| 词条 | Acute proliferative glomerulonephritis |
| 释义 |
| name = Acute proliferative glomerulonephritis | image = Post-infectious_glomerulonephritis_-_very_high_mag.jpg | caption = Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain. | symptoms = | complications = | onset = | duration = | causes =Caused by Streptococcus bacteria [1] | risks = | diagnosis =Kidney biopsy, Complement profile[1] | differential = | prevention = | treatment =Low-sodium diet, Blood pressure management[3] | medication = | prognosis = | frequency = 1.5 million (2015)[1] | deaths = }}Acute proliferative glomerulonephritis is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.[2] It can be a risk factor for future albuminuria.[3] In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used.[4] Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990 worldwide.[5] Signs and symptomsAmong the signs and symptoms of acute proliferative glomerulonephritis are the following:
CausesAcute proliferative glomerulonephritis (post-streptococcal glomerulonephritisis) is caused by an infection with streptococcus bacteria, usually three weeks after infection, usually of the pharynx or the skin, given the time required to raise antibodies and complement proteins.[10][11] The infection causes blood vessels in the kidneys to develop inflammation, this hampers the renal organs ability to filter urine.{{citation needed|date=September 2016}} Acute proliferative glomerulonephritis most commonly occurs in children.[11] PathophysiologyThe pathophysiology of this disorder is consistent with an immune-complex-mediated mechanism, a type III hypersensitivity reaction. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, via interaction with properdin, the complement is activated. Complement fixation causes the generation of additional inflammatory mediators[12] Complement activation is very important in acute proliferative glomerulonephritis. Apparently immunoglobulin (Ig)-binding proteins bind C4BP. Complement regulatory proteins (FH and FHL-1), may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the process of infection.[13] DiagnosisThe following diagnostic methods can be used for acute proliferative glomerulonephritis:[12]
Clinically, acute proliferative glomerulonephritis is diagnosed following a differential diagnosis between (and, ultimately, diagnosis of) staphylococcal and streptococcal impetigo. Serologically, diagnostic markers can be tested; specifically, the streptozyme test is used and measures multiple streptococcal antibodies: antistreptolysin, antihyaluronidase, antistreptokinase, antinicotinamide-adenine dinucleotidase, and anti-DNAse B antibodies.[14] Differential diagnosisThe differential diagnosis of acute proliferative glomerulonephritisis is based on the following:{{citation needed|date=October 2015}} {{columns-list|colwidth=30em|
}} PreventionIt is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis,[15] while others reject that antibiotics can prevent acute proliferative glomerulonephritis.[16] TreatmentAcute management of acute proliferative glomerulonephritis mainly consists of blood pressure (BP) control. A low-sodium diet may be instituted when hypertension is present. In individuals with oliguric acute kidney injury, the potassium level should be controlled.[17] Thiazide or loop diuretics can be used to simultaneously reduce edema and control hypertension; however electrolytes such as potassium must be monitored. Beta-blockers, Calcium channel blockers, and/or ACE inhibitors may be added if blood pressure is not effectively controlled through diureses alone.[12] EpidemiologyAcute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[5] References1. ^{{cite journal|last1=GBD 2015 Disease and Injury Incidence and Prevalence|first1=Collaborators.|title=Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015.