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CHEM PATH - Abbie > 9. Assessment of renal function / acute and chronic renal failure > Flashcards

9. Assessment of renal function / acute and chronic renal failure Flashcards

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1
Q

What is normal GFR?

A

120 ml/min (7.2 L/hr)

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2
Q

What is the age-related decline of kidney function?

A

1mL/min per year

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3
Q

What is clearance and what is it used for?

A

Clearance is the volume of plasma that can be completely cleared of a marker substance per unit time. Clearance can be used to calculate GFR.

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4
Q

What are three criteria that need to be fulfilled for a marker to be used to measure GFR?

A
  1. Marker is NOT bound to serum proteins. 2. Freely filtered by the glomerulus 3. NOT secreted or reabsorbed by tubular cells. If these conditions are fulfilled, then clearance = GFR
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5
Q

At any one point, clearance =

A

C = (U x V)/P where U = urinary concentration, P = plasma concentration.

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6
Q

Describe inulin

A

5.2 kDa fructose polymer, neutral charge, freely filtered, not processed by tubular cells

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7
Q

Why is inulin only used as a research tool?

A

This is technically the ‘perfect marker’. However, measurement of inulin concentrations is quite difficult and it requires a steady-state infusion.

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8
Q

What is a clinically viable measure of GFR?

A

Single injection plasma clearance measurements using: 51Cr-EDTA, 99Tc-DTPA, lohexol

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9
Q

How to measure GFR using single injection plasma clarance measurements?

A

You administer the injection, then you can either measure the urine collection using a gamma counter or you can take blood samples and look at the progressive reduction in radioactivity. This is still NOT how GFR is measured on a day to day basis. This test is only used under certain circumstances (e.g. if you want to have a good estimate of GFR before starting chemotherapy)

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10
Q

• You would ideally like to use endogenous markers that have similar characteristics to the ideal injectable marker. What are these three charactersitics?

A

Not plasma protein bound, freely filtered by the glomerulus, not modified by the tubules.

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11
Q

Blood urea was the first endogenous marker of GFR and is a by-product of protein metabolism. What are some issues with blood urea as a marker for GFR?

A
  1. Variable (30-60%) reabsorption by tubular cells
  2. Dependent on nutritional state, hepatic function, GI bleeding
  3. Very limited clinical value
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12
Q

Where is serum creatinine derived from, how is it filtered and how is it affected by tubular cells?

A

Derived from muscle cells (small amount from intestinal absorption), freely filtered, actively secreted into the urine by tubular cells.

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13
Q

What is the rate of generation of creatinine affected by?

A

Muscularity, age, sex, ethnicity

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14
Q

What is the Cockcroft-Gault equation?

A

• Derived equation to estimate creatinine clearance (NOT GFR directly).
May overestimate GFR, especially when < 30 mL/min

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15
Q

What is the estimated GFR equation?

A

Complex equation derived from cohort studies (MDRD). Requires information about age, sex, serum creatinine and ethnicity. May underestimate GFR if above average weight and young.

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16
Q

What are current recommendations for GFR?

A

CKD-Epidemiology Collaboration (CKD-EPI). The equation is based on the same four variables as MDRD but models the relationship between GFR and serum creatinine, age, sex and race differently. It is an improvement on MDRD but it is still imprecise at higher GFRs.

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17
Q

What is cystatin C? How is it produced? How is it generated? How is it filtered? How is it affected by tubular cells? What do NICE guidelines say?

A
  1. This is an alternative endogenous marker.
  2. This is constitutively produced by all nucleated cells
  3. It is generated at a constant rate
  4. Freely filtered
  5. Almost completely reabsorbed and catabolised by tubular cells
  6. NOTE: CKD NICE guidelines have included cystatin C, however, it is not used that frequently
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18
Q

Serum creatinine is an insensitive marker of GFR and other endogenous markers (cystatin C) are better, true or false?

A

true

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19
Q

Should GFR be used on a daily basis?

A

No, single injection GFR measurement is reserved for specific situations

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20
Q

What is the best compromise to measure GFR?

A

In practice, estimated GFR/creatinine clearance is the best compromise.

Constant rate infusion GFR measurement is a research tool.

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21
Q

What is the most useful purpose of serum creatinine measurement?

A

to determine change in kidney function within an individual over time

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22
Q

What is urine protein: creatinine ratio?

A

Quantitative assessment of the amount of proteinuria. Measurement of creatinine corrects for urinary concentration.

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23
Q

Spot PCR or 24 hr urine collecction?

