Nephritic syndrome

Last updated: July 26, 2023

Summarytoggle arrow icon

Nephritic syndrome is characterized by glomerular capillary damage leading to hematuria, pyuria, water retention, and subsequent hypertension and edema. It can be caused by a variety of conditions including autoimmune, hereditary, and infectious diseases. Nephritic diseases can manifest with varying degrees of severity, ranging from asymptomatic hematuria to systemic involvement, as in rapidly progressive glomerulonephritis. The urine sediment is typically characterized by red blood cell casts, mild to moderate proteinuria (< 3.5 g/day), and sterile pyuria. Diagnosis of the underlying disease is often based on presentation and laboratory values, although renal biopsy may be indicated for confirmation.

Definitiontoggle arrow icon

Nephritic syndrome is an inflammatory process that is defined as the presence of one or more of the following: [1]

NephrItic syndrome indicates glomerular Inflammation.

Overviewtoggle arrow icon

Diseases associated with nephritic syndrome
Epidemiology Clinical features Diagnostics
Poststreptococcal glomerulonephritis
  • Usually affects children 3–12 years of age and elderly patients [2]

IgA nephropathy (Berger disease)

Small vessel vasculitis

Granulomatosis with polyangiitis

  • Slightly more common in men
  • Peak incidence: 65–74 years [6]

Microscopic polyangiitis

  • Slightly more common in men
  • Peak incidence: 50–60 years [7]

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

Goodpasture syndrome (anti–GBM antibody disease)

  • Two peaks of occurrence [9]

Thin basement membrane nephropathy (benign familial hematuria)

  • Estimated to affect 5–10% of the general population [10]

Alport syndrome

Diffuse proliferative glomerulonephritis (DPGN)

Rapidly progressive glomerulonephritis (RPGN)

  • Renal function declines rapidly over days to weeks
  • Not a disease entity itself but a possible manifestation of glomerulonephritis
  • Poor prognosis: can progress to ESRD within weeks to months

Membranoproliferative glomerulonephritis (MPGN)

  • Primary disease occurs mainly in children
LM = light microscopy, IM = immunofluorescent microscopy, EM = electron microscopy

Low serum C3 levels are seen in poststreptococcal glomerulonephritis, lupus nephritis, and membranoproliferative glomerulonephritis.

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Diagnosticstoggle arrow icon

Glomerular hematuria is a typical finding in nephritic syndrome. It is characterized by acanthocytes, RBC casts, and mild to moderate proteinuria. Nonglomerular hematuria is characterized by bright red or pink urine, the occurrence of blood clots, normal RBC morphology, and the absence of RBC casts.

Differential diagnosestoggle arrow icon

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

Referencestoggle arrow icon

  1. Yuste C, Gutierrez E, Sevillano AM, et al. Pathogenesis of glomerular haematuria. World J Nephrol. 2015; 4 (2): p.185.doi: 10.5527/wjn.v4.i2.185 . | Open in Read by QxMD
  2. Goljan EF. Rapid Review Pathology. Mosby ; 2011
  3. Rose M. Ayoob and Andrew L. Schwaderer. Acute Kidney Injury and Atypical Features during Pediatric Poststreptococcal Glomerulonephritis. International Journal of Nephrology and Renovascular Disease. 2016.
  4. Prashanth Rawla; Faten Limaiem.. IgA Nephropathy. StatPearls. 2020.
  5. Ipek Kaplan Bulut, Sevgi Mir, Nida Dincel. Outcome results in children with IgA nephropathy: a single center experience. International Journal of Nephrology and Renovascular Disease. 2012.
  6. J. Barratt J. Feehally. Treatment of IgA nephropathy. Kidney International. 2006.
  7. R A Watts, S E Lane, G Bentham, D G Scott. Epidemiology of systemic vasculitis: a ten-year study in the United Kingdom. Arthritis & Rheumatology. 2000.
  8. Sharon A. Chung, MD, MAS and Philip Seo, MD, MHS. Microscopic Polyangiitis. Rheumatic diseases clinics of North America. 2010.
  9. Rebanta K. Chakraborty; Narothama R. Aeddula.. Churg Strauss Syndrome (Allergic Granulomatosis). StatPearls. 2020.
  10. Bethel Shiferaw, Viktor Miro, Zae Kim. Goodpasture’s Disease: An Uncommon Disease With an Atypical Clinical Course. Journal of Clinical Medicine Research. 2015.
  11. Rizwan A. Qazi and Bahar Bastani. Co-existence of thin basement membrane nephropathy with other glomerular pathologies; a single center experience. Journal of Nephropathology. 2015.
  12. Judy Savige, Deb Colville, Frances Flinter. Alport Syndrome in Women and Girls. Clinical Journal of the American Society of Nephrology. 2016.
  13. Ruchi H. Naik; Saed H. Shawar.. Rapidly Progressive Glomerulonephritis. StatPearls. 2020.
  14. Bassam Alchi and David Jayne. Membranoproliferative glomerulonephritis. Pediatric Nephrology. 2010.
  15. Goldman L, Schafer AI. Goldman-Cecil Medicine, 25th Edition. Elsevier ; 2016

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