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Unit 10 > Week 6 Renal pathology workshop > Flashcards

Week 6 Renal pathology workshop Flashcards

1
Q

What is the renal sinus?

A

A space around the hilar structures filled with loose connective tissue

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2
Q

What are the functions of a normal kidney?

A

Excretion of metabolic waste products and foreign chemicals
Regulation of water and electrolyte balance
Regulation of body fluid osmolarity and electrolyte concentrations
Regulation of arterial blood pressure
Regulation of acid-base balance
Secretion, metabolism and excretion of hormones
Bone metabolism
Gluconeogenesis

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3
Q

What are the five major parts of the nephron?

A

The glomerulus and Bowmans capsule
The proximal convoluted tubule
The loop of henle
The distal convoluted tubule
The collecting duct

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4
Q

What are the two types of nephrons?

A

The cortical nephron
The juxtamedullary nephron

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5
Q

What are the features of the cortical nephron?

A

85% of all nephrons
Located in the cortex

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6
Q

What are the features of juxtaglomerular nephrons?

A

15% of all nephrons
Located at the boundary of the cortex and the medulla tend to have a longer loop of Henle so play a greater role of regulation of blood volume.

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7
Q

Describe the vascular supply the the nephron?

A

From interlobular arteries branch the afferent arteriole the glomerulas then the efferent arteriole
From the efferent arteriole is the peritubular capillary that surrounds all the cortical nephrons, in the juxtaglomerular nephonrs due to their increased LOH length the peritibular capillary also branch to vasa recta to surround the LOH.
The venous end of the capillaries will drain into interlobular veins.

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8
Q

What are the components of the renal filtration barrier?

A

Endothelial cells
Basement membrane
Visceral epithelial cells/podocytes

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9
Q

What are the key features in the bowmans capsule/ glomerulus?

A

Afferent and efferent arteial
Mesangial cells
Endothelial cell fenestrations
Basmenent mebrane
Podocytes
Parietal cells in bowmans capsule.

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10
Q

What is teh function of mesangial cells in the renal nephron?

A

Maintain the structure of capillaries (endothelial cells) and aid filtration.
Found in the intercapilular space

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11
Q

Describe the structure of the bowmans capsule?

A

Consists of parietal cells that form the outer capsule covering
Consists of visceral cells also called podocytes that fuse with the basement membrane of endothelial cells to form part of the filtration barrier.

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12
Q

How does each component of the filtration barrier contribute to what can and can not pass through the filtration barrier?

A

Endothelial cells - have pores between them roughly 70-100nm in width this allows the movement of plasma proteins, fluid and solute but not rbcs.

Basement membrane - negative charge - repels most plasma proteins

Podocytes/visceral epithelial cells of bowmans capsule - attach to the basement membrane by foot processes with filtration slits between them that vary from 25 to 60nm in diameter

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13
Q

What is the typical content of the filtrate?

A

Water, glucose, small amino acids, ions, urea, hormones, vitamins and ketones.

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14
Q

What features of a substance may prevent it from being filtered into the bowmans space?

A

Molecular weight above 70 kilodaltons such as albumin
Is negatively charged
Shape - has a radius above 3.6nm in radius **

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15
Q

What are the four categories of renal disease?

A

Disease of glomeruli
Disease of tubules
Disease of interstitium
Disease of blood vessels

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16
Q

How does the general cause vary between the different types of renal disease?

A

Disease of the glomeruli - tends to be immunological in origin
Tubular and interstitial diseases - are normally caused by toxic or infectious agents.

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17
Q

What are the five different clinical manifestations of glomerular disease?

A

Nephrotic syndrome
Nephritic syndrome
Chronic renal failure
Rapidly progressive glomerulonephritis
Asymptomatic hematuria or proteinuria

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18
Q

What are the clinical presentations of nephritic syndrome?

A

Haematuria
Azotemia - build up of nitrogenous and other waste products in the blood due to kidney failing
Mild proteinuria
Oliguria - low urine output
Edema
Hypertension
Pyuria

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19
Q

What are the primary causes of nephritic syndrome?

A

Post infectious glomerulonephritis
Rapidly progressive or crescentric glomerulonephritis
IgA nephropathy

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20
Q

What are the secondary causes of nephritic syndrome?

A

SLE - systemic lupus erythymus
Vasculitis

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21
Q

What is the clinical presentation fo nephrotic syndrome?

