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Yr 4 - CCC > Renal: CKD & AKI > Flashcards

Renal: CKD & AKI Flashcards

1
Q

Give some causes of CKD

A

1) Diabetes
2) HTN
3) Medications (e.g. NSAIDs or lithium)
4) Glomerulonephritis
5) Polycystic kidney disease

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2
Q

Presenation of CKD?

A
  • Often asymptomatic
  • Fatigue
  • Pallor (due to anaemia)
  • Foamy urine (proteinuria)
  • Nausea
  • Loss of appetite
  • Pruritus (itching)
  • Oedema e.g. ankle swelling, weight gain
  • Hypertension
  • Peripheral neuropathy
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3
Q

What is estimated glomerular filtration rate (eGFR)?

A

It estimates the glomerular filtration rate (the rate at which fluid is filtered from the blood into Bowman’s capsule).

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4
Q

How is proteinuria quantified in CKD?

A

with a urine albumin:creatinine ratio (ACR).

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5
Q

What sample should be used for assessing proteinuria in CKD?

A

should be a first-pass morning urine specimen

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6
Q

What ACR is defined as clinically important proteinuria?

A

a confirmed ACR of 3 mg/mmol or more

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7
Q

What ACR is:
a) Normal to mildly increased
b) Moderately increased
c) Severely increased

A

a) <3
b) 3-30
c) >30

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8
Q

How can haematuria be assessed?

A

urine dipstick or microscopy.

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9
Q

Microscopic vs macroscopic haematuria?

A

Microscopic haematuria is when blood is identified on testing but not visible on inspection.

Macroscopic haematuria refers to visible blood in the urine.

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10
Q

What can haematuria indicate?

A

Infection, malignancy (e.g., bladder cancer), glomerulonephritis or kidney stones.

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11
Q

What investigations are required in CKD?

A

1) Renal ultrasound helps identify obstructions (e.g., kidney stones or tumours) and polycystic kidney disease.

2) Blood pressure (for hypertension)

3) HbA1c (for diabetes)

4) Lipid profile (for hypercholesterolaemia)

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12
Q

When can a diagnosis of CKD be made?

A

A diagnosis can be made when there are consistent results over three months of either:

1) Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2

2) Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol

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13
Q

CKD can be classified according to a ‘G score’ and an ‘A score’.

What is the G score based on?

What is the A score based on?

A

G score based on eGFR

A score based on the albumin:creatinine ratio.

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14
Q

Describe G stage 1 to 5 in CKD

A

G1: eGFR >90
G2: 60-80
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: under 15

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15
Q

Describe A stage 1 to 3 in CKD

A

A1: ACR under 3 mg/mmol

A2: 3-30 mg/mmol

A3: Above 30 mg/mmol

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16
Q

What is accelerated progression in CKD?

A

a sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2.

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17
Q

Complications of CKD?

A

1) Anaemia
2) Renal bone disease
3) Cardiovascular disease
4) Peripheral neuropathy
5) End-stage kidney disease
6) Dialysis-related complications

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18
Q

Most significant cause of anaemia in CKD?

A

reduced erythropoietin (EPO) levels.

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19
Q

What type of anaemia does CKD cause?

A

This is usually a normochromic (normal colour) normocytic (normal size) anaemia

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20
Q

At what eGFR does anaemia typically become apparent in CKD?

A

when the GFR is less than 35 ml/min (other causes of anaemia should be considered if the GFR is > 60 ml/min).

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21
Q

What does anaemia in CKD predispose to?

A

To the development of left ventricular hypertrophy (associated with a three fold increase in mortality in renal patients)

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22
Q

What is EPO?

A

A hormone produced by the kidneys that stimulates erythropoiesis in the bone marrow

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23
Q

How does reduced EPO in CKD lead to anaemia?

A

EPO is produced by the kidneys.

In CKD, there is less EPO reduced, meaning reduced RBC production.

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24
Q

Give some ways the CKD can cause bone problems

A

1) low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)

2) high phosphate

3) low calcium: due to lack of vitamin D, high phosphate

4) secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

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25
Q

Treatment of anaemia in CKD?

A

Erythropoiesis-stimulating agents, such as recombinant human erythropoietin.

Blood transfusions can sensitise the immune system (allosensitization), increasing the risk of future transplant rejection.

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26
Q

What is treated before using erythropoeitin in anaemia in CKD?

