Glomerulonephritis – symptoms and causes
Glomerulonephritis is bilateral diffuse nonpurulent inflammatory disease of the glomeruli (kidney’s bodies).
Causes of glomerulonephritis
The main reason for the development of glomerulonephritis is purulent angina. The disease develops in a mechanism similar to that of rheumatism.
Glomerulonephritis is kidney disease with immune genesis. In these diseases glomeruli are primarily affected and they are the principal manifestation of the disease. Primary glomerulonephritis usually is with diffuse involvement of glomeruli – over 80% of kidney bodies are affected. In secondary glomerulonephritis kidney bodies are damaged in the course of other diseases (systemic lupus erythematosus, diabetes mellitus, amyloidosis, polyarteritis nodosa, bacterial endocarditis, etc.). The dropping of the function of the damaged glomeruli because of the development of diffuse nephrosclerosis leads to chronic renal failure.
In 85% of cases there is immune glomerulonephritis genesis – caused by circulating immune complexes in blood. The same can be proven by fluorescence, iimmunohistochemical or electronmicroscopical study. In the remaining 15% of cases the participation of cytotoxic antibodies and cell-mediated immune responses is considered – by sensitized T cells, damaging the endothelium and basal membrane of glomeruli. There is also a genetic predisposition to develop certain types of glomerulonephritis – presence in the serum of so-called C3-nefritogen factor, abnormal secretion of IgA and others.
Mechanisms of immune damage of the glomeruli
In this case immune complexes don’t have high affinity to the kidney glomeruli but they turn out to be the “victims” of the immune conflict, as this happens in serum illness. About 70% of glomerulonephritis arise through the capture of circulating immune complexes formed somewhere else (immunocomplex mechanism).The localization of immune complexes is under the endothelium, inside the basal membrane, in the subepithelium and mesangium According to the localization of the changes, glomerulonephritis can be endocapillary glomerulonephritis (in endothelium and mesangium) mesangial (in mesangium) and extracapillary (in the urinary spaces).
Only in 10% of the cases the antigen itself is the basal membrane and immune complexes form in situ along her whole length. This is visualized by linear immunofluorescence.
Immune damage of glomeruli is done through:
Activation of complement – a traditional way and the formation of membrane attack complex (MAC – C5b-C9). Besides the classical cascade, complement can be activated by the alternative way in case C3 nephritogen factor (S3NeFN) presents in the body.
Organizing of neutrophil or monocyte attack. It can be complement-mediated (C3a and C5a) or complement-independent, for example big molecule complexes in blood circulation (mesangiocapillar glomerulonephritis, lupus nephritis, etc.)..
Fibrin deposition, thrombosis, necrosis and rupture of capillary walls (in extracapillary semilunar glomerulonephritis).
Stimulation of cell proliferation – mesangial cells, fibroblasts from periglomerular interstitium penetrate through the perforations of the Bowman capsule. Endothelial cells don’t proliferate, but podocytes can react with change of their configuration and with degenerative changes.
Damage to the glomerular basal membrane of complement may have progressive course when C5b-C9 fragment is embedded in it. New antigens are formed, called MAK neoantigens against which antibodies are formed further. Secondary chain immune response occurs with formation of new immune complexes “in place” in the glomeruli.
Main symptoms of glomerulonephritis
• Proteinuria – loss of more than 150 mg protein per day in urine. Due to increased permeability of the glomerular basal membrane.
• Hematuria – blood in the urine as a sign of impaired integrity of glomerular capillaries.
• Oliguria or anuria – the formation of urine is reduced or absent.
• Azotemia – reduced filtration of products of nitrogen metabolism, which leads to intoxication of the organism.
• Swelling – mainly on the face (eyelids) – due to poor glomerul-tubular balance, fluid retention, reduced intravascular oncotic pressure or increased capillary permeability.
• Hypertension (high blood pressure) – appears due to fluid retention and impairment of renopressor function(secretion of renin in the juxtaglomerular apparatus) and/or hypotensive function of the kidney (renomedular prostaglandins).
Symptoms of glomerulonephritis are combined into two main syndromes:
1. Nephritic syndrome
2. Nephrotic syndrome
• 3,5 g proteinuria per 24 hours
• hyperlipidemia and lipiduria
Glomerulonephritis symptoms appear only when at 75% of nephrons (kidney bodies) are severely affected by the pathological process.