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Metabolic > Renal > Flashcards

Renal Flashcards

1
Q

What are the 9 functions of the kidney?

A

Elimination of metabolic waste, water homeostasis, electrolyte homeostasis, acid-base balance, BP control, vitamin D synthesis, EPO synthesis, renin synthesis, drug excretion.

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2
Q

How is CKD characterised?

A

eGFR <60 or pathological kidney damage (proteinuria) for > 3 months.

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3
Q

Which stage of CKD can a patient present with symptoms due to impaired kidney function?

A

4 & 5

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4
Q

What are the causes of CKD?

A

Diabetes, hypertension, glomerulonephritis, atherosclerosis (renal artery stenosis), drugs (e.g. NSAIDs), infection, polycystic kidney disease, obstructive uropathy.

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5
Q

What are the complications of CKD?

A

CV disease, hypertension, salt/water retention, electrolyte abnormalities (e.g. hyperkalaemia), metabolic acidosis, renal bone disease, anaemia (EPO), uraemia, altered drug metabolism, peripheral neuropathy.

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6
Q

How is CKD managed?

A

Treat underlying cause, control BP, reduce proteinuria (ACEi/ARB), avoid nephrotoxic drugs, manage complications, renal replacement therapy.

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7
Q

How do ACEi/ARBs reduce proteinuria?

A

Lower intraglomerular pressure so reduce filtration.

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8
Q

How do ACEi decrease glomerular filtration?

A

They cause vasodilation of efferent arteriole.

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9
Q

How is AKI characterised?

A

Increase serum creatinine within hours/days or decrease urine output > 6 hours.

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10
Q

Name some nephrotoxic drugs

A

Diuretics, ACEi/ARBs, NSAIDs, gentamicin, vancomycin, chemotherapy.

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11
Q

What are the causes of AKI?

A

Pre-renal: perfusion failure.
Renal: damage to kidney tissue.
Post-renal: obstruction.

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12
Q

How is AKI treated?

A

Treat underlying cause, fluid balance, dietary restriction, stop nephrotoxic drugs, dialysis.

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13
Q

What are the signs of nephrotic syndrome?

A

Heavy proteinuria, peripheral oedema, hypoalbuminaemia, hyperlipidaemia.

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14
Q

Which part of the glomerular filtration barrier is damaged in nephrotic syndrome?

A

Podocytes and basement membrane.

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15
Q

Give some examples of diseases that cause nephrotic syndrome

A

Primary: focal segmental glomerulosclerosis, membranous nephropathy, minimal change disease.
Secondary: SLE, diabetes, amyloidosis, HIV.

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16
Q

What are the complications of nephrotic syndrome?

A

Thromboembolism, infection, hyperlipidaemia, malnutrition, CKD/AKI.

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17
Q

Treatment of nephrotic syndrome?

A

Treat underlying cause, loop diuretics, salt restriction, ACEi/ARB, thrombo-prophylaxis.

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18
Q

What are the signs of nephritic syndrome?

A

Proteinuria, haematuria, hypertension, impaired kidney function and oedema.

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19
Q

How is the glomerular endothelium damaged in nephritic syndrome?

A

By inflammation or immune mediated processes.

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20
Q

Give examples of diseases causing nephritic syndrome

A

ANCA vasculitis, anti-glomerular basement membrane disease (good pasture syndrome), post-streptococcal glomerulonephritis, IgA nephropathy, lupus nephritis.

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21
Q

Why is there haematuria in nephritic syndrome?

A

The damage to the endothelium allows RBC, albumin and large molecules to be filtered into urine.

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22
Q

How are the kidneys commonly imaged?

A

Ultrasound.

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23
Q

What are the risk factors for AKI?

A

Age > 65, Hx of AKI, CKD, HF, diabetes, liver disease, nephrotoxic drugs.

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24
Q

Name the pre-renal causes of AKI

A

Hypoperfusion such as dehydration, hypotension/shock, cardiac failure, hypovolaemia.

