EMJ NephrologyPub Date : 2015-07-14DOI: 10.33590/emjnephrol/10311578
D. Rebić, Almira Hadžović-Džuvo, A. Valjevac
{"title":"Chronic Kidney Disease and Endothelium","authors":"D. Rebić, Almira Hadžović-Džuvo, A. Valjevac","doi":"10.33590/emjnephrol/10311578","DOIUrl":"https://doi.org/10.33590/emjnephrol/10311578","url":null,"abstract":"The endothelial cell layer is responsible for molecular traffic between the blood and surrounding tissue, and endothelial integrity plays a pivotal role in many aspects of vascular function. Cardiovascular disease (CVD) is the main cause of death in patients with chronic kidney disease (CKD) and its incidence and severity increase in direct proportion with kidney function decline. Non-traditional risk factors for CVDs, including endothelial dysfunction (ED), are highly prevalent in this population and play an important role in cardiovascular (CV) events. ED is the first step in the development of atherosclerosis and its severity has prognostic value for CV events. Several risk markers have been associated with ED. Reduced bioavailability of nitric oxide plays a central role, linking kidney disease to ED, atherosclerosis, and CV events. Inflammation, loss of residual renal function, and insulin resistance are closely related to ED in CKD. ED may be followed by structural damage and remodelling that can precipitate both bleeding and thrombotic events. The endothelium plays a main role in vascular tone and metabolic pathways. ED is the first, yet potentially reversible step in the development of atherosclerosis and its severity has prognostic value for CV events. Therefore, evaluation of ED may have major clinical diagnostic and therapeutic implications. In patients with CKD, many risk factors are strongly interrelated and play a major role in the initiation and progression of vascular complications that lead to the high mortality rate due to CVD.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"122 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115780868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMJ NephrologyPub Date : 2015-07-14DOI: 10.33590/emjnephrol/10310549
H. Trimarchi
{"title":"Primary Focal Segmental Glomerulosclerosis: Why Are Pieces of This Puzzle Still Missing?","authors":"H. Trimarchi","doi":"10.33590/emjnephrol/10310549","DOIUrl":"https://doi.org/10.33590/emjnephrol/10310549","url":null,"abstract":"Focal segmental glomerulosclerosis (FSGS) can be classified as primary or secondary. Moreover, many causes of primary FSGS have been identified in recent years. In this regard, genetic circulating permeability factors and the abnormal podocyte expression of co-stimulatory molecules have been reported. However, the classification of this entity remains difficult to understand, mainly due to the fact that it describes a morphologic pattern of scarring. FSGS is a histological pattern shared by almost all the glomerulonephritides that describes a podocyte lesion and not a disease. Therefore, it should be reclassified according to the new pathophysiological findings and the biomarkers encountered in each triggered pathway.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127814095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMJ NephrologyPub Date : 2015-07-14DOI: 10.33590/emjnephrol/10314123
F. Berthoux, H. Mohey, N. Maillard, C. Mariat
{"title":"IgA Nephropathy: New Aspects in Pathophysiology and Pathogenesis","authors":"F. Berthoux, H. Mohey, N. Maillard, C. Mariat","doi":"10.33590/emjnephrol/10314123","DOIUrl":"https://doi.org/10.33590/emjnephrol/10314123","url":null,"abstract":"Knowledge of the pathophysiology of immunoglobulin A nephropathy (IgAN) has progressed significantly, with this disease being clearly identified as an autoimmune disease with a peculiar autoantigen (galactosedeficient IgA1 [Gd-IgA1]), specific autoantibodies (IgG and IgA1 anti-glycans), and formation followed by mesangial deposition of circulating immune complexes with the involvement of other players, such as mesangial transferrin receptor (TfR), monocyte Fcα receptor (CD89), and glomerular transglutaminase 2 (TG2). The pathogenesis still requires additional clarifications in order to explain the initiation of the disease and to establish the respective role of genetics, environment, and hazard concordance in the cascade of events/steps. The clinical application of this new knowledge is spreading slowly and includes possible measurement of serum Gd-IgA1, IgG anti-Gd-IgA1, IgA anti-Gd-IgA1, soluble CD89, and soluble TfR in the urine of patients with IgAN.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"8 1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132893100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMJ NephrologyPub Date : 2015-07-05DOI: 10.33590/emjnephrol/10311591
