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Kidney function and failure > PBL 33 > Flashcards

PBL 33 Flashcards

1
Q

Anatomical position of the kidneys (peritoneal?)

A

Retroperitoneal

T12-L3

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2
Q

Which of the kidneys is situated lower?

A

The right kidney due to the liver above it

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3
Q

What is the structure and function of the glomerulus

A

Structure: network of capillaries at the beginning of the nephron

Function: Filtering of blood in its formation of urine

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4
Q

Blood supply to and from the glomerulus

A

Afferent artery
- Branch of the interlobular artery in the cortex of the kidney

Efferent arteriole takes blood away
- Provides tighter control over the blood flow through the glomerulus as arterioles dilate and constrict more readily than venules due to the larger smooth muscle layer - tunica media

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5
Q

Lining of the glomerulus

A

Endothelial cells containing fenestrated pores to allow free filtration of fluid, plasma solutes and protein

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6
Q

Which substances are found in the glomerulus basement membrane & how are these synthesised?

A
  • Laminins
  • Type IV collagen
  • Agrin
  • Nidogen
  • Synthesised by endothelial cells and podocytes
  • This makes the basement membrane thicker than other types of tissue
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7
Q

The side of the basement membrane that faces outwards from the capillary is lined with folds called…, these are lined with folds of cytoplasm called….

A

Podocytes

Pedicles

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8
Q

The role of podocytes and pedicles

A

Filtration barrier from the capillary lumen into the Bowman’s space

  • Fluid from the blood in the glomerulus are filtered through the visceral layer of podocytes, resulting in the glomerular filtrate
  • Pedicles have a negatively charged coat (glycocalyx) that limits filtration of negatively charged molecules such as serum albumin
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9
Q

Which type of molecules (size and charge) will pass through more frequently through the glomerulus?

A
  • Small and positively charged ones
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10
Q

Which factors influence the permselectivity of the glomerulus?

A
  • Negative charge of the membrane
  • Podocytic epithelium
  • Pore size of the glomerular wall
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11
Q

Three categories of diseases that affect the kidneys (based on the way they affect different parts of the kidneys)

A
  1. Glomerulonephritis (incl. nephritic syndrome)
  2. Nephrotic syndrome
  3. Tubulointerstitial nephritis
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12
Q

What is tubulointerstitial nephritis?

A

Inflammation of the tubules and the tissues surrounding the tubules

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13
Q

What is the juxtaglomerular apparatus made of? Function?

A
  • A specialised structure formed by the DCT and the glomerular afferent arteriole
  • Function is to regulate blood pressure and filtration rate. Detects BP within glomerulus, detect salt levels within urine and secrete renin. It is in contact with the DCT and regulates the function of each nephron!
  • Composed of macula densa cells (MDC) which detect low BP and send signals to juxtaglomerular cells
  • Composed of juxtaglomerular cells which synthesise, store and secrete renin
  • Composed of extraglomerular mesangial cells
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14
Q

Renal corpuscule components

A

Glomerulus

Bowman’s capsule

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15
Q

Epithelium type in the Bowman’s capsule

A

Simple squamous

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16
Q

Renal tubule components

A

PCT
Loop of Henle
DCT

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17
Q

Flow of blood through the kidney (different arteries and arterioles)

A
  • Afferent arteriole
  • Efferent arteriole
  • Peritubular capillaries (surround the PCT & DCT, supply nutritents to renal cortex)
  • Vasa recta (surround Henle loops and supply nutrients to renal medulla)
  • Efferent venule
  • Renal vein
  • IVC
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18
Q

Epithelium type in the PCT

A

Simple cuboidal w/brush borders to increase area of absorption

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19
Q

Epithelium type in the ascending loop of Henle

A

Lower = simple squamous

Distal portion = simple cuboidal

20
Q

Two different classes of nephrons

A
  • Cortical nephrons (majority)

- Juxtamedullary nephrons

21
Q

Explain the process of glomerular filtration

A
  • Blood enters via renal artery
  • Diameter of afferent arteriole is greater than the efferent
  • The pressure of blood in the glomerulus is increased due to the difference in diameter of the incoming and out-going arterioles
  • In the glomerulus, blood filters into the Bowman’s capsule in a process called ultrafiltration.
22
Q

What is glomerular ultrafiltration?