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25
Q

Name the renal causes of AKI

A

Intrinsic kidney disease such as acute tubular necrosis, interstitial nephritis, glomerulonephritis, renal vascular damage.

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26
Q

Name the post-renal causes of AKI

A

Obstruction such as stones, tumours in pelvis/abdomen, ureter strictures, BPH/prostate cancer, blocked catheter.

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27
Q

List the main investigations for AKI

A

Urinalysis: blood, protein, glucose, nitrites, leukocytes.
Bloods: FBC, U&Es, bone profile, blood gas.
Imaging: ultrasound, CXR.
ECG.

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28
Q

What are the additional blood tests for an AKI?

A

CK, vasculitis screen (ANCA, ANA), blood film, blood/urine culture, virology (HBV, HCV), clotting, complement, immunoglobulins, serum electrophoresis.

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29
Q

What are the complications of AKI?

A

Hyperkalaemia, metabolic acidosis, fluid overload and uraemia.

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30
Q

What is the common presentation of minimal change disease?

A

Child, oedema (puffy face, swollen ankles), proteinuria (frothy urine), normal BP, no haematuria.

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31
Q

What is the commonest cause of nephrotic syndrome in adults and children?

A

Adults - focal segmental glomerulosclerosis.
Children - minimal change disease.

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32
Q

What is the most common type of glomerulonephritis overall?

A

Membranous nephropathy.

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33
Q

What is the histology of membranous nephropathy?

A

IgG and complement deposits on basement membrane.
Thickened basement membrane on light microscopy and sub-epithelial spikes on silver staining.

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34
Q

What is the histology of IgA nephropathy?

A

IgA deposits and glomerular mesangial proliferation.

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35
Q

Describe the classical presentation of IgA nephropathy

A

Individual in 20s presents with visible haematuria 1-2 days after URTI.

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36
Q

Name the condition with a mutation in GBM type 4 collagen

A

Alport syndrome.

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37
Q

Post-streptococcal glomerulonephritis is also known as…

A

Diffuse proliferate glomerulonephritis.

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38
Q

Describe the classical presentation of post-streptococcal glomerulonephritis

A

Child presents with haematuria, proteinuria and oedema 10-14 days after a throat or skin infection.

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39
Q

Name the subsets of rapidly progressive glomerulonephritis/ANCA-associated vasculitis

A

Granulomatosis with polyangitis (Wegener’s).
Microscopic polyangitis.

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40
Q

Describe the clinical presentation of anti-glomerular basement membrane disease (Goodpasture syndrome)

A

AKI (glomerulonephritis) and haemoptysis (pulmonary haemorrhage).

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41
Q

How would you distinguish between granulomatosis with polyangitis and anti-GBM disease?

A

Granulomatosis would present with wheeze, sinusitis and saddle-shaped nose as well as haemoptysis and AKI. Anti-GBM disease just haemoptysis and AKI.

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42
Q

What is the general treatment for glomerulonephritis?

A

Immunesuppression - steroids.
BP control - ACEi/ARBs.

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43
Q

What are the 2 types of fluids?

A

Crystalloids - electrolytes in water e.g. saline, dextrose saline, 5% dextrose, Hartmann’s.
Colloids - fluids with high molecular weight molecules - natural e.g. blood, albumin and synthetic e.g. gelatins, dextrans and hydroxyethyl starches (HES).

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44
Q

What is the pathophysiology of pyelonephritis?

A

Bacteria ascend from lower urinary tract or directly enter kidney from bloodstream.

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45
Q

What is the most common cause of pyelonephritis?

A

E.coli

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46
Q

What are the causes of catheter-associated pyelonephritis?

A

Enterococcus, Pseudomonas aeruginosa and Staphylococcus aureus.

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47
Q

Risk factors for pyelonephritis?

A

Female, structural abnormalities, vesico-uretic reflux, diabetes, immune compromised, catheters and recent sexual intercourse.

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48
Q

What are the main symptoms of pyelonephritis?

