Causes (Etiology)
The onset of the immunoinflammatory process in the kidneys is triggered by various factors. Although the exact cause is often difficult to establish, several groups of proven etiologic factors are distinguished:
- Infectious agents: bacteria (primarily streptococci) and viruses (hepatitis B and C, measles, rubella, cytomegalovirus, herpes simplex virus).
- Parasitic diseases: malaria, schistosomiasis.
- Chemical and toxic exposures: organic solvents, alcohol, and heavy metal poisoning (lead, mercury, cadmium).
- Drug-related factors: administration of vaccines and sera, use of gold preparations or penicillamine.
Note: the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics more frequently provokes tubulointerstitial nephritis, but in some situations can also initiate glomerulonephritis.
Pathogenesis and mechanisms of progression
The disease is based on immune disorders. The key mechanism is the formation of immune complexes (ICs) consisting of an antigen, an antibody, and complement. Most frequently, they circulate in the blood and then deposit in the renal filter. Less commonly, complexes form in situ (directly at the site), when antibodies attack the glomerular basement membrane's own structures. The deposition of ICs triggers inflammation, which determines the morphological type of nephritis (mesangial, membranous, fibroplastic, or minimal change disease).
The progression of glomerular sclerosis and nephron loss are driven by several factors:
- Role of the mesangium: activation and proliferation of mesangial cells lead to the excessive accumulation of extracellular matrix.
- Hemodynamic shifts: intraglomerular hypertension and hyperfiltration damage the filter, increasing protein loss.
- Toxicity of proteinuria: massive passage of plasma macromolecules exerts a direct toxic effect on the tubular epithelium. Activated tubular cells release pro-inflammatory factors, causing an interstitial reaction. It has been proven that the rate of CGN progression directly depends on the severity of these tubulointerstitial changes.
Clinical forms of CGN
Despite the introduction of morphological classification (based on biopsy), Russian clinical practice actively uses the E.M. Tareev classification, which distinguishes five forms depending on the leading syndrome:
- Latent: the most common form. There are no clinical symptoms; the pathology is detected only by urinary syndrome (microhematuria and mild proteinuria).
- Hematuric: erythrocyturia comes to the forefront (more than 20–30 red blood cells per high-power field in the urinary sediment), with periodic episodes of gross hematuria.
- Hypertensive: persistent blood pressure elevation dominates. Urinary syndrome is minimally expressed, but signs of target organ damage (funduscopic changes, left ventricular hypertrophy) are present.
- Nephrotic: characterized by massive protein loss (proteinuria > 3.5 g/day). Accompanied by marked edema (ranging from facial puffiness to anasarca with ascites, pleural effusion, and hydropericardium), oliguria, hypoalbuminemia, and hypercholesterolemia.
- Mixed: a combination of hypertensive and edematous-nephrotic syndromes. This is the prognostically most unfavorable and severe variant of the course.
Principles of treatment
Treatment of chronic glomerulonephritis requires a comprehensive approach. Etiotropic treatment (eliminating the root cause) is rarely performed because the trigger is often already inactive or unknown.
Main areas of therapy:
- Immunosuppression (pathogenetic therapy): use of glucocorticoids, cytostatics, and cyclosporine to suppress immune inflammation.
- Nephroprotection: strict maintenance of normal blood pressure (adequate antihypertensive therapy) to slow down glomerular sclerosis.
- Symptomatic care: prescription of diuretics for edema, and in resistant cases, plasma ultrafiltration.
- Dietary therapy: mandatory restriction of table salt (especially in hypertensive and nephrotic forms). With the onset of the first signs of renal failure, patients are restricted in their intake of animal proteins.
Memorizing the 5 clinical forms of CGN according to Tareev can be aided by focusing on the main symptom: "Urine" (latent — a little bit, hematuric — blood), "Pressure" (hypertensive), "Protein/Edema" (nephrotic), and "Everything at once" (mixed).
Class and exam questions
Why is proteinuria considered not only a symptom, but also a progression factor in CGN?
Filtered protein macromolecules exert a direct toxic effect on the epithelium of the renal tubules. This prompts tubular cells to produce pro-inflammatory factors, leading to interstitial inflammation and accelerating renal sclerosis.
What is the difference between glomerulonephritis and tubulointerstitial nephritis?
In glomerulonephritis, the morphological substrate is primary damage to the glomeruli. If damage to the tubules and interstitium initially predominates in the biopsy or clinical picture, tubulointerstitial nephritis is diagnosed.
Can chronic glomerulonephritis be completely cured?
As a rule, the disease has a chronic progressive course. The goal of treatment is to achieve stable remission, minimize protein loss, and maximally delay the onset of end-stage chronic kidney disease.
What else to study on this topic
- Pathomorphological classification of CGN (mesangial, membranous, fibroplastic types)
- Mechanisms of in situ immune complex formation
- Differential diagnosis of tubulointerstitial nephritis and CGN
- Criteria and complications of nephrotic syndrome
- Drugs for pathogenetic therapy of CGN (immunosuppression regimens)
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