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Books on the topic 'Glomerulonephritis, IGA'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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1

IgA nephropathy: From molecules to men. Karger, 1999.

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2

International Symposium on IgA Nephropathy (11th 2006 Tokyo, Japan). IgA nephropathy today. Edited by Tomino Yasuhiko 1949-. Karger, 2007.

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3

Dixhoorn, Mieneke G. A. van. IgA in experimental kidney disease. University of Leiden, 1998.

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4

R, Clarkson A., and Woodroffe A. J, eds. IgA nephropathy: Pathogenesis and treatment. Karger, 1995.

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5

Fijter, Johan Willem de. The mucosal immune response in primary IgA nephropathy. University of Leiden, 1998.

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6

R, Clarkson A., ed. IgA nephropathy. Nijhoff, 1987.

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7

Recent Advances in IGA Nephropathy. World Scientific Publishing Company, 2009.

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8

Tomino, Y. IgA Nephropathy Today. S. Karger AG (Switzerland), 2007.

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9

Iga Nephropathy: The 25th Year (Contributions to Nephrology). S. Karger Publishers (USA), 1993.

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10

(Editor), Rosanna Coppo, and Licia Peruzzi (Editor), eds. Moderately Proteinuric IgA Nephropathy in the Young (Biomedical and Health Research, V. 44). Ios Pr Inc, 2000.

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11

Rodriguez-Iturbe, Bernardo, and Mark Haas. Immunoglobulin A-dominant post-infectious glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0078_update_001.

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Immunoglobulin A (IgA)-dominant post-infectious glomerulonephritis is usually associated with infections with Staphylococcus aureus. It is most commonly seen in patients over 60, and particularly in men. The renal lesion is acute and severe, and commonly includes crescent formation, although the described histological features vary widely. IgA is the dominant immunoglobulin and in later phases when capillary deposits are resolving it may be impossible to distinguish the condition from IgA nephropathy without the use of electron microscopy. Diabetes appears to be a risk factor. Complement levels are frequently low but may be normal. Clinically there is often severe nephrotic syndrome and hypertension may be less prominent.
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12

Marie-Christine, Béné, Faure Gilbert, and Kessler M, eds. IgA nephropathy: The 25th year : international symposium, Nancy, August 31-September 2, 1992. Karger, 1993.

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13

1947-, Ballardie Francis W., ed. Autoimmunity in nephritis. Harwood Academic Publishers, 1992.

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14

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0065.

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Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis. It runs a slow and sometimes relentless clinical course with consequent end-stage renal failure in 35–40% of patients 25–30 years after first clinical presentation. The pathology is characterized by deposition of macromolecular (polymeric) IgA1 in the glomerular mesangium, proliferation of mesangial cells, increased synthesis of extracellular matrix, and infiltration of macrophage, monocytes, and T cells.
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15

Carton, James. Renal pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0010.

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This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.
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16

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Renal medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0017.

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Chapter 17 covers the basic science and clinical topics relating to ophthalmology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers renal basic science, pathophysiology of renal disease, the kidney as an 'endocrine' organ, renal investigations, acute kidney injury, chronic kidney disease/renal failure, renal replacement therapy, renal transplantation, haemodialysis, peritoneal dialysis, nephrotic syndrome, primary glomerular causes of nephrotic syndrome/proteinuria, rapidly progressive glomerulonephritis, IgA nephropathy, mesangiocapillary glomerulonephritis, tubulointerstitial nephritis, renal tubular disorders, urinary tract obstruction, renal stone disease, urinary tract infection in adults, renovascular disease, renal tumours, inherited renal disease, and renal disease and pregnancy.
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17

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy diagnosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0067_update_001.

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The defining histological hallmark of immunoglobulin A (IgA) nephropathy is the presence of IgA in the mesangium as the sole or dominant immunoreactant. Light microscopy appearances vary very widely. The most common appearance is mesangial cell proliferation and an increase in mesangial matrix. However, this is not diagnostic in the absence of immunohistology. Focal segmental proliferative or necrotizing glomerulonephritis may be seen in ‘vasculitic’ disease with or without the skin changes of Henoch–Schönlein purpura. Extracapillary proliferation and crescent formation may occur. Occasionally florid haematuria may cause renal failure through acute tubular injury. Most commonly the disease is slowly evolving and focal or global sclerosis and tubulointerstitial scarring develop. The Oxford classification scheme may give some prognostic weight to these changes. There are no reliable serological or urine tests for the disease. Although average levels of serum IgA are above the population average this is not diagnostically useful in individual patients. Promising biomarkers in urine and serum are under investigation.
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18

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0066_update_001.

