A procedure called plasmapheresis may sometimes be used for glomerulonephritis caused by immune problems. The fluid part of the blood that contains antibodies is removed and replaced with intravenous fluids or donated plasma (that does not contain antibodies). Removing antibodies may reduce inflammation in the kidney tissues.
Glomerulonephritis Ppt Download
Reich HN, Cattran DC. Treatment of glomerulonephritis. In: Yu ASL, Chertow GM, Luyckx VA, Marsden PA, Skorecki K, Taal MW, eds. Brenner and Rector's The Kidney. 11th ed. Philadelphia, PA: Elsevier; 2020:chap 33.
processing.... Drugs & Diseases > Nephrology Acute Glomerulonephritis Updated: Sep 22, 2022 Author: Malvinder S Parmar, MBBS, MS, FRCPC, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN more... Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Acute Glomerulonephritis Sections Acute Glomerulonephritis Overview Practice Essentials Background Pathophysiology Etiology Epidemiology Prognosis Patient Education Show All Presentation History Physical Examination Complications Show All DDx Workup Approach Considerations Initial Blood Tests Complement Levels Urinalysis and 24-Hour Urine Study Streptozyme Test Blood and Tissue Culture Other Laboratory Tests Radiography and Computed Tomography Ultrasonography and Echocardiography Kidney Biopsy Histologic Findings Show All Treatment Approach Considerations Pharmacologic Therapy Diet and Activity Long-Term Monitoring Show All Medication Medication Summary Antimicrobials (Antibiotics) Loop Diuretics Vasodilators Calcium Channel Blockers Show All Questions & Answers Media Gallery References Overview Practice Essentials Acute glomerulonephritis (AGN) comprises a specific set of kidney diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium. Acute nephritic syndrome is the most serious of these syndromes. AGN progresses to chronic glomerulonephritis in about 30% of adults. [1]
Acute poststreptococcal glomerulonephritis (PSGN) is the archetype of AGN. In recent decades, however, the incidence of PSGN has fallen in the United States and other developed countries, while glomerulonephritis associated with staphylococcal infection has risen, due to the increase in antibiotic-resistant Staphylococcus aureus infections. [2, 3, 4]
Historically, the classification of glomerulonephritis was based on the histopathological patterns of injury. With increased understanding of underlying etiology, glomerulonephritis is more frequently classified as follows [5] :
Treatment of PSGN is mainly supportive, because there is no specific therapy for renal disease. When AGN is associated with chronic infections, the underlying infections must be treated. This article addresses the aspects of glomerulonephritis that are relevant to its acute management.
Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft because of the proliferation of endothelial, mesangial, [7] and epithelial cells. The proliferation may be endocapillary (ie, within the confines of the glomerular capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial cells). In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive glomerulonephritis.
Antibody levels to nephritis-associated protease (NAPR) are elevated in streptococcal infections (group A, C, and G) associated with glomerulonephritis but are not elevated in streptococcal infections without glomerulonephritis, whereas anti-streptolysin-O titers are elevated in both circumstances. These antibodies to NAPR persist for years and perhaps are protective against further episodes of PSGN. In a study in adults, the two most frequently identified infectious agents were streptococci (27.9%) and staphylococci (24.4%). [10]
PSGN usually develops 1-3 weeks after acute infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The incidence of glomerulonephritis is approximately 5-10% in persons with pharyngitis and 25% in those with skin infections.
Nonstreptococcal postinfectious glomerulonephritis may also result from infection by other bacteria, viruses, parasites, or fungi. Bacteria other than group A streptococci that can cause AGN include the following:
Attributing glomerulonephritis to a parasitic or fungal etiology also requires the exclusion of a streptococcal infection. Identified organisms include Coccidioides immitis and the following parasites:
Membranoproliferative glomerulonephritis (MPGN) - This is due to the expansion and proliferation of mesangial cells as a consequence of the deposition of complements. Type I refers to the granular deposition of C3; type II refers to an irregular process.
