Which findings are commonly observed in the child who is in the acute phase of Poststreptococcal glomerulonephritis?

Acute post streptococcal glomerulonephritis is an immunologic response of the kidney to infection, characterized by the sudden appearance of edema, hematuria, proteinuria and hypertension . It is essentially a disease of childhood that accounts for approximately 90% of renal disorders in children. The disease occurs especially in children between the ages of 2 and 12 years and young adults, and more often in male than in female .

Acute post streptococcal glomerulonephritis are caused by group A beta haemolytic streptococci and follow upper airway infections such as pharyngitis or tonsillitis, by 14 to 21 days and 3-6 weeks after skin infection especially in warmer climates .

In recent decades the number of patients with post streptococcal glomerulonephritis has decreased considerably in the United States and Europe industrialized countries. In other parts of the world ,some developing communities. the incidence of post streptococcal glomerulonephritis has remained high. post streptococcal glomerulonephritis is one of the leading cause requiring hospital admissions in children , and it is also an important cause of acute renal failure in developing countries. Though deaths due to this disease are rare, it can cause serious complications such as hypertensive emergency, congestive cardiac failure, renal failure, encephalopathy and retinopathy .

Acute post streptococcal glomerulonephritis can also progress to rapidly progressive glomerulonephritis which is defined as''a syndrome that progresses rapidly within a few weeks or months to renal failure and is accompanied by urinary findings of nephritis.'' The clinical concept of rapidly progressive glomerulonephritis includes various renal diseases that cause renal function to deteriorate over a subacute course. Necrotizing crescentic glomerulonephritis is often observed in histopathological findings .

Acute post streptococcal glomerulonephritis was diagnosed in the presence of :

features of acute nephritic syndrome. evidence of recent streptococcal infection. lower serum complement three levels. Anti streptolysin o titre >200 units/ml was considered as evidence of recent streptococcal infection

Intervention Details:

• Diagnostic Test: anti streptolysin o titre and serum complement test

Primary Outcome Measures :

1. number of patients with full recovery or having complication at time of discharge and after 8 week [ Time Frame: one year ]

   serum complementary test by ELISA

   
   

This study will be done on children attending at Assiut University Children Hospital with clinical manifestation of acute post streptococcal glomerulonephritis during one year period .

In addition to meticulous history taking and thorough clinical examination , all the cases will be subjected to the following laboratory investigations :

Complete blood count on admission, urine analysis, blood urea, serum creatinine, serum albumin, serum cholesterol, urine spot protein creatinine ratio, antistreptolysin O , Erythrocyte sedimentation rate , C-reactive protein and serum complement C3 levels on admission and after 8 weeks.

Inclusion Criteria:

• Children in the age groups of 2-15 years. presenting with clinical manifestation of acute nephritic syndrome will be included in the study.

Exclusion Criteria:

• Children having history suggestive of chronic renal and cardiac disease in the past
• Children with congenital renal anomalies .
• Children with clinical manifestation of nephrotic syndrome .
• Children with clinical manifestation of acute nephritic syndrome due to other causes .

Publications of Results:

Arimura Y, Muso E, Fujimoto S, Hasegawa M, Kaname S, Usui J, Ihara T, Kobayashi M, Itabashi M, Kitagawa K, Hirahashi J, Kimura K, Matsuo S. Evidence-based clinical practice guidelines for rapidly progressive glomerulonephritis 2014. Clin Exp Nephrol. 2016 Jun;20(3):322-41. doi: 10.1007/s10157-015-1218-8. No abstract available.

Additional relevant MeSH terms:

Post-streptococcal glomerulonephritis (PSGN) is an immunologically-mediated sequela of pharyngitis or skin infections caused by nephritogenic strains of Streptococcus pyogenes. S. pyogenes are also called group A Streptococcus (group A strep).

Etiology

PSGN is usually an immunologically-mediated, nonsuppurative, delayed sequela of pharyngitis or skin infections caused by nephritogenic strains of S. pyogenes. Reported outbreaks of PSGN caused by group C streptococci are rare. 1,2

S. pyogenes are gram-positive cocci that grow in chains (see figure 1). They exhibit β-hemolysis (complete hemolysis) when grown on blood agar plates. They belong to group A in the Lancefield classification system for β-hemolytic Streptococcus, and thus are called group A streptococci.1

Clinical features

The clinical features of acute glomerulonephritis include:

• Edema (often pronounced facial and orbital edema, especially on arising in the morning)
• Hypertension
• Proteinuria
• Macroscopic hematuria, with urine appearing dark, reddish-brown
• Complaints of lethargy, generalized weakness, or anorexia

Figure 1. Streptococcus pyogenes (group A Streptococcus) on Gram stain. Source: Public Health Image Library, CDC

Laboratory examination usually reveals:

• Mild normocytic normochromic anemia
• Slight hypoproteinemia
• Elevated blood urea nitrogen and creatinine
• Elevated erythrocyte sedimentation rate
• Low total hemolytic complement and C3 complement

Patients usually have decreased urine output. Urine examination often reveals protein (usually <3 grams per day) and hemoglobin with red blood cell casts.

