Post-infectious glomerulonephritis is a type of glomerulonephritis, and thus an important cause of nephritic syndrome. It predominantly occurs in children and is a sequela of streptococcal throat or skin infections. The implicated organism is almost always, group A streptococcus.
Children older than 3 years are the most susceptible to post-infectious glomerulonephritis (PIGN), with boys affected twice as much as girls. A history of throat infection, tonsillitis or strep throat, for example, about 1 to 2 weeks prior to presentation, or up to 6 weeks in the case of suppurative skin infections such as impetigo, is always present. Only nephritogenic variants of group A streptococcus (GAS) can lead to PIGN . Patients may not always have a record of treatment, as symptoms may have been mild, or resolved quickly, not warranting a hospital visit. Non-specific symptoms seen include tiredness, gastrointestinal upset (nausea, vomiting, abdominal pain), loss of appetite and malaise. Fever is not a common finding and its presence should alert the clinician of ongoing infection.
The usual presenting complaints are some or all of the symptoms characterizing nephritic syndrome namely gross hematuria often described as cola or tea colored urine, microscopic hematuria, hypertension, periorbital edema, and markedly decreased urine output. In some patients, the only sign of the disease is microscopic hematuria; in endemic areas, this alone should raise the suspicion of PIGN .
Hypertension and fluid overload can lead to further morbidity; acute confusion, lethargy, seizures, shortness of breath and coughing with or without hemoptysis are amongst the findings  . These may indicate the presence of encephalopathy, heart failure or pulmonary-renal syndrome . Other complications include uremia, thrombotic microangiopathy, and nephrotic syndrome after PIGN has been adequately treated . Complications such as these are considerably more frequent in adults than in children. The elderly, diabetics and alcoholics are at an increased risk of developing PIGN.
Entire Body System
- Rapidly Progressive Glomerulonephritis
The clinical presentation of PIGN varies from a benign asymptomatic condition to rapidly progressive glomerulonephritis requiring dialysis. In most cases, PIGN is self-limiting and the evidence base for the treatments used is quite weak. [ncbi.nlm.nih.gov]
95% recover with conservative therapy; 1% develop rapidly progressive glomerulonephritis, 1 - 2% develop chronic glomerulonephritis Poor prognosis more likely if massive proteinuria and abnormal GFR; 2 - 5% die from pulmonary edema, hypertensive encephalopathy [pathologyoutlines.com]
抄録 A 55-year-old man developed rapidly progressive glomerulonephritis and nephrotic syndrome. [jstage.jst.go.jp]
progressive glomerulonephritis Findings Light microscopy: glomeruli appear enlarged and hypercellular (infiltration of monocytes and polymorphonuclear cells) Immunofluorescent microscopy: granular deposits ( IgG, IgM, C3 complement ) Electron microscopy [amboss.com]
- Dark Urine
Symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic. Diagnosis is made through a series of lab tests. [medical-dictionary.thefreedictionary.com]
They may also leak blood and protein in to the urine. The damage may cause dark urine, swelling, high blood pressure, or even kidney failure. Some patients get kidney damage from strep, but it is so mild they never know. [pascalelane.wordpress.com]
urine, typical of the condition, may not be noticed by children. [bpac.org.nz]
Symptoms include: pink or dark urine due to blood in your urine (hematuria) foamy urine due to too much protein (proteinuria) high blood pressure fluid retention fatigue kidney failure PANDAS PANDAS stands for Pediatric Autoimmune Neuropsychiatric Disorders [healthline.com]
- Smoky Urine
Patients with overt disease demonstrate gross hematuria characterized by red or smoky urine, headache, and generalized symptoms such as anorexia, nausea, vomiting, and malaise. 32 Swelling of the renal capsule can cause flank or back pain. [aafp.org]
A family history of PIGN, especially among siblings, should be inquired about, as this increases the likelihood of the diagnosis by at least 10% . A preceding streptococcal infection is imperative to the diagnosis of PIGN; this might be evident in the patient history. However, in cases where it is unclear, the following laboratory tests are carried out, as they provide evidence of said infection:
- Serum titers of antistreptolysin O and anti-DNAse will be elevated and have a high detection rate for recent streptococcal infection. The streptozyme test is even more sensitive, as it detects levels of the aforementioned antibodies and, in addition, antihyaluronidase, anti nicotinamide adenine dinucleotidase and antistreptokinase .
- Serum complement levels are usually low, especially complement component 3 (C3).
- Other tests can also be ordered, including more specialized immune response proteins and autoantibodies such as rheumatic factor  .
Testing for renal functions may reveal elevated levels of urea and creatinine. Urinalysis is particularly useful and may show white blood cells, microscopic hematuria, red cell casts, epithelial cells as well as hyaline casts. Proteinuria is rarely present, and even when present, it is rarely in the nephrotic range. Imaging studies have no role in diagnosing or treating PIGN. Moreover, renal biopsy is not usually needed and is only done if an alternative diagnosis is suggested by unusual symptoms.
