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Summary Lecture 19 + 20 - Nephropathology II
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Lecture 19 20 - Nephropathology II
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Principles and practice of Human Pathology – Lecture 17 + 18 (21-6-2018):Nephropathology II
Filtration barrier:
Consists out of three layers:
1. Podocytes
2. Basement membranes
3. Fenestrated endothelium
Large molecules should stay inside the circulation, while small molecules should be
filtered out (e.g. electrolytes).
The basement membrane is negatively charged, so it is easier for positively charged
molecules to pass through the membrane.
In a normal urine specimen, there should be no albumin.
Podocyte injury causes heavy proteinuria:
- This can be caused by mechanical, genetic, toxic, viral, immune-complexes,
other causes)
If there is something wrong with your podocytes, you get albuminuria
proteinuria.
Nephrotic syndrome:
- Heavy albuminuria when a patient loses a lot of albumin
- Edema (because of low circulating albumin concentrations), hyperlipidemia,
pro-thrombotic state (loss of anti-thrombotic factors, because of the leaky
kidney)
- (initially) Normal renal function (clearance)/GFR (glomerular filtration rate).
Glomerulopathies that cause nephrotic syndrome:
- Minimal change glomerulopathy (MCN)
- Focal and segmental glomerulosclerosis (FSGS)
- Membranous glomerulopathy (MG)
- Others (deposition diseases, diabetes)
1. Minimal change glomerulopathy:
- Mild and transient podocyte injury, multiple causes
- Normal light microscopy no morphological changes can be observed.
- Extensive effacement of podocyte foot-processes (EM) de-differentiation of
the footprocesses can be observed under the EM.
- Steroid sensitive
- Does not lead to fibrosis/chronic damage.
2. Focal and segmental glomerulosclerosis:
- More severe/prolonged podocyte injury, multiple causes (e.g. medication,
virus – very similar causes to minimal change glomerulopathy)
- Focal = not all the glomeruli are affected, segmental = only a part of the
glomerulus is affected.
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