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Acute Nephritis and Nephrosis
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- Nephritis essentially means inflammation of the kidney. Nephritis may involve the glomerulus, tubule, or the interstitial renal tissue.
- When inflammation involves the glomeruli it is called glomerulonephritis.
- When kidney disease involves structures in the kidney outside the glomerulus, it is broadly referred to as tubulointerstitial disease. This disease generally involves the tubules and/or the interstitium of the kidney and spares the glomeruli.
- When inflammation affects the area of the kidney between the nephrons (the renal interstitium) it is known as interstitial nephritis, or sometimes tubulo-interstitial nephritis.1
- Nephrosis is a descriptive histopathological term for renal disease without an inflammatory component.
Renal disease can present in a number of different ways, including as:
- Nephritic syndrome (nephritis)
- Nephrotic syndrome (nephrosis)
- Acute renal failure
- Chronic renal failure
- Hypertension
- Renal pain and dysuria
Interstitial nephritis can be acute or chronic. Acute interstitial nephritis is commonly due to a drug hypersensitivity reaction and presents as sudden onset acute renal failure.1 Acute interstitial nephritis is discussed in detail in the separate article Interstitial Nephritides and Nephrotoxins.
So, nephritis and nephrosis are responses to renal disease or injury. There are a number of underlying disease processes that can lead to both nephritic and nephrotic syndromes. This article gives an overview of acute nephritis and nephrosis. There are also separate articles on:
Acute nephritic syndrome is the most serious and potentially devastating form of the various renal syndromes.2
Clinical features
The key clinical features of acute nephritic syndrome are:
- Haematuria
- Reduced urine output
- Fluid retention and oedema (including periorbital, pedal and pulmonary oedema)
- Proteinuria
- Hypertension
- Uraemic symptoms (including anorexia, pruritus, lethargy, nausea)
- Deteriorating renal function
Causes2
- Post-infection with nephritogenic strains of group A beta-haemolytic streptococcus (typically occurs in children)
- Any of the other causes of glomerulonephritis
- Other bacterial infections - e.g. typhoid, secondary syphilis, MRSA infection, pneumococcal pneumonia, infective endocarditis
- Viral infections - e.g. hepatitis B, mumps, measles, infectious mononucleosis, varicella, coxsackievirus
- Parasitic infections - e.g. malaria, toxoplasmosis
- Multisystem systemic diseases - e.g. systemic lupus erythematosus, vasculitis, Henoch-Schönlein purpura, Goodpasture syndrome, Wegener granulomatosis
- Primary glomerular diseases - e.g. Berger disease (IgA nephropathy), membranoproliferative glomerulonephritis
- Guillain-Barré syndrome
- Diphtheria-pertussis-tetanus vaccine
Management
In primary care:
- Take a history - ask about onset of symptoms, uraemic symptoms, look for a clue to underlying cause e.g. recent streptococcal infection, other infection, multisystem disease.
- Measure blood pressure.
- Assess for peripheral, periorbital and pulmonary oedema.
- Perform urine dipstick for protein and blood.
- If acute nephritic syndrome is suspected, patients should be referred to secondary care. Acute admission may be required.
In secondary care:
- Investigations are focused on assessing severity of renal injury and looking for the underlying cause. They are discussed in detail in the article entitled Glomerulonephritis.
- Management depends on the underlying cause and is also discussed in the same article.
Prognosis
- This depends on the underlying cause.
- Nephritic syndrome caused by acute post-streptococcal glomerulonephritis in children is generally excellent.2
Clinical features
The key clinical features of nephrotic syndrome are:
- Proteinuria (formerly defined as >3.5 g/day but there appears to be individual variation around this cut-off figure)
- Hypoalbuminaemia as a result of urinary protein loss (albumin levels usually in range <25–30 g/l)
- Peripheral oedema due to hypoalbuminaemia
- Hypercholesterolaemia/dyslipidaemia
Causes
- Primary renal diseases
- Minimal-change nephrotic syndrome (~85% of childhood cases)
- Focal segmental glomerulosclerosis (~9% of childhood cases)
- Mesangial proliferative glomerulonephritis (~2% of childhood cases)
- Membranous nephropathy (~3% of childhood cases)
- Membranoproliferative glomerulonephritis
- Secondary renal diseases
- Postinfectious causes, e.g. Group-A beta-haemolytic streptococci, TB, malaria, syphilis, viruses such as VZV, HBV, HIV, infectious mononucleosis
- Collagen vascular diseases, e.g. SLE, rheumatoid arthritis, polyarteritis nodosa, Henoch-Schönlein purpura, vasculitides
- Metabolic diseases, e.g. diabetes mellitus, amyloidosis
- Inherited disease, e.g. Alport's syndrome, hereditary nephritis, sickle cell disease
- Malignant disease, e.g. multiple myeloma, leukaemia, lymphoma, carcinoma of breast/lung/colon/stomach
- Medications, e.g. NSAIDs, captopril, lithium, gold, diamorphine, interferon-alpha, penicillamine, probenecid and many others
- Toxins, e.g. bee sting, snake bites, phytotoxins
- Pregnancy, e.g. pre-eclampsia
- Transplant rejection
Management
In primary care:
- Take a history - onset of symptoms may be gradual over a few weeks, look for a clue to underlying cause, some patients describe their urine as frothy, there may be associated lethargy and anorexia.
- Measure blood pressure (although hypertension is not usually found).
- Assess for peripheral, periorbital and pulmonary oedema and ascites.
- Look for deep vein thrombosis can occur due to a hypercoagulable state.3
- Perform urinalysis which will show gross proteinuria.
- If nephrotic syndrome is suspected, patients should be referred to secondary care. However, most do not require acute admission.
- The separate article on Nephrotic Syndrome (click here) discusses investigations and management in more detail.
Document references
- Alper Jr AB, Meleg-Smith S; Nephritis, Interstitial. eMedicine. Last Updated Jun 10, 2008.
- Parmar MS; Acute Glomerulonephritis. eMedicine. Last Updated Jul 2, 2008.
- Agraharkar M, Gala G; Nephrotic Syndrome. eMedicine, February 2007.
DocID: 1763
Document Version: 20
DocRef: bgp548
Last Updated: 19 Aug 2008
Review Date: 19 Aug 2010
The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.
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