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Renal Flashcards

1
Q

What is an AKI?

A
  1. Abrupt loss of kidney function (<48 hours)
  2. Resulting in retention of urea and other waste products
  3. Dysregulation of extracellular volume and electrolytes
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2
Q

3 criteria that define AKI?

A
  1. Increase serum creatinine >26umol/L above baseline
  2. Increase in serum creatinine 1.5x baseline
  3. Oliguria <0.5mK/kg/hr for >6hr
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3
Q

Which groups of patients are at high risk of AKI?

A
  1. CKD
  2. Diabetes
  3. Atherosclerotic disease
  4. Heart failure
  5. Multiple myeloma
  6. Elderly
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4
Q

How can the causes of AKI be classified?

A
  1. Pre-renal
  2. Renal
  3. Post-renal
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5
Q

What are the pre-renal causes of AKI?

A
  1. Volume depletion (bleeding, D&V, burns)
  2. Oedematous states (cardiac failure, cirrhosis, nephrotic syndrome)
  3. Hypotension (sepsis, shock)
  4. Medications (NSAIDs, COX-2 inhibitors, ACEi, ARBs)
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6
Q

What are the renal causes of AKI?

A
  1. Glomerular disease (glomerulonephritis, thrombosis)
  2. Tubular injury (prolonged ischaemia, nephrotoxins)
  3. Acute interstitial nephritis (drugs, infection, autoimmune disease)
  4. Vascular disease (polyarteritis nodosa, vasculitis, renal artery stenosis, eclampsia)
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7
Q

What are the post-renal causes of AKI?

A
  1. Prostatic hypertrophy
  2. Calculus
  3. Blood clot
  4. Urethral stricture
  5. Tumour
  6. Pelvic malignancy
  7. Radiation fibrosis
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8
Q

What are the drugs known to cause AKI?

A
  1. NSAIDs
  2. Gentamicin
  3. Antifungals
  4. Antivirals
  5. Radio-iodine contrast
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9
Q

Which group of patients is most commonly affected by AKI?

A

Elderly

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10
Q

Give 3 risk factors for AKI

A
  1. Age >65
  2. CKD with eGFR <60
  3. Prev AKI
  4. Co-morbidities (CCF, liver disease, diabetes)
  5. Neuroimpairment
  6. Hypovolaemia, sepsis
  7. Symptoms of urological obstruction
  8. Nephrotoxic meds (inc contrast)
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11
Q

Metabolic changes in AKI?

A

^Urea and Creat
Hyponatraemia
Hyperkalaemia
Metabolic acidosis

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12
Q

Symptoms of AKI?

A
  1. Oliguria/anuria
  2. Nausea and vomiting
  3. Dehydration
  4. Confusion
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13
Q

Signs of AKI?

A 
HTN
Large painless bladder
Fluid overload (^JVP, oedema)
Postural hypotension and dehydration
Pallor, rash, bruising
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14
Q

Investigations required for an AKI?

A
  1. Urinalysis and urine microscopy
  2. Creatinine
  3. Blood film
  4. Immunology (Bence Jones proteins, ANCA, complement)
  5. US (if obstruction suspected)
  6. Other radiology for systemic disease
  7. Biopsy
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15
Q

How does CKD differ from AKI?

A
  1. Longer duration of Sx
  2. Nocturia
  3. Absence of illness
  4. Anaemia
  5. Hyperphosphataemia
  6. Reduced renal size
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16
Q

Management of AKI?

A

Supportive:

  1. Treat underlying cause
  2. Stop nephrotoxic drugs
  3. Monitor fluids and electrolytes
  4. Treat acute complications (^K+, acidosis, pulmonary oedema, bleeding)
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17
Q

Indications for dialysis (renal replacement therapy)?

A
  1. Hyperkalaemia
  2. Pulmonary oedema resistant to medical management
  3. Severe metabolic acidaemia due to kidney failure
  4. Progressive renal failure (^Creat)
  5. Uraemic complications (pericarditis, altered mental state)
  6. Fluid overload
  7. Renal transplant
  8. CKD 4 or 5
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18
Q

What is the AKI management bundle?