Idiopathic rapidly progressive glomerulonephritis - This form of glomerulonephritis is characterized by the presence of glomerular crescents. Three types have been distinguished: Type I is an antiglomerular basement membrane disease, type II is mediated by immune complexes, and type III is identified by antineutrophil cytoplasmic antibody (ANCA).
The prognosis for nonstreptococcal postinfectious glomerulonephritis depends on the underlying agent, which must be identified and addressed. Generally, the prognosis is worse in patients with heavy proteinuria, severe hypertension, and significant elevations of creatinine level. Nephritis associated with methicillin-resistant Staphylococcus aureus (MRSA) and chronic infections usually resolves after treatment of the infection.
In a pooled analysis of poststaphylococcal glomerulonephritis, only 44.7% of patients achieved remission; 22.9% progressed to end-stage renal disease (ESRD) and remained dialysis-dependent, and 14.5% died. Older age and diabetes mellitus were risk factors for adverse outcomes. [2]
Murakami and colleagues examined the clinical characteristics and pathological patterns of postinfectious glomerulonephritis in 72 HIV-infected patients. The most common infectious agent was Staphylococcus. During a median of 17 months of follow-up, pathological patterns had no significant effects on renal outcomes. Mortality occurred in 14 patients overall, and mortality rates were significantly elevated among the 28 patients with healed postinfectious glomerulonephritis. [23]
In a retrospective study of 101 patients with severe lupus and rapidly progressive glomerulonephritis and 200 lupus patient controls who were followed for a median of 4 years, rapidly progressive glomerulonephritis was associated with poorer treatment response, atrophy and fibrosis, severe renal manifestations, serious sclerotic and crescentic glomeruli lesions, severe tubulointerstitial inflammation, and prominent leukocyte infiltration. Serum creatinine levels and the proportion of crescents were the most important predictors of developing ESRD. [24]
It is not clear why the immune system causes diseases such as glomerulonephritis. There may be some trigger that makes the immune system go wrong, such as an infection or cancer. Often it is not known why glomerulonephritis occurs.
Many other conditions can cause the glomeruli to be damaged. High blood pressure or diabetes are common examples, so your kidney specialist will ask a lot of questions and perform lots of blood tests if glomerulonephritis is suspected.
Most commonly there are no symptoms, in other words someone with glomerulonephritis feels completely well. Although they may have symptoms if other organs are injured too (eg rash, sinusitis, joint pain and swelling). The only sign of damage to the glomeruli may be small amounts of blood or protein that have passed through the damaged filters into the urine, and can only be detected when tests are performed by a doctor or nurse.
Doctors consider glomerulonephritis in anyone with kidney disease, but problems such as infection are much commoner. If glomerulonephritis is suspected, some blood tests will be performed to look for abnormal antibodies in the blood. However, it is not possible to make an accurate diagnosis in most cases by blood tests alone. To be sure of making a diagnosis, a Kidney biopsy must be performed. A biopsy is the removal of a tiny fragment of kidney to examine under the microscope. This test carries a small risk of bleeding, and not everyone with possible glomerulonephritis requires a biopsy. Some of these conditions run in the family.
Treatment varies according to the type of glomerulonephritis. Some types of glomerulonephritis will respond to treatment that reduces the action of the immune system, but other types are very difficult to treat. Many treatments, because they attack the whole immune system and not just the abnormal part, can cause serious side effects.
Most people with glomerulonephritis do not have anyone else in the family with the condition. However, it is always worth asking your specialist if the type of glomerulonephritis you have could be inherited. It is simple to test people for glomerulonephritis with a urine test, so sometimes a specialist will advise checks on the family to be on the safe side. There are some types of glomerulonephritis that run very strongly in families, and if one of these is diagnosed the specialist will certainly advise about the chances of family members being affected, and how screening should be done.
A form of inherited glomerulonephritis called Alport syndrome, which affects both men and women; men are more likely to have kidney problems. Treatment focuses on preventing and treating high blood pressure and preventing kidney damage.
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