Glomeruli are basically filters. When things go wrong, they:
- Leak (protein, RBCs, etc)
- Don’t work (no filtrate)
1. Nephrotic syndrome (leaky filter)
- Heavy proteinuria (>3.5g/day) (importantly, albumin is one of the proteins lost)
- Hypoalbuminaemia (basically an effect of renal albumin loss)
- Severe oedema (an effect of low serum albumin – low serum oncotic pressure)
- Hyperlipidaemia
- Lipiduria (urine lipid loss)
2, Nephritic syndrome (leaky + cannot filter)
- Haematuria (usually gross – RbCs pass through leaky filter)
- Mild to moderate proteinuria (due to leaky gloms)
- Oliguria (due to poor filtering function)
- Oedema (from fluid retention due to poor filtration)
- Hypertension (due to fluid retention)
- Azotaemia (biochemical abnormality characterised by raised creatinine levels)
3. Asymptomatic haematuria and/or proteinuria (mild leak)
- Usually associated with mild glomerular abnormalities
4. Acute renal failure (Rapidly progressive glomerulonephritis / Crescentic glomerulonephritis) – (suddenly unable to filter)
- There is:
i. Rapid development of anuria/severe oliguria
ii. Rise in serum creatinine
iii. Over 3 months or less
5. Chronic renal failure (progressive inability to filter)
Many of the glomerular diseases causing the above clinical syndromes can progress to chronic renal failure.
This chart is taken from Robbins. Take note that some are Primary while others are Secondary (non-primary eg. systemic conditions)
How do we correlate clinical presentation with specific glomerular diseases and morphology?
Here is a Mindmap that helps tie in the clinicopathologic correlation. Many of the conditions mentioned in this mindmap are Primary Glomerular diseases. There are secondary and systemic conditions that can also cause nephrotic and nephrotic syndrome, mentioned in your lecture notes
For specific disease aetiologies, pathogenesis and clinical course, please refer to your notes.