Majority Of Chronic Kidney Disease Research Articles

Osteoprotegerin and Inflammation in Incident Peritoneal Dialysis Patients.

Objectives: Osteoprotegerin (OPG) is a member of the tumor necrosis factor receptor family involved in processes in many inflammatory states. OPG concentration is enhanced in the majority of chronic kidney disease (CKD) patients and those undergoing renal replacement therapy. The aim of the study was to assess the relation of OPG and chronic inflammation in peritoneal dialysis (PD) patients and to evaluate whether OPG concentrations in plasma and dialysate were related to plasma and dialysate levels of proinflammatory mediators (interleukin 6 (IL-6), high-sensitivity C-reactive protein (hsCRP), interleukin 33 (IL-33) and interleukin 1 receptor-like 1IL-1RL1 (IL-1RL1, sST2)). Methods: The study included 37 patients of the Peritoneal Dialysis Center, Department of Nephrology, Transplantology and Internal Medicine, Szczecin, Poland, 4-6 weeks after the onset of peritoneal dialysis therapy. During a peritoneal equilibration test, plasma (at 2 h) and dialysate (at 4 h) OPG, IL-33, 1IL-1RL1 (sST2), IL-6 and hsCRP concentrations were determined. Results: Plasma concentration of OPG did not correlate with dialysate OPG level (Rs = 0.04, p = 0.8). There was a strong positive correlation between plasma OPG concentrations and plasma IL-1RL1 (sST2) (Rs = 0.41; p = 0.01), plasma IL-6 (Rs = 0.38; p = 0.01) and plasma hsCRP (Rs = 0.35; p = 0.02). Dialysate OPG concentrations were positively associated with dialysate IL-1RL1 (sST2) (Rs = 0.37; p = 0.02) and dialysate IL-6 levels (Rs = 0.44; p = 0.005). Multivariate analysis showed that higher IL-1RL1 (sST2) (ß = +0.38, p = 0.006), higher plasma hsCRP (ß = +0.32, p = 0.02) and older age (ß = +0.35, p = 0.01) were independent determinants of higher plasma OPG concentration and that higher concentrations of dialysate IL-6 (ß = +0.37, p = 0.02) were independent determinants of higher dialysate OPG concentration. Conclusions: Both plasma and dialysate OPG levels are associated with the severity of systemic and local inflammation illustrated by the plasma and dialysate concentrations of IL-1RL1 (sST2), hsCRP and IL-6, suggesting that OPG might have a pivotal role in explaining the milieu of systemic and intraperitoneal inflammation.

Evaluation of Serum Lipoprotein (a) Levels and Novel Lipid Indices in Patients with Chronic Kidney DiseaseA Case-control Study

Introduction: Majority of Chronic Kidney Disease (CKD) patients are more likely to die of cardiovascular complications, before reaching End Stage Renal Disease (ESRD). Although there are many risk factors contributing to pathogenesis of cardiovascular disease in CKD subjects, dyslipidemia represents one of the modifiable risk factors. American Heart Association has recommended that CKD patients should be classified in the highest risk group for developing cardiovascular events. Kidney Disease: Improving Global Outcome (KDIGO) recommends, these patients should be evaluated for dyslipidemia and for treatment to reduce the risk of cardiovascular events. Aim: To evaluate serum Lipoprotein (a) {Lp(a)} levels and assess the significance of novel lipid indices in non dialysis patients of CKD. Materials and Methods: This analytical case-control study was conducted from January 2016 to June 2016 at Government Stanley Medical College and Hospital, Chennai, Tamil Nadu, India. It included 70 non dialysis CKD subjects and 70 healthy control subjects, adhering to inclusion and exclusion criteria. Fasting Blood Samples (FBS) were collected and analysed for: Fasting blood glucose, Fasting Lipid Profile, Serum Lp(a). Serum Lp(a) was estimated by immunoturbidimetry method and lipid profile by enzymatic method. Estimated Glomerular Filtration Rate (eGFR) was calculated using Modification of Diet in Renal Disease (MDRD) formula and staging of CKD subjects was done, based on KDIGO guidelines. Novel lipid indices were calculated using appropriate formula. Statistical analysis of the tabulated data was done using Social Sciences of the Statistical Package (SPSS) software. Results: There were significant differences in the levels of FBS, Triglycerides (TG), Lp(a) between controls and non dialysis CKD subjects (p<0.001). Among Lipid Indices, Atherogenic Index of Plasma (AIP) and Lipid Tetrad Index (LTI) values were significantly higher in CKD subjects compared to controls (p<0.001), but there was no significant difference was seen in Atherogenic Coefficient (AC), Castelli’s Risk Index-I (CRI-I) and CRI-II values. AIP and LTI showed significant positive correlation with Lp(a). LTI had the highest Positive Predictive Value (PPV) (77.8%) and Negative Predictive Value (NPV) (72.7%); AIP had PPV of 65.3% and NPV of 66.2%. Conclusion: The present study concludes that, among lipid indices, AIP and LTI are the most suitable for assessment of atherogenicity in non dialysis CKD. In developing countries like India, owing to high cost of tests like Serum Lp(a), novel lipid index AIP can serve as a cost-effective screening tool for monitoring cardiovascular disease risk in CKD patients.

