Nephritic is inflammatory with haematuria; nephrotic is leaky with heavy proteinuria
Mnemonic
“Nephritic is blood, nephrotic is protein”:
| Nephritic | Nephrotic | |
|---|---|---|
| Hallmark | Haematuria, red cell casts | Proteinuria over 3.5 g/day |
| Protein | Under 3.5 g | Over 3.5 g |
| Blood pressure | Raised | Normal or low |
| Oedema | Mild, periorbital | Marked, generalised |
| Albumin | Normal or slightly low | Low, under 30 |
| Lipids | Normal | Raised |
| Mechanism | Inflammatory, proliferative | Podocyte damage, non-inflammatory |
Nephritic causes: post-streptococcal, IgA nephropathy, rapidly progressive glomerulonephritis, lupus, membranoproliferative, Alport’s.
Nephrotic causes: minimal change (children), membranous (adults, and the commonest secondary to malignancy), focal segmental glomerulosclerosis, diabetes, amyloid.
Nephrotic syndrome carries specific complications worth remembering: thrombosis (loss of antithrombin III, classically renal vein thrombosis), infection (loss of immunoglobulin, especially encapsulated organisms), hyperlipidaemia and vitamin D deficiency.
Expansion
| Feature | Nephritic | Nephrotic |
|---|---|---|
| Mechanism | Inflammation | Podocyte injury |
| Proteinuria | Modest, under 3.5 g/day | Over 3.5 g/day |
| Haematuria | Yes, with red cell casts | Absent or minimal |
| Blood pressure | Raised | Normal or low |
| GFR | Reduced | Often preserved initially |
| Oedema | Periorbital, mild | Marked, generalised |
Nephritic causes: post-streptococcal glomerulonephritis, IgA nephropathy (the commonest worldwide), rapidly progressive glomerulonephritis, lupus nephritis, anti-GBM disease.
Nephrotic causes: minimal change disease (commonest in children, steroid responsive, normal light microscopy with foot process effacement on electron microscopy), membranous nephropathy (commonest in adults, anti-PLA2R antibodies), focal segmental glomerulosclerosis, diabetic nephropathy, amyloid.
Complications of nephrotic syndrome follow from urinary protein loss: thrombosis (loss of antithrombin III, classically renal vein thrombosis), infection (loss of immunoglobulin), hyperlipidaemia (compensatory hepatic synthesis), and vitamin D deficiency.
Distinguishing IgA nephropathy from post-streptococcal disease is a common question: IgA follows infection within days (synpharyngitic), post-streptococcal follows after 1 to 3 weeks with low complement.