Nephritic Syndrome

This condition lies on a spectrum of glomerular disorder (glomerulonephritis).

– It reflects inflammatory damage to the glomerulus, due to the release of cytokines.

– It increases the permeability to proteins and blood giving proteinuria + haematuria.


Protein and blood loss give characteristic signs of nephritic syndrome:

– Haematuria (with small amounts of proteinuria <3.5g/24h)

– Excessive salt retention –> Hypertension and blurred vision

– Oliguria – low urine output

– Azotemia – increased serum urea and creatinine

– Can progress onto renal failure


There are many specific conditions which give rise to nephritic syndrome, which have specific treatments:

IgA nephropathy

This is the most common cause of nephritic syndrome, called Berger’s disease

– Due to IgA immune complexes being deposited in the glomerulus, due to unknown etiology

– Whilst usually seen in young males, it is also associated with alcohol and GI diseases (coeliac disease)


In young people as recurrent macroscopic haematuria, usually 1-2 days after an URTI

– However, the condition carries a good prognosis and is unlikely to lead to CKD


Renal biopsy taken –> shows IgA deposition in glomerulus


 Corticosteroids + Fish Oil

Henoch-Schonlein purpura (HSP)

This is similar to IgA nephropathy, but in addition it also causes IgA deposition in skin/joints too


IgA Nephropathy + Arthritis + Rash on extensor surfaces


Steroids + Analgesia for joint pain (it is usually self-limiting)

Post-Streptococcal Glomerulonephritis

This arises 1-2 weeks after infection with group A B-hemolytic Streptococcus bacterial infection

– Antibodies produced against the bacteria lead to immune complex formation which then end up getting deposited in the glomerulus causing inflammation

– Usually resolves in children, but some adults can get rapidly progressing glomerulonephritis.


Haematuria + other signs of full nephritic syndrome (hypertension + proteinuria/oedema)


– Evidence of streptococcal infection e.g. anti-streptolysin antibodies or DNase antibodies

– Renal biopsy –> Endothelial proliferation of neutrophils giving granular “starry sky” appearance


Antibiotics to clear bacteria + supportive treatment for renal dysfunction

Rapidly progressive glomerulonephritis

This is an aggressive Glomerulonephritis, which is characterized by a sudden decrease in renal clearance, which can present with renal failure

– Due to many conditions e.g. Wegener’s Granulomatosis + Goodpasture’s disease + Lupus nephritis


– Renal biopsy –> shows breaks in basement membrane allow influx of inflammatory cells

This leads to the formation of crescents (crescenteric GN) and red cell casts in urine

Goodpasture’s disease (anti-GBM disease)

A disease due to autoantibodies against type IV collagen

– This causes damage to the exchange surfaces which rely on the basement membrane (lungs + kidney)


Rapidly progressive nephritic syndrome + bleeding in lungs (SOB, hemoptysis)


Anti-GBM autoantibodies in blood test + linear IgG deposits in membrane on renal biopsy


Plasmapheresis to remove antibodies form blood + Immunosuppression (steroids)

Alport syndrome

This is a genetic X-linked dominant condition the protein chain of type IV collagen

– This causes the glomerular basement membrane to be excessively thin, meaning it can easily tear.


– Presents in childhood with microscopic haematuria, progressing to renal failure

Ears –> Bilateral Sensorineural hearing loss

– Eyes –> Retinitis Pigmentosa and blindness


Renal biopsy –> Splitting of lamina densa


Can develop anti-GBM antibodies which causes rejection of kidney transplants


Image 1: Mnokel at Arabic Wikipedia / Public domain