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]
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 or crescentic glomerulonephritis; children with [pathologyoutlines.com]
抄録 A 55-year-old man developed rapidly progressive glomerulonephritis and nephrotic syndrome. [jstage.jst.go.jp]
hematuria and RBC casts, mild proteinuria ) Ultrasound : enlarged kidneys Renal biopsy (not performed in most cases) Indication: suspected rapidly progressive glomerulonephritis Findings Light microscopy: glomeruli appear enlarged and hypercellular [amboss.com]
- Dull Chest Pain
His shortness of breath had worsened over the previous 2 days, and was associated with substernal dull chest pain and hemoptysis. [dovepress.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]
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. Other infections can cause GN, although less commonly than strep. [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.
- Abnormal Renal Function
However, the patient reported here had abnormal renal function. Further PCR analyses indicated that he was infected with M. pneumoniae. Although his ASO was in the normal range, the serum C3 at poststreptococcal glomerulonephritis was decreased. [ijpmonline.org]
- Burr Cell
Laboratory evaluation revealed micro-angiopathic anaemia with burr cells, thrombocytopenia, elevated lactic dehydrogenase and low complement C3. Urinalysis showed marked proteinuria and haematuria. [ncbi.nlm.nih.gov]
QT, RR, ST Intervals
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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.