Renal 5 Flashcards
(23 cards)
Q1: Describe the normal structure and filtration function of the glomerulus.
Model Answer:
The glomerulus is a capillary tuft within the nephron where blood filtration begins. It includes:
Fenestrated endothelium (allows passage of water/small solutes)
=> Blocks blood cells
Glomerular basement membrane (GBM) – collagenous and negatively charged, repels proteins like albumin
=> Acts as a charged, size-selective barrier
Podocytes (visceral epithelial cells) – create slit diaphragms to aid filtration
=> attach to GBM via foot processes
=> Create filtration slits with negatively charged proteoglycans that repel proteins like albumin
Mesangial cells –
They sit between capillary loops, stabilizing the glomerular tuft (like internal scaffolding).
provide structural support, contractile and immune functions
These components ensure selective ultrafiltration into Bowman’s space
Modified vascular smooth muscle cells (contractile,
phagocytic)
=>Can alter capillary surface area by contracting — affects GFR indirectly.
Remove trapped residues or immune complexes from the glomerular basement membrane (like housekeeping).
Ø Proliferate, secrete cytokines (yields inflammation)
Participate in immune signaling and inflammation, especially in glomerulonephritis.
Q2: Define azotemia, proteinuria, hematuria, and hypoalbuminaemia.
Model Answer:
Azotemia: Elevated blood urea and creatinine due to reduced renal function.
Proteinuria: Abnormal protein in urine, especially albumin.
Hematuria: Presence of blood in urine.
Hypoalbuminaemia: Low serum albumin from protein loss via urine, often seen in nephrotic syndrome.
Compare and contrast nephritic and nephrotic syndromes.
Onset
Proteinuria
Hematuria
BP and edema
GBM damage
Cellularity
Nephritic Syndrome
Acute
Mild to moderate
Present (often gross)
Acute hypertension, localized edema
Sporadic, with immune deposits (IgA, C3)
Hypercellular glomeruli
Compare and contrast nephritic and nephrotic syndromes.
Onset
Proteinuria
Hematuria
BP and edema
GBM damage
Cellularity
Nephrotic Syndrome
Chronic/slow
Severe (>3.5g/day)
Rare or microscopic
Chronic hypertension, generalized edema
Diffuse thickening, podocyte loss
No hypercellularity, fibrosis over time
Q4: Explain the immunological mechanisms behind glomerulonephritis.
Model Answer:
Immune complex deposition in the glomerulus (either circulating or formed in situ) initiates inflammation. These deposits activate complement (C3, C5) and recruit leukocytes, causing:
GBM disruption
Podocyte effacement
Altered charge and permeability
The site and type of deposition influence whether the condition presents as nephritic (e.g. acute post-infectious GN) or nephrotic (e.g. membranous GN).
Q5: Describe the features of acute post-infectious glomerulonephritis.
Model Answer:
Follows Group A Streptococcal infection (1–4 week latency)
Presents with: hematuria (coca-cola urine), fever, malaise, oliguria
Histology: hypercellular glomeruli, sporadic IgG/C3 “humps”, endothelial swelling
Prognosis: often self-limited in children; worse in adults
Describe the features of membranous glomerulonephritis.
Chronic immune complex deposition along the GBM
==> This triggers:
Inflammation (via complement activation)
Podocyte injury
Protease and oxidant release from local cells
REsult:
Loss of podocytes
Thickened GBM from deposits
Loss of charge and size selectivity → severe proteinuria
Histology: thickened capillary walls, “spike and dome” pattern on silver stain
Leads to podocyte loss and severe proteinuria
Often idiopathic (no known cause).) may be linked to autoimmune conditions, drugs, or infections
How do histological features differ between nephritic and nephrotic cases?
Model Answer:
Nephritic: Hypercellularity, immune deposits, disrupted GBM with red cell leakage
Nephrotic: Diffuse GBM thickening, podocyte effacement, absence of leukocyte infiltration, widespread protein leakage
azotemia definition
- increases in blood creatinine and urea concentration
indicative of renal dysfunction
- haematuria
- blood in the urine
- proteinurea
- elevated protein in the urine
- hypoalbuminaemia
- low albumin content in the circulation* Hyperlipidaemia and associated lipiduria - excessive circulating lipid
presenting as elevated urinary lipid levels
Useful terminology
- Hyperlipidaemia and associated lipiduria -
excessive circulating lipid
presenting as elevated urinary lipid levels
Useful terminology
Glomerular Basement Membrane (GBM): charged, size selective barrier
GBM Negatively Charged
=> GBM contains proteins called proteoglycans.
(These proteins have attached sugar chains with sulfate or carboxyl groups, giving them a net negative charge.)
.
🚫 What Does the Negative Charge Do?
It repels negatively charged molecules, like albumin (a major blood protein that also has a net negative charge).
This helps prevent protein loss in urine under normal conditions.
What Does ‘Size-Selective Barrier’ Mean?
The GBM has a Meshwork structure
Physically sieves by size
It allows: Water, ions (Na⁺, Cl⁻), glucose, urea, Small peptides
It blocks: Large proteins (like albumin), Blood cells (red and white)
Nephrotic syndrome and nephrici difference
Type of immune complex
Site of deposition
Result
Nephritic syndrome (acute):
* acute onset of haematuria, acute onset of inflammation with cellular proliferation,
inflammatory white cells and capillary damage.
Nephrotic syndrome (slow chronic) = Proteinuria in excess
Characterised by slow, progressive damage to filtration by immune mechanisms
(eg Ab/AIg/complement deposition).
