Glomerulonephritis acute postinfectious N08.0

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 14.06.2022

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Acute postinfectious glomerulonephritis; Acute postinfectious infectious glomerulonephritis; PIGN; Postinfectious acute infectious glomerulonephritis; postinfectious glomerulonephritis; Post-streptococcal glomerulonephritis; PSGN

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Acute, immune-mediated, post-infectious inflammation of the renal glomerula, which mainly affects children between 5 and 15 years (Wang D et al. 2017).

The main causes are streptogenic infections of the mouth and throat (angina tonsillaris, pharyngitis), skin and bones (erysipelas, impetigo, possibly osteomyelitis, etc.).

Also possible in cases of bacterial endocarditis, infections of ventriculo-atrial or ventriculo-jugular shunts.

Less frequent pathogens are "non-streptococcal bacteria" such as: staphylococci. (Remark: versch. Authors consider "post-staphylococcal glomerulonephritis" as a separate, IgA-mediated entity - Glassock RJ et al. 2015), viruses (e.g. HBV, parvovirus B19 - Marco H et al. 2016), parasites, rickettsia, fungi and malaria pathogens.

In adults, leading infection precursors are (staphylogenic) skin infections, followed by pneumonia and urinary tract infections.

Besides staphylococci, streptococci and Gram-negative germs are the main causes (Nasr SH et al. 2011).

In rare cases, scabies infections were the triggering cause in adults. (Wang D et al. 2017)

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Rather rare in developed countries, of significant relevance in developing countries (Kambham N 2012) or among certain indigenous peoples (Ramanathan G et al. 2017). For adults: m:w=2.8:1.

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Unknown; it is postulated that microbial antigens bind to the glomerular basement membrane; they activate the alternating complement pathway directly or by binding of circulating IgG antibodies and induce a site-bound, initially neutrophilic, later neutrophilic/monocytic inflammation. Furthermore, infection-associated circulating immune complexes may be deposited at the glomerular basement membrane, also inducing focal granulocytic-monocytic inflammation. Such a process can be observed analogously in capillaries of the skin (principle of leukocytoclastic vasculitis, - clinical picture of palpable purpura).

Other antigens known to play a role in the pathogenesis of PIGN are the "Nephritis-associated plasmin receptor" (NAPlr) and the "Streptococcal pyrogenic exotoxin B" (SPeB). Both antigens are characterized by an affinity to glomerular proteins and are also able to activate the alternative complement pathway (Balasubramanian R et al.2017).

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About 5%-10% of patients with streptococcal pharyngitis and about 25% of patients with impetigo develop a PIGN.

Clinical features
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50% of cases of PIG in children and adolescents are completely asymptomatic or clinically undiagnosed. The other half of patients become symptomatic after a latency period of 6-21 days (rarely longer up to 6 weeks). Typically, the patient feels significantly ill again after a normal postinfectious convalescence period. However, fever is rare.

  • Obligatory symptoms are: microhematuria + proteinuria (<3.0g/24h).

Optional symptoms are:

  • Edema (especially periorbital), hypertension.
  • Headache, pain in limbs, pain in lumbar region (renal capsular tension).
  • Macrohaematuria (urine becomes dark brown, smoky or purely bloody; detectable in about 50% of cases).
  • Neurological symptoms: epileptic seizures, somnolence (cerebral edema)
  • Complicative: hypertensive crisis with dyspnea and pulmonary edema. Renal failure with fluid overload and cardiac failure may occur in 1-2% of patients with severe hypertension (pulmonary syndrome with haematuria and haemoptysis).
  • Rarely, a nephrotic syndrome (proteinuria > 3.0-3.5g/24h) may persist after the acute phase has resolved.

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Urine status: mostly moderate proteinuria (0.5-2.0 g/24h), dysmorphic erythrocytes, leucocytes, renal tubule cells, possibly erythrocyte, leucocyte granulocyte cylinders and renal tubule cells.

Serum creatinine: may initially rise rapidly.

ASL: increased in 50%.

Imaging: Sonography: Large swollen kidneys


  • Complement: C3- decreased during the active phase. Normalization in 80% of PIGN cases within 6-8 weeks. C1q, C2 and C4 levels are usually normal.
  • Cryoglobulins: Rare is a mostly passagere (few months) cryoglobulinemia.
  • Anti-DNAse-B (=ADB-titer) in 90% increased in streptococcal infections (Impetigo contagiosa) of the skin.