Anatomy and embryology of congenital surgical anomalies: Congenital Anomalies of the Kidney and Urinary Tract

Congenital anomalies of the kidney and urinary tract or “CAKUT” describes a spectrum of developmental disorders with a range of associated clinical presentations and functional consequences. CAKUT underlies the majority of chronic kidney disease and kidney replacement therapy requirement in children, but functional deterioration can also emerge in adulthood. Understanding the normal embryological processes involved in kidney development allows us to appreciate the timing and sequence of critical events implicated when things go wrong. In this review, we will describe the normal developmental mechanisms and relate this to what we currently know about the pathological processes involved in various forms of CAKUT. We will also review the proposed etiological factors, in particular genetics, involved in CAKUT.

Integrating pediatric trauma care into a national system of trauma care

Congenital anomalies of the kidney and urinary tract or “CAKUT” describes a spectrum of developmental disorders with a range of associated clinical presentations and functional consequences. CAKUT underlies the majority of chronic kidney disease and kidney replacement therapy requirement in children, but functional deterioration can also emerge in adulthood. Understanding the normal embryological processes involved in kidney development allows us to appreciate the timing and sequence of critical events implicated when things go wrong. In this review, we will describe the normal developmental mechanisms and relate this to what we currently know about the pathological processes involved in various forms of CAKUT. We will also review the proposed etiological factors, in particular genetics, involved in CAKUT.

Urologic care and progression to end-stage kidney disease: a Chronic Kidney Disease in Children (CKiD) nested case–control study

Children with chronic kidney disease (CKD) risk progressing to end-stage kidney disease (ESKD). The majority of CKD causes in children are related to congenital anomalies of the kidney and urinary tract, which may be treated by urologic care. To examine the association of ESKD with urologic care in children with CKD. This was a nested case-control study within the Chronic Kidney Disease in Children (CKiD) prospective cohort study that included children aged 1-16 years with non-glomerular causes of CKD. The primary exposure was prior urologic referral with or without surgical intervention. Incidence density sampling matched each case of ESKD to up to three controls on duration of time from CKD onset, sex, race, age at baseline visit, and history of low birth weight. Conditional logistic regression analysis was performed to estimate rate ratios (RRs) for the incidence of ESKD. Sixty-six cases of ESKD were matched to 153 controls. Median age at baseline study visit was 12 years; 67% were male, and 7% were black. Median follow-up time from CKD onset was 14.9 years. Seventy percent received urologic care, including 100% of obstructive uropathy and 96% of reflux nephropathy diagnoses. Cases had worse renal function at their baseline visit and were less likely to have received prior urologic care. After adjusting for income, education, and insurance status, urology referral with surgery was associated with 50% lower risk of ESKD (RR 0.50 [95% confidence interval [CI] 0.26-0.997), compared to no prior urologic care (Figure). After excluding obstructive uropathy and reflux nephropathy diagnoses, which were highly correlated with urologic surgery, the association was attenuated (RR 0.72, 95% CI 0.24-2.18). In this study, urologic care was commonly but not uniformly provided to children with non-glomerular causes of CKD. Underlying specific diagnoses play an important role in both the risk of ESKD and potential benefits of urologic surgery. Within the CKiD cohort, children with non-glomerular causes of CKD often received urologic care. Urology referral with surgery was associated with lower risk of ESKD compared to no prior urologic care but depended on specific underlying diagnoses.