A

Haemodynamic restoration (fluids and inotropes)
Treatment of ^K+
Fluid balance monitoring
Urinalysis
Stop nephrotoxins, drugs with haemodynamic effect, reduce doses of renally excreted drugs

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19
Q

What is CKD?

A

Abnormal kidney function (eGFR <60ml/min/1.73m^2) for longer than 3 months
OR
Kidney damage

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20
Q

Risk factors for CKD?

A
  1. ^Age
  2. Diabetes
  3. CVD, HTN
  4. Proteinuria, AKI
  5. Smoking
  6. African, afro-Caribbean or Asian ethnicity
  7. Chronic NSAID use
  8. Untreated outflow obstruction
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21
Q

Classification of CKD?

A

Stages:

  1. Normal (eGFR >90ml/min/1.72m2) with other evidence of chronic kidney damage
  2. Mild (eGFR 60-89)
    3a. Moderate (eGFR 45-59)
    3b. Moderate (eGFR 30-44)
  3. Severe (eGFR 15-29)
  4. Established Renal Failure (ERF) (eGFR <15) or on dialysis
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22
Q

What persistent findings may indicate CKD?

A 
Persistent microalbuminaemia
Persistent proteinuria
Persistent haematuria
Structural abnormalities (ie PCKD)
Biopsy proven glomerulonephritis
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23
Q

How does CKD present?

A

Usually incidentally on routine blood/urine test

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24
Q

Symptoms of severe CKD?

A 
Anorexia, nausea, vomiting, fatigue, insominia, pruritis
Pulmonary oedema, dyspnoea
Muscle cramps, headache
Nocturia
Sexual dysfunction
Pericarditis
Coma, seizures
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25
Q

RFs that require screening for CKD?

A
  1. AKI
  2. CVD
  3. IHD, chronic HF, PAD
  4. Structural renal tract disease, BPH
  5. Multisystem disease (SLE)
  6. FHx of CKD
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26
Q

Investigations for CKD?

A
  1. eGFR
  2. Biochemistry: ^K+, low bicarb, ^phos
  3. Haematology: anaemia
  4. Autoantibodies serology: ANA, c-ANCA, p-ANCA, anti-GBM
  5. Virology (hepatitis, HIV)
  6. Urinalysis
  7. Imaging: renal US
  8. Retrograde pyelogram
  9. Renal radionuclide scan
  10. CT (renal artery stenosis)
  11. Biopsy
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27
Q

Management of CKD?

A
  1. Explanation and education
  2. Medication review
  3. Monitoring of eGFR
  4. Immunise against influenza and pneumococcus
  5. CVD prevention and BP control
  6. Lifestyle advice (diet, exercise)
  7. Manage and monitor bone and mineral disorders; treat with Vit D supplementation if required
  8. Treat ^phosphate with calcium acetate
  9. Renal replacement therapy (RRT) if required
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28
Q

When should a patient with CKD be referred?

A
  1. GFR <30mL/min/1.73m2
  2. Albumin:Creatinine ratio (ACR) >70mg/mmol (unless known DM and treated)
  3. Sustained decrease GFR of 25% within 12 months
  4. Poorly controlled HTN despite >4 drugs
  5. Known/suspected rare/genetic causes of CKD
  6. Suspected renal artery stenosis
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29
Q

Give 3 potential complications of CKD

A
  1. Anaemia
  2. Coagulopathy
  3. Hypertension
  4. Fluid overload (pulmonary oedema)
    Others: ^CaPO4 - CVD, arthropathy, soft tissue calcification; renal osteodystrophy; neurological Sx (uraemic encephalopathy, neuropathy); dialysis amyloid (bone pain, carpal tunnel syndrome); malnutrition
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30
Q

What is hyperkalaemia?

A

Plasma K+ >5.5mmol/L

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31
Q

What is mild hyperkalaemia, and when should blood tests be repeated?

A

5.5-5.9mmol/L

Re-check in a week

32
Q

What is moderate hyperkalaemia, and when should the bloods be repeated?

