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Chemical Pathology - Path > Assessment of renal function 2 > Flashcards

Assessment of renal function 2 Flashcards

1
Q

What are the main differences between AKI and CKD?

A

AKI:

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

CKD:

  • Longstanding decline in GFR
  • Irreversible
  • Treatment targeted to prevention of complications of CKD and limitation of progression
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2
Q
  1. Define Acute kidney injury (AKI)
A

AKI is defined as a rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis.

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3
Q

What are the stages of AKI, by serial measurements of serum creatinine?

A
  • AKI Stage 1: Increase in sCr by ≥26 µmol/L, or by 1.5 to 1.9x the reference 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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4
Q

What are the 3 types of AKI?

A
  • Pre-renal
  • Intrinsic renal
  • Post-renal
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5
Q

Describe the hallmark features of pre-renal AKI

A
  • Hallmark is reduced renal perfusion
    • as part of generalized reduction in tissue perfusion
    • or selective renal ischaemia
  • No structural abnormality
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6
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 –>
  • Vasoconstriction, increased cardiac output, renal sodium retention

Pre-renal AKI occurs when normal adaptive mechanisms fail to maintain renal perfusion

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7
Q

How is renal perfusion pressure controlled?

A

Renal perfusion pressure normally controlled by two autoregulation intrarenal phenomena. The myogenic response means the afferent arteriole constricts with elevation in systemic pressure and dilates with reduction in systemic pressure. The tubuloglomerular feedback mechanism means that an increase in chloride ions in the early distal tubule, which is caused by an increase in GFR, leads to afferent arteriole constriction and hence a decrease in GFR and a decrease in chloride ions in the distal tubule.

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8
Q

What are the causes of pre-renal AKI?

A
  • True volume depletion
  • Hypotension
  • Oedematous states
  • Selective renal ischaemia
  • Drugs affecting glomerular blood flow
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9
Q

What does this image show?

A

Renal artery stenosis

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10
Q

Which class of drugs may predispose patients to developing pre-renal AKI?

A.NSAIDs

B.Calcineurin inhibitors

C.ACEi or ARBs

D.Diuretics

E.All of the above

A

E. All of the above

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11
Q

Describe how the following drugs potentially lead to developing pre-renal AKI?

  1. NSAIDs
  2. Calcineurin inhibitors
  3. ACEi or ARBs
  4. Diuretics
A
  1. NSAIDs - decrease afferent arteriolar dilatation
  2. Calcineurin inhibitors - decrease afferent arteriolar dilatation
  3. ACEi or ARBs - decrease efferent arteriolar constriction
  4. Diuretics – affect tubular function, decrease preload
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12
Q

Describe the differences between Pre-renal AKI and acute tubular necrosis

A
  • Pre-Renal AKI is not associated with structural renal damage and responds immediately to restoration of circulating volume
  • Prolonged insult leads to ischaemic injury in Pre-renal AKI
  • Acute Tubular Necrosis does not respond to restoration of circulating volume
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13
Q

Define acute tubular necrosis and most common causes

A

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. Common causes of ATN include low blood pressure and use of nephrotoxic drugs.

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14
Q

A 68 year old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys. What is the likely cause of his AKI?

A.Right-sided kidney stone

B.Left ureteric transitional cell carcinoma

C.Membranous glomerulonephropathy

D.Benign prostatic hypertrophy

E.Amyloid

A

A. Right sided kidney stone

The image shows hydronephrosis of the kidney, which can occur in both kidneys if one is obstructed by, for example, a kidney stone

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15
Q
  1. What is the hallmark of post-renal AKI?
  2. What are some common causes of post-renal AKI?
A
  1. Hallmark is physical obstruction to urine flow
  2. Common causes
  • (Intra-renal obstruction)
  • Ureteric obstruction (bilateral)
  • Prostatic / Urethral obstruction
  • Blocked urinary catheter
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16
Q

What is obstrcutive uropathy and what can it lead to?