A

More than 3.5g proteinuria (specifically albumin)
Hypoalbumineia (in blood)
Severe edema
Hyperlipidemia
Lipiduria
Hypercoagulability
Risk of infection - loss of antibodies (also a protein)

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22
Q

What are the primary causes of nephrotic syndrome?

A

Membranous glomerulonephritis
Minimal change disease
Focal segmental glomerulosclerosis

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23
Q

What are the secondary causes of nephrotic syndrome?

A

Diabetes
Amyloid

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24
Q

What is the mechanism of nephrotic syndrome?

A
  1. Glomerular injury occurs - damages the filtration barrier so albumin (more than 3.5 grams a day) is able to cross the barrier and enter the bowman capsule
  2. Plasma hypoalbulimea activates the liver to increase protein production. Excess protein filtered across the barrier may be catabolised by PCT limiting protein in urine to around 3.5g a day.
  3. Liver synthesised more lipids - resulting in hyperlipidemia/ dyslipidemia. Lipids can be lost in urine (lipiduria)
  4. Liver increases anti-thrombin 3 - which increases the risk of renal artery thrombosis
  5. Increased transferrin, and leaks about into Bowmans space - leads to iron deficiency.
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25
Q

What are the consequences of hypoalbuminemia in nephrotic syndrome?

A

Low oncotic pressure in the blood - results in hypotension and oedema as less reabsorption from nephron and interstitial fluid.
Water and electrolytes may also move into the interstitial fluid..
Decreases venous return and cardiac output
This reduced blood flow to the kidney and decreases GFR - which results in RAAS activation - resulting in vasoconstriction so high BP and this results in severe odema (as more water retention from nephron then lost into interstitial again as hypoalbuminemia). **

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26
Q

What is the clinical presentation of chronic renal failure?

A

Azotemia and uremia progressing for years, end result of all chronic renal diseases.

Presents as:
- hyperkalemia
- acidosis
- azotemia
- hypertension
- renal osteodystrophy
- anaemia

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27
Q

What is uremia?

A

Build up of toxins in the blood

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28
Q

What is azotemia?

A

Build up of nitrogenous products, creatinine and other waste products in the blood.

29
Q

What is the clinical presentation of rapidly progressive glomerulonephritis?

A

Acute nephritis, proteinuria and acute renal failure with microscopic hematuria, dysmorphic red blood cells and casts in the urine.

30
Q

What is the clinical manifestation of asymptomatic hematuria or proteinuria?

A

Glomerular hematuria
Subnephrotic proteinuria

31
Q

What is the pathology of nephritic syndrome?

A
  1. Inflammation of hte glomerulus - reduced barrier integrity
  2. RBCs pass through filtration barrier, as pass through tubules can become dysmorphic
  3. RBCs clump together in renal tubule forming rbc casts
  4. Damaged podocytes cause proteinuria (less than 3.5grams in the day)
  5. Immune cells are attracted to the area and may leak through barrier and into the urine
  6. Inflammation reduces the GFR - result in oliguria, and acute kidney injury (increased creatinine), and azotemia and RAAS activation -which can result in hypertension
32
Q

What are the different pathogenic explanations for glomerular injury?

A

Non-immunological

Immunological - 1.cell mediated (CD4 CD8 inflammatory cells and monocytes) 2.Antibody mediated - in situ immune complex deposition or circulating immune complex deposition
3. Alternative pathway - C3

Deposition of these in the filtration barriers, thickens it and can cause glomerular injury by decreasing GFR

33
Q

What is diabetic nepthopathy?

A

A chronic kidney disease defined by structural and functional changes that result due to microvascular complications associated with long standing or poorly controlled diabetes

Leading cause of chronic kidney disease and end stage renal disease worldwide. 27.5% of diabetic patients will develop ESRD in the UK

34
Q

What is the main risk factor for diabetic nephropathy?

A

Hypertension

35
Q

What are the symptoms associated with diabetic nephropathy?

A

Persistent albuminiuria (first sign) - resulting in peripheral odema (first symptoms)
Decline in GFR
Raised arterial blood pressure

36
Q

What are the three main branches of diabetic nephropathy?