A

Fever, loin pain and nausea/vomiting. As well as dysuria, suprapubic pain, increased frequency and urgency.

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49
Q

What are the investigations for pyelonephritis?

A

Urine dipstick, midstream urine, bloods and imaging.

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50
Q

What is the management for pyelonephritis?

A

Antibiotics for 7-10 days: cefalexin, co-amoxiclav, trimethoprim, ciprofloxacin.
Sepsis six if admitted to hospital.

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51
Q

Describe sepsis six

A

3 in: IV fluids, IV antibiotics, oxygen.
3 out: lactate, blood cultures and urine output.

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52
Q

What are the complications of pyelonephritis?

A

Urosepsis and chronic pyelonephritis (leading to CKD).

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53
Q

Define polyuria

A

Abnormally high urine output.

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54
Q

Define oliguria

A

Abnormally low urine output - <400mls/day or <0.5ml/kg(body weight)/hour.

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55
Q

Define anuria

A

No urine output - <50mls/day.

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56
Q

How do NSAIDs contribute towards an AKI?

A

They reduce GFR by inhibiting the prostaglandin-mediated vasodilation of the afferent arteriole.

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57
Q

What is the pathophysiology of uraemia and what are the symptoms/signs?

A

Kidneys fail to remove metabolic waste so urea builds up in the blood to toxic levels.
Symptoms/signs - anorexia, change in taste, nausea/vomiting, pruritis, neuropathy, pericarditis, confusion, encephalopathy and coma.

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58
Q

What is the pathophysiology of sodium retention in kidney failure?

A

Production of renin and failure to regulate sodium and water homeostasis leads to oedema and hypertension. Treatment - loop diuretic and salt restriction.

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59
Q

What is the pathophysiology of anaemia in kidney failure?

A

Reduction in EPO production —> decreased rbc synthesis.

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60
Q

What is the pathophysiology of bone disease in kidney failure?

A

Increased phosphate in blood and decreased production of vitamin D in kidney failure stimulates PTH to release calcium from bones into the blood. This leads to vascular calcification and renal osteodystrophy.

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61
Q

What are the changes seen in diabetic nephropathy?

A

Mesangial cell expansion, podocytopathy, GBM thickening and sclerosis.

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62
Q

CKD patients are usually asymptomatic - true or false?

A

True - incidental finding.

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63
Q

What are the symptoms of CKD?

A

Anorexia, nausea, fatigue, weakness, muscle cramps, pruritus, dyspnoea, oedema.

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64
Q

What are the signs of CKD?

A

Pallor, hypertension, fluid overload, skin pigmentation, excoriation marks, peripheral neuropathy.

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65
Q

End stage renal failure is classified by a GFR of…

A

<15

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66
Q

Describe the main investigations for CKD

A

Urine dipstick, ACR, U&Es, FBC, bone profile, renal USS.

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67
Q

Why does renal bone disease occur with CKD?

A

Decreased vitamin D synthesis —> hypocalaemia —> increased PTH production —> bone resorption/osteoclast activity.

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68
Q

Which drug can control BP and reduce proteinuria in CKD?

A

ACEi

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69
Q

How would you treat the complications of CKD?

A

Acidosis - sodium bicarbonate.
Anaemia - iron & EPO.
Bone disease - vitamin D.
Hyperkalaemia - calcium gluconate (stabilise myocardium) & insulin/dextrose (drive potassium into cell).
Fluid overload - restrict salt intake and diuretics.

70
Q

How does Alport syndrome present in male patients?

A

Haematuria, proteinuria, renal failure, sensorineural hearing loss and eye problems.

71
Q

What is the universal donor blood group?

A

O-

72
Q

What is the universal recipient blood group?

A

AB+

73
Q

A rise in urea that is proportionally greater than the rise in creatinine is characteristic of…

A

Dehydration

74
Q

How can a fall or prolonged epileptic seizure cause an AKI?

A

Being immobilised on the floor for many hours can cause rhabdomyolysis. Myoglobins released from muscles are toxic to kidneys producing an AKI.

