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:
- Post-streptococcal (most frequent)
- Autoimmune (especially SLE)
- 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.
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.
- Kidney swelling
- 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 and normal reabsorption causes large amounts of fluid to be retained, causing hypervolaemia and resulting hypertension and possibly oedema. Also, the macula densa sense a low amount of sodium in the urine (because very little urine is being filtered), causing them to activate RAAS, furthering the hypertension.
If the damage to the glomeruli is severe enough, especially the scarring can chronic renal failure develop. Many of the causes of acute GN are chronic, so if acute GN occurs repeatedly is the chance for CRF high.
74. Acute tubular nephropathy
76. Compensation of pH-abnormalities (plasma and intracellular puffers, respiration, kidney) and their disturbances