A

Iron deficiency –> IV iron is usually given, particularly in dialysis patients.

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27
Q

Cause of increased phosphate in CKD?

A

Reduced phosphate excretion by kidneys

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28
Q

Cause of low vit D in CKD?

A

Healthy kidneys metabolise vitamin D into its active form.

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29
Q

Cause of low serum calcium in CKD?

A

1) Active vitamin D is essential in calcium absorption in the intestines and reabsorption in the kidney

2) Also responsible for regulating bone turnover and promoting bone reabsorption to increase the serum calcium level

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30
Q

How do parathyroid glands react to low serum calcium and high serum phosphate in CKD?

A

Excrete more PTH, causing secondary hyperparathyroidism.

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31
Q

Impact of PTH on bone?

A

Parathyroid hormone stimulates osteoclast activity, increasing calcium absorption from bone.

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32
Q

Bone complications in CKD?

A

1) Osteomalacia: due to increased turnover of bones without adequate calcium supply

2) Osteosclerosis: occurs when the osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone (due to the low calcium level, this new bone is not properly mineralised)

3) Osteitis fibrosa cystica (aka hyperparathyroid bone disease)

4) Adynamic: reduction in cellular activity (both osteoblasts and osteoclasts) in bone (may be due to over treatment with vitamin D)

5) Osteoporosis: treat with bisphosphonates

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33
Q

Characteristic xray finding in renal bone disease?

A

Rugger jersey spine

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34
Q

What is Rugger jersey spine?

A

This involves sclerosis of both ends of each vertebral body (denser white) and osteomalacia in the centre of the vertebral body (less white).

The name refers to the stripes found on a rugby shirt.

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35
Q

What is osteosclerosis?

A

Osteosclerosis is a disorder that is characterized by abnormal hardening of bone and an elevation in bone density.

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36
Q

Management of renal bone disease?

A
  • Low phosphate diet
  • Phosphate binders
  • Active forms of vitamin D (alfacalcidol and calcitriol)
  • Ensuring adequate calcium intake
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37
Q

Overall aim of management in renal bone disease?

A

reduce phosphate and parathyroid hormone levels.

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38
Q

1st line for HTN in CKD?

A

ACEi - these are particularly helpful in proteinuric renal disease e.g. diabetic nephropathy

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39
Q

How can ACEi affect creatinine?

What rise is acceptable?

A

As these drugs tend to reduce filtration pressure a small fall in glomerular filtration pressure (GFR) and rise in creatinine can be expected.

NICE suggest a rise in creatinine of up to 30% is acceptable.

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40
Q

ACEi are offered to ALL patients with:

A

1) Diabetes plus a urine ACR above 3 mg/mmol

2) Hypertension plus a urine ACR above 30 mg/mmol

3) All patients with a urine ACR above 70 mg/mmol

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41
Q

What needs to be monitored in CKD patients on ACEi?

A

potassium (risk of hyperkalaemia)

42
Q

2 drugs used for proteinuria in CKD?

A

1) ACEi (or ARBs)

2) SGLT-2 inhibitors

43
Q

What drug is 1st line in patients with ACR > 70 mg/mmol (regardless of the patient’s blood pressure)?

A

ACEi

44
Q

What drug is 1st line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol?

A

ACEi

45
Q

What is the SGLT-2 inhibitor licensed for CKD?

A

Dapagliflozin

46
Q

Role of SGLT-2 inhibitors in CKD?

A

They primarily act by blocking reabsorption of glucose in the proximal tubule –> lowers the renal glucose threshold –> glycosuria

They also reduce intraglomerular pressure.

47
Q

SGLT-2 inhibitors are offered to all patients with CKD with…

A

Diabetes plus a urine ACR above 30 mg/mmol

48
Q

SGLT-2 inhibitors are considered in patients with with…

A

1) Diabetes plus a urine ACR or 3-30 mg/mmol
2) Non-diabetics with an ACR of 22.6 mg/mmol or above

48
Q

What investigation can differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD)?

A

Renal US

49
Q

Describe typical kidneys in CKD?

A

Bilateral small kidneys

50
Q

Most patients with CKD have bilateral small kidneys.

What are 4 exceptions to this?

A

1) autosomal dominant polycystic kidney disease

2) diabetic nephropathy (early stages)

3) amyloidosis

4) HIV-associated nephropathy

51
Q

What calcium level may indicate CKD over AKI?