A

Obstructive uropathy is blockage of urinary outflow, which can affect one or both kidneys

Obstruction can lead to hydronephrosis which dilation of the renal pelvis, and affect both kidneys

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17
Q

What is the pathophysiology of obstructive uropathy?

A
  • GFR is dependent on hydraulic pressure gradient
  • Obstruction results in increased tubular pressure
  • Immediate decline in GFR
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18
Q

What are the risk factors for developing obstructive uropathy?

A
  • benign prostatic hyperplasia (BPH)
  • constipation
  • medication (anticholinergic agents, narcotic analgesia, alpha receptor agonists)
  • urolithiasis (ureteric calculi)
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19
Q
  1. What is immediate management for obstructive uropathy?
  2. What can it lead to if not treated?
A
  1. Treatment is immediate relief of osbtruction, which in most cases restores GFR fully, with no structural damage
  2. Prolonged obstruction results in structural damage:
  • Glomerular ischaemia
  • Tubular damage
  • Long term interstitial scarring
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20
Q

Describe instrinsic ‘renal’ AKI

A

Pathophysiologically more diverse group

May represent abnormality of any part of nephron

–Vascular Disease e.g. vasculitis

–Glomerular Disease e.g. glomerulonephritis

–Tubular Disease e.g. ATN

–Interstitial Disease e.g. analgesic nephropathy

21
Q

Describe some common mechanims of DIRECT tubular injury

A
  • Most common ischaemic
  • Endogenous toxins
    • Myoglobin
    • Immunoglobulins
  • Exogenous toxins - contrast, drugs
    • Aminoglycosides
    • Amphotericin
    • Aciclovir
22
Q

A 40 year old female presents with a rash 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

B. systemic vasculitis

23
Q

What arecommon mechanisms of renal injury?

A
  • Immune dysfunction causing renal inflammation
  • Glomerulonephritis
  • Vasculitis

Infiltration / Abnormal protein deposition

  • Amyloidosis
  • Lymphoma
  • Myeloma-related renal disease
24
Q

What two measures do we use to define severity of acute kidney injury?

A

Urine output and serum creatinine levels

25
Q

Describe how AKI damage is resolved - some AKI resolves and some don’t

A

•Acute wounds heal via four phases:

  • Haemostasis
  • Inflammation
  • Proliferation
  • Remodeling
  • Pathological responses to renal injury are characterized by imbalance between scarring and remodeling
  • Replacement of renal tissue by scar tissue results in chronic disease
26
Q

What are the stages of CKD?

A
27
Q

What are the commonest causes of CKD?

A
  • Diabetes
  • Atherosclerotic renal disease
  • Hypertension
  • Chronic Glomerulonephritis
  • Infective or obstructive uropathy
  • Polycystic kidney disease
28
Q

What are the roles of the kidney?

A
  • Excretion of water-soluble waste
  • Water balance
  • Electrolyte balance
  • Acid-base homeostasis
  • Endocrine functions

EPO, RAS, Vit D

29
Q

What are the consequences of CKD?

A

1]Progressive failure of homeostatic function

  • Acidosis
  • Hyperkalaemia

2]Progressive failure of hormonal function

  • Anaemia
  • Renal Bone Disease

3]Cardiovascular disease

  • Vascular calcification
  • Uraemic cardiomyopathy

4]Uraemia and Death

30
Q

Describe renal acidosis and what it can result in, and treatment

A
  • Metabolic acidosis
  • Failure of renal excretion of protons
  • Results in:
  • Muscle and protein degradation
  • Osteopenia due to mobilization of bone calcium
  • Cardiac dysfunction

•Treated with oral sodium bicarbonate

31
Q

Regarding hyperkalaemia, which of the following is true

A.It can lead to ECG changes such as peaked p waves and flattened t waves.

B.In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.

