Glomerular Diseases

Glomerular diseases could be primary (i.e., there is a primary abnormality in the glomerulus) or secondary (to systemic diseases).

Clinical manifestations:

1. nephritic syndrome, which would result in azotemia, hematuria, HTN and proteinuria less than 3.5 grams/day.

2. nephritic syndrome, which would result in proteinurua >3.5 grams/day, hypoalbuminemia, edema(due to decreased oncotic pressure), and hyperlipidemia (compensatory mechanism by the liver to loss of protein).

We can separate these two syndromes by the definitions above, but, in reality, these two often overlap. (why can’t anything ever be simple?)

As a result of insult to glomerulus, we could see the following changes:

1. Cellular proliferation of endothelial, epithelial, and/or mesangial cells and deposition of mesangial matrix, which would appear pink on H&E stain.

2. Leukocytic infiltration: PMNs. Ex: proliferative glomerulonephritis

3. BM (basement membrane) will thicken as a result of deposition of immune complexes. Ex: membranous glomerulonephritis

4. End stage changes will include fibrosis, or sclerosis/hyalinization (histological term) of the glomeruli.

A few terms before we go on discussing glomerular diseases (btw, this is a better term than glomerulonephritis, since we don’t really have an inflammation of the glomerulus, but rather IC (immune complex) deposition, etc., (see below in pathogenesis of glomerular diseases for other causes) in the glomerulus.

(diffuse vs. focal, describing how many glomeruli are involved)

Diffuse GN: all glomeruli are involved

Focal: only several glomeruli are involved

(global vs. segmented, describing whether a whole glomerulus or only part of it is involved)

Global: the whole glomerulus is involved

Segmental: only part of glomerulus is involved

Category: Nephrology Notes , Pathology Notes