Additionally, some evidence from epidemic situations indicates that subclinical cases of PSGN may occur. Thus, some individuals may have symptoms that are mild enough to not come to medical attention.1

Transmission

As a delayed sequela of group A strep infection, PSGN is not contagious. However, people mostly commonly spread group A strep through direct person-to-person transmission. Typically, transmission occurs through saliva or nasal secretions from an infected person. Symptomatic people are much more likely to transmit the bacteria than asymptomatic carriers. Crowded conditions — such as those in schools, daycare centers, or military training facilities — facilitate transmission.  Although rare, spread of group A strep infections may also occur via food. Foodborne outbreaks of pharyngitis have occurred due to improper food handling. Environmental transmission via surfaces and fomites was historically not thought to occur. However, evidence from outbreak investigations indicate that environmental transmission of GAS may be possible, although it is likely a less common route of transmission.

Humans are the primary reservoir for group A strep. There is no evidence to indicate that pets can transmit the bacteria to humans.

Incubation period

PSGN occurs after a latent period of approximately 10 days following group A strep pharyngitis. Generally, PSGN occurs up to 3 weeks following group A strep skin infections.1

Risk factors

The risk factors for PSGN are the same as for the preceding group A strep pharyngitis or skin infection. PSGN is more common in children, although it can occur in adults. Pharyngitis-associated PSGN is most common among children of early school age. Pyoderma-associated PSGN is most common among children of pre-school age.

There are no known risk factors specific for PSGN. However, the risk of PSGN is increased if a nephritogenic strain of group A strep is introduced into a household.

Diagnosis and testing

The differential diagnosis of PSGN includes other infectious and non-infectious causes of acute glomerulonephritis.  Clinical history and findings with evidence of a preceding group A strep infection should inform a PSGN diagnosis. Evidence of preceding group A strep infection can include1

• Isolation of group A strep from the throat
• Isolation of group A strep from skin lesions
• Elevated streptococcal antibodies

Treatment

Treatment of PSGN focuses on managing hypertension and edema. Additionally, patients should receive penicillin (preferably penicillin G benzathine) to eradicate the nephritogenic strain. This will prevent spread of the strain to other people.1

Prognosis and complications

The prognosis of PSGN in children is very good; more than 90% of children make a full recovery. Adults with PSGN are more likely to have a worse outcome due to residual renal function impairment.1

Prevention

There is insufficient evidence to determine if antimicrobial therapy can prevent PSGN.1,2 Thus, it is important to prevent the primary group A streptococcal skin or pharyngeal infection. However, treating PSGN patients with antibiotics can stop a nephritogenic strain from circulating in a household. Thus, treating PSGN patients can prevent additional infections among close contacts.

Good hand hygiene and respiratory etiquette can reduce the spread of all types of group A strep infection. Hand hygiene is especially important after coughing and sneezing and before preparing foods or eating. Good respiratory etiquette involves covering your cough or sneeze. Treating an infected person with an antibiotic for 12 hours or longer generally eliminates their ability to transmit the bacteria. Thus, people with group A strep pharyngitis or impetigo should stay home from work, school, or daycare until:

• They are afebrile
  AND
• At least 12 hours after starting appropriate antibiotic therapy

Epidemiology

Humans are the only reservoir for group A strep. One 1960s study found a 10% to 15% attack rate of PSGN following throat or skin infection with a nephritogenic strain of group A strep.5 An estimated 470,000 cases of PSGN and 5,000 deaths from PSGN occur each year globally.3

1. Sainato RJ, Weisse ME. Poststreptococcal glomerulonephritis and antibiotics: A fresh look at old data. Clin Ped. 2019;58(1):10–12.
2. Bateman E, Mansour S, Okafor E, Arrington K, Hong B, Cervantes J. Examining the efficacy of antimicrobial therapy in preventing the development of postinfectious glomerulonephritis: A systematic review and meta-analysis. Infect Dis Rep. 2022;14(2):176–83.
3. Carapetis JR. The current evidence for the burden of group A streptococcal diseases. World Health Organization. Geneva. 2005.
4. Committee on Infectious Diseases. Group A streptococcal infections. In Kimberlin DW, Brady MT, Jackson MA, Long SS, editors. 30th ed. Red Book: 2015 Report of the Committee on Infectious Diseases. Elk Grove Village (IL). American Academy of Pediatrics. 2015;732–44.
5. Anthony BF, Kaplan EL, Wannamaker LW, Briese FW, Chapman SS. Attack rates of acute nephritis after Type 49 streptococcal infection of the skin and of the respiratory tract. J Clin Invest. 1969;48(9):1679–704.