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YEAR 5: Chemical Pathology SM > 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.

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3
Q

What are the three stages of AKI?

A

Stage 1: increase in serum creatinine by 1.5-1.9 times baseline

Stage 2: increase in serum creatinine by 2-2.9 times baseline

Stage 3: increase in serum creatinine by >3 times baseline

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4
Q

What is pre-renal AKI?

A

AKI caused by reduced renal perfusion

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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 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
  • Hypotension
  • Oedematous state
  • Selective renal ischaemia (e.g. renal artery stenosis)
  • Drugs affecting renal blood flow
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8
Q

List some drugs that affect renal blood flow.

A
  • ACE inhibitors - reduce efferent arteriolar constriction
  • NSAIDs - decreased afferent arteriolar constriction
  • Calcineurin inhibitors - decrease afferent arteriolar constriction
  • Diuretics - affect tubular funciton 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

What causes post-renal AKI?

A

Physical obstruction of urine flow

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12
Q

List some sites of urine obstruction.

A
  • Intra-renal
  • Ureteric
  • Prostatic/urethral
  • Blocked urinary catheter
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13
Q

Outline the pathophysiology of post-renal AKI.

A
  • GFR is dependent on a hydraulic pressure gradient
  • Obstruction results in increased tubular pressure
  • This results in an immediated decline in GFR
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14
Q

What are some consequences of prolonged renal obstruction?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long-term interstitial scarring
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15
Q

List the possible sites of disease in intrinsic AKI.

A
  • Vascular (e.g. vasculitis)
  • Glomerular (e.g. glomerulonephritis)
  • Tubular (e.g. ATN)
  • Interstitial (e.g. AIN)
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16
Q

What can cause direct tubular injury?

A
  • Ischaemia (MOST COMMON)
  • Endoengous toxins (e.g. myoglobin, immunoglobulin)
  • Exogenous toxins (e.g. aminoglycosides, amphotericin, aciclovir)
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17
Q

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

A
  • Amyloidosis (associated with nephrotic syndrome)
  • Lymphoma
  • Myeloma
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18
Q

List the possible outcomes of AKI.

A
  • Partial recovery of renal function
  • Discharged with increased serum creatinine
  • Discharged requiring chronic dialysis
  • Death
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19
Q

What are the biochemical definitions of AKI?

A
  • Increase in serum creatinine > 26.5µmol/L within 48 hours
  • Increase in serum creatinine > 1.5 times baseline within the previous 7 days
  • Urine volume < 0.5 ml/kg/hr for 6 hours
20
Q

What are the four processes of acute wound healing?

A
  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodelling
21
Q

Why does wound healing matter in AKI

A

Determines Scarring

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

22
Q

How is severity of AKI measured

A

By creatinine (in clinical practice)

and Urine output

23
Q

What are the stages of CKD?

A
  • eGFR - mL/min
  • Stage 1: >90
  • Stage 2: 60-89
  • Stage 3: 30-59
  • Stage 4: 15-29
  • Stage 5: <15
24
Q

List some causes of CKD.

A
  • Diabetes mellitus
  • Hypertension
  • Chronic glomerulnephritis
  • Atherosclerotic renal disease
  • Infective or obstructive uropathy
  • Polycystic kidney disease
25
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)
26
Q

Outline the consequences of CKD.

A
  • Progressive failure of homeostatic function (acidosis, hyperkalaemia)
  • Progressive failure of hormonal function (anaemia, renal bone disease)
  • Cardiovascular disease (vascular calcifiction, uraemic cardiomyopathy)
  • Uraemia and death
27
Q

Why CKD causes acidosis

A

Kidney cannot excrete H+ ions

28
Q

What are the consequences of renal acidosis?

A
  • 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 dysfunction (arrhythmia) (flat P, Tall T, wide QRS)
  • Muscle dysfunction

NOTE: hyperkalaemia causes membrane depolarisation

31
Q

Which medications can cause hyperkalaemia?

A
  • ACE inhibitors
  • Spironolactone
  • Potassium-sparing diuretics
32
Q

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

A

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

NSAIDs will also increase levels ok K

33
Q

What type of anaemia does chronic renal disease cause?

A

Normochromic, normocytic anaemia

34
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 deficiency, malignancy, B12 deficiency etc.

35
Q

Why Anaemia in CKD

A

Less EPO

usually when GFR <30

Often given ESA - erythropoietin stimulating agents
(monthly injection)

36
Q

List some types of renal bone disease.

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

Outline the pathophysiology of renal bone disease.

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
  • To try and get rid of the excess phosphate, the body will produce more PTH
  • Furthermore, to try and increase levels of vitamin D, the body will produce more PTH (i.e. there are two stimuli for PTH release)
  • 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

39
Q

What is adynamic bone disease?

A

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

40
Q

Outline the treatment of renal bone disease.

A
  • Phosphate control - dietary, phosphate binders
  • Vitamin D activators - 1-alpha calcidol, paricalcitol -
    cant activate 25 vit D
  • Direct PTH suppression - cinacalcet (works by increasing the sensitivity of the calcium sensing receptor)
41
Q

What is the most important consequence of CKD?

A

Cardiovascular disease - this is most likely to kill them

Marked calcification of arteries

Uraemic cardiomyopathy

42
Q

What are the three phases of uraemic cardiomyopathy?

A
  • LV hypertrophy
  • LV dilatation
  • LV dysfunction
43
Q

What are the treatment options for patients with CKD?

A
  • Transplantation
  • Haemodialysis
  • Peritoneal dialysis
44
Q

Describe Haemodialysis

A
  • 90% of dialysis
  • 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
45
Q

Describe peritoneal dialysis

A
  • filtration occurs within the patient’s abdomen
  • 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
46
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 SM (29 decks)

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