NEPHRITIC
Often IgA
Mesangial or subendothelial
Acute inflammation, hematuria
NEPHROTIC
Often IgG
Subepithelial (beneath podocytes)
Chronic damage, proteinuria
glomerulonephritis
ITIS : Glomerulonephritis = inflammation and damage of the glomeruli, caused primarily by the immune system.
Antibodies (Ab)
Antigen-antibody (immune) complexes
Complement system
Immune cells
🧪 1. What Triggers It?
Infection (e.g., Strep A) or autoimmune disorders can trigger your immune system.
Your body makes antibodies to fight off foreign antigens.
Sometimes, these antibodies + antigens stick together = immune complexes.
🎯 2. Where Do These Immune Complexes Go?
They travel in the blood and may get trapped in the glomerulus.
OR, the immune response happens right in the kidney (in situ reaction = Antibodies bind directly to kidney antigens (e.g. anti-GBM disease).
💣 3. What Damage Do They Cause?
Once stuck, immune complexes trigger:
Complement activation (C3, C5)
Recruitment of white blood cells (neutrophils, T cells)
Release of enzymes and oxidants
➡ This damages glomerular structures:
GBM disruption → alters filtration
Podocyte effacement → loss of slit diaphragm
Loss of negative charge → albumin leaks out → proteinuria
🧫 Acute Post-Infectious Glomerulonephritis (APIGN)
EXAMPLE of nephritis
🦠 1. What Causes It?
Triggered by infection with Group A β-haemolytic streptococci — the same bacteria that cause strep throat or skin infections.
The body creates antibodies to fight the infection.
These antibodies bind to bacterial antigens, forming immune complexes.
==> immune complexes trigger
* Complement activation (esp. C3)
* White blood cell infiltration
* Inflammation
This leads to:
* Damage to GBM → hematuria
* Reduced GFR → oliguria (less urine)
* Swelling and capillary injury
⏳ 4. Why Is There a Latent Period?
Symptoms appear 1–4 weeks after the infection because:
It takes time for the immune system to build up enough antibodies.
Immune complexes need time to form and deposit in the kidney.
symptoms :
Mild proteinuria Small protein leakage; not as high as nephrotic syndrome
Periorbital edema Swelling around the eyes from fluid retention
Hypertension Due to reduced kidney function and salt/water retention
morphological feature and symptom occurs in acute nephritic syndrome : sporadically thickened wall
🔹 1) Sporadically Thickened Glomerular Capillary Walls
* Cause: Deposition of immune complexes (IgA, IgG, C3) on the glomerular basement membrane (GBM).
* These deposits are not evenly distributed, so the wall thickening is sporadic.
* ➤ Why? The immune complexes don’t deposit uniformly — they settle in certain areas depending on blood flow and capillary structure.
morphological feature and symptom occurs in acute nephritic syndrome : hypercellularity
🔹 2) Marked Increase in Glomerular Cellularity (Hypercellularity)
* Cause: Inflammation from immune complex deposition recruits:
o Leukocytes (especially neutrophils)
o Mesangial cell proliferation
o Sometimes endothelial swelling
* ➤ Why? The immune system sees the immune complex as “foreign” → activates complement → attracts immune cells → causes swelling + extra cells.
morphological feature and symptom occurs in acute nephritic syndrome : IgA & C3
🔹 4) Sporadic Deposits of IgA & C3 → Podocyte Effacement
* Cause: The immune deposits cause local inflammatory stress and disrupt podocyte attachment.
* ➤ Why?
o Podocytes normally help maintain the selective filtration barrier.
o When immune complexes accumulate beneath podocytes, it pushes them off the GBM (this is called effacement).
o Result = loss of filtration control, leading to proteinuria.
morphological feature and symptom occurs in acute nephritic syndrome : hematuria
🔹 3) Hematuria with Variable Proteinuria
* Cause:
o Hematuria: GBM damage allows red blood cells to leak into Bowman’s space.
o Proteinuria: Some podocyte disruption allows limited protein leakage.
* ➤ Why?
o RBCs are leaking because the endothelial barrier is inflamed and compromised.
o Albumin (a protein) leaks only partially because podocyte disruption is not complete or widespread.
Glomerulonephritis” vs. Nephritic & Nephrotic Syndromes
🔷 1. Glomerulonephritis (GN) = Umbrella Term
GN means inflammation of the glomeruli.
It refers to a group of diseases involving immune-mediated injury to glomerular structures.
GN includes both:
Nephritic syndromes
Nephrotic syndromes
🧬 Why Inflammation Happens in Nephritic but Not (Usually) in Nephrotic Syndrome
🔥 Nephritic Syndrome = Inflammatory
Immune complexes deposit in the subendothelial or mesangial space.
These areas are exposed to circulating immune cells and plasma proteins.
This triggers:
Complement activation (C3, C5a) → chemoattracts neutrophils
Leukocyte infiltration
Cytokine release and cell proliferation
The result is inflammation, capillary wall damage, and hematuria.
❄️ Nephrotic Syndrome = Non-Inflammatory (Usually)
Immune complexes deposit in the subepithelial space — beneath podocytes, on the urinary side of the GBM.
These deposits are hidden from circulating immune cells and complement proteins to some extent.
There’s little to no leukocyte recruitment.
Damage is structural, not inflammatory:
Podocyte foot process effacement
Loss of slit diaphragm integrity
Loss of negative charge of GBM
