MEDI7111 Lecture Notes - Lecture 2: Focal Segmental Glomerulosclerosis, Peripheral Edema, Iga Nephropathy
Renal 2
Pathology of the Kidney and Urinary Tract
Nephritic Syndrome
Nephrotic Syndrome
Haematuria
- blood may be microscopic or
macroscopic
- Red cell casts: distinguishing feature,
form in nephrons and indicate
glomerular damage
- Dysmorphic red cells → indicates
glomerulus as the site of bleeding
- Podocytes develop large pores which
allow blood and protein through
Some proteinuria
Mild Hypertension
Azotaemia
- Abnormally high blood urea & nitrogen
(BUN)
- Leads to decreased blood flow,
decreased in GFR, stimulation of RAS
Oliguria
Lesions causing nephritic syndrome all have
increased cellularity within the glomeruli,
accompanied by a leukocyte infiltrate.
This causes inflammation which injures capillary
walls which let red blood cells leak into urine.
This hemodynamic change causes decreased GFR
and stimulation of RAS.
Proteinuria (> 3.5g in 24hrs)
Hypoalbuminaemia
- Albumin is lost in urine
- Binds cations, water, hormones, fatty
acids, and others to regulate the osmotic
pressure of blood
- Gaps between podocytes allow proteins
to escape
Oedema
- Due to loss of albumin (Intravascular
oncotic pressure decreased → Fluid leaks
out of vessels)
- Ascites, non-pitting peripheral oedema,
periorbital oedema
Hyperlipidaemia
- Due to loss of albumin, liver has to
compensate for lower products in the
blood and uses lipids to bulk it out
- Fatty changes in the liver are also present
Nephrotic is often more dangerous than
nephritic.
Conditions presenting with Nephritic Syndrome
Post streptococcal GN
IgA Nephropathy
Rapidly progressive/ crescentic GN
Membranoproliferative GN
Goodpastures Syndrome
Vasculitis disorders – Wegners Granulomatosis,
Microscopic Polyangiitis, Churgg-Strauss disease,
Henoch-Schönlein purpura
Conditions presenting with Nephrotic Syndrome
Primary causes
Minimal change Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranous Glomerulonephritis.
Secondary causes
SLE, Hep B & C, HIV
Diabetes Mellitus
Malignancy (particularly CML)
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Document Summary
Red cell casts: distinguishing feature, form in nephrons and indicate glomerular damage. Dysmorphic red cells indicates glomerulus as the site of bleeding. Binds cations, water, hormones, fatty acids, and others to regulate the osmotic pressure of blood. Podocytes develop large pores which to escape allow blood and protein through. Abnormally high blood urea & nitrogen (bun) Leads to decreased blood flow, decreased in gfr, stimulation of ras. Lesions causing nephritic syndrome all have increased cellularity within the glomeruli, accompanied by a leukocyte infiltrate. This causes inflammation which injures capillary walls which let red blood cells leak into urine. This hemodynamic change causes decreased gfr and stimulation of ras. Due to loss of albumin (intravascular oncotic pressure decreased fluid leaks out of vessels) Due to loss of albumin, liver has to compensate for lower products in the blood and uses lipids to (cid:858)bulk(cid:859) it out. Fatty changes in the liver are also present.
