Acute glomerulonephritis

Acute glomerulonephritis (AGN), i.e. acute post-infectious glomerulonephritis, short for acute nephritis, clinically presents as acute onset with hematuria, proteinuria, edema, hypertension and reduced GFR; the vast majority is acute post-streptococcal glomerulonephritis. It is the commonest kidney disease in children, aged 3-14, rare under 2, male:female about 2:1. AGN usually follows infection; the commonest pathogen is beta-hemolytic streptococcus, occasionally staphylococcus, pneumococcus, typhoid bacillus, diphtheria bacillus and protozoa such as plasmodium, schistosome and viruses. Clinically acute post-streptococcal GN is commonest; AGN appears 1-3 weeks after group A beta-hemolytic streptococcal pharyngeal or skin infection, rarely secondary to other infection (staphylococcus, pneumococcus, group C streptococcus, viruses or parasites).

Common Symptoms

Hematuria; Yi Yupin; urine protein; nephrotic syndrome; dizziness; anuria; nausea; oliguria; anorexia; proteinuria

Causes

(1) Etiology. AGN usually follows infection; the commonest pathogen is beta-hemolytic streptococcus, occasionally staphylococcus, pneumococcus, typhoid and diphtheria bacilli and protozoa such as plasmodium and schistosome; acute post-streptococcal GN is commonest, appearing 1-3 weeks after group A beta-hemolytic pharyngeal or skin infection. (2) Mechanism. The exact mechanism is unclear; it is an immune-complex disease marked by anti-streptococcal antibody formation and complement immune-complex deposition on the kidney. AGN occurs only after group A beta-hemolytic nephritogenic strains; typical strains' antibodies target wall antigens M types 1, 2, 4, 12, 18, 25, 49, 55, 57, 60. Evidence for immune-complex disease: ① the incubation period after precursor streptococcal infection equals the time for immune response; ② early positive circulating immune complexes and low serum complement; ③ granular IgG and C3 deposition in mesangium and capillary loops. Studies show proliferative GN has marked glomerular and interstitial inflammatory infiltration, while non-proliferative GN has few; monocytes and T cells correlate with proteinuria. Immune deposits activate complement; C3a, C5a and anaphylatoxins cause histamine release and capillary permeability increase; the terminal C5b-C9 membrane attack complex acts on the basement membrane; C3a-C5a stimulate platelets to secrete serotonin (5-HT) and thromboxane B, macrophages to secrete phospholipids and arachidonic acid, and mesangial cells to secrete prostaglandins, proteases, phospholipases and oxygen radicals, all inflammatory mediators. Evidence supports that one or more streptococcal antigens with glomerular affinity implant early, and after 10-14 days host antibodies bind them; candidate antigens include nephritis strain-associated protein and nephritis-associated plasmin receptor.

Treatment

Medication, TCM treatment, supportive treatment

Prevention

Actively preventing streptococcal infection markedly reduces incidence; isolate respiratory patients to prevent scarlet fever and purulent tonsillitis; keep skin clean to prevent impetigo. Once infection occurs, use effective antibiotics promptly; adequate penicillin stops nephritogenic strains and reduces nephritis incidence.

Recommended Department

It is recommended to visit the nephrology department; before the visit you may first book an appointment and connect with experts through this platform.

Warm reminder: The above information is provided for health education reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek care at a regular hospital in time.