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Diagnosis:

Acute postinfectious glomerulonephritis

Acute postinfectious glomerulonephritis (APGN) most comonly affects children and young adults, although no age group is exempt; between 30% and 50% of patients are over the fourth decade of life. Males are affected more than females (ratio 2:1). Although the distribution of APGN is worldwide, it is more frequent in developing countries. For diagnosis, a preceding infective episode is required. The microorganism is usually Streptococcus pyogenes, however, the same glomerulonephritis has been described with other organisms: bacteria, fungi, and viruses.

APGN usually presents as acute nephritic syndrome. Glomerular lesions reult in reduced blood flow with low fractional excretion of sodium, low urinary sodium concentrations, salt and water retention with dilutional anemia, hypertension, and edema. Progession of the lesions may result in oliguria or anuria.

In many cases the APGN the disease is subclinical with transient depression of serum complement and/or mild urinary anormalities.

In most cases, the outcome of APGN is favorable: more than 90% of patients have no later effect. However, from 30% to 60% of adults and one-third of children suffer from irreversible changes, such as proteinuria, high blood pressure, and impaired renal function. Complications in the acute phase of the disease include hypertensive encephalopathy, and acute renal and heart failure. Hypertension, edema, electrolyte imbalance, anemia, and complement activation products may influence cardiac function and structure. Heart involvement, as well as proteinuria and high blood pressure, are factors that influence the
outcome of renal diseases.

In the present case the histologic features are tipical, with proliferative endocapillary GN, polymorphonuclear leukocytes and other leokocytes. In a variable proportion of cases there are crescents; in our case there is this extracapillary proliferation in seven of nineteen glomeruli. This lesion do not indicate a poor prognosis, although it can associate with low glomerular filtration rate. Cellular crescent (as in the present case) can resolve without major side effects.

We do not see humps in this case. The immunofluorescence was negative for IgA, IgM and C1q, but some cases can show positivity for this antigens.

See the chapter [Proliferative endocapillary glomerulonephritis] with atlas and text (only in spanish).

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References

• El-Husseini AA, Sheashaa HA, Sabry AA, Moustafa FE, Sobh MA. Acute postinfectious crescentic glomerulonephritis: clinicopathologic presentation and risk factors. Int Urol Nephrol. 2005;37:603-9. PubMed link
• Ozaltin F, Besbas N, Bakkaloglu A, Gucer S, Topaloglu R, Ozen S, Kale G, Caglar M. Apoptosis and proliferation in childhood acute proliferative glomerulonephritis. Pediatr Nephrol. 2005;20:1572-7. PubMed link
• Batsford SR, Mezzano S, Mihatsch M, Schiltz E, Rodriguez-Iturbe B. Is the nephritogenic antigen in post-streptococcal glomerulonephritis pyrogenic exotoxin B (SPE B) or GAPDH? Kidney Int. 2005;68:1120-9. PubMed link
• Ozaltin F, Besbas N, Bakkaloglu A, Gucer S, Topaloglu R, Ozen S, Kale G, Caglar M. Apoptosis and proliferation in childhood acute proliferative glomerulonephritis. Pediatr Nephrol. 2005;20:1572-7. PubMed link
• Hahn RG, Knox LM, Forman TA. Evaluation of poststreptococcal illness. Am Fam Physician. 200515;71:1949-54. PubMed link / Free full text
• Haas M. Incidental healed postinfectious glomerulonephritis: a study of 1012 renal biopsy specimens examined by electron microscopy. Hum Pathol. 2003;34:3-10. PubMed link
• Ferrario F, Rastaldi MP. Histopathological atlas of renal diseases: Acute post-streptococcal glomerulonephritis. J Nephrol. 2004;17:747-8. PubMed link / Free full text
• Sotsiou F. Postinfectious glomerulonephritis. Nephrol Dial Transplant. 2001;16 Suppl 6:68-70. PubMed link / Free full text link
• Rodriguez-Iturbe B. Postinfectious glomerulonephritis. Am J Kidney Dis. 2000 Jan;35(1):XLVI-XLVIII. PubMed link

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