A

Change in biochemistry of the body
1. Metabolic factors
2. Hemmodynamic factors
3. Inflammatory factors

37
Q

What is the role of high blood glucose on biochemistry that leads to diabetic nephropathy? (metabolic pathway)

A
  1. Hyperglycemia
  2. Blood glucose binds with protein forming advanced glycosation end-products (AGEs)
  3. These can bind to RAGE or can act directly to cause
  4. Increased ECM synthesis, increases production of ROS and cross linking with ECM proteins
  5. This results in thickening of the basement membrane and increased mesangial matrix.
38
Q

What is the role of glomerular hypertension in diabetic nephropathy?

A

Results in glomerular hyperfiltration (Causes sclerosis of glomerulus reducing renal blood flow resulting in activation of RAAS)
Increased blood flow into the glomerulus results in increased pressure in the glomerulus
Angiotensin 2 causes vasoconstriction of the efferent arteriole resulting in glomerular capillary hypertension and an increase in glomerular size
The basement membrane becomes thicker to withstand the pressure
results in the leakage of a small amount of albumin across a thicker but more porous basement membrane and decreased GFR

THis is a hemodynamic pathway

39
Q

What is the role of tubuloglomerular feedback in diabetic nephropathy?

A

Hyperglycemia means increased glucose in the proximal convoluted tubule - leads to increased SGLT2 activity so more sodium ion reabsorption
Less sodium ions are delivered to the macula densa cells, low Na+ leads to impaired tubuloglomerular feedback - RAAS activation resulting in a premature increase in GFR.

THis is a hemodynamic pathway

40
Q

What do all three branches of diabetic nephropathy lead to?

A

Three branches - metabolic, inflammatory and haemodynamic
Leads to the production of cytokines, chemokines, endothelial factors and interluekins - this triggers signalling pathways that lead to
Mesangial cell proliferation/expansion
Tubulo-intesinal fibrosis
THickening of BM
Glomerulosclerosis
Podocyte injury
Endothelial cell dysfunction

41
Q

What is the hemodynamic pathway of diabetic nephropathy?

A

Hyperglycemia causes increased glucose load to kidney - results in increased activity of SGLT2, so less Na+ delivery to macular densa - this impairs tubuloglomerular feedback resulting in vasodilation of the afferent arteriole which temporarily increases GFR.
Increased blood volume and pressure in the glomerulus leads to hyperfiltration - this pressure causes sheer damage to the glomerulus (DAMPs can attract immune cells causing inflammatory damage and depositions)
Pressure results in podocyte loss and increased basement membrane permeability to albumin - resulting in albuminuria
Mesangial matrix expansion occurs
Tubular fiboris resulting in decreased GFR and diabetic nephropathy

42
Q

What is the metabolic pathway causes diabetic nephropathy?

A

Hyperglycemia causes increased uptake of glucose and glycolysis in glomerular and tubular cells
Results in AGE formation, accumulation of glycolytic intermediates and overwhelming the mitochondrial membrane - results in accumulation of free radicals causing oxidative stress
This activates pro-inflammatory processes and signalling, attraction of immune cells into the area.
result in deregulation the extracellular matrix - increased deposition in the ECM, this thickness the basement membrane and causes fibrosis
Can cause tubular fibrosis and decreased GFR causing diabetic nephropathy.

43
Q

What are the five different stages of diabetic nephropathy?

A
  1. Very early stage or hyperfiltration
  2. Developing/silent stage
  3. microalbuminuria stage
  4. Overt nephropathy
  5. Uremia
44
Q

What occurs in Stage 1 of diabetic nephropathy?

A

Hyperfiltration stage

Hypertension and hyperglycemia causes hyperfiltration with increased glomerular pressure (activates RAAS)
Causes increased GFR
Glomerular hypertrophy and Increased renal size.

45
Q

What occurs in stage 2 of diabetic nephropathy?

A

Developing/silent stage

Continued hyperfiltration and hypertrophy
GFR remain elevated throughout or return to normal
No evidence of albuminuria
Glomerular damage in the form of basement membrane thickening and mesangial expansion

46
Q

What occurs in stage 3 of diabetic nephropathy?

A

Microalbuminuria stage

Urinary albumin excretion rate increases
Renal functions could be normal or reduced (affect plasma creatinine)
Hypertension develops during this stage (RAAS activation)

47
Q

What occurs in stage 4 of diabetic nephropathy?

A

Overt nephropathy

Urinary albumin excretion is more than 300mg and creatine levels in the blood rise
Have systemic hypertension
If untreated rapidly cycles to develop into renal impairment leading to end-stage renal disease.

48
Q

What is stage 5 of diabetic nephropathy?