C.NSAIDs can lower potassium levels

D.Hyperaldosteronism is a common cause

E.All of the above

A

B.In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.

32
Q
  1. Whats the importance of potassium?
  2. What are the common causes of hyperkalaemia?
A

1.

Potassium is the major intracellular cation

Hyperkalaemia causes membrane depolarization

  • Cardiac function
  • Muscle function
  1. Common causes:

Common sequelae of CKD

Especially among diabetics

Medications

  • ACEi
  • Spironolactone
  • ’Potassium-sparing’ diuretics
33
Q

Describe the changes on ECG for hyperkalaemia

A
34
Q

Describe anaemia of chronic renal disease

A
  • Progressive decline in erythropoietin-producing cells with loss of renal parenchyma
  • Usually noted when GFR<30mL/min
  • Normochromic, normocytic anaemia
  • Distinguish from other causes of anaemia, which are common

–iron deficiency

–B12 and/or folate deficiency

35
Q

Name some common erythropoiesis-stimulating agents (ESAs)

A
  • Erythropoietin alfa (Eprex)
  • Erythropoietin beta (NeoRecormon)
  • Darbopoietin (Aranesp)
36
Q

Your patient with CKD has been started on an ESA but does not respond. What could be the cause?

A.Iron deficiency

B.TB

C.Malignancy

D.B12 and folate deficiency

E.Hyper-parathyroidism

F.Any of the above

A

F. Any of the above

37
Q

What can happen in renal bone disease?

A

Complex entity resulting in reduced bone density, bone pain and fractures:

  • Osteitis fibrosa
  • Osteomalacia
  • Adynamic bone disease
  • Mixed osteodystrophy
38
Q

How does hyperparathyroidism develop in CKD?

A
  • CKD causes phosphate retention and low levels of 1,25(OH)2D3 (precursor to vitamn D)
  • Both of these changes causes hypocalcemia
  • To increase Ca, hyperparathyroidism occurs
39
Q

What is osteitis fibrosa?

A

Osteoclastic resorption of calcified bone and replacement by fibrous tissue

Can occur due to hyperparathyroidism

40
Q

What does this image show?

A

Osteitis fibrosa

41
Q

What is osteomalacia?

A

Insufficient mineralization of bone osteoid

42
Q

What does this image show?

A

Osteomalacia

43
Q

What is adynamic bone disease?

A

Excessive suppression of PTH results in low turnover and reduced osteoid

44
Q

How is renal bone disease managed/treated?

A

•Phosphate control

  • Dietary
  • Phosphate binders

Vit D receptor activators

  • 1-alpha calcidol
  • Paricalcitol

•Direct PTH suppression

  • Cinacalcet - calcimimetic and activates the Ca senor receptors
45
Q

What are the two main cardiovascular disease consequences of CKD?

A
  • Vascular calcification
  • Uraemic cardiomyopathy

The most important group of consequences of CKD

  • Risk of cardiac event is directly predicted by GFR
46
Q

What is vascular calcification?

A

Calcified plaques that build up in cardiac vasculature. More commonly seen in renal vascular lesions than the traditional lipid-rich atheroma in obese, high cholesterol risk individuals

47
Q
  1. What is uraemic cardiomyopathy?
  2. What are the three phases?
A
  1. pathological cardiac hypertrophy, indicating the influence of impaired renal function on the myocardium.
  2. Three phases
  • Left ventricle hypertrophy
  • LV dilation
  • LV dysfunction

Can lead to cardiac arrhythmias

48
Q

Say whether the following are contraindicated for a kidney transplant

  1. HIV positive
  2. BMI >30
  3. Active sepsis
  4. Aged above 65 years
  5. Any malignant disease
A
  1. NO
  2. NO
  3. YES
  4. NO
  5. YES
49
Q

What are the main two types of dialysis?

A
  • Haemodialysis
  • Peritoneal dialysis

Chemical Pathology - Path (18 decks)

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