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YEAR 5: Chemical Pathology PM > ChemPath: Assessment of Renal Function 2 > Flashcards

ChemPath: Assessment of Renal Function 2 Flashcards

1
Q

AKI vs CKD

A

AKI

  • Abrupt decline in GFR
  • Potentially reversible
  • Treatment to precise diagnosis and reversal of disease

CKD

  • Longstanding decline of GFR
  • Irreversible
  • Treatment targeted to prevention of complications and limiting progression
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2
Q

Define AKI.

A

Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis.

It is a medical emergency necessitating referral to a nephrologist for diagnosis and treatment

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3
Q

What are the three stages of AKI, defined by serum creatinine?

A
  • Stage 1: increase in serum creatinine by 1.5-1.9x baseline (or by >26.5 µmol/L)
  • Stage 2: increase in serum creatinine by 2-2.9x baseline
  • Stage 3: increase in serum creatinine by ≥3x baseline
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4
Q

What is pre-renal AKI?

A

AKI caused by reduced renal perfusion

No structural abnormality

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5
Q

Describe the normal response to reduced circulating volume.

A
  • Activation of central baroreceptors and renin-angiotensin system
  • Release of vasopressin
  • Activation of sympathetic system

Results in vasoconstriction, increased cardiac output and renal sodium retention

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6
Q

Name and describe the two autoregulatory mechanisms that maintain renal blood flow despite changes in systemic blood pressure.

A
  • Myogenic stretch - if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that pressure to the glomerulus
  • Tubuloglomerular Feedback - high chloride concentration in the early distal tubule (suggestive of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and, hence, chloride concentration
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7
Q

List some causes of pre-renal AKI.

A
  • True volume depletion (dehydration)
  • Hypotension (e.g. septic shock)
  • Cardiac failure
  • Selective renal ischaemia (e.g. BILATERAL renal artery stenosis)
  • Drugs affecting renal blood flow
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8
Q

List some drugs that affect renal blood flow.

A
  • NSAIDs - decreased afferent arteriolar dilatation
  • Calcineurin inhibitors - decrease afferent arteriolar dilatation
  • ACE inhibitors - reduce efferent arteriolar constriction
  • Diuretics - affect tubular function and decrease preload
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9
Q

What is a consequence of prolonged pre-renal insult?

A

Acute tubular necrosis (ATN)

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10
Q

What might be seen on urine microscopy in a patient with ATN?

A

Epithelial cell casts

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11
Q

List the possible sites of disease in intrinsic (renal) AKI.

A
  • Vascular (e.g. vasculitis)
  • Glomerular (e.g. glomerulonephritis)
  • Tubular (e.g. ATN)
  • Interstitial (e.g. AIN)
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12
Q

What can cause direct tubular injury?

A

Ischaemia (MOST COMMON)

Toxins

  • Endoengous: myoglobin, immunoglobulin
  • Exogenous toxins: aminoglycosides, amphotericin, aciclovir

Ischaemia = pre-renal progressing to ATN

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13
Q

Which diseases can cause intrinsic AKI due to immune dsyfunction?

A
  • Glomerulonephritis e.g. lupus, Goodpasture’s
  • Vasculitis e.g. GPA
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14
Q

Which diseases can cause intrinisc AKI due to infiltration/abnormal protein deposition?

A
  • Amyloidosis (associated with nephrotic syndrome)
  • Lymphoma
  • Myeloma
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15
Q

What causes post-renal AKI?

A

Physical obstruction of urine flow

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16
Q

List some sites of urine obstruction.

A
  • Intra-renal
  • Ureteric
  • Prostatic/urethral
  • Blocked urinary catheter
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17
Q

Outline the pathophysiology of post-renal AKI.

A
  • GFR is dependent on a hydrostatic pressure gradient
  • Obstruction results in increased tubular pressure
  • This results in an immediated decline in GFR
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18
Q

What are some consequences of prolonged renal obstruction?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long-term interstitial scarring

Immediate relief of short-term obstruction restores GFR fully, with no structural damage

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19
Q

What is the most common cause of AKI?
What are 2 important causes of iatrogenic AKI?

A

Decreased renal perfusion is the most common cause of AKI

Iatrogenic causes:
- Medications
- Radiographic contrast

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20
Q

List the possible outcomes of AKI.

A
  • Complete recovery of renal function
  • Partial recovery of renal function
  • Discharged with increased serum creatinine
  • Discharged requiring chronic dialysis
  • Death
21
Q

What are the biochemical definitions of AKI?

A
  • Increase in serum creatinine >26.5µmol/L within 48 hours
  • Increase in serum creatinine >1.5x baseline within the previous 7 days
  • Urine volume < 0.5 ml/kg/hr for 6 hours
22
Q

What are the four processes of acute wound healing?

A
  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodelling
23
Q

Why does wound healing matter in AKI

A

Determines scarring

i.e. whether a patient will recover kindey function or have chronically impaired kidney function

24
Q

What is used to classify CKD and what are the stages?

A

eGFR - mL/min

  • Stage 1: >90
  • Stage 2: 60-89
  • Stage 3: 30-59
  • Stage 4: 15-29
  • Stage 5: <15 or dialysis (end-stage renal failure)
25
Q

List some causes of CKD.

