Causes and mechanisms of development
The disease is caused by Group A beta-hemolytic Streptococcus (GABHS), specifically its "nephritogenic" strains. Less commonly, group C streptococcus is the cause. The pathology is based on immune-complex mechanisms.
There are three main theories regarding the development of the pathological process:
- Formation of in situ complexes (considered the most likely): streptococcal antigens, such as nephritis-associated plasmin receptor or pyrogenic exotoxin B, become fixed in the glomeruli. Autoantibodies then bind to them, activating the complement system.
- Deposition of circulating immune complexes (CICs): preformed complexes enter the glomeruli from the bloodstream.
- Molecular mimicry: antibodies attack kidney tissues due to their structural similarity to streptococcal antigens.
Morphological picture
Light microscopy reveals diffuse proliferative endocapillary glomerulonephritis. A prominent infiltration of capillaries by leukocytes (mainly neutrophils) is characteristic. Proliferation of endothelial cells, mesangial cells, and epithelial cells is observed.
Immunofluorescence shows granular deposits of immunoglobulin G (IgG) and the C3 complement fraction. On electron microscopy, dense subepithelial deposits—"humps"—are pathognomonic. The appearance of "crescents" in Bowman's capsule is considered an extremely unfavorable prognostic sign.
Clinical manifestations
The disease begins abruptly. The onset may feature nonspecific signs of intoxication: pallor, weakness, nausea, decreased appetite, and low-grade fever. Due to inflammatory edema, the kidneys enlarge, stretching the fibrous capsule, which causes lower back pain.
The classic acute nephritic syndrome includes:
- Edema: morning facial edema is typical; in infants, ascites or hydrothorax may occur (a consequence of sodium and water retention due to decreased glomerular filtration).
- Hematuria: an obligate symptom. Gross hematuria occurs in 50% of cases ("smoky" or cola-colored urine in an alkaline environment, or dark brown in an acidic one).
- Arterial hypertension (AH): occurs in 75% of patients due to hypervolemia and increased peripheral resistance.
- Oliguria: decreased urine output against the background of a drop in the glomerular filtration rate (GFR).
- Proteinuria: usually moderate, rarely in the nephrotic range.
Urinary sediment often reveals erythrocyte casts, confirming the glomerular origin of bleeding, while abacterial lymphocytic leukocyturia is possible at the onset of the disease.
Laboratory diagnostics and complications
The diagnosis is confirmed serologically: high titers of antibodies to streptococcus (ASO, anti-DNase B) and hypocomplementemia (decrease in the C3 fraction within 4–8 weeks). Blood tests show leukocytosis, elevated ESR, and a "false" decrease in hemoglobin and platelets due to hemodilution.
In severe cases, life-threatening conditions may develop:
- Hypertensive encephalopathy (eclampsia): cerebral vasospasm and edema, manifesting as seizures, vomiting, and loss of consciousness. It threatens intracranial hemorrhage.
- Acute kidney injury (AKI): a drop in GFR down to anuria, azotemia, and hyperhydration.
The triad of acute nephritic syndrome: AHE — Edema, Hematuria, Arterial hypertension.
Class and exam questions
What is an obligate clinical and laboratory sign of acute poststreptococcal glomerulonephritis?
Hematuria (ranging from micro- to macrohematuria) is a basic and obligate symptom.
Why does lower back pain occur in glomerulonephritis?
Pain occurs due to inflammatory edema of the renal parenchyma, which leads to stretching of the fibrous capsule, which is rich in pain receptors.
What are "humps" in the morphological picture?
This is a pathognomonic electron-microscopic sign: dome-shaped subepithelial immune deposits in the glomeruli.
What else to study on this topic
- Modern (acyclic) course of the disease
- Timeline for the resolution of urinary syndrome and extrarenal symptoms
- Differential diagnosis with nephrotic syndrome
- Features of immunological shifts (hypocomplementemia)
- Infections preceding the development of glomerulonephritis
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