Diagnose first, then localise the lesion. A nephritic child - smoky/cola urine, $RBC$ casts, oedema and hypertension - presenting roughly two weeks after pharyngitis (or six weeks after skin infection) with a nephritogenic strain of group A streptococcus has post-streptococcal glomerulonephritis.
The pathology is immune-complex mediated. Antigen-antibody complexes lodge on the outer, subepithelial aspect of the glomerular basement membrane, producing discrete dome-shaped electron-dense deposits the classic literature calls humps. Immunofluorescence corroborates this with coarse granular $IgG$ and $C3$ in a starry-sky distribution; serum complement ($C3$) is transiently low.
Each distractor belongs elsewhere: tram-tracking with subendothelial deposits is membranoproliferative GN, universal foot-process effacement without deposits is minimal change disease, and a smooth linear GBM pattern is anti-GBM disease.
\[\boxed{\text{PSGN} \Rightarrow \text{subepithelial electron-dense humps on EM}}\]