Chronic kidney disease among human immunodeficiency virus positive patients on antiretroviral therapy in sub-Saharan Africa: A systematic review and meta-analysis

Human immunodeficiency virus (HIV)-infected patients are at risk for renal disease as a consequence of complications of antiretroviral treatment. Particularly, the complication of kidney disease is high in patients who switched to Tenofovir Disoproxil Fumarate. The treatment is associated with nephrotoxicity, decrease in glomerular filtration rate, leading to kidney disease. This review focused on assessing the effect of antiretroviral therapy (ART) on kidney function among HIV-positive patients. Initially, the study protocol was registered on Prospero and given a unique identification number of CRD42018087686. We then conducted a systematic search of PubMed, Google Scholar, the Cochrane library, and Google from 2008 to September 2018. We found 742 study results eligible for this review. After stringent filtration mechanism, 15 qualified studies were used for systematic review and meta-analysis process. Cross-sectional, cohort, randomized controlled trials, and prospective studies were eligible for inclusion in the study. The overall pooled prevalence found in this meta-analysis was 6.42% with high statistical heterogeneity (I2 = 96.7%). The highest subgroup prevalence was reported from Ghana, with subgroup prevalence of 13.65% without statistical heterogeneity (I2 = 0.0%). Majority of chronic kidney disease (CKD) was in stage 3 with subgroup prevalence of 6.78% and tolerable statistical heterogeneity (I2 = 66.7%). There was high pooled prevalence of CKD among HIV-positive patients on ART in Sub-Saharan Africa. The highest subgroup prevalence was reported from Ghana. Majority of CKD was reported in stage 3.

The surgical aspect of renal hyperparathyroidism: a summary of the guidelines

Renal hyperparathyroidism is a common disease affecting the vast majority of chronic kidney disease (CKD) patients. With effective medical treatment, only 5-10% of CKD patients require surgical treatment. The medical treatment includes a wide variety of medications to replace the inactive vitamin D, suppress the hyperactive parathyroid glands and also to counteract the hyperphosphatemia. Based on publications from Egypt, the financial difficulties the CKD patients are suffering from does not allow the delivery of successful medical treatment. This is mainly due to the inability to use an effective and more expensive phosphate binder and active vitamin D (1). Also, calcimimetic therapy (e.g cinacalcet) is unaffordable and needs life-long administration. This has led to an increased prevalence of the florid disease compared to developed countries (2). The situation was made worse by the lack of understanding of the principles of diagnosis and surgical treatment of renal hyperparathyroidism among many clinicians. Surgeons rely mainly on imaging in the localization of the hyperplastic glands, which is well known to be not sensitive enough in this multi-gland disease (3). This often led to inadequate surgical management of this disease. Also, the multicentric nature of this condition (multi-gland, rather than a single-gland disease) is often undermined. The published reports from Egypt showed only a few centres dealing with this disease; however the number of patients reported is quite small with variable outcomes (4). The reported outcome demonstrates that more patients require surgery for the poorly controlled hyperparathyroidism that unmasks the lack of appropriate surgical experience in many district areas of Egypt.

Whole-exome resequencing distinguishes cystic kidney diseases from phenocopies in renal ciliopathies

Rare single-gene disorders cause chronic disease. However, half of the 6,000 recessive single gene causes of disease are still unknown. Because recessive disease genes can illuminate, at least in part, disease pathomechanism, their identification offers direct opportunities for improved clinical management and potentially treatment. Rare diseases comprise the majority of chronic kidney disease (CKD) in children but are notoriously difficult to diagnose. Whole exome resequencing facilitates identification of recessive disease genes. However, its utility is impeded by the large number of genetic variants detected. We here overcome this limitation by combining homozygosity mapping with whole exome resequencing in 10 sib pairs with a nephronophthisis-related ciliopathy, which represents the most frequent genetic cause of CKD in the first three decades of life. In 7 of 10 sib-ships with a histologic or ultrasonographic diagnosis of nephronophthisis-related ciliopathy we detect the causative gene. In six sib-ships we identify mutations of known nephronophthisis-related ciliopathy genes, while in two additional sib-ships we found mutations in the known CKD-causing genes SLC4A1 and AGXT as phenocopies of nephronophthisis-related ciliopathy. Thus whole exome resequencing establishes an efficient, non-invasive approach towards early detection and causation-based diagnosis of rare kidney diseases. This approach can be extended to other rare recessive disorders, thereby providing accurate diagnosis and facilitating the study of disease mechanisms.

Assessment of dyslipidemia in pre-dialysis patients in south-west Nigeria.

