- Clinical science
Renal glomeruli excrete urinary substances and excess water as an ultrafiltrate into the urine by selectively filtering the blood. Any damage to the glomeruli disrupts the filtration process and results in the appearance of blood components (proteins and red blood cells) in the urine. Glomerular damage is commonly caused by immune-mediated processes, which often lead to glomerulonephritis. Non-inflammatory causes, such as metabolic disease (e.g., diabetes, amyloidosis), can also result in significant damage to the glomeruli. The pathophysiology of glomerular diseases is complex; most patients present with either nephritic syndrome (low-level proteinuria, microhematuria, oliguria, and hypertension) or nephrotic syndrome (high-level proteinuria and generalized edema). All glomerular diseases can progress to acute or chronic renal failure. Thus, quick diagnosis and immediate initiation of immunosuppressive therapy are required to prevent irreversible kidney damage.
Terminology of glomerular diseases
- Diffuse: all glomeruli are affected
- Focal: only a number of glomeruli are affected
- Global: the entire glomerulus is affected
- Segmental: only part of the glomerulus is affected
- Proliferative: an increased number of cells in the glomerulus
- Sclerosing: scarring of the glomerulus
- Necrotizing: cell death within the glomerulis
- Crescentic: accumulation of cells such as macrophages, fibroblasts, and epithelial cells in Bowman's space
- The glomerular filtration barrier consists of 3 parts
- Initial segment: Fenestrated glomerular capillary endothelium prevents large proteins from passing through.
- Second segment: The glomerular basement membrane (GBM) contains a negative charge produced by heparan sulfate.
- Final segment: Visceral epithelial cells produce/maintain the GBM and contain intercellular junctions created by podocytes that prevent further protein loss.
Damage to the glomeruli → disruption of the glomerular filtration barrier → can lead to nephritic or nephrotic syndrome