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Enlarged and hypercellular glomeruli, initially with neutrophil, later with mononuclear infiltrates. Possible are cellular proliferation and edema of the glomeruli; crescent formations (by proliferation of the Bowman capsule epithelium); severe narrowing of the capillary light. Mesangial spaces often considerably enlarged by edema formation; they contain neutrophil cells and cell debris.

Direct Immunofluorescence DIF): Detection of immune complex deposits, IgG (more rarely IgA) and complement fractions, which are detectable as "humps" on the outside of the basement membrane (Mascarenhas R et al. 2016).

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Evidence of previous infection, characteristic clinic, laboratory; possibly kidney biopsy (only in case of rapid and high increase of retention values) to exclude an RPGN (Rapid Progressive GN).

Differential diagnosis
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Rapid progressive glomerulonephritis (retention levels remain high); IgA nephropathy (macrohematuria).

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Basically the treatment of uncomplicated PIGN is conservative, supportive. It includes physical protection, a restriction of the protein, sodium and fluid intake (Kanjanabuch T et al. 2009). Furthermore: antibiotic therapy (3 mega penicilin/day for 10 days). Further symptom-oriented therapies:

  • Possible treatment with antibiotics (the sense is controversially discussed).
  • Edema: Diuretic therapy (loop diuretics)
  • Hypertension: ACE inhibitor or Sartane
  • Severe course/complications: glucocorticoids, possibly intermittent dialysis

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Symptomatic therapy with monitoring of kidney function is usually sufficient in children and leads to healing within 6-8 weeks (!) in 90% of cases without consequences (Sethi S et al. 2012). The GFR normalizes during this time. A mild proteinuria can persist for 6-12 months, a microscopic hematuria for several years. Renal cell proliferation disappears within weeks, but sclerosis usually persists. In about 50% of the cases a restriction of the renal function remains. In immunocompromised patients this value is >50%.

Adults (often associated with diabetes mellitus) have a significantly worse prognosis than children. 46% of adult patients become acutely dependent on dialysis (Nasr SH et al. 2011).

In 1% of children and 10% of adults, PIGN develops into a rapidly progressive GN (Rapid progressive GN). The cause for this atypical course is still unclear. Dysregulations of the alternative complement pathway are being discussed, such as mutations in the genes of the complement building blocks and in antibody formation against C3-convertase (Sethi S et al. 2012).

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Early and sufficiently long antibiotic therapy for infections with beta-hemolytic Group A Streptococci.

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Basically, PIGN should be considered in children and adolescents with microhematuria and mild proteinuria (as well as other optional PIGN symptoms), recent history of infections (streptococcal tonsillitis, pharyngitis impetigo or erysipelas) who feel sick again and impaired performance. Evidence of hypocomplementemia is essential confirmation. Biopsy may confirm the diagnosis but is rarely required. Supportive treatment generally leads to recovery of renal function

Further comment. Immune complex glomerulonephritis may also develop during persistent infection: e.g. endocarditis or soft tissue abscesses.

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  1. Balasubramanian R et al.(2017) Post-infectious glomerulonephritis. Paediatr Int Child Health 37:240-247.
  2. Glassock RJ et al (2015) Staphylococcus-related glomerulonephritis and poststreptococcal glomerulonephritis: why defining "post" is important in understanding and treating infection-related glomerulonephritis. At J Kidney Dis. 65:826-832.
  3. Kambham N (2012) Postinfectious glomerulonephritis. Adv Anat Pathol 19:338-347.
  4. Kanjanabuch T et al (2009) An update on acute postinfectious glomerulonephritis worldwide. Nat Rev Nephrol 5:259-269.
  5. Marco H et al (2016) Postinfectious glomerulonephritis secondary to Erythrovirus B19 (Parvovirus B19): case report and review of the literature. Clin Nephrol 85:238-244.
  6. Mascarenhas R et al (2016) IgA dominant postinfectious glomerulonephritis. Clin Pediatr (Phila) 55:873-876.
  7. Nasr SH et al (2011) Postinfectious glomerulonephritis in the elderly. J Am Soc Nephrol 22:187-195.

  8. Ramanathan G et al (2017) Analysis of clinical presentation, pathological spectra, treatment and outcomes of biopsy-proven acute postinfectious glomerulonephritis in adult indigenous people of the Northern Territory of Australia. Nephrology (Carlton) 22:403-411.

  9. Sethi S et al (2012) Atypical postinfectious glomerulonephritis is associated with abnormalities in the alternative pathway of complement. Kidney Int 83:293-299
  10. Wang D et al (2017) Acute postinfectious glomerulonephritis associated with scabies in the elderly: A case report. Parasitol Int 66:802-805.


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Last updated on: 14.06.2022