OF STUDY: Traditional molecular biology can only explain the local part of the biological system, and difficult to make comprehensive exploration of the whole biological system in the chronic kidney disease (CKD). In this study, we gave an explicit elucidation of dysregulated protein coding genes by the analysis of microarray datasets in GEO database. We have presented a novel approach using weighted gene correlation network analysis (WGCNA) to explore the DEGs which implicated in CKD process. In this study, we conducted WGCNA to explore the potential mechanisms of renal tubular damage, and provided novel biomarkers associated with the molecular mechanisms underlying renal tubulointerstitial injury in CKD.

Scientific reports 10(1), 21260 (2020). doi:10.1038/s41598-020-78209-1, Published by Macmillan Publishers Limited, part of Springer Nature, London

Background Quantitative evaluation of renal cortical echogenicity (RCE) has been tried and developed in human and veterinary medicine. Objectives The objective of this study was to propose a method for evaluating RCE quantitatively and intuitively, and to determine associations between ultrasonographic renal structural distinction and estimated glomerular filtration rate (eGFR) in canine chronic kidney disease (CKD). Methods Data were collected on 63 dogs, including 27 with normal kidney function and 36 CKD patients. Symmetric dimethylarginine and creatinine concentrations were measured for calculating eGFR. RCE was evaluated as 3 grades on ultrasonography images according to the distinction between the renal cortex and outer medulla. The RCE grade of each kidney was measured. Results There was a significant difference in eGFR between the group normal and CKD (p < 0.001). As mean of RCE grades (the mean values of each right and left kidney's RCE grade) increases, the proportion of group CKD among the patients in each grade increases (p < 0.001). Also, severity of RCE (classified as "high" if any right or left kidney evaluated as RCE grade 3, "low" otherwise) and eGFR is good indicator for predicting group CKD (p < 0.001). Conclusions The degree of distinction between the renal cortex and the outer medulla is closely related to renal function including eGFR and the RCE grade defined in this study can be used as a method of objectively evaluating RCE.

This study tested whether resting state alpha rhythms (8-13 Hz) may characterize mild cognitive impairment due to Alzheimer's disease (ADMCI) compared with MCI due to chronic kidney disease (CKDMCI). Clinical and resting state eyes-closed electroencephalographic (rsEEG) rhythms from 40 ADMCI, 29 CKDMCI, and 45 cognitively normal elderly (Nold) subjects were available in a national archive. Age, gender, and education were matched in the three groups, and Mini-Mental State Evaluation (MMSE) score was paired in the ADMCI and CKDMCI groups. Delta (

Objective Febuxostat, a novel non-purine selective xanthine oxidase inhibitor, is a recommended treatment option for patients with chronic kidney disease (CKD) and hyperuricemia. There are only a few trials on the long-term use of allopurinol and febuxostat for CKD. In this study, we compared the efficacy of allopurinol and febuxostat and their effects on renal function in patients with CKD and hyperuricemia. Materials and methods This was a retrospective study of adult patients with hyperuricemia and CKD (estimated glomerular filtration rate (eGFR) ≤ 60 mL/min/1.73m2) treated with febuxostat or allopurinol. The proportion of patients who achieved the treatment goal and the difference in efficacy between different drug doses were evaluated. Further, the effects on cardiovascular and renal functions were assessed. Cardiovascular risk is defined as cardiovascular events occurring after treatment initiation. Results We enrolled 316 patients in the study, with 83 and 233 patients in the allopurinol and febuxostat groups, respectively. The application of linear mixed model for analysis revealed that febuxostat 40 mg was more effective than allopurinol 100 mg in reducing the serum uric acid level. The results indicated that the long-term eGFR slope of the febuxostat group was positive, whereas that of the allopurinol group was negative. Conclusion The results showed that, in patients with CKD and hyperuricemia, febuxostat can be used to reduce the serum uric acid level. The long-term use of febuxostat may exert a protective effect on the kidneys. Moreover, there were no obvious adverse reactions and the patients tolerated the drug well.

The endogenous cannabinoids anandamide and 2-arachidonoylglycerol bind to the cannabinoid receptors of type 1 and 2. These receptors are also the binding sites for exogenous, both natural and synthetic, cannabinoids that are used for recreation purposes. Until recently, cannabinoids and cannabinoid receptors have attracted little interest among nephrologists; however, a full endocannabinoid system (ECS) is present in the kidney and it has recently emerged as an important player in the pathogenesis of diabetic nephropathy, drug nephrotoxicity, and progressive chronic kidney disease. This newly established role of the ECS in the kidney might have therapeutic relevance, as pharmacological modulation of the ECS has renoprotective effects in experimental animals, raising hope for future potential applications in humans. In addition, over the last years, there has been a number of reported cases of acute kidney injury (AKI) associated with the use of synthetic cannabinoids that appear to have higher potency and rate of toxicity than natural Cannabis. This poorly recognized cause of renal injury should be considered in the differential diagnosis of AKI, particularly in young people. In this review we provide an overview of preclinical evidence indicating a role of the ECS in renal disease and discuss potential future therapeutic applications. Moreover, we give a critical update of synthetic cannabinoid-induced AKI.

Background: Patients with chronic kidney disease (CKD) often have CD4+ regulatory T cells (Tregs) dysfunction and chronic inflammation. We aim to investigate the effect, function, and related mechanism of low-dose IL-2 on CD4+ regulatory T cells expansion in vitro from patients with CKD. Methods: A total of 148 newly diagnosed patients with CKD at Stage III and 35 healthy volunteer subjects were recruited into our studies. The number of peripheral Tregs in peripheral blood mononuclear cells isolated from CKD patients, which were characterized by FACS as CD4+CD25hi and CD4+CD25+FoxP3+. The effect of low-dose IL-2 on expansion of Tregs, and the suppressive function of expanded Tregs were also analyzed by FACS. The levels of FoxP3 mRNA were detected by qRT-PCR. The activation of IL-2 induced Stat5 and blocking experiments were assessed by Western Blotting and FACS. Results: We found that the frequency of peripheral Tregs from CKD patients was significantly lower than that in healthy volunteer subjects. We also showed that IL-2 selectively expanded CD4+CD25hi and CD4+CD25+FoxP3+ regulatory T cells, and also upregulated the expression of FoxP3 mRNA. Our in vitro studies demonstrated that expanded CD4+ regulatory T cells from CKD patients suppressed proinflammatory Th1 and Th17 cell response. Furthermore, STAT5 activation is required for IL-2-induced expansion of regulatory T cells and expression of FoxP3 mRNA from CKD patients. Conclusions: Our findings support the clinical Treg defects in CKD patients with glomerular diseases, and the rationale of evaluating low-dose IL-2 treatment for selectively modulating CD4+ Tregs.