A

hypocalcaemia (due to lack of vitamin D)

52
Q

What is an AKI?

A

Acute kidney injury (AKI) refers to a rapid drop in kidney function

53
Q

How is an AKI diagnosed?

A

By measuring serum creatinine

54
Q

Who is AKI most common in?

A

acutely unwell patients (e.g., infections or following surgery).

55
Q

Criteria for diagnosing an AKI?

a) Rise in creatinine
b) Urine output

A

a) Rise in creatinine of more than 25 micromol/L in 48 hours
OR
Rise in creatinine of more than 50% in 7 days

b) Urine output of less than 0.5 ml/kg/hour over at least 6 hours

56
Q

Risk factors for developing an AKI?

A
  • Older age (e.g., above 65 years)
  • Sepsis
  • Chronic kidney disease
  • Heart failure
  • Diabetes
  • Liver disease
  • Cognitive impairment (leading to reduced fluid intake)
  • Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
  • Radiocontrast agents (e.g., used during CT scans)
57
Q

What can the causes of AKI be separated into?

A

pre-renal, renal, and post-renal

58
Q

What is the most common group of causes of AKI?

A

Pre-renal

59
Q

Mechanism behind pre-renal causes of AKI?

A

Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood

60
Q

Pre-renal causes of AKI?

A

1) Dehydration
2) Shock (e.g., sepsis or acute blood loss)
3) Heart failure
4) hypovolaemia secondary to diarrhoea/vomiting
5) renal artery stenosis

61
Q

Mechanism behind renal causes of AKI?

A

Renal causes are due to intrinsic disease in the kidney.

62
Q

Renal causes of AKI?

A
  • Acute tubular necrosis (ATN)
  • Glomerulonephritis
  • Acute interstitial nephritis (AIN)
  • Haemolytic uraemic syndrome
  • Rhabdomyolysis
  • Tumour lysis syndrome
63
Q

Mechanism behind post-renal causes of AKI?

A

Post-renal causes involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function (obstructive uropathy)

64
Q

Causes of post-renal causes of AKI?

A
  • Kidney stones
  • Tumours (e.g., retroperitoneal, bladder or prostate)
  • Strictures of the ureters or urethra
  • Benign prostatic hyperplasia (benign enlarged prostate)
  • Neurogenic bladder
  • External compression of ureter
65
Q

What drugs can lead to an AKI?

A

NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics

66
Q

How is the risk of AKI reduced in patients undergoing an investigation requiring contrast (if they’re high risk)?

A

IV fluids

ALSO certain drugs such as ACE inhibitors and ARBs may also be temporarily stopped.

67
Q

What are 3 of the key ways that an AKI may be detected?

A

1) Reduced urine output: oliguria is <0.5 ml/kg/hr

2) Fluid overload

3) Rise in molecules that the kidney normal excretes/maintains a careful balance of e.g. potassium, urea and creatinine

68
Q

Many patients with early AKI may experience no symptoms. However, as renal failure progresses, what symptoms may be seen?

A

1) reduced urine output

2) pulmonary and peripheral oedema

3) arrhythmias (secondary to changes in potassium and acid-base balance)

4) features of uraemia (for example, pericarditis or encephalopathy)

69
Q

Investigations in AKI?

A

1) U&Es

2) Urinalysis

3) Renal US within 24 hours: if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction

70
Q

What drugs should be stopped in AKI as may worsen renal function?

A

1) ACEi

2) Diuretics

3) NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)

4) Angiotensin II receptor antagonists

5) Aminoglycosides e.g. gentamicin

71
Q

What drugs may have to be stopped in AKI due to increased risk of toxicity (but don’t usually worsen AKI themself)?

A

1) Metformin
2) Lithium
3) Digoxin

72
Q

Are loop diuretics recommended in AKI (to artificially boost urine output)?

A

No - except in patients who experience significant fluid overload.

73
Q

There are 3 methods of treatment of hyperkalaemia (in AKI).

What are they?

A

1) Stabilisation of cardiac membrane

2) Short-term shift in potassium from extracellular to intracellular fluid compartment

3) Removal of potassium from the body

74
Q

What is used to stabilise cardiac membrane in hyperkalaemia?

A

IV 10% 10ml calcium gluconate

75
Q

What is used for a short-term shift in potassium from extracellular to intracellular fluid compartment in hyperkalaemia?