A

Spot urine PCR correlates pretty well with 24 hr urine collection. 24 hr Urine Collection is cumbersome and messy. Highly inaccurate without specific patient education. The estimation of proteinuria by 24 hr urine collection has been superseded by PCR.

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24
Q

Types of single sample urine exams:

A

Dipstick testing, microscopic examination, proteinuria quantification, electrolyte estimation

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25
Q

Types of 24 hour collection urine exams:

A

Creatinine clearance estimation, stone forming elements, (proteinuria quantification and electrolyte estimation)

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26
Q

If the dipstick is negative for blood, it reliably excludes haematuria. Haematuria is NOT the only cause of a positive dipstick for blood, what else can be a cause?

A

Haematuria can also be caused by myoglobinuria in cases of rhabdomyolysis

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27
Q

What is specific gracity?

A

a measure of the concentration of the urine (ranges between 1.003 to 1.035 in urine dipstick testing)

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28
Q

How does centrifuge occur in urine microscopy?

A

Centrifuge at 3000 rpm for 5-10 mins

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29
Q

What to look at the sediment for in urine microscopy and centrifuge?

A

Crystals, red blood cell, white blood cells, casts, bacteria

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30
Q

Clinical case: A 50 y/o, known alcoholic, presents generally unwell, seemingly intoxicated, with acute kidney injury. Urine microscopy reveals calcium oxalate crystals, what diagnosis do you expect and explain findings?

A

This is a classic case of ethylene glycol poisoning (anti-freeze). It gets converted to oxalic acid which will then precipitate with calcium in the renal tubules and the ureters.

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31
Q

What are examples of renal imaging?

A
  1. Plain KUB films
  2. IV urogram (Tends to be done more in paediatrics to look for anatomical defects) 3. Ultrasound KUB
  3. CT KUB (FIRST CHOICE for kidney stones)
  4. MRI KUB
  5. Functional imaging (static and dynamic renograms)
    NOTE: renal biopsy is often necessary for various diagnoses which can be ultrasound or CT guided.
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32
Q

Differences between AKI and CKD in terms of decline, reversibility, and treatment target

A

In AKI there is an abrupt decline in GFR and in CKD there is a longstanding decline in GFR. AKI is potentially reversible, CKD is irreversible. Treatment for AKI is targeted to precise diagnosis and reversal of disease. Treatment for CKD is targeted to prevention of complications of CKD and limitation of progression.

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33
Q

What is the definition of an AKI?

A

Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis. (It is a MEDICAL EMERGENCY needing referral to a nephrologist for diagnosis and treatment).

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34
Q

What is the standardised definition of AKI?

A

NHS England standardised the definitions of AKI based on serial measurements of serum Creatinine (sCr) as follows:

  • AKI Stage 1: Increase in sCr by >= 26 μmol/L, or by 1.5 to 1.9x the references sCr
  • AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr
  • AKI Stage 3: Increase in sCr by >=3x the reference sCr, or increase by >=354 μmol/L
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35
Q

Why is one-off creatinine measurements not very useful?

A

You need to see how creatinine changes because it is a relative measure

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36
Q

What is the hallmark of pre-renal AKI?

A

Reduced renal perfusion. This could occur as a generalised reduction over the whole body (e.g. shock) or it could be selective renal ischaemia.

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37
Q

Pre-renal AKI has structural abnormality, true or false?

A

False

38
Q

What is the normal response to reduced circulating volume?

A

Activation of central baroreceptors, activation of RAS, release of vasopressin, activation of sympathetic system

39
Q

What happens as a result of the normal response to reduced circulating volume?

A

Vasoconstriction, increased cardiac output, renal sodium retention

40
Q

What two main mechanisms allow renal blood flow to stay constant over a huge range of pressures?

A

Myogenic stretch and tubuloglomerular feedback.

IMPORTANT: Pre-renal AKI occurs when the normal adaptive mechanisms FAIL to maintain renal perfusion

41
Q

What is the myogenic stretch mechanism?

A

If the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that high pressure into the Bowman’s capsule, thereby keeping the GFR steady

42
Q

What is the tubuloglomerular feedback?

A

High chloride concentration in the early distal tubule (sign of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and reduced chloride level in the distal tubule

43
Q

What are the causes of pre-renal AKI?

A

True volume depletion (e.g. haemorrhage), hypotension, oedematous state, selective renal ischaemia (e.g. renal artery stenosis), drugs affecting renal blood flow.

44
Q

What are examples of drugs that affect renal blood flow thurs causing pre-renal AKI??

A

ACE inhibitors, NSAIDs, calcineurin inhibitors, diuretics

45
Q

How do ACEi cause pre-renal AKI?

