Usually the patients present with manifestations of acute nephritic
syndrome with oliguria, smoky urine, puffiness of the face and headache
(as a result of hypertension). 20% of patients may manifest as nephrotic
syndrome, 5% may present as rapidly progressive glomerulonephritis and
some patients may be with asymptomatic urinary abnormalities.
Some patients may develop encephalopathy as a result of severe
hypertension or hyponatraemia or they develop heart failure because of
hypertension and fluid retention.
Pathogenesis:
- Nephritogenic strains of streptococci may secrete substances e.g.
neuraminidase and sialic acid which may modify autologous
immunoglobulin for which antibodies are formed by the patient
(autoantibodies) and immune complexes are formed which will be
trapped by the renal glomeruli and cause the disease. - Streptococcal antigens stimulate the body to form antibodies against
them with the subsequent immune complex formation.
Laboratory investigations:
- Urine may show red cell casts, proteinuria (less than in nephrotic
syndrome), haematuria or leucocyturia. - Pharyngeal or skin culture may show streptococci.
- Markers of streptococcal infection as ASO titre and C-reactive
protein are positive. - Hypocomplementaemia (C3, C4) which is transient (for few weeks
only). - Serum creatinine is usually high.
- Kidney biopsy (Fig. 3.8) may show diffuse proliferative
glomerulonephritis with neutrophil and monocyte infiltration of the