Paradoxically, the treatment of glomerulonephritis has become even more complicated in the recent years, after the introduction of a number of newer immunosuppressive drugs. [books.google.com]
Antibiotic treatment was administered with improved respiratory symptoms, but worsening renal function. [revistanefrologia.com]
Treatment Treatment is supportive and may include restriction of dietary protein, sodium, and fluid and, in more severe cases, treatment of edema and hypertension. Dialysis is occasionally necessary. [merckmanuals.com]
[…] of antiviral treatment. [panafrican-med-journal.com]
[…] and immunosuppressive treatment. 1. [ijpmonline.org]
PSGN was the most common etiology [65(90.3 %)] among the PIGN cases. Pyodermas, upper respiratory infections and varicella preceded hematuria in 58 (80.6 %), 4 (5.6 %) and 2 (2.8 %) cases respectively. [ncbi.nlm.nih.gov]
Etiology Occurs approximately 10–30 days following an acute infection The most common cause is a prior infection with group A beta-hemolytic streptococci It occurs less frequently following other bacterial, viral infections, or malaria. [amboss.com]
Epidemiology and Etiology [ ✎ edit | edit source ] Typical age is 2-12 years. Patients usually have streptococcal pharyngitis or impetigo 5-21 days before PSAGN manifestation. [wikilectures.eu]
Etiology Postinfectious glomerulonephritis (PIGN), a nephritic syndrome, is the most common cause of a glomerular disorder in children between 5 and 15 yr; it is rare in children 2 yr and uncommon in adults > 40 yr. [merckmanuals.com]
licensee BioMed Central Ltd. 2014 Received: 22 February 2014 Accepted: 10 September 2014 Published: 13 September 2014 Abstract Background Posterior reversible encephalopathy syndrome is a clinical radiographic syndrome of heterogeneous etiologies. [bmcresnotes.biomedcentral.com]
The aim of this study was to evaluate the epidemiological, clinical and biologic features of APIGN in a Tunisian center. [ncbi.nlm.nih.gov]
References:    Epidemiological data refers to the US, unless otherwise specified. [amboss.com]
This Review focuses on acute postinfectious glomerulonephritis, and covers its epidemiology, presentation, pathology, pathogenesis, treatment and outcomes. [nature.com]
Definition / general Also called post streptococcal or acute glomerulonephritis; a type of diffuse endocapillary proliferative glomerulonephritis Pathophysiology Deposition of immune complexes from antibodies against organisms elicits acute inflammatory [pathologyoutlines.com]
[ edit ] The pathophysiology of this disorder is consistent with an immune -complex-mediated mechanism, a type III hypersensitivity reaction. [en.wikipedia.org]
References:   Pathophysiology Infection with nephritogenic strains of group A beta-hemolytic streptococci → immune complexes containing the streptococcal antigen deposit within the glomerular basement membrane ; (likely involves molecular mimicry [amboss.com]
Pathophysiology [ ✎ edit | edit source ] There are some antigenes produced by Streptococcus pyogenes the most important is NSAP-streptokinase (nephritogen strains associated protein), M-protein and endostreptosin. [wikilectures.eu]
PIGN is generally a self-limiting form of glomerulonephritis with activation of the alternative complement pathway as the main pathophysiological background. [karger.com]
Prevention is also key and involves encouraging individuals to seek early diagnosis and treatment of sore throats and skin lesions, particularly in children. [medical-dictionary.thefreedictionary.com]
Antibiotics Help Prevent Spreading the Infection to Others Prevent spreading group A strep infections to others. [cdc.gov]
Prevention The best means of preventing PSGN is to prevent the spread of group A streptococcal infection. At present, there is no vaccine available to prevent group A streptococcal infection. [ada.com]
Regular follow-up and monitoring of blood pressure, renal function test, and urine for hematuria and proteinuria every 3-6 months after the acute phase for at least a year is recommended to prevent progression to chronic renal failure.  Prevention [ijhas.in]
[ edit ] It 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 [en.wikipedia.org]
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- Rodríguez-Iturbe B, Katiyar VN, Coello J. Neuraminidase activity and free sialic acid levels in the serum of patients with acute poststreptococcal glomerulonephritis. The N Engl J Med. 1981;304(25):1506–1510
- Adikari M, Priyangika D, Marasingha I, et al. Post-streptococcal glomerulonephritis leading to posterior reversible encephalopathy syndrome: a case report. BMC Res Notes. 2014;7:644.
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- Kakajiwala A, Bhatti T, Kaplan BS, et al. Post-streptococcal glomerulonephritis associated with atypical hemolytic uremic syndrome: to treat or not to treat with eculizumab?. Clin Kidney J. 2016;9(1):90-96.
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- Parra G, Rodriguez-Iturbe B, Batsford S, et al. Antibody to streptococcal zymogen in the serum of patients with acute glomerulonephritis: a multicentric study. Kidney Int. 1998;54(2):509-517.