A
  • Filtration occurring under pressure, due to the afferent and efferent arterioles
  • Afferent arteriole at proximal glomerulus dilates whilst the efferent arteriole constricts. Causing a pressure gradient through the glomerulus, causing filtration under pressure
  • Filtration rate of molecules of the same charge across the filtration barrier is inversely related to their molecular weight!
23
Q

The increased pressure of the glomerulus helps force which components of blood out of the capillaries?

A
  • Water
  • Salts
  • Glucose
  • Urea
  • Water and salts are called GLOMERULAR FILTRATE
24
Q

What is glomerular filtration rate?

A

The volume of fluid filtered from the renal glomerular capillaries into the Bowman’s capsule

  • (urine conc x urine flow) / plasma conc
25
Q

3 mechanisms via which tubular reabsorption occurs

A
  1. Osmosis
  2. Diffusion
  3. Active transport
26
Q

What is reabsorbed in the PCT?

A 
Glucose 100%
Amino acids 100%
Urea 50%
Sodium 70%
Water 70%
Potassium 90%
Phosphate 70%
Calcium 70%
Magnesium 30%
27
Q

What is reabsorbed in the loop of Henle?

A

Descending: permeable to water and less to salts and urea, therefore water moves out into the interstitium

Thick ascending: 
25% sodium
25% potassium
25% calcium
60% magnesium
28
Q

What is reabsorbed in the DCT?

A

5% sodium
8% calcium
5% magnesium
- Water, urea and salts contained within the ascending loop pass into the DCT

29
Q

Function of the major and minor callices

A

Minor calyx: collects urine from the pyramids

Major calyx: formed by the merging of several minor callices

  • Urine passes through the callices into the renal pelvis, a flattened, funnel-shaped structure
  • Renal pelvis –> ureter –> bladder
30
Q

Blood supply to the kidneys & venous drainage

A
  • Abdominal aorta –> left and right renal artery. Immediately distal to the origin of the superior mesenteric artery
  • The right renal artery is slightly longer due to the abdominal aorta being slightly left of the midline
  • Vena cava lies anteriorly to the abdominal aorta, so the right and left renal veins are anterior to the renal arteries
  • The renal artery has segmental branches that supply the renal parenchyma. Each segmental arteries divides to form interlobar arteries either side of each renal pyramid.
  • Interlobar arteries undergo further division to form arcuate arteries
  • Interlobular arteries arise 90 degrees to the arcuate arteries, which pass through the cortex and divide to form the afferent arterioles!

Venous drainage:

  • Left and right renal veins
  • They leave the hilum ANTERIORLY to the renal arteries
  • Empty into the IVC
  • Vena cava lies slightly to the right, so the left renal vein is longer and travels anteriorly to the abdominal aorta below the origin of the superior mesenteric artery
31
Q

What is the line of Brodel? Significance?

A

Imaginary line along the lateral and slightly posterior border of the kidney which delineates the segments of the kidney supplied by the anterior and posterior divisions of the renal artery.
- Renal artery anterior division supplies 75% and the posterior division supplies 25% of the kidney

  • Significance: important access route for both open and endoscopic surgical access of the kidney as it minimises risk of damage to the major arterial branches
32
Q

Pathophysiology of glomerulonephritis

  1. Mechanism
  2. Causes
  3. Risk/trigger factors
  4. Signs and symptoms
  5. Diagnostic factors
  6. Treatment
A
  1. Mechanism
    - Immune-mediated mechanism
    - Consequent inflammatory response which paves the way for fibrotic events
    - Activation of common inflammatory pathways, such as complement system and coagulation cascade, which cause the generation of pro-inflammatory cytokines and complement products, results in the proliferation of glomerular cells
  2. Causes
    - Can be primary (originate in kidney) or secondary
    - Can be acute or chronic

Acute:
- Most often occurs as a result of streptococcus infection of the throat or skin. This type typically develops in children between 2 and 10 y/o after they recover from the infection

  • Infections from other bacteria such as staphylococcus and pneumococcus, viral infections (such as chicken pox), and parasitic infections (such as malaria), can also cause GN
  • Non-infectious disorders such as IgA nephropathy, lupus, Goodpasture syndrome, and membranoproliferative GN can also cause GN

Chronic:

  • IgA nephropathy
  • Membranoproliferative GN
  • Hereditary nephritis
  1. Risk/trigger factors
    - High BP
    - Diabetes
    - Cancer
    - Strep throat
    - > than normal dose of NSAIDs
    - Bacterial infection of heart
    - Viral infections: HIV, Hep B and Hep C
    - Immune diseases: lupus, Goodpasture syndrome, IgA nephropathy
    - Hereditary nephritis
  2. Signs and symptoms
    - About 50% have no symptoms
    - Oedema
    - Proteinuria
    - Haematuria
    - High BP
    - Rapidly progressive GN patients develop weakness, fever, loss of appetite, vomiting/nausea, abdo pain and joint pain
    - About 50% have flu-like symptoms in the month before kidney failure develops
  3. Diagnostic factors
    - Blood tests
    - Urine tests
    - Kidney biopsy
  • Look for protein and blood cells
  • Look for urea and creatine in blood
  • Look for casts (clumps of RBCs or WBCs)
  1. Treatment
    - Treat the causative disorder = infection
    - For rapidly progressive GN, suppression of the immune system . Corticosteroids are given IV. Cyclophosphamides
  • For acute GN - treat cause. Diuretics to reduce high BP. Antibiotics but may be ineffective because GN starts 1-6 weeks after the infection
  • For chronic GN, Acei or Ang II blocker and reduce dietary sodium (to reduce BP)
33
Q

Pathophysiology of nephrotic syndrome

  1. Cause
  2. Signs and symptoms
  3. Complications
  4. Risk factors
  5. Diagnostic factors
  6. Treatment
A

Nephrotic triad: proteinuria, hypoalbuminaemia, oedema. Also hyperlipidaemia

  1. Cause
    - Nephrotic syndrome can be primary or secondary
    - Primary: GN
    - Secondary: diabetes mellitus, lupus, viral infections
    - Nephrotoxic drugs, especially NSAIDs
    - Certain allergies to insect bites, poison ivy
    - Minimal change disease: most common cause in children.
    - Amyloidosis - amyloid proteins accumulate
    - Membranous nephropathy - result of thickening membranes within the glomeruli
  2. Signs and symptoms
    - Malaise
    - Oedema (feet and ankles) - can move around as it is affected by gravity, accumulating in eyelids in the night and the lower body during the night
    - Abdominal pain
    - Frothy urine
    - Weight gain
    - SoB due to fluid accumulating in the pleural space
    - Nutritional deficiencies because of nutrients being excreted in the urine
  3. Complications
    - Thromboembolism - DVT/PE. Renal vein thrombosis
    - Infection
    - Hyperlipidaemia
    - Malnutrition
    - AKI
    - CKD
  4. Risk factors
    - Any condition that damages kidneys: diabetes, lupus and amyloidosis
    - Medications such as NSAIDs and drugs used for infections
    - Certain infections: HIV, Hep B, Hep C, and malaria
  5. Diagnostic tests
    - Urine tests
    - Blood test
  6. Treatment
    - Ace inhibitor (decrease proteinuria)
    - Ang II receptor blocker (decrease proteinuria)
    - Treat the cause
    - Treat the complication
    - Statins to reduce cholesterol
    - Diuretics for high BP
34
Q

Why does hypoalbuminaemia cause oedema, hyperlipidaemia and high BP?

A

Albumin maintains colloid osmotic pressure, keeping fluid in your bloodstream so that it does not leak into tissues.

  • Without albumin in blood, fluid enters the tissues, leading to oedema
  • Hypoalbuminaemia also causes the liver to compensate and increase production of albumin which also has a side effect of lipid production
  • Fluid leaving the bloodstream causes kidneys to compensate by making more sodium, which increases the blood pressure
35
Q

Nephrotic vs nephritic

A

Nephrotic:

  1. Proteinuria
  2. Hypoalbuminaemia
  3. Oedema
  4. Hyperlipidaemia

Nephritic:

  1. Haematuria - due to podocytes developing large pores, allowing blood and protein through
  2. Proteinuria
  3. Mild hypertension
  4. Low urine volume
  5. Oliguria
36
Q

Causes of nephritic syndrome

A
  1. Auto-immune disorders
    - SLE
    - ANCA vasculitis
    - Anti-glomerular basement membrane antibody disease
  2. Infection related
    - Post-infectious glomerulonephritis
    - Bacterial endocarditis
    - HCV
37
Q

Acute vs chronic renal failure

A

Acute:

  • Rapid progressive loss of kidney function
  • When blood supply to kidneys is suddenly interrupted or kidneys become overloaded with toxins
  • Recognised by significant elevation of serum creatinine within hours or days, or significant decrease in urine output for more than 6 hours

Chronic:

  • Long term consequence of irreversible acute disease or part of a disease progression
  • Most common causes are diabetes type 2, long-term uncontrolled hypertension, and polycystic kidney disease
  • Recognised by the presence of structural kidney damage or a GFR <60ml/min/1.73^2 for more than 3 months
38
Q

