Table 1.
Classical features of nephritic and nephrotic syndrome
| Nephritic syndrome | Nephrotic syndrome |
|---|---|
| Salt-water retention edema (increased hydrostatic pressure) | Loose part edema (decreased oncotic pressure edema) |
| • Starts in the dependent part (legs, ankles) Edema in other parts at a later stage | • Starts with loose tissue (upper eyelids, genitalia) Edema in dependent parts at a later stage |
| New onset or accelerated hypertension | Pleural effusion, ascites, hyperlipidemia, hypoalbuminemia |
| Dysmorphic RBC in UA | Usually, no RBC in UA, not dysmorphic if presented |
| RBC cast | Oval fat body (degenerating tubular epithelial cells filled that contain refractile fat droplets) |
| Nephrotic or sub-nephrotic range proteinuria | Nephrotic range proteinuria |
| Usually with elevated Cr/decreased eGFR | Meet all the criteria of nephrotic syndrome |
| 1. Generalized edema | |
| 2. Nephrotic range proteinuria (≥3.5 g/d) | |
| 3. Hypoalbuminemia (<3.0-3.5 g/dL, depends on assay) |
Table 2.
| USA/Canada (n = 23,391) Survey 2012–2013 | Europe (n = 15,042) Survey 2012–2013 | Latin America (n = 2,561) Survey 2012–2013 | Japan (n = 28,728) 2007–2017 | Thailand (n = 5,893) 2000–2014 |
|---|---|---|---|---|
| FSGS (19%) | IgAN/HSP (22%) | LN (38%) | IgAN/HSP (33%) | LN (32%) |
| DN (19%) | FSGS (15%) | FSGS (16%) | MN (9%) | IgAN/HSP (21%) |
| IgAN/HSP (12%) | MN (13%) | MN (11%) | FSGS/NS (9%) | MCD (8%) |
| MN (12%) | LN (10%) | MCD (7%) | DN (6%) | DN (8%) |
| LN (10%) | Pauci-immune GN (8%) | IgAN/HSP (6%) | Pauci-immune GN (6%) | FSGS (7%) |
| Pauci-immune GN (5%) | DN (7%) | Pauci-immune GN (5%) | MCD (6%) | MN (7%) |
| MCD (4%) | MCD (6%) | DN (4%) | LN (5%) | TI disease (4%) |
| Alport syndrome/TBM (3%) | Amyloidosis (4%) | MPGN (3%) | TI disease (4%) | Infection-related GN (3%) |
| TMA (3%) | MPGN (4%) | MesProlif GN (2%) | Amyloidosis (2%) | Pauci-immune GN (3%) |
| MPGN (3%) | TMA (2%) | Infection-related GN (2%) | Alport syndrome/TBM (1%) | MPGN (2%) |
1 DN, diabetic nephropathy; FSGS, focal segmental glomerulosclerosis; GN, glomerulonephritis; HSP, Henoch-Schönlein purpura; IgAN; IgA nephropathy; LN, lupus nephritis; MCD, minimal change disease; MesProlif, mesangial proliferative; MN, membranous nephropathy; MPGN, membranoproliferative glomerulonephritis; NS, nephrosclerosis; TBM, thin basement membrane disease; TI, tubulointerstitial; TMA, thrombotic microangiopathy.
Figure 1.
Overview of nephritic syndrome, listing common causes of GN and their classical presentations. ANA, anti-nuclear antibody; ANCA, anti-neutrophil cytoplasmic antibodies; ASO, anti-streptolysin-O; DDD, dense deposition disease; DN, diabetic nephropathy; EGPA, eosinophilic granulomatosis polyangiitis; ENT, ear-nose-throat; FSGS, focal segmental glomerulosclerosis; GBM, glomerular basement membrane; GN, glomerulonephritis; GPA, granulomatosis polyangiitis; HBV, hepatitis B virus; HCDD; heavy chain deposition disease; HCV, hepatitis C virus; HIV, human immunodeficiency virus; HSP, Henoch-Schönlein purpura; IBD, inflammatory bowel disease; IE, infective endocarditis; Ig, immunoglobulin; IgAN, IgA nephropathy; LCDD, light chain deposition disease; LHCDD, light-heavy chain deposition disease; MCD, minimal change disease; MesProlif, mesangial proliferative; MN, membranous nephropathy; MPA, microscopic polyangiitis; MPGN, membranoproliferative glomerulonephritis; MPO, myeloperoxidase; NS, nephrosclerosis; PR3, proteinase-3; PSC, primary sclerosing cholangitis; RPGN, rapidly progressive glomerulonephritis; SLE, systemic lupus erythematosus; TBM, thin basement membrane disease; TI, tubulointerstitial; TMA, thrombotic microangiopathy.
Table 3.
Complement levels in GN with classical and alternative pathway
| Pathway | Disease | C3 | C4 |
|---|---|---|---|
| Classical | LN | ↓ | ↓↓ |
| pathway | Mixed cryoglobulinemic GN | ↓ or ↔ | ↓↓ |
| Alternative | C3 GN | ↓ or ↔ | ↔ |
| pathway | Infection-related GN | ↓ | ↓ or ↔ |
| Atypical hemolytic-uremic syndrome | ↓ | ↔ | |
| Atheroembolic disease | ↓ or ↔ | ↓ or ↔ | |
| Other non-GN conditions that cause hypocomplementemia | |||
| • Severe sepsis | |||
| • Malnutrition | |||
| • Hepatic failure |
Figure 2.
Overview of glomerular diseases according to their typical onset and clinical phenotypes. Brown represents diseases with predominantly nephritic features, while blue represents diseases with predominantly nephrotic features. (Adapted with permission from Dr. Ali Poyan Mehr) [45]. AKI, acute kidney injury; DN, diabetic nephropathy; FSGS, focal segmental glomerulosclerosis; GBM, glomerular basement membrane; GN, glomerulonephritis; MCD, minimal change disease; MN, membranous nephropathy; RBC, red blood cell.
Figure 3.
Overview of nephrotic syndrome, listing common causes of GN and their classical presentations. AKI, acute kidney injury; CMV, cytomegalovirus; CNI, calcineurin inhibitor; DKD, diabetic kidney disease; eGFR, estimated glomerular filtration rate; FSGS, focal segmental glomerulosclerosis; GN, glomerulonephritis; HBV, hepatitis B virus; HCV, hepatitis C virus; HIV, human immunodeficiency virus; LN, lupus nephritis; LVH, left ventricular hypertrophy; MCTD, mixed connective tissue disease; MN, membranous nephropathy; mTORi, mammalian target of rapamycin inhibitor; NSAID, non-steroidal anti-inflammatory drug; PLA2R, phospholipase A2 receptor; RBC, red blood cell; SARS-COV-2, severe acute respiratory syndrome coronavirus 2; WBC, white blood cell.