A

reduce efferent arteriolar constriction

46
Q

How do NSAIDs cause pre-renal AKI?

A

decrease afferent arteriolar dilatation

47
Q

How do calcineurin inhibitors cause pre-renal AKI?

A

decrease afferent arteriolar dilatation

48
Q

How do diuretics cause pre-renal AKI?

A

affect tubular function, decrease preload

49
Q

Pre-renal AKI vs. acute tubular necrosis

A
  • Pre-Renal AKI is NOT associated with structural renal damage and responds immediately to restoration of circulating volume.
  • Prolonged insult will lead to ischaemic injury (ATN)
  • ATN, on the other hand, does NOT respond to restoration of circulating volume.
  • Epithelial cell casts would be seen in the urine on microscopy
50
Q

What is the hallmark of post-renal AKI?

A

physical obstruction of urine flow

51
Q

What are sites of obstruction?

A

Intra-renal obstruction, ureteric obstruction, prostatic/urethral obstruction, blocked urinary catheter

52
Q

What is the pathophysiology of post-renal AKI?

A

GFR is dependent on the hydraulic pressure gradient, obstruction results in increased tubular pressure, this results in an immediate decline in GFR

53
Q

Immediate relief of obstruction restores GFR with no structural damage. What can prolonged obstruction result in?

A

Glomerular ischaemia, tubular damage and long-term interstitial scarring

54
Q

In intrinsic renal AKI, pathophysiology is more diverse. Abnormality can be anywhere in the nephron such as:

A

Vascular disease (e.g. vasculitis), glomerular disease (e.g. glomerulonephritis), tubular disease (e.g. ATN), interstitial disease (e.g. analgesic nephropathy)

55
Q

Direct tubular injury (common) is most commonly ischaemic. What endogenous toxins may cause it?

A

Myoglobin, immunoglobulins

56
Q

Direct tubular injury (common) is most commonly ischaemic. What exogenous toxins may cause it?

A

Aminoglycosides, amphotericin, acyclovir

57
Q

What are examples of immune dysfunction causing renal inflammation (common)?***

A

Glomerulonephritis, vasculitis

58
Q

What are examples of infiltration/abnormal protein deposition?

A

Amyloidosis (causes nephrotic syndrome), lymphoma, myeloma-related renal disease

59
Q

Patient has a new onset AKI. Presenting symptoms: dark, brown urine, and large purple skin discoloration on leg. What is the likely diagnosis?

A

Rhambdomyolysis. This is what myoglobin looks like in the urine.

60
Q

Q. A 40 year old female presents with a rash (widespread purpura on legs) and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?
A. NSAIDs
B. Systemic vasculitis
C. Amyloidosis
D. Tumour lysis syndrome following chemotherapy for lymphoma
E. Myeloma

A

Purpura is classic of systemic vasculitis

61
Q

What are complications of AKI?

A

Partial recovery of renal function, discharged with increased serum creatinine, discharged requiring chronic dialysis, death (20%)

62
Q

What is the KDIGO definition of AKI?

A

AKI is defined as any of the following (not graded):

  • Increase in sCr by >= 0.3 mg/dl (>+ 26.5 μmol/l)
  • Increase in sCr by >= 1.5 times baseline, which is known or presumed to have occured within the prior 7 days
  • Urine volume < 0.5 ml/kg/h for 6 hours

(also staged for severity)

63
Q

Acute wounds heal via 4 processes, what are they?

A

Haemostasis, inflammation, proliferation, remodelling

64
Q

Why do some AKIs resolve and others don’t?

A

Pathological responses are characterised by an imbalance between scarring and remodelling. Replacement of renal tissue by scar tissue results in chronic disease.

65
Q

What are the stages of CKD and what is the GFR in ml/min?

A

Stage 1 - Kidney damage with normal GFR - >90; stage 2 - mild decrease in GFR - 60-89; stage 3 - moderate decrease in GFR - 30-59; stage 4 - severe decrease in GFR - 15-29; stage 5 - end-stage kidney failure - <15 or dialysis.

66
Q

What is the prevalence of each stage?

A

Stage 1 - 3.3 %, stage 2 - 3%, stage 3 - 4.3%, stage 4 - 0.2%, stage 5 - 0.2%

67
Q

Why does stage 3 have a lower prevalence than stages 1 and 2 of CKD?

A

Stages 1 and 2 are undiagnosed

68
Q

CKD common risk factors:

A

Diabetes mellitus, atherosclerotic renal disease, hypertension, chronic glomerulonephritis, infective or obstructive uropathy, polycystic kidney disease

69
Q

List 5 normal roles of the kidney

A

Excretion of water-soluble waste, water balance, electrolyte balance, acid-base homeostasis, endocrine functions (EPO, RAS, Vitamin D)

70
Q

What are the consequences of CKD?

