Question
A 6 year old school going boy was brought by his father to the Paediatric OPD with complaints of swelling in the face and leg for the past one week with passing of reduced amount of high coloured urine since 3 days. The father also gave a past history of the boy having scabies, detected and treated in his school health programme. On examination the boy is under nourished, periorbital edema present, pedal edema present. His Blood pressure was 130/100 mm of Hg.Pulse rate was 94/mt regular.
- (a) What is your provisional diagnosis 1 mark(s)
- (b) Aetiopathogenesis of this condition 4 mark(s)
- (c) List the investigations and their interpretations to support your diagnosis 4 mark(s)
- (d) What is the prognosis of this condition e) Enumerate the common complication of this condition 1 mark(s)
Answer
(a) Provisional diagnosis: Acute Post-Streptococcal Glomerulonephritis (PSGN) — the presentation of facial and leg (periorbital and pedal) oedema, reduced high-coloured urine output (oliguria with haematuria), hypertension (130/100 mmHg), in a child with a recent antecedent skin infection (scabies, which can become secondarily infected with nephritogenic streptococci), is classic for acute PSGN (post-streptococcal, in this case likely following impetiginization of scabies lesions rather than pharyngitis).
(b) Aetiopathogenesis: PSGN follows infection with nephritogenic strains of Group A beta-haemolytic Streptococcus (skin strains, e.g., type 49, are classically linked to impetigo-associated PSGN, as may be relevant here given the scabies history predisposing to secondary bacterial skin infection). It is an immune-complex mediated (Type III hypersensitivity) glomerulonephritis: streptococcal antigens are either planted in the glomerular basement membrane or form circulating immune complexes that deposit in the glomeruli, after a latent period of 1–4 weeks. This activates complement, attracting neutrophils and monocytes that damage glomerular capillaries, producing a diffuse proliferative glomerulonephritis — reducing GFR (oliguria, azotaemia) and allowing red cells to leak into urine (high-coloured/smoky urine).
(c) Investigations and interpretation:
- Urinalysis: haematuria (RBC casts pathognomonic of glomerular bleeding), mild-to-moderate proteinuria.
- Renal function tests: elevated blood urea and serum creatinine (reflecting reduced GFR).
- Serum complement (C3): characteristically low, normalizing within 6–8 weeks.
- ASO titre / anti-DNase B: elevated, supporting recent streptococcal infection (anti-DNase B more reliable than ASO after skin infections).
- Throat/skin swab culture, if still active infection present.
- Renal biopsy (if atypical course): diffuse proliferative GN with subepithelial “humps” on EM and granular IgG/C3 deposits on immunofluorescence.
(d) Prognosis: Excellent in children — over 95% recover completely with conservative management (rest, salt/fluid restriction, diuretics and antihypertensives as needed). A small minority may progress to rapidly progressive GN or, rarely, chronic glomerulonephritis.
(e) Common complications: Hypertensive encephalopathy, acute kidney injury, pulmonary oedema/congestive heart failure (from fluid overload), and (rarely) progression to rapidly progressive glomerulonephritis.