75
Q

Which drug reduces the rate of CKD progression in autosomal dominant polycystic kidney disease?

A

Tolvaptan - vasopressin antagonist that slows down cyst formation.

76
Q

A patient who is receiving haemodialysis for end stage renal failure complains of headache, fatigue, nausea, vomiting and drowsiness. Lung fields are clear and bloods are normal. What complication of haemodialysis should be considered?

A

Dialysis disequilibrium syndrome.

77
Q

How would you differentiate between AKI vs CKD?

A
  • Ultrasound of urinary tract - reduced kidney size in CKD (exception polycystic kidney disease and early diabetic nephropathy) and normal in AKI.
  • CKD has hypocalcaemia.
78
Q

‘Muddy brown casts’ are pathognomonic in…

A

Acute tubular necrosis.

79
Q

Causes of acute tubular necrosis?

A

Ischaemia (shock, sepsis, dehydration - hypoperfusion) and toxins (radiology contrast dye, gentamicin, NSAIDs, myoglobin secondary to rhabdomyolysis).

80
Q

Causes of acute interstitial nephritis and how does it present?

A
  • Hypersensitivity reaction to drugs (penicillin, rifampicin, NSAIDs, allopurinol, furosemide) or infection.
  • Presents with rash, fever and eosinophilia. Also raised urinary WCC, IgE, and eosinophils, alongside impaired renal function and hypertension.
81
Q

What are complications of polycystic kidney disease?

A

Liver cysts, cerebral berry aneurysms, cysts in other organs (e.g. pancreas, spleen, liver and ovaries), mitral valve prolapse.

82
Q

Membranous nephropathy is frequently associated with what?

A

Malignancy.

83
Q

What is the histology of focal-segmental glomerulosclerosis?

A

Foot process effacement.

84
Q

Which bacteria is commonly responsible for peritonitis secondary to PD?

A

Staphylococcus epidermidis or staphylococcus aureus.

85
Q

How is metabolic acidosis commonly classified?

A

Anion gap

86
Q

How is the anion gap calculated?

A

(Na+ + K+) - (Cl- + HCO3-)

87
Q

What is the normal range for an anion gap?

A

8-14 mmol/L

88
Q

What are the causes of a normal anion gap (hyperchloraemic metabolic acidosis)?

A
  • GI bicarbonate loss (prolonged diarrhoea, fistula, ureterosigmoidostomy).
  • Renal tubular necrosis.
  • Addison’s disease.
  • Drugs: e.g. acetazolamide.
  • Ammonium chloride injection.
89
Q

What are the causes of a raised anion gap?

A
  • Lactate (shock, sepsis, hypoxia).
  • Ketones (DKA, alcohol).
  • Urate (renal failure).
  • Acid poisoning (salicylates, methanol).
  • 5-oxoproline: chronic paracetamol use.
90
Q

What are the signs of acute graft failure in a renal transplant?

A

Usually asymptomatic and picked up by a rising creatinine, pyuria (leukocytes in urine) and proteinuria. Acute rejection occurs within 6 months.

91
Q

What is the most common cause of acute renal failure in first few weeks post renal transplant?

A

Acute tubular necrosis of graft.

92
Q

What is the MOA of calcium gluconate in the management of hyperkalaemia?

A

Stabilises cardiac membrane.

93
Q

What is the MOA of calcium resonium in the management of hyperkalaemia?

A

Removes potassium from the body.

94
Q

What is the MOA of insulin/dextrose in the management of hyperkalaemia?

A

Intracellular shift of potassium ions.

95
Q

What is the first-line treatment for minimal change disease?

A

Oral corticosteroids e.g. prednisolone.

96
Q

How does Henoch-Schonlein purpura classically present?

A

Abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs.

97
Q

What is Henoch-Schonlein purpura (HSP)?

A

IgA mediated small vessel vasculitis.

98
Q

What is the 2 week referral criteria for haematuria?