A

6-6.4mmol/L

Re-check following week

33
Q

What is severe hyperkalaemia, and when should the bloods be repeated?

A

> 6.5

Requires urgent investigation

34
Q

What can cause hyperkalaemia?

A

Metabolic acidosis
Hyperglycaemia Hyperosmolar State
Medication (K+ sparing diuretics)
Tissue breakdown (e.g. crush injury)

Spurious (sample haemolysis, clenched fist, contamination with purple top tube, length of storage, cold storage)

35
Q

What are the renal causes of hyperkalaemia?

A

AKI, CKD
Hyperkalaemic RTA
Mineralocorticoid deficiency (eg Addisons)
Medicines that interfere with RAAS

36
Q

What drugs can cause hyperkalaemia?

A 
K+ sparing diuretics (e.g. spironolactone)
Drugs that affect RAAS (e.g. ACEi, ARBs)
NSAIDs, Cyclosporine, Tacrolimus
Heparin
Pentamidine 
Co-trimoxazole
Herbal remedies
37
Q

What are some exogenous causes of hyperkalaemia?

A
  1. Potassium supplementation

2. Increased consumption of bananas, oranges, watermelons, aubergine, peas, potatoes

38
Q

Endogenous causes of hyperkalaemia?

A
  1. Tumour lysis syndrome
  2. Rhabdomyolysis (often associated with crush injury)
  3. Trauma
  4. Burns
  5. Crush syndrome
39
Q

Causes of pseudohyperkalaemia?

A 
Prolonged tourniquet time
Difficulty collecting sample
Clenched fist 
Test tube haemolysis
Excessive cooling/storage of specimen
Leukocytosis and thrombocytosis
40
Q

How does hyperkalaemia present?

A
  1. Often asymptomatic
  2. Palpitations, Paraesthesia, Muscle weakness
  3. Flaccid paralysis (ascending)
  4. Oliguria
41
Q

Investigations required for hyperkalaemia?

A

ECG!

  1. 24hr urine volume and electrolytes
  2. FBC
  3. Capillary blood glucose
  4. ABG (if ^K caused by metabolic acidosis - i.e. if Bicarb is low)
42
Q

ECG findings of hyperkalaemia?

A
  1. Tall, tented T waves (all leads)
  2. Small/absent P wave
  3. Wide QRS
43
Q

What is the concentration of K+:

  1. Intracellularly?
  2. Extracellularly?
A
  1. 150mmol/L

2. 4.5mmol/L

44
Q

Why might someone clenching their fist lead to a rise in their serum potassium?

A

Potassium is released from muscle cells during contraction

45
Q

Why might someone with CLL have pseudohyperkalaemia?

A

Lymphocytosis; the lymphocytes are frail so break easily, releasing potassium into the blood

46
Q

What arrhythmia may be caused by hyperkalaemia?

A

Ventricular fibrillation

47
Q

What is a common cause of metabolic acidosis?

A

Diabetic ketoacidosis (DKA)

48
Q

Initial management of hyperkalaemia? (detailed)

A
  1. IV Calcium Gluconate 10%
    - 10mls over 1-2 mins (to protect cardiac muscle)
    - This can be repeated every 30-60 mins
  2. 10-20 units insulin in 500mL 10% dextrose IV over 60 mins
  3. Nebulised albuterol (beta 2 agonist)
49
Q

Initial management of hyperkalaemia? (simple)

A
  1. Calcium gluconate 10%
  2. Insulin in 10% dextrose
  3. Nebulised albuterol
50
Q

How can the excess potassium be removed from the body?

A
  1. Diuretic, e.g. furosemide
  2. GI cation exchanger, e.g. Patiromer or Kayexalate (binds K+ in colon in exchange for Ca or Na)
  3. Haemodialysis
51
Q

What is Parotimer? What does it do?

A

A gastrointestinal cation exchanger

It binds to potassium in the colon in exchange for calcium

52
Q

What can cause tumour lysis syndrome?

A

Radiation or cytotoxic therapy for leukaemia or lymphoma

53
Q

What is Addison’s disease?