Background:Majority of chronic kidney disease (CKD) patients are more likely to die of cardiovascular complications before reaching end stage renal disease. The Kidney Disease Outcomes Quality Initiative (K/DOQI) recommends that all CKD patients should be evaluated for dyslipidemia and for treatment to reduce the risk of cardiovascular events.Patients and Methods:A cross-sectional case control study to determine the frequency of occurrence of lipid abnormalities in patients with CKD and compare these abnormalities with that of normal controls. A total of 100 patients and 100 controls were recruited for the study. Demographic and clinical data were obtained using structured questionnaire. Weight, height and waist circumference, body mass index (BMI) and blood pressure were also obtained. Subjects had their fasting lipid profile and fasting plasma glucose assayed after overnight fast of 8-14 hours. Low-density lipoprotein (LDL) was obtained using Friedwald formula.Result:The study revealed that total cholesterol (TC) was elevated above normal levels in 44% of cases compared with 6% in controls (P < 0.001), with the mean (SD) value of 5.82 ± 3.28 mmol/l for cases compared with 3.9 ± 1.0 mmol/l (P < 0.001) in controls. Low density lipoprotein was elevated in 48% of cases compared with 14% in controls (P < 0.001), with the mean (SD) values of 4.15 ± 2.74 mmol/l and 2.57 ± 0.95 mmol/l for cases and controls, respectively, (P < 0.001). Triglyceride (TG) was elevated above normal level in 26% of cases compared with none in the controls (P < 0.001), with the mean (SD) values of 1.41 ± 1.10 mmol/l and 0.64 ± 0.24 mmol/l for cases and controls, respectively (P < 0.001). All Lipid fractions except HDL also correlated significantly with levels of proteinuria TC (r = 0.345, P = 0.001), TG (r = 0.268, P = 0.011) LDL (r = 0.366, P = 0.001).Conclusion:Dyslipidemia is common among patients with CKD. Regular evaluation of all CKD patients for dyslipidemia and treatment need be instituted.

Vitamin D Therapy in Cardiac Hypertrophy and Heart Failure

Vitamin D3 is made in the skin, modified in the liver to form 25(OH)D, and then further hydroxylated in the kidney to form the active hormone, 1,25-dihydroxyvitamin D3 (calcitriol). Calcitriol binds to and activates the vitamin D receptor (VDR), a nuclear receptor, to regulate numerous downstream signaling pathways in different cells and tissues. Emerging evidence suggests that VDR plays an important role in modulating cardiovascular, immunological, metabolic and other functions. Data from preclinical, epidemiological and clinical studies have shown that deficiency in VDR activation is associated with an increased risk for cardiovascular disease (CVD). Results from interventional trials using either nutritional vitamin D or VDR agonists (VDRAs) support the idea that VDR activation is beneficial for improving the underlying factors of CVD such as hypertension, endothelial dysfunction, atherosclerosis, vascular calcification, cardiac hypertrophy and progressive renal dysfunction. Furthermore, a majority of chronic kidney disease (CKD) patients die of CVD and VDRA therapy is associated with a survival benefit in both pre-dialysis and dialysis CKD patients. Most of the studies measured serum 25(OH)D as an indication for vitamin D deficiency, which does not truly reflect the VDR activation status. Although VDR plays an important role in regulating cardiovascular function and VDRAs may be potentially useful for treating CVD, at present VDRAs are not indicated for the treatment of CVD.