A

Aged >= 45 with unexplained visible haematuria without UTI or visible haematuria that persists after successful treatment of UTI.
Aged >= 60 with unexplained non-visible haematuria and either dysuria or raised WCC.

99
Q

What are the routine maintenance fluid requirements for potassium, sodium and chloride?

A

1 mmol/kg/day

100
Q

What is the maintenance fluid requirement for water?

A

25-30 ml/kg/day

101
Q

What is the maintenance fluid requirement for glucose?

A

50-100 g/day

102
Q

How would you reduce the risk of contrast-induced nephropathy?

A

Volume expansion with IV 0.9% NaCl pre- and post- procedure.

103
Q

Describe the first line treatment for patients with severe hyperkalaemia (>= 6.5 mmol/L) or with ECG changes

A

IV calcium gluconate.
Insulin/dextrose infusion.

104
Q

Severe hyperkalaemia in the context of AKI requires what treatment after been given IV calcium gluconate and insulin/dextrose infusion?

A

Haemodialysis

105
Q

What is the most common extra-renal manifestation of ADPKD?

A

Liver cysts

106
Q

How long does it take for an AV fistula to be fully functioning?

A

6-8 weeks

107
Q

Prolonged vomiting can lead to…

A

Metabolic alkalosis

108
Q

Define type 1 respiratory failure

A

Hypoxia without hypercapnia

109
Q

Define type 2 respiratory failure

A

Hypoxia with hypercapnia

110
Q

What is the investigation of choice in patients presenting with an AKI of unknown aetiology?

A

Renal tract ultrasound.

111
Q

Stage 1 and stage 2 of CKD can only be diagnosed when…

A

There are markers of kidney disease including proteinuria, haematuria, electrolyte abnormalities or structural abnormalities detected.

112
Q

Rhabdomyolysis is only diagnosed if creatinine kinase is how many times the upper limit of normal?

A

5 times

113
Q

What are the causes of crescentic glomerulonephritis on renal biopsy?

A

Goodpasture’s syndrome, lupus nephritis and ANCA-associated vasculitis (e.g. Wegener’s granulomatosis).

114
Q

Describe the NICE guidelines for AKI diagnostic criteria

A

↑ creatinine > 26µmol/L in 48 hours.
↑ creatinine > 50% in 7 days.
↓ urine output < 0.5ml/kg/hr for more than 6 hours.

115
Q

What is the cellular pathology behind myoglobinuria causing renal failure?

A

Tubular cell necrosis.

116
Q

A 63-year-old man attends for a GP appointment and states that he has had two episodes of visible blood in his urine. One episode occurred last week and the other this morning. There was not any pain. He denies any lower urinary tract symptoms. A urinalysis shows +++ blood and is negative for all other markers. What investigation should be requested?

A

Cystoscopy

117
Q

Is warfarin safe to continue in AKI?

A

Yes

118
Q

What test would confirm the diagnosis of a recent streptococcal infection?

A

Raised anti-streptolysin O titre.

119
Q

What is the first line screening test for polycystic kidney disease?

A

Renal ultrasound

120
Q

Name some side effects of EPO

A

Bone aches, flu-like symptoms and skin rashes.

121
Q

What is the most causative organism in peritonitis secondary to peritoneal dialysis?

A

Staphylococcus epidermidis

122
Q

How much does CK need to be elevated by to support a diagnosis of rhabdomyolysis?

A

At least 5 times upper limit of normal.
Elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology.

123
Q

Can statins cause a rise in CK?

A

Yes (statin-induced myopathy). They can also cause rhabdomyolysis.

124
Q

What is the definitive treatment for hyperacute graft rejection?

A

Removal of graft.

125
Q

What are the causes of hyperacute graft rejection?

A

Recipient has preformed Abs to donor kidney.

126
Q

What is the pathophysiology of acute graft rejection?

A

Cytotoxic T cell medicated.

127
Q

What is the treatment of acute graft rejection?

A

Steroids and immunosuppressants.

128
Q

What is the usual immunosuppressant regime for renal transplant?

A

Tacrolimus, mycophenolate, prednisolone.