A
  1. Progressive failure of homeostatic function -> acidosis, hyperkalaemia;
  2. progressive failure of hormonal function -> anaemia and renal bone disease;
  3. cardiovascular disease -> vascular calcification and uraemic cardiomyopathy;
  4. uraemia and death
71
Q

What is renal acidosis?

A

Metabolic acidosis, failure of renal excretion of protons

72
Q

What does renal acidosis result in?

A

Muscle and protein degradation, osteopaenia due to mobilisation of bone calcium (because protons can be stored in bone), cardiac dysfunction

73
Q

What is the treatment for renal acidosis?

A

Oral sodium bicarbonate

74
Q

What is the most common consequence of CKD especially amongst diabetics?

A

Hyperkalaemia - causes membrane depolarisation and impacts cardiac function, muscle function

75
Q

What medications can cause hyperkalaemia in those with CKD?

A

ACE inhibitors, spironolactone, potassium-sparing diuretics

76
Q

Why does anaemia of chronic renal disease occur?

A

Progressive decline in EPO-producing cells with loss of renal parenchyma, usually occurs when GFR < 30 ml/min

77
Q

How can you distinguish anaemia of chronic renal disease with other causes of anaemia?

A

Causes normochromic, normocytic anaemia

78
Q

What is treatment for anaemia of chronic renal disease?

A

Use artificial erythropoiesis-stimulating agents: erythropoietin alfa (Eprex), erythropoietin beta (NeoRecormon), darbopoietin (Aranesp)

79
Q

Reasons for CKD not responding to an erythropoiesis-stimulating agent?

A

Iron deficiency, TB, malignancy, B12 and folate deficiency, hyperparathyroidism

80
Q

What is renal bone disease?

A

Result of CKD. Complex entity resulting in reduced bone density, bone pain and fractures, includes osteitis fibrosa cystica, osteomalacia, dynamic bone disease and mixed osteodystrophy

81
Q

What is the pathophysiology of renal bone disease (in CKD patients)?

A
  1. Unable to excrete phosphate from the kidneys. Also unable to make activated vitamin D.
  2. The phosphate retention stimulates production of FGF23 and Klotho which also lowers the levels of activated vitamin D.
  3. In an attempt to get rid of phosphate, the body will produce PTH (hyperparathyroidism)
  4. In addition, to try to increase activated vitamin D, PTH will be increased (i.e. there are two stimuli that are driving PTH release up)
  5. The increased phosphate in the blood will complex with calcium, which lowers the amount of free calcium in the blood
  6. In response to the high levels of circulating PTH, the bone will become resistant to PTH
82
Q

Osteitis fibrosa cystica is an effect of CKD. What is it?

A

Caused by osteoclastic resorption of calcified bone and replacement by fibrous tissue. This is a feature of hyperparathyroidism.

83
Q

Osteomalacia is an effect of CKD. What is it?

A

Characterised by insufficient mineralisation of the bone osteoid because the body is trying to mobilise the calcium from the bone.

84
Q

Adynamic bone disease is an effect of CKD. What is it?

A

Excessive suppression of PTH (from overtreatment) results in low turnover and reduced osteoid

85
Q

What treatments can be used for renal bone disease?

A

Phosphate control (lower it), through diet and phosphate binders. Vitamin D receptor activators such as 1-alpha calcidol and paricalcitol. Direct PTH suppression such as cinacalcet which works by increasing the sensitivity of the calcium-sensing receptors

86
Q

What is the most important consequence of CKD and likely to kill pt?

A

Cardiovascular disease

87
Q

What is the risk of CVD in CKD?

A

The risk of a cardiac event seems to be directly related to GFR. Traditional risk factors such as cholesterol and hypertension contribute towards the risk.

88
Q

How do you characterise renal vascular lesions?

A

Heavily calcified plaques (rather than traditional lipid-rich atheroma)

89
Q

What are the three phases of uraemic cardiomyopathy?

A

LV hypertrophy, LV dilatation, LV dysfunction

90
Q

What are the options for people with progressive CKD?

A

Transplantation, haemodialysis, peritoneal dialysis.

91
Q

Briefly explain how haemodialysis works.

A

Blood is passed through a dialyser which removed most waste products. It is done about 3 x per week for around 6 hours. You can have home dialysis.

92
Q

Briefly explain how peritoneal dialysis works.

A

This can be done at home. The peritoneal cavity is filled with fluid and the peritoneal membrane is used as the dialysing membrane.

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