|journal=Lancet|date=8 October 2016|volume=388|issue=10053|pages=1545–1602|pmid=27733282|doi=10.1016/S0140-6736(16)31678-6|pmc=5055577}} 2. ^{{cite journal |author =Baltimore RS |title=Re-evaluation of antibiotic treatment of streptococcal pharyngitis |journal=Curr. Opin. Pediatr. |volume=22 |issue=1 |pages=77–82 |date=February 2010 |pmid=19996970 |doi=10.1097/MOP.0b013e32833502e7 }} 3. ^{{cite journal |vauthors=White AV, Hoy WE, McCredie DA |title=Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life |journal=Med. J. Aust. |volume=174 |issue=10 |pages=492–6 |date=May 2001 |pmid=11419767 |doi= |url=http://www.mja.com.au/public/issues/174_10_210501/white/white.html}} 4. ^{{cite journal | author=Nasr SH |author2=Radhakrishnan J |author3=D'Agati VD | journal=Kidney Int | title=Bacterial infection-related glomerulonephritis in adults |date=May 2013 | volume=83 | issue=5 | pages=792–803 | doi=10.1038/ki.2012.407 | pmid=23302723}} 5. ^1 {{cite journal|last1=GBD 2013 Mortality and Causes of Death|first1=Collaborators|title=Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.|journal=Lancet|date=17 December 2014|pmid=25530442|doi=10.1016/S0140-6736(14)61682-2|volume=385|issue=9963|pmc=4340604|pages=117–71}} 6. ^{{cite book|last=Tasic |first=Velibor |title=Comprehensive Pediatric Nephrology |date=2008 |publisher=Elsevier |isbn=9780323048835 |pages=309–317 |chapter=Postinfectious Glomerulonephritis|doi=10.1016/B978-0-323-04883-5.50026-X }}{{Subscription or libraries|sentence|via=ScienceDirect}} 7. ^{{Cite book|title = Handbook of Signs & Symptoms|url = https://books.google.com/books?id=57YxBgAAQBAJ|publisher = Lippincott Williams & Wilkins|date = 2015-01-16|isbn = 9781496310545|first = Lippincott Williams &|last = Wilkiins}} 8. ^1 {{Cite book|title = Critical Care Transport|url = https://books.google.com/books?id=rJcpF54JNGIC|publisher = Jones & Bartlett Learning|date = 2009-11-13|page=959|isbn = 9780763712235|first = American Academy of Orthopaedic|last = Surgeons|first2 = American College of Emergency|last2 = Physicians}} 9. ^{{Cite book|title = Pediatric Clinical Advisor: Instant Diagnosis and Treatment|url = https://books.google.com/books?id=pwajBQAAQBAJ|publisher = Elsevier Health Sciences|date = 2007-07-05|page=223|isbn = 9780323070584|first = Lynn C.|last = Garfunkel|first2 = Jeffrey|last2 = Kaczorowski|first3 = Cynthia|last3 = Christy}} 10. ^Marianne Gausche-Hill, Susan Fuchs, Loren Yamamoto, American Academy of Pediatrics, American College of Emergency Physicians. "APLS: The Pediatric Emergency Medicine Resource". Jones & Bartlett Learning; 2004. 11. ^1 {{Cite web|title = Post-streptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia|url = https://www.nlm.nih.gov/medlineplus/ency/article/000503.htm|website = www.nlm.nih.gov|accessdate = 2015-10-31}} 12. ^1 2 3 4 {{Cite journal|title = Acute Poststreptococcal Glomerulonephritis: Background, Pathophysiology, Epidemiology|url = http://emedicine.medscape.com/article/980685-overview#a3|date = 2018-12-05}} 13. ^{{Cite journal|title = Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet|url = http://www.nature.com/ki/journal/v71/n11/full/5002169a.html|journal = Kidney International|date = 2007-03-07|issn = 0085-2538|pages = 1094–1104|volume = 71|issue = 11|doi = 10.1038/sj.ki.5002169|first = B.|last = Rodríguez-Iturbe|first2 = S.|last2 = Batsford|pmid=17342179}} 14. ^{{Cite web|title = Acute Poststreptococcal Glomerulonephritis Workup: Approach Considerations, Hematologic and Blood Chemistry Studies, Urine Studies|url = http://emedicine.medscape.com/article/980685-workup|website = emedicine.medscape.com|accessdate = 2015-10-31}} 15. ^{{Cite journal|title = The Current State of Poststreptococcal Glomerulonephritis|url = http://jasn.asnjournals.org/content/19/10/1855|journal = Journal of the American Society of Nephrology|date = 2008-10-01|issn = 1046-6673|pmid = 18667731|pages = 1855–1864|volume = 19|issue = 10|doi = 10.1681/ASN.2008010092|first = Bernardo|last = Rodriguez-Iturbe|first2 = James M.|last2 = Musser}} 16. ^Allan H Goroll, Albert G Mulley, Jr. Primary Care Medicine: Office Evaluation and Management of The Adult Patient, 6th ed. Lippincott Williams & Wilkins; 2011. 17. ^1 {{Cite journal|title = Acute Poststreptococcal Glomerulonephritis Treatment & Management: Approach Considerations, Consultations, Long-Term Monitoring|url = http://emedicine.medscape.com/article/980685-treatment|date = 2018-12-05}} Further reading
External links{{Medical condition classification and resources| DiseasesDB = 29306| ICD10 = {{ICD10|N00.8}} | ICD9 = {{ICD9|580.0}} | ICDO = | OMIM = | MedlinePlus = 000503 | eMedicineSubj = med | eMedicineTopic = 889 | MeshID = }}{{Nephrology}}{{Medicine}}{{DEFAULTSORT:Acute Proliferative Glomerulonephritis}} 2 : Kidney diseases|Disorders causing edema |
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