A

GFR has fallen to 15ml/min or lower
Require renal replacement therapy

49
Q

What are some symptoms of uremia?

A

Shortness of breath
Ithcing
Fatgiue
Change in mental status (uremia encephalopathy)
Vomitting

50
Q

What are the different types of lesions that can occur due to diabetic nephropathy?

A

Glomerular lesion - diffuse or nodular - glomerulosclerosis
Vascular lesion - renal atherosclerosis (lipid deposition) or renal arteriosclerosis (loss of elastic)
Tubular and interstial lesions - papillary necrosis, tubular atrophy

51
Q

How does a diffuse glomerular lesion in diabetic nephropathy present?

A

Most common type of lesion, involves whole glomeruli

  1. Thickening of glomerular basement membrane
  2. Increased in mesangial matrix and mild proliferation of mesangial cells
  3. Fibrin caps - over between BM and Endothelial cells
  4. Capsular drop (accumulation of plasma proteins)- between BC parietal cells and visceral cells
52
Q

How does a focal/nodular glomerular lesion in diabetic nephropathy present?

A

More specific to type 1 diabetes, develops in 15-30% of patients

  1. Nodule formation that are normally spherical and in the glomerulus. Is a hyaline acelluar mass - this can be called Kimmestiel-Wilson disease

Are identifiable by PAS (periodic Acid Shieff stain) or PAS +ve.

53
Q

What is the pathogenesis of vascular lesions in diabetic nephropathy?

A

Arteriole hyalinosis in the afferent and efferent arteriole ( this is the thickening of the arterial wall with a substance that appears eosinophilic or glass like on H&E staining)
Arteries may also show varying degrees of intimal fibrosis

54
Q

What different tests should be used to assess renal function?

A

Glomerular filtration rate
Urine Albumin: creatininte ratio
Serum creatininte
Serum blood Urea Nitrogen (BUN)
Creatinine clearance
Imaging studies/biopsies of the kidney

55
Q

How does the GFR help assess renal function?

A

Best marker for overall function
Does not indicate cause of disease
Cannot be measured directly so reliant on surrogate markers
GFR changes with age and other physiology such as pregnancy
Stable GFR can be present in disease

56
Q

How does GFR value relate to chronic kidney disease?

A

Is very specific to chronic kidney disease
90 or higher is normal
less than 60 may indicate kidney disease
Bel01 15 indicates renal failure

57
Q

How is urine albumin:creatinine ratio used to assess renal function?

A

Also known as urine microalbumin
Sensitive for glomerular disease/damage
Correlates with cardiovascular risk
3g/24hr higher indicates heavy proteinuria or nephrotic

58
Q

How is serum creatinine used to assess renal function?

A

Creatinine is a chemical waste product from muscle metabolism
Normal is 0.6-1.3mg/dL

59
Q

How is serum blood urea nitrogen used to assess renal function?

A

Urea nitrogen is a waste product
Normal - 6-24mg/dL
Increase suggests kidney dysfunction

60
Q

What treatments are offered for stage 1 diabetic nephropathy?

A

Tight glucose and blood pressure control

61
Q

What treatments are offered for stage 2 diabetic neprhropathy?

A

Tight glucose and blood control
Smoking cessation
Weight reduction
Exercise
Annual eye examination

62
Q

What are the treatments for stage 3 diabetic nephropathy?

A

ACE inhibitors or angiotensin receptor blokcers
Restirction of dietary protein
Anti-hyperlipidemic medications

63
Q

What are the treatments for stage 4 diabetic nephropathy?

A

Treat manifestatino of nephrotic syndrome and chronic renal insufficiency
Prevent anemia
prevention of calcium and phosphorous

64
Q

What are the treatment for stage 5 diabetic nephropathy?

A

Renal replacement therapy.

65
Q

What are the life style and self management for diabtiec nephropathy?

A

Diet
Exercise
Smoking cessation
Weight loss if needed

66
Q

What are the first line drugs in diabetic nephropathy?

A

MetforminSGLT2 inhibitors
RAS blockade
Statin

67
Q

What are the additional drugs offred to diabetics with heart and kidney problems?

A

GLP-1 agonists
Antiplatelet therapies (reduce risk of CVD)
ns-MRA (antagnoist of aldosterone)

68
Q

What are some risk factor controls for diabetic patients with CKD?

A

Lipid management
Glycemic control
Blood pressure control

Unit 10 (37 decks)

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