A

1) Combined insulin/dextrose infusion

2) Nebulised salbutamol

76
Q

What is used for the removal of potassium from the body in hyperkalaemia?

A

1) Calcium resonium (orally or enema)

2) Loop diuretics

3) Dialysis

77
Q

Management of all patients with suspected AKI secondary to urinary obstruction?

A

prompt review by a urologist.

78
Q

When is renal replacement therapy (e.g. haemodialysis) used in AKI?

A

When a patient is not responding to medical treatment of complications, for example refractory hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).

79
Q

What is acute tubular necrosis (ATN)?

A

Acute tubular necrosis refers to damage and death (necrosis) of the epithelial cells of the renal tubules.

80
Q

What is the most common intrinsic cause of AKI?

A

ATN

81
Q

Via what 2 ways can damage to kidney cells occur in ATN?

A

1) Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)

2) Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)

82
Q

What confirms ATN on urinalysis?

A

Muddy brown casts (renal tubular epithelial cells may also be seen)

83
Q

Is ATN reversible?

A

Can be - the epithelial cells can regenerate

84
Q

What is urinalysis looking for in AKI?

A

1) Leucocytes and nitrites: suggest infection

2) Protein and blood: suggest acute nephritis (but can be positive in infection)

3) Glucose: suggests diabetes

85
Q

What investigation is required if a post-renal cause of AKI is suspected?

A

Renal US

86
Q

Management of AKI?

A

Involves reversing the underlying cause and supportive management, for example:

1) IV fluids for dehydration and hypovolaemia

2) Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)

3) Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)

4) Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)

5) Dialysis may be required in severe cases

87
Q

Are ACEi nephrotoxic?

A

No.

ACEi should be stopped in an AKI, as they reduce the filtration pressure.

Hwever, ACE inhibitors have a protective effect on the kidneys long-term.

They are offered to certain patients with hypertension, diabetes and chronic kidney disease to protect the kidneys from further damage.

88
Q

Complications of AKI?

A

1) Fluid overload, heart failure and pulmonary oedema

2) Hyperkalaemia

3) Metabolic acidosis

4) Uraemia (high urea), which can lead to encephalopathy and pericarditis

89
Q

What is pre-renal uraemia (‘azotemia’)?

A

Prerenal azotemia is caused by hypoperfusion to the kidneys. However, there is no inherent kidney disease. It can occur following hemorrhage, shock, volume depletion, congestive heart failure, adrenal insufficiency, and narrowing of the renal artery among other things.

90
Q

Define azotemia

A

Azotemia is elevation, or buildup of, nitrogenous products (BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body.

91
Q

Urine sodium in pre-renal uraemia vs ATN?

A

Pre-renal uraemia: <20 mmol/L i.e. low (kidneys hold on to sodium to preserve volume)

ATN: >40 mmol/L i.e high

92
Q

Urine osmolality in pre-renal uraemia vs ATN?

A

Pre-renal uraemia: >500 (high i.e. very conc)

ATN: <350 (low)

93
Q

Response to fluid challenge in pre-renal uraemia vs ATN?

A

Pre-renal uraemia: Good

ATN: Poor

94
Q

Serum urea:creatinine ratio in pre-renal uraemia vs ATN?

A

Pre-renal uraemia: Raised

ATN: Normal

95
Q

What Abx can increase the risk of AKI?

A

Aminoglycosides are nephrotoxic

96
Q

Criteria for diagnosing AKI?

A

1) Rise in creatinine of 26µmol/L or more in 48 hours OR

2) >= 50% rise in creatinine over 7 days OR

3) Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR

4) >= 25% fall in eGFR in children / young adults in 7 days.

97
Q

What criteria is used to stage AKI?

A

The Kidney Disease: Improving Global Outcomes (KDIGO)

98
Q

How many stages of AKI are there according to KDIGO?

A

3

99
Q

Stage 1, 2 and 3 of AKI according to KDIGO:

A

Stage 1:
- Increase in creatinine to 1.5-1.9 times baseline, or
- Increase in creatinine by ≥26.5 µmol/L, or
- Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

Stage 2:
- Increase in creatinine to 2.0 to 2.9 times baseline, or
- Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours

Stage 3:
- Increase in creatinine to ≥ 3.0 times baseline, or
- Increase in creatinine to ≥353.6 µmol/L or
- Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
- The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

100
Q
A

Yr 4 - CCC (54 decks)

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