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PATH FINAL > ChemPath: Assessment of Renal Function 2 > Flashcards

ChemPath: Assessment of Renal Function 2 Flashcards

1
Q

Distinguish between AKI and CKD

A

AKI
* Abrupt decline in GFR
* Defined and staged using serum creatinine and urine output
* Potentially reversible
* Tx targetted to precise dx + reversal of disease

CKD
* Longstsanding decline in GFR
* Defined and graded using GFR
* Irreverisble
* Tx targeted to prevent complications and limit 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

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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 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
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5
Q

3 broad causes of AKI

A

Pre-renal (commonest)
Renal
Post-renal

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6
Q

What is pre-renal AKI?

A

AKI caused by reduced renal perfusion (either by generalised reduction in tissue perfusion OR selective renal ischaemia) WITH NO structural abnormality

AKI occurs when normal adaptive mechanisms of kidneys fail. Note that kidneys are good at maintainig adequate profusion even as pressure lowers due to RAAS + activation of sympathic nervous sytem. However when pressure lowers so much these adaptive mechanisms no longer compensate ==> pre-renal AKI!

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7
Q

Describe the normal renal 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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8
Q

List some causes of pre-renal AKI.

A
  • True volume depletion (severe dehydration)
  • Hypotension (e.g. blood loss = generalised low tissue perfusion)
  • Oedematous state (e.g. heart failure where fluid is stuck in wrong place hence low perfusion)
  • Selective renal ischaemia (e.g. renal artery stenosis)
  • Drugs affecting renal blood flow
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9
Q

List how common drugs (ACEi/ARBs, NSAIDs, Diuretics, CalcineurinI) may cause a pre-renal AKI.

A
  • ACE inhibitors - reduce efferent arteriolar dilatation
  • NSAIDs - decreased afferent arteriolar constriction
  • Calcineurin inhibitors - decrease afferent arteriolar constriction
  • Diuretics - affect tubular funciton and decrease preload
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10
Q

Broad treatment regime for AKI

A

Responds well to restoration of normal circulating volume and perfusion to kidney.

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11
Q

What is a consequence of prolonged pre-renal insult?

A

Acute tubular necrosis (ATN)
= ischaemia results in renal necrosis and no longer responds to restoration of circulating volume

ATN is NOT a type of pre-renal AKI as it involves structural abnormalities (necrosis) in kidney.

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12
Q

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

A

Epithelial cell casts

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13
Q

List the possible sites of disease in renal AKI.

A
  • Vascular (e.g. vasculitis)
  • Glomerular (e.g. glomerulonephritis)
  • Tubular (e.g. ATN)
  • Interstitial (e.g. AIN)
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14
Q

List the 3 main pathophysiological pathways resulting in renal AKI

A
  • Direct tubular injury
  • Immune dysfunction causing renal impairment
  • Infiltration of abnormal protein deposits
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15
Q

What can cause direct tubular injury in renal AKI?

A
  • Ischaemia (MOST COMMON)
  • Endoengous toxins (e.g. myoglobin in rhabdomyolisis, immunoglobulin in myeloma)
  • Exogenous toxins (e.g. aminoglycosides, aciclovir)
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16
Q

Diseases that can cause renal AKI through immune dysfunction

A

Glomerulonephritis
Vasculitis (rash + AKI!)

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17
Q

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

A
  • Amyloidosis (associated with nephrotic syndrome)
  • Lymphoma (plasma cell infiltration)
  • Myeloma (plasma cell infiltration - note that myeloma can cause renal AKi in two diff ways)
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18
Q

What causes post-renal AKI?

A

Physical obstruction of urine flow

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19
Q

List some sites of urine obstruction.

A
  • Intra-renal (stones in PUJ)
  • Ureteric (stones - unilateral usually)
  • Prostatic/urethral (bilateral changes seen)
  • Blocked urinary catheter
20
Q

Outline the pathophysiology of post-renal AKI.

A
  • GFR is dependent on a hydraulic pressure gradient (high pressure in blood but low in filtrate)
  • Obstruction results in increased tubular pressure (increased pressure in filtrate)
  • This results in an immediated decline in GFR and rise in serum creatinine
21
Q

What happens to GFR in cases where there is immediate removal of obstruction

A

GFR returns to normal with NO structural damange to kidneys

22
Q

What are some consequences of prolonged renal obstruction?