Causes of acute renal failure (pre-renal, renal and post-renal)

A
  1. Pre-renal
    - Hypovolemia (blood loss)
    - Extremely low blood pressure (Shock)
    - Heart failure
    - Decreased renal perfusion due to vasoactive mediators
    - Dehydration
  2. Renal
    - Acute tubular necrosis caused by: prolonged renal ischaemia, exposure to nephrotoxic drugs, organic solvents, disorders affecting nephrons such as GN or tubulointerstitial nephritis & sepsis
  3. Post-renal
    - Ureteral/bladder obstruction (enlarged prostate/bladder cancer)
    - Kidney/bladder stones
39
Q

Risk factors for AKI

A
  1. Older age
  2. Diabetes mellitus
  3. Hypertension
  4. Heart disease
  5. Liver disease
  6. CKD
  7. Medication:
    - Diuretics
    - ACEi/ARB
    - NSAID
    - Gentamycin
    - Vancomycin
    - Chemotherapy
40
Q

5 stages of kidney failure

A
  1. Stage 1
    - Very mild
    - May experience no symptoms and have no visible complications yet damage is still present
    - Maintain a healthy lifestyle to manage and slow progression
    - GFR >=90 renal function
  2. Stage 2
    - Still quite mild
    - Detectable issues such as proteinuria or physical damage to kidneys may be more obvious
    - Same lifestyle approaches used as in stage 1
    - GFR = 60-89
  3. Stage 3
    - Moderate
    - Kidneys aren’t working as they should
    - Peripheral oedema
    - Back pain
    - Changes to urination
    - GFR 30-59
  4. Stage 4
    - Moderate - severe
    - Anaemia
    - Hypertension
    - Bone disease
    - Healthy lifestyle is vital
    - GFR 15-29
  5. Stage 5
    - Severe
    - Nearing complete failure
    - Symptoms of loss of function evident, including vomiting/nausea, trouble breathing, itchy skin and more
    - Require regular dialysis or transplant
    - GFR < 15
41
Q

Causes of chronic renal failure

A
  1. Type 2 diabetes
  2. Hypertension
  3. Glomerular diseases (IgA nephropathy)
  4. Type 1 diabetes
  5. Genetic diseases (polycystic kidneys)
  6. Nephritis
  7. Obstruction (tumours, stones)
  8. Drugs (NSAIDs)
  9. Infection (HIV, HBV, HCV, TB)
42
Q

Symptoms of kidney failure

A
  • Sometimes no symptoms
  • Reduced urine
  • Swelling if legs, ankles and feet due to failure of water waste elimination
  • SoB
  • Drowsiness or fatigue
  • Persistent nausea
  • Confusion
  • Pain or pressure in the chest
  • Seizures
  • Coma
43
Q

Early signs of kidney failure

A
  • Decreased urine output
  • Fluid retention that leads to limb oedema
  • SoB
44
Q

Complications of AKI

A
  1. Death - mainly sepsis
  2. Infection - main cause of death
  3. Hypertension
  4. Salt/water retention
  5. Electrolyte abnormalities
  6. Metabolic acidosis
  7. Anaemia (EPO)
  8. Uraemia
  9. CKD
45
Q

Clinical manifestations of chronic renal failure

A
  • Alterations in water, electrolyte and acid-base balance
  • Mineral and skeletal disorders
  • Anaemia and coagulation disorders
  • Hypertension and altered cardiovascular function
  • GI disorders
  • Neurologic complications
  • Disorders of skin integrity
46
Q

5 types of kidney failure

A
  1. Acute pre-renal kidney failure
    - Insufficient blood flow to the kidneys as the kidney can’t filter toxins from the blood without enough flow
  2. Acute intrinsic kidney failure
    - Direct trauma such as physical impact
    - Toxin overload
    - Ischaemia (caused by severe bleeding, shock, renal blood vessel obstruction and glomerulonephritis)
  3. Chronic pre-renal kidney failure
    - Not enough blood flow for a prolonged period of time, the kidneys shrink and lose function
  4. Chronic intrinsic kidney failure
    - Long term damage due to intrinsic disease. Intrinsic develops from a direct trauma to the kidneys such as severe bleeding or lack of oxygen.
  5. Chronic post-renal kidney failure
    - Long-term blockage in the urinary tract prevents urination. This causes pressure and eventual kidney damage

Kidney function and failure (12 decks)

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