Figure 1.
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.](https://sciendo-parsed.s3.eu-central-1.amazonaws.com/69970fb10883ce575fb68836/j_abm-2025-0036_fig_002.jpg?X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Credential=ASIA6AP2G7AKPUIYSOQF%2F20260220%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Date=20260220T203131Z&X-Amz-Expires=3600&X-Amz-Security-Token=IQoJb3JpZ2luX2VjEND%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEaDGV1LWNlbnRyYWwtMSJGMEQCIDF1pDSD9d1%2FPtk45tRAI0kLW6b7VhWWX9DZ8p6YtTYjAiBpkDLP9bTY0lN6UNr1RjXuZETqXZpXdFA%2Fk68Hyc3odyrGBQiZ%2F%2F%2F%2F%2F%2F%2F%2F%2F%2F8BEAIaDDk2MzEzNDI4OTk0MCIMf1LT%2Fo92UnXNnGZaKpoFEyUc0aumWN9%2F%2BZNSIp3TXJ5oyGhro0pG9L2Ca8Wg%2BiDP4ZaOXbmBxHGK7TSjDydr4XJcSZEHC4BHarLNlom%2BlXntLjfogkvOhACUqthsAMfS2Q2IJpclJWTLZoUSCSq6cEns%2FxEeSThXMtzRK28vDugaJ6tGbbgFlmCAozj5G4ANbe3%2F7s8xjd2NRi3RTxuRuuTTUyCZ8S1TLoiCfjrsdHXANl5VBPA1NPclFgs15GSPIDWD1KR9rKNppVkP%2FyNw42OElkRt5ra2GXLCxncB%2BGqRmKJ8UMXQpz1kn7MWqPTxeNYLqyLgwb8WVUM3KmKGHaROCWqyUFCeXFkvQvf%2FBj4qBHD4%2FinNVdXJt1B2KgMkh%2FdPiBpCwrN8sZB117KRHuyl%2FBSTTz3BXH4Xv18yKo73gCN0hDqYa01vZOZBM8AasFCtpDl2D4AHUtZUMBCpz6AkM1Yx4%2FamqsS1k6QyBW3DOGzvBfVLxX7EdhYOqn7hH0nWywXW8rj4HwbGpC8HFESCLSaVeuIpjW4PEBClmWrTI4QeoJvkxZl2FZ%2FpRck2U6t7hI17wPGnTDVVy5IZdKjzFKXBYWITeX%2F9762M57k0C%2FCSbBaVliIIW%2BLLiXHgIvA5AmZqwMLNtZf9NCeuo7g0nLDUXNfC6CUBDP12YCfC20z3B44m4YUhKxnUzwsWM6%2FBDxfr9KGiURpU2nP5fkrHj%2B9S1Di92AAsRUz3B2JEvffWqGw7IFXTVHFpDZUDqXkalokdzrgziyvxPINBHOf2fVWvm69%2BUHUKja5bl%2F%2Bbazq0Lh2qlYTg2j0UScVKH5YIxUTQO3T0AQYK5nghApTsy8VMav6%2F%2F5oRitRlWaF58efelhf9feylkLyCkgB3DMNQCpmoOFLDMPqB4swGOrIBQKpXtlB%2FMc0bBmLHcVMJM0eFeWZWebfQfSy%2F%2F06P29WGIxDUr7VWQvYc27NsYwpMIOMvM9BXu975coOL5%2BQnxqYEmk6rst36axGgmpdsEy99NgO8%2BK7iZTO82FtgZS8yOhZOzt4i4IzgdQH4RN20ufKIsYiMYnbM9UB2u%2BoUy3bBt%2FcbgJjxLM8k8qlQWbXG2N15U8sBM4NYoazIenMIZ2FciIEjzOx3zrZ%2BDcdDy2gg8g%3D%3D&X-Amz-Signature=1968d6247201fb4cb2507f75c65e5d57ee91cdc89d57cf9aa2a5cda1fee99ce2&X-Amz-SignedHeaders=host&x-amz-checksum-mode=ENABLED&x-id=GetObject)
Figure 3.
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) |
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 |
Prevalence of kidney biopsy pathological diagnosis (top 10 most common) [28–30]
| 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%) |