Urinary: Pathology Flashcards

1
Q

Which areas can pathology in kidney affect?

A
  • Glomerulus
  • Tubular compartment
  • Interstitium
  • Vascular
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2
Q

What can the glomerular filter leaking cause?

A
  • Proteinuria
  • Haematuria

One or both

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3
Q

What is area of the glomerulus is affected in nephrotic syndrome?

A

Podocyte/Sub-epithelial damage

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4
Q

How is nephrotic syndrome managed?

A

Oedema - Salt and fluid restriction, diuretics
Proteinuria - ACE inhibitors
Hypercholesteraemia - Statins

Treat the underlying cause

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5
Q

What are the common primary causes of nephrotic syndrome?

A
  • Minimal change glomerulonephritis
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
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6
Q

What are the features of minimal change glomerulonephritis?

A
  • Usually arises in childhood and adolescence.
  • Responds to steroid but may recur if the steroid are stopped
  • Doesn’t usually progress to renal failure
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7
Q

What is minimal change glomerulonpehritis?

A
  • Damage to podocyte layer so patient can’t selectively filter so proteins pour out of the glomerulus.
  • Thought to be immune associated
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8
Q

What is focal segmental glomerulosclerosis?

A
  • Damage to podocyte layer so patient can’t selectively filter so proteins pour out of the glomerulus.
  • Heals by scarring after being damaged by circulating factors in the blood (haven’t found out which it is)
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9
Q

What are the features of focal segmental glomerulosclerosis?

A
  • Scarring of the glomerulus occurs
  • Less effectively treated by steroids
  • Progression rapidly to renal failure
  • Patients can get FSGS even after they have a kidney transplant
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10
Q

What is membranous glomerulonephritis?

A
  • Autoimmune

- Immune complex deposits on sub-epithelial layer causing damage to the podocyte layer

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11
Q

What are the features of membranous glomerulonephritis?

A
  • Rule of thirds
  • Commonest in adults
  • May be secondary for example lymphoma
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12
Q

What are secondary causes of nephrotic syndrome?

A
  • Amyloidosis

- Diabetes Mellitus

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13
Q

What are the pathological changes that occur in diabetes mellitus?

A
  • Hyperfiltation/Capillary hypertension
  • Glomerular basement membrane thickening Mesangial expansion
  • Podocyte injury
  • Glomerular sclerosis
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14
Q

Why does hyperfiltation/capillary hypertension occur in diabetes mellitus?

A

Occurs in early course of disease.Related to hyperglycaemia

  • Increase in glucose levels
  • Upregulates SGLT2 transporter
  • Less glucose passed out in urine
  • Increase in reabsorption of sodium
  • Less sodium gets to the macula densa
  • Less effect on JGA
  • Afferent vasodilation
  • Efferent vasoconstriction
  • Glomerular hypertension occurs as a result
  • GFR increases
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15
Q

What are the risk factors for diabetes mellitus?

A
  • Genetic susceptibility
  • Race
  • Hypertension
  • Hyperglycaemia
  • High level of hyper-filtration
  • Increasing age
  • Duration of diabetes
  • Smoking
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16
Q

What are the stages of of diabetic nephropathy?

A
  1. Hyperfiltration and hypertrophy
  2. Latent stage
  3. Microalbuminuria
  4. Overt proteinuria
  5. ESRD
17
Q

What happens in the latent stage of diabetic nephropathy?

A
  • Normal albuminuria

- GBM thickening and mesangial expansion

18
Q

What happens in the microalbuminuria stage of diabetic nephropathy?

A
  • Variable mesangial expansion/sclerosis
  • Increase GBM thickening
  • Podocyte changes
  • GFR normal
19
Q

What happens in the overt proteinuria phase of diabetic nephropathy?

A
  • Diffuse histopathological changes
  • Systemic hypertension
  • Falling GFR
  • Mesangial expansion/sclerosis leads to reduced surface area for filtration
  • Microvascular changes (hyalinosis of arterioles) leads to tissue ischaemia
20
Q

What is the primary prevention of diabetic nephropathy?

A
  • Tight blood pressure control
  • SGLT2 inhibitors (Reduced hyper-filtration)
  • Statin therapy
  • Cardiovascular risk management (diet, exercise)
  • Moderate protein intake
21
Q

How is diabetic nephropathy managed?

A
  1. Hyper-filtration & hypertrophy – primary prevention
  2. Latent stage – primary prevention
  3. Microalbuminuria -RAAS Blockage to reduced glomerular hyper filtration. Hyperkalaemia limits use with advanced CKD
  4. Overt proteinuria
  5. ESRD
22
Q

What are the clinical features of hypertensive renal disease?

