Acute nephritic syndrome and glomerulonephritis

A six-year-old boy presents with smoky, cola-coloured urine and puffy eyes. Two weeks earlier he had a sore throat. This is the classic face of acute glomerulonephritis, and it is the pattern every paediatric trainee is expected to reason through at viva. The syndrome itself is simply the visible result of glomerular capillary inflammation: the inflamed filter leaks red cells and protein, holds back salt and water, and, when severe enough, fails. ^[2]

This page owns the acute nephritic syndrome as a presentation and glomerulonephritis as the underlying inflammation. It treats post-streptococcal GN in enough depth to contrast it with every other nephritic cause, and points to the dedicated post-infectious-glomerulonephritis and IgA-nephropathy-and-IgA-vasculitis-nephritis leaves for their full standalone detail. ^[1]

Overview & Definition

The acute nephritic syndrome is defined by its clinical tetrad: haematuria (gross or microscopic), proteinuria (usually below the nephrotic range), oedema and hypertension, with or without a fall in glomerular filtration rate. It is a syndrome, not a disease — several different glomerular disorders produce it. ^{[1] [2]}

Glomerulonephritis (GN) is the histological word behind the syndrome: inflammation of the glomerulus, most often from immune-complex deposition. The KDIGO 2021 Glomerular Diseases guideline frames GN by both its clinical presentation (nephritic, nephrotic, rapidly progressive, or chronic with asymptomatic haematuria) and its immunopathological pattern (immune-complex, pauci-immune, or anti-GBM). The same histology can show up in more than one clinical box, which is why the two frames are not interchangeable. ^[1]

The key distinction at the bedside is between a self-limiting post-infectious cause (which needs supportive care alone) and a continuing inflammatory disease (which needs biopsy and specific treatment). The serum complement, the tempo of renal failure, and the presence of systemic features are the three levers that move a child from one column to the other. ^{[2] [11]}

References12ShowHide

1. [1]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int, 2021.PMID 34556256
2. [2]Sethi S; De Vriese AS; Fervenza FC Acute glomerulonephritis. Lancet, 2022.PMID 35461559
3. [3]Rodriguez-Iturbe B; Musser JM The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol, 2008.PMID 18667731
4. [4]Rodriguez-Iturbe B Autoimmunity in Acute Poststreptococcal GN: A Neglected Aspect of the Disease. J Am Soc Nephrol, 2021.PMID 33531351
5. [5]Nasr SH; Fidler ME; Valeri AM; et al Postinfectious glomerulonephritis in the elderly. J Am Soc Nephrol, 2011.PMID 21051737
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7. [7]Oda T; Yoshizawa N Factors Affecting the Progression of Infection-Related Glomerulonephritis to Chronic Kidney Disease. Int J Mol Sci, 2021.PMID 33477598
8. [8]Pinto SW; do Nascimento Lima H; de Abreu TT; et al Twenty-year Follow-up of Patients With Epidemic Glomerulonephritis due to Streptococcus zooepidemicus in Brazil. Kidney Int Rep, 2022.PMID 36090503
9. [9]Reamy BV; Servey JT; Williams PM Henoch-Schonlein Purpura (IgA Vasculitis): Rapid Evidence Review. Am Fam Physician, 2020.PMID 32803924
10. [10]Mary AL; Clave S; Rousset-Rouviere C; et al Outcome of children with IgA vasculitis with nephritis treated with steroids: a matched controlled study. Pediatr Nephrol, 2023.PMID 37154959
11. [11]Iyengar A; Kamath N; Radhakrishnan J; et al Infection-Related Glomerulonephritis in Children and Adults. Semin Nephrol, 2023.PMID 38242806
12. [12]Wang Y; He Y; Cheng F; et al Optimal drug treatment for children with IgA vasculitis nephritis: a systematic review and network meta-analysis. Transl Pediatr, 2025.PMID 41502882