- What is Glomerulonephritis (GN)
- Statistics on Glomerulonephritis (GN)
- Risk Factors for Glomerulonephritis (GN)
- Progression of Glomerulonephritis (GN)
- Symptoms of Glomerulonephritis (GN)
- Clinical Examination of Glomerulonephritis (GN)
- How is Glomerulonephritis (GN) Diagnosed?
- Prognosis of Glomerulonephritis (GN)
- How is Glomerulonephritis (GN) Treated?
- Glomerulonephritis (GN) References
What is Glomerulonephritis (GN)
Glomerulonephritis is a general term for a group of disorders in which there is bilateral, symmetrical immunologically mediated injury to the glomerulus.
A renal glomerulus consists of a capillary plexus invaginating the blind end of the proximal renal tubule. There are about one million glomeruli in each kidney. The glomerular capillaries are lined by a glomerular basement membrane.
Statistics on Glomerulonephritis (GN)
- Minimal change glomerulopathy – early childhood (mostly 1-6yo).
- Acute post-streptococcal glomerulonephritis – sporadically or endemic. Sporadic is more common and affects children more than adults with the peak incidence from age 2-6.
- Anit-glomerular basement membrane glomerulonephritis – 20% of rapidly progressive glomerulonephritis and probably less than 1% of all diagnostic biopsies.
- IgA nephropathy – very common in many countries (20-25% of all glomerulonephritis in Southern Europe and Australia and 30-40% in Japan and Singapore).
- Membranoproliferative glomerulonephritis – uncommon.
The frequencies of the associated disorders vary widely. Diabetic nephropathy is a common cause of nephrotic syndrome in the adult, lupus nephritis is moderately common in young women but the majority of the disorders are quite rare.
Risk Factors for Glomerulonephritis (GN)
The aetiology of the vast majority of these conditions is unknown. Two chief pathogenic mechanisms are recognised:
- Deposition or in situ formation of immune complexes (antigen-antibody complexes).
- The antigen may be exogenous (beta-haemolytic streptococci) or endogenous (seen in systemic lupus erythematosus).
- Deposition of antiglomerular basement membrane antibody. Anti-GBM reacts with an antigen in the GBM producing glomerular damage.
In some cases there is no evidence of immune complex deposition, eg. Granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis) and microscopic polyangiitis. Injury is mediated by a vasculitis.
Systemic diseases causing secondary glomerulonephritis:
- Immunologic diseases: Systemic lupus erythematosus, polyarteritis, Granulomatosis with polyangiitis, mixed connective tissue disease, Henoch-Schonlein purpura.
- Genetic-metabolic diseases: Diabetes mellitus, amyloidosis, sickle cell disease.
- Haematologic-oncologic diseases: Multiple myeloma, macroglobulinaemia, light chain disease, cryoglobulinaemia, thrombotic thrombocytopaenia purpura, haemolytic-uraemic syndrome, lymphoma, leukaemias and carcinomas.
- Infectious diseases: Post-streptococcal, endocarditis, occult abscesses, hepatitis B and C, malaria, schistosomiasis.
- Others: Drug-induced.
Progression of Glomerulonephritis (GN)
The natural history of these glomerulonephritides is quite variable. Rapidly progressive glomerulonephritis of whatever cause is associated with a rapidly progressive course to terminal renal failure while the chronic glomerulopathies associated with nephrotic syndrome (Membranous glomerulopathy) and microscopic haematuria (IgA nephropathy) have a more indolent course. Many of these patients remain stable for long periods and even may show complete remission.
Prognosis usually favourable, especially in children, with less than 1% of patients dying from the acute disease. When progressive renal failure occurs, focal glomerulosclerosis and the less frequent IgM nephropathy are the usual lesions responsible. Patients with mild proteinuria do better than those who are nephrotic.
The prognosis of most of these secondary forms has improved over the past decades. This is because of better knowledge, care, earlier detection and better follow-up and increased patient education. The risk of developing end-stage renal failure at 5 years after the appearance of flomerular disease is approximately 20% for proliferative lupus nephritis. It is nearer 50% for the vasculitic forms and higher in systemic sclerosis.
Symptoms of Glomerulonephritis (GN)
- Altered urine volumes,
- Foamy urine, and
- Oedema (generalised swelling).
How is Glomerulonephritis (GN) Diagnosed?
- Urinalysis – first morning, freshly voided.
- Urea and electrolytes – renal function.
- Albumin – may be low.
- Lipids – may be hyperlipidaemia.
- Coagulation profile – may be hypercoagulability.
Prognosis of Glomerulonephritis (GN)
Specific features used to refine prognositic estimates include: clnical evidence of rapidly progressive or crescentic glomerulonephritis, severe hypertension, complicated nephrotic syndrome and a background of chronic atrophic and sclerosing renal pathology.
How is Glomerulonephritis (GN) Treated?
- Corticosteroids (prednisolone) – minimal change nephropathy is the only case that has a predictable response (>90% urine protein excretion reduced to normal).
- Treatment for acute post-streptococcal glomerulonephritis is symptomatic – give antibiotics (penicillin) to family members or contacts. Immunosuppressive therapy has no role.
- Rapidly progressive glomerulonephritis – consider IV pulse prednisolone.
- Anti-glomerular basement membrane disease – benefit with plasma exchange plus immunosuppressive agents.
- IgA nephropathy – consider fish oil
- Angiotensin converting enzyme (ACE) inhibitors- may be of benefit in preserving glomerular function.
Glomerulonephritis (GN) References
- Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001
- Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
- Haslet C, Chiliers ER, Boon NA, Colledge NR. Principles and Practice of Medicine. Churchill Livingstone 2002.
- Hurst JW (Editor-in-chief). Medicine for the practicing physician. 4th edition Appleton and Lange 1996.
- Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002 Pg 427-430.
- Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford Universtiy Press. 2001
- McLatchie G and LEaper DJ (editors). Oxford Handbook of Clinical Surgery 2nd Edition. Oxford University Press 2002.
- Raftery AT Churchill’s pocketbook of Surgery. Churchill Livingsone 2001.