A
  • Diabetes mellitus
  • Atherosclerotic renal disease
  • Hypertension
  • Chronic glomerulnephritis
  • Infective or obstructive uropathy
  • Polycystic kidney disease
26
Q

What are the normal roles of the kidney?

A
  • Excretion of water-soluble waste
  • Water balance
  • Electrolyte balance
  • Acid-base homeostasis
  • Endocrine (EPO, RAS, vitamin D)
27
Q

Outline the consequences of CKD.

A

Failure of homeostasis

  • Acidosis
  • Hyperkalaemia

Failure of endocrine function

  • Anaemia
  • Renal bone disease

Cardiovascular disease

  • Vascular calcifiction
  • Uraemic cardiomyopathy

Uraemia and death

28
Q

Why CKD causes acidosis?
What are the consequences of renal acidosis?

A

Kidney cannot excrete H+ ions

  • Muscle and protein degradation
  • Osteopaenia due to mobilisation of bone calcium
  • Cardiac dysfunction
29
Q

How is renal acidosis treated?

A

Oral sodium bicarbonate

30
Q

What are the consequences of hyperkalaemia?

A
  • Cardiac arrhythmia - flat P, Tall T, wide QRS
  • Muscle dysfunction

NOTE: hyperkalaemia causes membrane depolarisation

31
Q

Which medications can cause hyperkalaemia?

A
  • ACE inhibitors, ARB
  • Potassium-sparing diuretics
32
Q

What other factors may affect a CKD patient’s potassium levels

A

Diet - patients often need to be seen by dietician on a regular basis

NSAIDs will also increase levels potassium levels

33
Q

What is the mechanism of anaemia of chronic kidney disease and what type of anaemia is it?

A

Progessive loss of EPO-producing cells with loss of renal parenchyma
Causes normochromic, normocytic anaemia

34
Q

At what GFR does anaemia of chronic renal disease start to occur?

A

<30 ml/min

35
Q

How is anaemia of chronic renal disease treated?

A
  • Erythropoietin alfa (Eprex)
  • Erythropoietin beta (NeoRecormon)
  • Darbopoietin (Aranesp)

NOTE: if CKD is not responding to erythropoiesis stimulating agents, consider iron, B12, folate deficiency or malignancy

36
Q

List some types of renal bone disease.

A
  • Osteitis fibrosa cystica
  • Osteomalacia
  • Adynamic bone disease
  • Mixed osteodystrophy
37
Q

Outline the pathophysiology of hyperparathyroidism in CKD

A
  • Damaged kidneys are unable to excrete phosphate and activate vitamin D
  • Phosphate retention stimulates the production of FGF-23 and Klotho
  • This lowers the levels of activated vitamin D
  • Low vitamin D levels leads to hypocalcaemia
  • High phosphate and low calcium both stimulate PTH secretion
  • High levels of PTH will result in the bone becoming resistant to PTH
38
Q

What is osteitis fibrosa cystica?

A

Caused by osteoclastic resoprtion of calcified bone and replacement by fibrous tissue (feature of hyperparathyroidism)

Brown tumours seen on X-ray

39
Q

What is adynamic bone disease?

A

Overtreatment leading to excessive suppression of PTH results in low bone turnover and reduced osteoid

Differetiated from osteomalacia because osteoid bone levels are also low (where in osteomalacia they are relatively high)

40
Q

Outline the treatment of renal bone disease.

A

Phosphate control

  • Dietary
  • Phosphate binders

Active vitamin D

  • Alfacalcidol
  • Paricalcitol

Direct PTH suppression

  • Cinacalcet (works by increasing the sensitivity of the CaSR)
41
Q

What is the most important consequence of CKD?

A

Cardiovascular disease - most relevant for CKD related mortality

  • Vascular calcification
  • Uraemic cardiomyopathy
42
Q

How do vascular plaques differ in CKD?

A

In CKD, plaques are characterised by calcification, rather than traditional lipid-rich atheroma

43
Q

What are the three phases of uraemic cardiomyopathy?

A
  • LV hypertrophy
  • LV dilatation
  • LV dysfunction
44
Q

What are the treatment options for patients with CKD?

A
  • Transplantation
  • Haemodialysis
  • Peritoneal dialysis
45
Q

What are the indications for haemodialysis in renal disease?

A
  • Refractory pulomary oedema
  • Refractory hyperkalaemia
  • Refractory acidosis
  • Uraemic symptoms
46
Q

Describe Haemodialysis

A
  • Regular filtration of the blood through a dialysis
  • 8 weeks before the commencement of treatment, the patient must undergo surgery to create an arteriovenous fistula

90% of dialysis

47
Q

Describe peritoneal dialysis

A
  • Filtration occurs within the patient’s abdomen (peritoneal cavity)
  • Dialysis solution is injected into the abdominal cavity through a permanent catheter
  • High dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum
  • After several hours of dwell time, the dialysis solution is then drained, removing the waste products from the body, and exchanged for new dialysis solution
48
Q

Types of peritoneal Dialysis

A

Continuous ambulatory peritoneal dialysis (CAPD) - as described above, with each exchange lasting 30-40 minutes and each dwell time lasting 4-8 hours. The patient may go about their normal activities with the dialysis solution inside their abdomen

Automated peritoneal dialysis (APD) - a dialysis machine fills and drains the abdomen while the patient is sleeping, performing 3-5 exchanges over 8-10 hours each night

YEAR 5: Chemical Pathology PM (27 decks)

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