AUA Pathology PDF → Step 1 map

Nephrotic Syndrome, without the renal fog.

A tappable review built from the 27-page PDF: criteria, mechanism, primary glomerular diseases, microscopy clues, thrombotic traps, and quick exam checks.

Proteinuria >3.5 g/dayOval fat bodiesPodocyte injurySpikes / Foot effacement / Tram-tracks

Central idea: the filter leaks protein

Diagnostic criteria to memorize

Heavy proteinuria>3.5 g/day; core driver of syndrome.

A↓

HypoalbuminemiaSerum albumin <3 g/dL after urinary loss.

Generalized edemaFace, legs, ascites from low oncotic pressure.

L↑

HyperlipidemiaLiver compensates by increasing lipoprotein production.

✦

LipiduriaOval fat bodies, Maltese cross under polarized light.

Source: PDF pp. 3, 5–6.

Mechanism chain

Filtration barrier damaged

Podocyte/GBM injury increases protein permeability.

Albumin leaks into urine

Proteinuria becomes the measurable clue.

Plasma oncotic pressure falls

Fluid shifts into tissues → edema.

Liver overproduces lipoproteins

Hyperlipidemia, then lipiduria with fatty casts.

Tap a cause → lock the buzzwords

The PDF focuses on primary glomerular causes. For Step 1, make the age + microscopy + association your instant triad.

Microscopy pattern recognition

Most renal pathology questions are “name that pattern.” Pair each disease with LM, EM, IF and classic context.

Why membranous gets scary

Thrombosishighest reported in membranous nephropathy

PDF flags renal vein thrombosis, pulmonary embolism, and DVT as key complications in membranous nephropathy.

Source: PDF p. 12.

Exam traps to avoid

Nephrotic ≠ nephritic

Nephrotic is heavy protein/lipid/edema. Nephritic is hematuria, RBC casts, azotemia, hypertension. MPGN can mix both.

Minimal change looks normal on light microscopy

The pathology is podocyte foot process effacement on EM; no immune deposits on IF.

FSGS has worse steroid response than MCD

Think HIV, obesity, sickle cell, Hispanic/African ancestry; can progress to ESRD.

Dense deposit disease is alternative complement chaos

C3 nephritic factor stabilizes C3 convertase → persistent C3 activation → hypocomplementemia.

Nephrotic Syndrome Canvas