Nephritic Syndrome Flashcards
What is nephritic syndrome?
Nephritic syndrome or acute nephritic syndrome refers to a group of symptoms, not a diagnosis. When we say a patient has “nephritic syndrome” it simply means they fit a clinical picture of having inflammation of their kidney and it does not represent a specific diagnosis or give the underlying cause.
Unlike nephrotic syndrome, there are no set criteria.
What are the clinical features of nephritic syndrome?
- Haematuria (microscopic or macroscopic)
- Oliguria
- Proteinuria
- Fluid retention
With regards to proteinuria, what is classed as nephritic syndrome?
In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Briefly describe IgA nephropathy (Berger’s syndrome)
Note: overview, presentation, diagnosis and treatment
Commonest primary GN in high income countries:
Presentation: asymptomatic non-visible haematuria or episodic visible haematuria. Proteinuria usually <1g. Peak age in 20s.
Diagnosis: IgA deposition in mesangium.
Treatment: ACEI/ ARB to reduced proteinuria and protect renal function. In addition to this, corticosteroids.
Briefly describe Henoch-Schonlein purpura (HSP)
Note: overview, presentation, diagnosis and treatment
Small vessel vasculitis and systemic variant of IgA nephropathy with IgA deposition in skin/ joints and gut (in addition to the kidneys).
Presentation: purpuric rash on extensor surfaces, flitting polyarthritis, abdominal pain and nephritis.
Diagnosis: usually clinical, confirmed with positive IF for IgA and C3 in skin. Renal biopsy is identical to IgA nephropathy.
Treatment: ACEi/ ARB reduce proteinuria and protect renal function. In addition to this, corticosteroids.
Briefly describe post-streptococcal GN
Note: overview, presentation, diagnosis and treatment
Occurs after a throat (~2 weeks) or skin (~3-6 weeks) infection. Streptococcal antigen deposits in the glomerulus leading to immune complex formation and inflammation.
Presentation: varies from haematuria to acute nephritis: haematuria, oedema, hypertension and oliguria.
Diagnosis: evidence of streptococcal infection.
Treatment: supportive, antibiotics to clear nephritogenic bacteria. Most make a full recovery.
Briefly describe anti-GBM disease
Note: overview, presentation, diagnosis and treatment
Previously known as Goodpasture’s disease. Rare. Auto-antibodies attack the glomerulus and pulmonary basement membrane.
Presentation: renal disease (oliguria/ anuria, haematuria, AKI and renal failure) and lung disease (pulmonary haemorrhage).
Diagnosis: anti-GBM in circulation/ kidney.
Treatment: plasma exchange, corticosteroids and cyclophosphamide.
Briefly describe rapidly progressive GN
Note: overview, diagnosis and treatment
Any aggressive GN, rapidly progressing to renal failure over days or weeks. Causes include small vessel/ ANCA vasculitis, lupus nephritis and anti-GBM disease.
Diagnosis: breaks in the GBM allow an influx of inflammatory cells so that cresents are seen on renal biopsies (may be referred to as crescenteric GN).
Treatment: corticosteorids and cyclophosphamide. Other treatments depend on specific aetiology e.g. plasma exchange for anti-GBM/ ANCA vasculitis and possible role for monoclonal antibodies for lupus nephritis.
If a patient presented with AKI and haemoptysis, what disease may this be?
f you come across a patient in your exam with the combination of acute renal failure and haemoptysis, think of two conditions: Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis).
Goodpasture syndrome is associated with anti-GBM antibodies, whereas Wegener’s granulomatosis is a type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA). Patients with Wegener’s granulomatosis may also have a wheeze, sinusitis and a saddle-shaped nose.