L. Di Lullo, V. Barbera, A. Bellasi, M. Cozzolino, A. De Pascalis, D. Russo, L. Russo, F. Santoboni, A. Santoboni, C. Ronco
{"title":"Vascular and Valvular Calcifications in Chronic Kidney Disease: An Update","authors":"L. Di Lullo, V. Barbera, A. Bellasi, M. Cozzolino, A. De Pascalis, D. Russo, L. Russo, F. Santoboni, A. Santoboni, C. Ronco","doi":"10.33590/emjnephrol/10311591","DOIUrl":"https://doi.org/10.33590/emjnephrol/10311591","url":null,"abstract":"In chronic kidney disease (CKD) and end-stage renal disease patients cardiovascular disease is the main cause of morbidity and mortality, with incidence of cardiac related mortality increasing as renal function declines. Even after controlling for traditional cardiovascular risk factors such as smoking, age, gender, dyslipidaemia, and arterial hypertension, patients with CKD have a higher incidence of major cardiovascular events. CKD is characterised by the presence of many other non-traditional cardiovascular risk factors, such as chronic inflammation and accelerated atherosclerosis, oxidative stress, and especially, secondary hyperparathyroidism. This review will summarise the current evidence on vascular calcifications and valvular heart disease in CKD patients, from pathophysiology to therapeutic strategies.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"41 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125347526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMJ NephrologyPub Date : 2015-07-05DOI: 10.33590/emjnephrol/10312231
A. Lunn
{"title":"Automatic Reporting of Creatinine-Based Estimated Glomerular Filtration Rate in Children: Is this Feasible?","authors":"A. Lunn","doi":"10.33590/emjnephrol/10312231","DOIUrl":"https://doi.org/10.33590/emjnephrol/10312231","url":null,"abstract":"Creatinine, although widely used as a biomarker to measure renal function, has long been known as an insensitive marker of renal impairment. Patients with reduced renal function can have a creatinine level within the normal range, with a rapid rise when renal function is significantly reduced. As of 1976, the correlation between height, the reciprocal of creatinine, and measured glomerular filtration rate (GFR) in children has been described. It has been used to derive a simple formula for estimated glomerular filtration rate (eGFR) that could be used at the bedside as a more sensitive method of identifying children with renal impairment. Formulae based on this association, with modifications over time as creatinine assay methods have changed, are still widely used clinically at the bedside and in research studies to assess the degree of renal impairment in children.\u0000\u0000Adult practice has moved in many countries to computer-generated results that report eGFR alongside creatinine results using more complex, but potentially more accurate estimates of GFR, which are independent of height. This permits early identification of patients with chronic kidney disease. This review assesses the feasibility of automated reporting of eGFR and the advantages and disadvantages of this in children.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"205 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123416537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EMJ NephrologyPub Date : 2015-07-01DOI: 10.33590/emjnephrol/10314170
M. Kiremit, S. Guven, R. Horuz, B. Erkurt, S. Albayrak
{"title":"Home Nephrology Retrograde Intrarenal Surgery for Complex Stones in a Toddler with…\u0000Retrograde Intrarenal Surgery for Complex Stones in a Toddler with Congenital Renal Anomalies: Technical Details","authors":"M. Kiremit, S. Guven, R. Horuz, B. Erkurt, S. Albayrak","doi":"10.33590/emjnephrol/10314170","DOIUrl":"https://doi.org/10.33590/emjnephrol/10314170","url":null,"abstract":"We report herein the management of a challenging case due to anatomic and stone-related complications in a 37-month-old Caucasian toddler with megacalycosis and complex stone in the left kidney and duplicated ureter on the right side.","PeriodicalId":348431,"journal":{"name":"EMJ Nephrology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2015-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125424465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}