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Immunoglobulin A (IgA) nephropathy characteristically causes haematuria and may present as a nephritic illness in older children and young adults. However, it may occur at any age and is commonly asymptomatic, associated first with haematuria alone, later progressing in some patients to hypertension, proteinuria, and progressive loss of glomerular filtration. While this evolution is characteristically slow, over decades, in some it is rapid, leading to early end-stage renal failure. It is common for the disease to present late, as advanced renal disease, or malignant hypertension. It may present with acute kidney injury caused by crescentic disease, but acute kidney injury caused by haematuria may be confused clinically with the same. Henoch–Schönlein purpura is a type of small vessel vasculitis that is most commonly seen in children, but which occurs at all ages, that is associated with IgA deposition. In older children and most adults it merges closely into IgA nephropathy after the acute event. Outcomes in adults are less good. IgA nephropathy is the most common type of glomerulonephritis in most developed countries. The disease is more common in men, and appears to be much less common in black people. The detected incidence is strongly influenced by biopsy policies; the lower your threshold to biopsy patients with haematuria, the more of this condition you discover. There are clear genetic tendencies but the strongest risk seems to come from genes in the human leucocyte antigen complex.
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19

Fabrizi, Fabrizio, and Patrice Cacoub. The patient with cryoglobulinaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0151.

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AbstractCryoglobulinaemia is characterized by the presence in the blood of proteins showing the that precipitate when serum is cooled. Clinically recognised cryoprecipitates are predominantly immunoglobulin-containing. In Type 1 cryoglobulinaemia, the precipitate is formed from a monoclonal paraprotein, usually IgG. In Type 2, a monoclonal IgM binds IgG to form a mixed precipitate. Type 3 cryoglobulins do not contain a monoclonal element.Type 1 cryoglobulins are a rare cause of renal disease, but cause a membranoproliferative glomerulonephritis (MPGN) with nephrotic syndrome and haematuria and usually with severe cutaneous involvement.Type 2 is most typically associated with renal disease, again characterized by MPGN and haematuria, with variable cutaneous signs and vasculitis in other organs. Many cases are associated with Hepatitis C virus (HCV) infection – but not all.Therapeutic approaches include optimal antiviral regimen, immunosuppressive therapy (corticosteroids, rituximab, and cytotoxic agents), and plasma exchange. Treatment of HCV-related mixed cryoglobulinaemia vasculitis should be adjusted according to the clinico-biological presentation.
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20

Fabrizi, Fabrizio. Hepatitis C. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0186.

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Hepatitis C virus (HCV) is associated with a large spectrum of histopathological lesions in both native and transplanted kidneys. The exact frequency of kidney damage in HCV-infected patients remains unknown, but the most frequent associated renal lesion is membranoproliferative glomerulonephritis (MPGN) with deposition of immunoglobulin and complement (MPGN type 1), usually in the context of type II mixed cryoglobulinaemia associated with a monoclonal IgM which binds IgG.Various approaches have been tried for the treatment of HCV-related glomerulonephritis, including immunosuppressive therapy (corticosteroids and cytotoxic agents), plasma exchange, and antiviral agents. Use of antiviral drugs for treatment of HCV-associated glomerulonephritis has shown encouraging results. Immunosuppressive therapy is recommended for cryoglobulinaemic kidney disease. Two distinct approaches should be considered for the treatment of HCV-associated cryoglobulinaemic glomerulonephritis according to the level of proteinuria and kidney failure. Preliminary evidence on rituximab therapy for HCV-related cryoglobulinaemic glomerulonephritis exists but several questions related to its use remain unclear.
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21

Muche, Marion, and Seema Baid-Agrawal. Hepatitis B. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0185_update_001.

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Hepatitis B virus (HBV) has been causally linked to a variety of renal diseases, the most common being glomerular diseases and systemic autoimmune disease. Membranous nephropathy (MN) is the commonest HBV-associated glomerulonephritis (HBV-GN), followed by membranoproliferative glomerulonephritis (MPGN), mesangial proliferative glomerulonephritis, immunoglobulin (Ig)-A nephropathy, and focal segmental glomerulosclerosis (FSGS). Polyarteritis nodosa is a rare manifestation. The incidence of HBV-associated renal diseases seems to be decreasing with the introduction of vaccination programmes.HBV-MN is the most frequent cause of nephrotic syndrome in children in countries with high endemicity of HBV infection. The clinical course is usually benign in children with high rates of spontaneous remission rates and low risk of progression to renal failure. The prognosis is worse in adults. Of the systemic autoimmune disorders associated with HBV infection that involve the kidneys, the strongest link has been found with polyarteritis nodosa (PAN), a lesion that causes arteritis of medium-sized renal vessels. HBV-associated PAN (HBV-PAN) usually manifests in the first year after infection, and is clinically indistinguishable from classic PAN.Diagnosis of HBV-GN or -PAN is based on the clinical picture, histological findings, evidence of viral replication in serum and/or liver and detection of HBV antigens or DNA in the tissue. Besides deposition of immune complexes, other mechanisms such as virus-induced cytopathic damage have been proposed to explain the pathogenesis.HBV-GN and HBV-PAN appear to respond to antiviral treatment. Both show remission after HBeAg seroconversion. The available studies predominantly employed first-generation agents like interferon alpha and lamivudine, which showed suppression of viral replication and clinical remission of HBV-associated renal disease. Immunosuppressive therapy appears to be inevitable for the control of severe HBV-PAN and could be helpful in addition to antiviral treatment for cases of HBV-GN not responding clinically to antiviral treatment.
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