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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
What are the normal roles of the kidney?
* Excretion of water-soluble waste * Water balance * Electrolyte balance * Acid-base homeostasis * Endocrine (EPO, RAS, vitamin D)
26
Outline the consequences of CKD.
* 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
Why CKD causes acidosis
Kidney cannot excrete H+ ions
28
What are the consequences of renal acidosis?
* Muscle and protein degradation * Osteopaenia due to mobilisation of bone calcium * Cardiac dysfunction
29
How is renal acidosis treated?
Oral sodium bicarbonate
30
What are the consequences of hyperkalaemia?
* Cardiac dysfunction (arrhythmia) (flat P, Tall T, wide QRS) * Muscle dysfunction NOTE: hyperkalaemia causes membrane depolarisation
31
Which medications can cause hyperkalaemia?
* ACE inhibitors * Spironolactone * Potassium-sparing diuretics
32
What other factors may affect a CKD patient's K levels
Diet - Patients often need to be seen by dietician on a regular basis NSAIDs will also increase levels ok K
33
What type of anaemia does chronic renal disease cause?
Normochromic, normocytic anaemia
34
How is anaemia of chronic renal disease treated?
* 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
Why Anaemia in CKD
Less EPO usually when GFR \<30 Often given ESA - erythropoietin stimulating agents (monthly injection)
36
List some types of renal bone disease.
* Osteititis fibrosa cystica * Osteomalacia * Adynamic bone disease * Mixed osteodystrophy
37
Outline the pathophysiology of renal bone disease.
* 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
What is osteitis fibrosa cystica?
Caused by osteoclastic resoprtion of calcified bone and replacement by fibrous tissue (feature of hyperparathyroidism) Brown tumours
39
What is adynamic bone disease?
Overtreatment leading to excessive suppression of PTH results in low bone turnover and reduced osteoid
40
Outline the treatment of renal bone disease.
* 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
What is the most important consequence of CKD?
Cardiovascular disease - this is most likely to kill them Marked calcification of arteries Uraemic cardiomyopathy
42
What are the three phases of uraemic cardiomyopathy?
* LV hypertrophy * LV dilatation * LV dysfunction
43
What are the treatment options for patients with CKD?
* Transplantation * Haemodialysis * Peritoneal dialysis
44
Describe Haemodialysis
* 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
Describe peritoneal dialysis
* 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
Types of Peritoneal Dialysis
* **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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