China
Africa
Explore chapters and articles related to this topic
IgA nephropathy
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jan Novak, Bruce A. Julian, Jiri Mestecky
Currently, a definitive diagnosis of IgA nephropathy requires renal biopsy because there is no valid noninvasive test that can be reliably used as a diagnostic alternative. Unfortunately, renal biopsy entails a risk for serious bleeding complications. Consequently, early detection of the disease is frequently not possible, and monitoring disease activity is compromised. Some patients with IgA nephropathy will progress to end-stage renal disease, even when the initial histology display shows relatively minor glomerular abnormalities. Consequently, a reliable noninvasive diagnostic test will be very useful for detecting subclinical IgA nephropathy, assessing activity, monitoring the progression or reduction in renal damage, and evaluating the response to treatment.
Transplant Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
David van Dellen, Zia Moinuddin, Hussein Khambalia, Brian KP Goh
A 25-year-old patient with end-stage renal failure due to IgA nephropathy is being assessed for renal transplantation. Apart from being on haemodialysis he is in reasonably good health. How would your assessment of his cardiac risk differ from the previous diabetic patient with asymptomatic ischaemic heart disease?The relative risk of cardiovascular death is disproportionately high in young dialysis patients.Assessment of this patient would therefore proceed along the lines of assessment for any asymptomatic high-risk patient with end-stage renal failure.He should have a routine ECG and echocardiogram (despite his young age). He would not have a routine myocardial perfusion scan or dobutamine stress echo and CPEX testing unless there was a definitive indication or a strong family history.The high-risk group includes: Age >50DiabetesCoronary revascularisation >3 years agoEvidence of cerebrovascular or peripheral vascular diseaseAbnormal resting ECG or echocardiogramSmoker
Glomerular solidification is associated with nephritis-related clinical parameters in IgA nephropathy
Published in Renal Failure, 2019
Tsutomu Inoue, Yankun Luo, Takeru Seto, Hiromichi Suzuki, Hirokazu Okada
IgA nephropathy is the most prevalent primary chronic glomerular disease worldwide. It is defined immunohistochemically by a predominance of IgA deposits, either alone or in conjunction with IgG, IgM, or both, in the glomerular mesangium [1]. Histological findings range from a virtually normal appearance by light microscopy to severe necrotizing, crescentic glomerulonephritis, or advanced glomerulosclerosis and tubular atrophy with interstitial fibrosis. Similar to the histological heterogeneity observed, the clinical course of IgA nephropathy is also variable. There is a common understanding that some patients with IgA nephropathy will show a progressive course and have a poor prognosis, which will eventually reach end-stage renal disease (ESRD). Several histological lesions have been reported to be of prognostic value. Generally, reports have shown that, where the clinical outcome is the time to ESRD/dialysis, chronic lesions, including tubular atrophy, interstitial fibrosis, and glomerulosclerosis, are the most important histological predictors [2,3]. Global glomerulosclerosis correlates well with tubulointerstitial alterations, and the presence of lesions has been proposed to be a poor prognostic factor, although interstitial fibrosis and tubular atrophy were stronger predictors compared with global glomerulosclerosis when the Oxford classification was used [2,3] because quantification is less susceptible to errors resulting from the presence of few glomeruli.
The role of phosphorylcholine-specific immune responses in the tonsils and peripheral blood on IgA nephropathy
Published in Acta Oto-Laryngologica, 2018
Junichiro Ohori, Tomohiro Jimura, Yuichi Kurono
PC-specific IgA is known to be associated with the induction of IgA nephropathy in animal models. When pneumococcal C polysaccharide containing PC was administered with PC-specific IgA (TEPC-15), the immune complex deposited in the renal glomerulus [9]. However, TEPC-15 does not recognize PC expressed on normal cells of the host and reacts only with cells that have undergone apoptosis because of inflammation, and thus plays an important role in biological defence and the maintenance of homeostasis [16,17]. Because PC is the target of CRP and CRP levels were higher in patients in the super-high-risk group of IgA nephropathy, the production of PC was increased in the tonsils of those patients possibly because of inflammation and the number of PC-specific IgA-producing cells was increased to eliminate damaged cells from the tonsils. Further, remarkably lower numbers of PC-specific IgA-producing cells in the peripheral blood than in the tonsils suggest that PC-specific IgA-producing cells do not circulate in the blood vessels and are not directly related to the pathogenesis of IgA nephropathy.
The comprehensive analysis of clinical trials registration for IgA nephropathy therapy on ClinicalTrials.gov
Published in Renal Failure, 2022
Yan Cui, Ya-ling Zhai, Yuan-yuan Qi, Xin-ran Liu, Ya-fei Zhao, Fu Lv, Li-pei Han, Zhan-Zheng Zhao
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerular disease in the world, with IgA depositing in the glomerular mesenterium as the main pathological feature [1]. IgAN may occur in patients of any age, but principally in young adults, and clinically characterized by asymptomatic hematuria with or without proteinuria. As a chronic kidney disease, IgAN almost cannot be cured completely presently and is one of the leading causes of end-stage renal disease (ESRD) [2]. In recent years, we have made great progress in the treatment of IgA nephropathy. The role of renin-angiotensin system (RAS) blockade in IgAN has been well-recognized, which can effectively control blood pressure and reduce urinary protein and thus slow the deterioration of renal function [3]. Therefore, an angiotensin-converting enzyme inhibitor (ACEi) or an angiotensin II-receptor blocker (ARB) is considered as a first-line treatment for IgAN. Additionally, more and more studies explore the role of immunosuppressive agents in the treatment of IgAN, such as corticosteroids, cyclophosphamide, and mycophenolate mofetil. But there still exists some controversy regarding their use in treating IgAN due to many side effects associated with immunosuppressive therapy [4]. Studies about exploring the effect of some novel drugs in IgAN have been the focus of researchers, such as Nefecon, complement inhibitors, drugs targeting cytokines and chemokines, and so on [5]. Nevertheless, 20–40% of patients with IgAN will still progress to ESRD, despite having received systematic management [6,7]. Therefore, improving the treatment for IgAN patients is still needed to establish an optimal management system to prolong renal survival and improve quality of life.