A

Primary adrenal insufficiency

54
Q

How are serum levels of potassium affected in Addison’s disease?

A

Hyperkalaemia due to low aldosterone stimulating renin secretion

55
Q

How is the diagnosis of Addison’s disease confirmed?

A
  1. Low serum ACTH
  2. Low serum cortisol
  3. Low aldosterone levels
  4. High renin levels
56
Q

Management of Addisons?

A

Replacement treatment with fludrocortisone

57
Q

How can mannitol cause hyperkalaemia?

A

Causes hyperosmolality which pulls water out of the cells and increases the K+ gradient

58
Q

What is hypokalaemia?

A

Plasma K+ <3.5mmol/L

59
Q

Give 5 common causes of hypokalaemia

A
  1. Low potassium intake
  2. Laxative abuse / diarrhoea
  3. Vomiting
  4. Metabolic alkalosis
  5. Diuretics (both loop and thiazides)
60
Q

What are the serum levels of potassium in mild hypokalaemia?

A

3.1-3.5 mmol/L

61
Q

What are the serum levels of potassium in moderate hypokalaemia?

A

2.5-3 mmol/L

62
Q

What are the serum levels of potassium in severe hypokalaemia?

A

<2.5 mmol/L

63
Q

Give 3 potential causes of decreased potassium intake

A
  1. Inadequate K+ replacement on IV fluids whilst NBM
  2. Total parenteral nutrition
  3. Malnutrition
  4. Anorexia nervosa
64
Q

How does hypokalaemia present?

A

Generally asymptomatic, but may have:

  • Fatigue
  • Weakness
  • Myalgia
  • Constipation
65
Q

How does severe hypokalaemia present?

A

Severe muscle paralysis (ascending)

66
Q

Investigations in hypokalaemia?

A
  1. ECG!
  2. 24hr urinary potassium (or urinary potassium to creatinine ratio)
  3. ABG
67
Q

If metabolic acidosis is associated with a low urine K+ to creatinine ratio, what is the likely cause of hypokalaemia?

A

GI, e.g. laxative abuse

68
Q

If metabolic acidosis is associated with a high urine K+ to creatinine ratio, what is the likely cause of hypokalaemia?

A

DKA

Type 1 or 2 renal tubular acidosis

69
Q

If metabolic alkalosis is associated with a low urine K+ to creatinine ratio, what is the likely cause of hypokalaemia?

A

Vomiting

70
Q

If metabolic alkalosis is associated with a high urine K+ to creatinine ratio, what is the likely cause of hypokalaemia?

A 
Diuretics
Renal syndromes (Bartter and Gitelman)
71
Q

What changes are seen on an ECG in hypokalaemia?

A

ST depression
Flat T waves
U waves (best seen in leads V4-V6)

72
Q

Management of hypokalaemia?

A
  1. Oral potassium
    (Metabolic ALKALOSIS: Potassium Chloride; Metabolic ACIDOSIS: Potassium Bicarbonate)
  2. K+ sparing diuretic (if cause is renal)
  3. Check serum K+ every 2-4 hrs; continue treatment until K+ above 3.5
73
Q

AKI. Angiotensin II mediates prostaglandin E2. How does prostaglandin E2 affect kidney perfusion?

A

Increases it by dilating the efferent arteriole

74
Q

AKI. How do ACEi and ARBs affect kidney perfusion?

Should they be stopped in AKI?

Should they be stopped in CKD?

A

Reduce perfusion. They prevent affect AngII and prevent PGE2 from dilating the efferent arteriole.

Stop in AKI

No. In CKD, glomerular perfusion pressure is elevated. Reducing this pressure is beneficial, so ACEi and ARBs are helpful.

75
Q

Does oral aspirin affect kidney function?

A

No

76
Q

What factors may affect creatinine levels?

A

Muscle mass, catabolism

77
Q

^urea > ^creatinine may indicate?

A

^production urea (GI bleed)
Dec blood flow to kidneys (dehydration, haemorrhage)

Or both - sepsis

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