A
  • Microalbuminuria is the first sign
  • Slow and progressive
  • Disease of exclusion (no evidence of hypertensive disease elsewhere)
23
Q

What is the management of hypertension renal disease?

A
  • Slow progression
  • Good BP control
  • ACE inhibitors or angiotensin receptor blockers with albimunuria
24
Q

What are the histoligcal changes that occur in hypertensive nephrosclorosis?

A
  • Vascular changes
  • Fibro-elastic intimal thickening leading to lumen narrowing
  • Hyalinosis of the afferent arterial wall (diabetes affects efferent as well)
  • Secondary insult causing glomerular changes such as wrinkling of glomerulus and glomerulosclerosis
  • Leads to CKD
25
Q

What is renal disease associated with acute severe hypertension?

A
  • Damage to endothelium leading to haematuria
  • Activation of RAAS
  • Glomerulus is punched out so acute kidney injury.
  • Fibrinoid necrosis of arterioles so ischaemia which leads to activation of RAAS
  • Haemolytic anaemia due to shearing of blood vessels
  • Associated with Scleroderma and Haemolytic uraemic syndrome
  • Leads to AKI
26
Q

What are the differentiating factors between hypertensive renal disease and renal vascular disease?

A
  • Hypertension is often more acute in renal vascular disease and refractory to treatment
  • Decline in GFR often more rapid
  • Evidence of atherosclerosis elsewhere
  • Acute worsening with RAAS blockade leads to reduction in GFR even more as kidney thinks its hypovolaemia
27
Q

What are the primary features of nephritic syndrome?

A
  • Loss of protein
  • Blood in urine
  • Acute renal failure usually
  • Hypertensive
  • Low GFR
28
Q

How is nephritic syndrome managed?

A
  • Blood pressure control
  • Treatment of oedema
  • Cardiovascular risk management
  • Disease specific treatment such as immunosuppressant
29
Q

What are the conditions that cause nephritic syndrome?

A
  • Anti-GBM disease

- Vasculitis

30
Q

What are the site affected by glomerular injury?

A
  • Basement membrane
  • Podocyte
  • Sub-epithelial
  • Sub-endothelial
31
Q

What are the causes of haematuria?

A

Blood vessels are commonly injured

Non nephrological

  • IgA Nephropathy
  • Thin glomerular basement membrane nephropathy
  • Hereditary Nephropathy (Alport)

Cancer

  • Renal cell carcinoma (RCC)
  • Upper tract transitional cell carcinoma (TCC)
  • Bladder cancer
  • Advanced prostate carcinoma

Other causes

  • Stones
  • Infection
  • Inflammtion
  • Benign prostatic hyperplasia
32
Q

How is IgA nephropathy managed?

A
  • Can detect abnormal IgA

- No effective treatment. ACE inhibitors can slow it down but not that underlying cause

33
Q

What is IgA nephropathy?

A
  • Commonest glomerular membrane
  • IgA is naturally secreted into mucosal membrane. IgA deposited in the kidney. If you get infected you produce more IgA.
  • IgA is deposited in the mesangium as there is nothing to stop it getting into the mesangium
  • Causes the capillary loop to become fragile as a result which leads to haematuria (visible/invisible)
  • Can also get protein in urine
34
Q

What are the features of thin glomerular basement membrane nephropathy?

A
  • Doesn’t progress

- Benign

35
Q

What is Hereditary Nephropathy (Alport syndrome) ?

A
  • X-linked
  • Abnormal collagen 4
  • Associated with deafness as collagen 4 is used in the ear
  • Abnormal appearing glomerular basement membrane
  • Progress to renal failure
36
Q

What are the symptoms of chronic kidney disease?

A
  • Fatigue / malaise
  • Loss of appetite / Loss of weight
  • Acute illness / recent infection
  • Ankle swelling
  • Haematuria / nocturia
37
Q

What are the symptoms of acute kidney disease?

A
  • Dysuria
  • Change in urine –amount / colour
  • Pain (supra-pubic / loin / joints)
  • S/E of drugs with renal metabolism
  • Nausea & vomiting
  • Ankle swelling / SoB
  • Fatigue / Malaise
  • Fever
38
Q

What are risk factors of acute kidney disease?

A
  • Ishaemic heart disease
  • Hypertension
  • Cerebrovascular disease
  • Known CKD (risk factor for AKI)
  • Diabetes mellitus
  • In younger patient – enuresis in childhood, problems in pregnancy
39
Q

What examination are undertaken for acute kidney disease?

A
  • Blood pressure
  • Urine dipstick
  • Urine microscopy if dipstick positive