184 AMNIOTIC FLUID STEM CELLS AND CHRONIC KIDNEY DISEASE

You have accessJournal of UrologyStem Cell Research1 Apr 2011184 AMNIOTIC FLUID STEM CELLS AND CHRONIC KIDNEY DISEASE Sargis Sedrakyan, Laura Perin, Stefano Da Sacco, Liron Shiri, Kevin Lemley, and Roger De Filippo Sargis SedrakyanSargis Sedrakyan Los Angeles, CA More articles by this author , Laura PerinLaura Perin Los Angeles, CA More articles by this author , Stefano Da SaccoStefano Da Sacco Los Angeles, CA More articles by this author , Liron ShiriLiron Shiri Los Angeles, CA More articles by this author , Kevin LemleyKevin Lemley Los Angeles, CA More articles by this author , and Roger De FilippoRoger De Filippo Los Angeles, CA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.253AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Alport Disease, the model used in our experiments, is characterized by a hereditary form of glomerulonephritis, wherein an abnormal level of glomerular basement membrane (GBM) is produced, gradually leading to interstitial fibrosis and eventual loss of renal function. At present, there is no definitive therapy to delay progression of fibrosis, which is the hallmark in a majority of chronic kidney disease (CKD) cases. Stem-cell based therapies may provide alternative therapeutic opportunities. Amniotic fluid stem cells (AFSCs) are well established to have both pluripotential and paracrine functions and represent a possible alternative approach to current therapies for CKD. METHODS In this study we have applied AFSCs in an in vivo model of chronic Alport Disease. Intracardiac injections of AFSCs have been performed on Alport mice between 2 and 3 months after birth. Changes in BUN, creatinine levels and albuminuria have been compared between injected mice and not injected siblings. Real Time PCR and Western Blotting have been used to evaluate cytokine expression. Immunohistochemistry and immunofluorescence have been performed to follow morphological modifications, extracellular matrix deposition and cast formation. RESULTS Systemic injection of the cells provides beneficial effects; we found decreased levels of albuminuria, creatinine and BUN as well as significant increase in the life-span of the treated mice as compared to their untreated controls. Additionally, treated mice present lower number of macrophage infiltration, lower myofibrostast trasformation in the kidney interstitial space, accompanied with downregulated expression of chemokines such as MPC-1, IP-10 and cytokines such as IL-1, TNF-α and TGF-α. CONCLUSIONS In this study we have shown that AFSCs are capable of slowing down the progression of Alport disease by incurring structural and functional benefits to the kidney. These cells may present an alternative approach to treat various medical conditions where currently therapeutic options are either limited or inadequate. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e76 Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sargis Sedrakyan Los Angeles, CA More articles by this author Laura Perin Los Angeles, CA More articles by this author Stefano Da Sacco Los Angeles, CA More articles by this author Liron Shiri Los Angeles, CA More articles by this author Kevin Lemley Los Angeles, CA More articles by this author Roger De Filippo Los Angeles, CA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Chronic kidney disease after liver, cardiac, lung, heart–lung, and hematopoietic stem cell transplant

Patient survival after cardiac, liver, and hematopoietic stem cell transplant (HSCT) is improving; however, this survival is limited by substantial pretransplant and treatment-related toxicities. A major cause of morbidity and mortality after transplant is chronic kidney disease (CKD). Although the majority of CKD after transplant is attributed to the use of calcineurin inhibitors, various other conditions such as thrombotic microangiopathy, nephrotic syndrome, and focal segmental glomerulosclerosis have been described. Though the immunosuppression used for each of the transplant types, cardiac, liver and HSCT is similar, the risk factors for developing CKD and the CKD severity described in patients after transplant vary. As the indications for transplant and the long-term survival improves for these children, so will the burden of CKD. Nephrologists should be involved early in the pretransplant workup of these patients. Transplant physicians and nephrologists will need to work together to identify those patients at risk of developing CKD early to prevent its development and progression to end-stage renal disease.

Chronic Kidney Disease in Long-Term Survivors of Hematopoietic Cell Transplantation

High-dose myeloablative hematopoietic cell transplantation is becoming an increasingly common treatment modality for a variety of diseases. Patient survival may be limited by substantial treatment-related toxicities, including chronic kidney disease (CKD). Although the majority of CKD after transplantation is idiopathic, thrombotic microangiopathic syndromes and nephrotic syndrome have been described. Epidemiology, pathogenesis, and potential treatment options for the various clinical syndromes that are associated with CKD in hematopoietic cell transplantation patients is reviewed. As the indications for and the numbers of transplants that are performed worldwide increases, so will the burden of CKD. The nephrologists and oncologists will have to work together to identify patients who are at risk for CKD early to prevent its development and progression to end-stage kidney disease.

Secondary Hyperparathyroidism in the Diabetic Patient with Chronic Kidney Disease

In the US, diabetic nephropathy accounts for the majority of chronic kidney disease (CKD). It contributes significantly to morbidity and mortality among the diabetic population1,2and accounts for approximately 40% of patients with end-stage renal disease.3The earliest manifestation of renal involvement in diabetes is the presence of microalbuminuria, as defined by urine albumin excretion of 30–300mg/day.4Progression to overt proteinuria (urine albumin excretion greater than 300mg/day) and diabetic nephropathy occur more frequently in those with poor glycemic control, glomerular hyperfiltration, and hypertension.5