A
  • Glomerular ischaemia
  • Tubular damage
  • Long-term interstitial scarring
23
Q

List the possible outcomes of AKI.

A
  • Partial recovery of renal function
  • Discharged with increased serum creatinine
  • Discharged requiring chronic dialysis
  • Death
24
Q

Why do some AKIs solve and others do not and result in renal damage

A

Some patients have a pathological response to AKI characterised by imbalance between scarring and remodelling. Replacement of renal tissue by scar tissue therefore leads to chronic disease.

25
Q

What are the stages of CKD?

A

BASED ON GFR:
* Stage 1: >90
* Stage 2: 60-89
* Stage 3: 30-59
* Stage 4: 15-29
* Stage 5: <15

26
Q

What else must be interpreted with GFR to predict risk of adverse outcomes in CKD

A

Interpret GFR alongisde Albumin:Creatinine ratio

27
Q

List some causes of CKD.

A
  • Diabetes mellitus (commonest!!)
  • Hypertension
  • Chronic glomerulnephritis (younger cohort)
  • Atherosclerotic renal disease
  • Infective or obstructive uropathy (acute on chronic usually from prostastic disease)
  • Polycystic kidney disease

increasing in incidence and prevalence

28
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)
29
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
30
Q

Why may renal acidosis occur in CKD and what are its consequences?

A

Renal acidosis may occur due to decreased renal excretion of H+

Concequences
* Muscle and protein degradation
* Osteopaenia due to mobilisation of bone calcium
* Cardiac dysfunction

31
Q

How is renal acidosis treated?

A

Oral sodium bicarbonate

32
Q

Why may hyperkalaemia occur in CKD and what are its consequences?

A

Decreased excretion of K+ (coupled with increase K+ in diet alongisde medications)

Concequences
* Cardiac dysfunction (arrhythmia)
* Muscle dysfunction

NOTE: hyperkalaemia causes membrane depolarisation

33
Q

Which medications can exacerbate hyperkalaemia in CKD patients?

A
  • ACE inhibitors
  • Potassium-sparing diuretics (e.g. spironolactone)
34
Q

What type of anaemia does chronic renal disease cause?

A

Normochromic, normocytic anaemia

35
Q

How can CKD result in anaemia

A

Loss of renal parenchyma decreases EPO producing cells therefore decrease in EPO release.

This is noted when GFR falls below 30.

36
Q

How is anaemia of chronic renal disease treated?

A

Erythropoesis Stimulating Agent (ESA)

  • 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.

37
Q

List some types of renal bone disease.

A
  • Osteititis fibrosa cystica
  • Osteomalacia
  • Adynamic bone disease
  • Mixed osteodystrophy
38
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 FDF23 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
39
Q

What is osteitis fibrosa cystica?

A

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

40
Q

What is osteomalacia

A

Decreased bone mineralisation due to decreased Vitamin D

41
Q

What is adynamic bone disease?

A

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

42
Q

Outline the treatment of renal bone disease.

A
  • Phosphate control - dietary, phosphate binders
  • Vitamin D activators - Alfacalcidol (1-alpha calcidol - can bypass the renal 1-α-hydroxylase due to its pre-existing hydroxyl group so just requires liver 25 hydroxylase to be activated),
  • Direct PTH suppression - cinacalcet (works by increasing the sensitivity of the calcium sensing receptor)
43
Q

What complication from CKD has the highest mortality?

A

Cardiovascular disease due to vascular calcification and subsequent atherosclerosis - this is most likely to kill patients with CKD

44
Q

What are the three phases of uraemic cardiomyopathy?

A
  • LV hypertrophy
  • LV dilatation
  • LV dysfunction
45
Q

What are the treatment options for patients with CKD?

A
  • Transplantation
  • Haemodialysis
  • Peritoneal dialysis (uses peritoneum as dialysis membrane)
46
Q

Contraindicaiton for renal transplant

A

Active sepsis

(BMI>30, HIV, Age are NOT contraindicaitons!)

PATH FINAL (36 decks)

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