75. Acute diffuse glomerulonephritis

Last updated on January 24, 2021 at 23:28

Acute (diffuse) glomerulonephritis (acute GN) is a term for many disorders that can cause acute inflammation of the glomeruli. It comprises 10% of the cases of parenchymal acute renal failure.

There can be many causes for acute glomerulonephritis. Most of them have immunological background. Common for all of them is that the glomeruli are damaged.

Common causes include:

  • Immunological
    • Post-streptococcal (most frequent)
    • Autoimmune (especially SLE)
  • Vasculitis
    • Wegener granulomatosis
    • Polyarteritis nodosa
    • Henoch-Schönlein purpura
    • Goodpasture syndrome
  • IgA nephropathy

The most common form is post-streptococcal acute GN. This occurs around three weeks after a streptococcus infection, due to immune complexes formed with the streptococcal antigens.

Pathomechanism

No matter the aetiology is the reason for damage and inflammation immune complex deposition in the glomeruli. When these immune complexes bind to the capillary wall will complement be activates, which recruits leukocytes and causes inflammation. Acute inflammatory cells produce lysosomes and free radicals that damage the wall and basement membrane of the capillaries, which decreases the filter surface.

Injured endothelium produces more vasoconstrictors and less vasodilators, so the capillary perfusion decreases. Coagulation increases.

Mesangial cells are activated and proliferate due to the inflammation. They contract and therefore increase the permeability of proteins.

The inflammation is healed by fibrosis, causing scarring and sclerosis of the glomeruli.

Clinical consequences
  • Kidney swelling
  • Oliguria
  • Proteinuria
  • Haematuria
  • Hypertension
  • Possibly chronic renal failure

The glomeruli will swell, causing the whole kidney to be swollen.

The tubules are untouched, so the smaller GFR will cause oliguria and the tubules will concentrate the urine. The increased capillary permeability allows protein and blood to enter the urine.

The decreased filtration but normal reabsorption causes large amounts of fluid to be retained, causing hypervolaemia and resulting hypertension and possibly oedema. Also, the macula densa senses the decreased GFR, causing it to activate RAAS, furthering the hypertension.

If the damage to the glomeruli is severe enough, (especially the scarring) can chronic renal failure may develop. Many of the causes of acute GN are chronic, so if acute GN occurs repeatedly the chance for CRF is high.


Previous page:
74. Acute tubular nephropathy

Next page:
76. Compensation of pH-abnormalities (plasma and intracellular puffers, respiration, kidney) and their disturbances

2 thoughts on “75. Acute diffuse glomerulonephritis”

  1. Hi,
    In the paragraph before the last one, you said “macula densa sense decreased amount of sodium, causing them to activate RAAS”
    But as far as I know RAAS will increase sodium and water retention ( which cause hypertension), then why would Macula activate RAAS to an already decreased amount of sodium filtrate?

    Regards

    1. The macula densa does not really “care” about sodium in the urine, it cares about the GFR. When the GFR is low, which the macula densa detects by monitoring the amount of sodium which reaches it, the macula densa will activate the RAAS, which normally increases the GFR.

Leave a Reply

Your email address will not be published.