129
Q

Is diabetic nephropathy nephrotic or nephritic?

A

Nephrotic - proteinuria.

130
Q

What is the most common cause of CKD in UK?

A

Diabetic nephropathy.

131
Q

Describe the pathophysiology of diabetic nephropathy

A

The chronic high level of glucose passing through the glomerulus causes scarring (glomerulosclerosis).

132
Q

What is the treatment for diabetic nephropathy?

A

ACEi

133
Q

Define interstitial nephritis

A

Inflammation of the space between cells and tubules (the interstitium) within the kidney.

134
Q

Define acute tubular necrosis

A

Necrosis of the epithelial cells of the renal tubules.
Epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.

135
Q

What is the most common cause of AKI?

A

Acute tubular necrosis

136
Q

Define renal tubular acidosis

A

Metabolic acidosis due to pathology in the tubules of the kidney.

137
Q

Define type 1 renal tubular acidosis

A

Pathology in the distal tubule, meaning it is unable to excrete hydrogen ions.

138
Q

Define type 2 renal tubular acidosis

A

Pathology in the proximal tubule, meaning it is unable to reabsorb bicarbonate from the urine into the blood. Therefore excessive bicarbonate is excreted in the urine. Fanconi’s syndrome is the main cause.

139
Q

Define type 3 renal tubular acidosis

A

Combination of type 1 and type 2 with pathology in the proximal and distal tubule.

140
Q

Define type 4 renal tubular acidosis

A

Caused by reduced aldosterone production secondary to adrenal insufficiency, medications (e.g. ACEi and spironolactone) or systemic conditions such as SLE, diabetes or HIV.

141
Q

What is the treatment for type 4 renal tubular acidosis?

A

Fludrocortisone

142
Q

What is haemolytic uraemic syndrome (HUS) and how is it triggered?

A
  • Thrombosis in small blood vessels.
  • Triggered by shiga toxin (E.coli 0157).
143
Q

Describe the classic triad of symptoms for HUS

A
  • Haemolytic anaemia.
  • Acute kidney injury.
  • Thrombocytopenia.
144
Q

Describe the symptoms a patient might experience with HUS

A

Brief gastroenteritis with dysentery. 5 days after the diarrhoea patient presents with: reduced urine output, haematuria, abdominal pain, lethargy, confusion (uraemia), hypertension and bruising.

145
Q

How can rhabdomyolysis cause hyperkalaemia?

A

Apoptosis of myocytes releases potassium.

146
Q

List some causes of rhabdomyolysis

A
  • Prolonged immobility (particularly frail patients that fall and spend time on the floor before being found).
  • Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition).
  • Crush injuries.
  • Seizures.
147
Q

Myoglobinurea gives the urine what colour?

A

Red-brown colour.

148
Q

What is the mainstay of treatment for rhabdomyolysis?

A

IV fluids to rehydrate the patient and encourage filtration of the breakdown products.

149
Q

What is the main complication of hyperkalaemia?

A

Cardiac arrhythmias such as VF.

150
Q

Describe the investigations for hyperkalaemia

A
  • U&Es.
  • ECG if potassium is > 6mmol/L.
151
Q

Describe the ECG changes in hyperkalaemia

A
  • Tall peaked T waves.
  • Flattening or absence of P waves.
  • Broad QRS complexes.
152
Q

What is the most common extra-renal manifestation of autosomal dominant polycystic kidney disease?

A

Liver cysts

153
Q

What is the most common cause of HUS?

A

E.coli 0157

154
Q

Which medications have an increased risk of toxicity during an AKI (but doesn’t usually worsen AKI itself)?

A

Metformin, lithium and digoxin.

155
Q

Which investigation is required in a patient presenting with an AKI of unknown aetiology?

A

Renal US

156
Q

What ABG finding would you find in a patient with prolonged diarrhoea?

A

Metabolic acidosis associated with hypokalaemia

157
Q

Describe the histology of membranous glomerulonephritis

A
  • Basement membrane thickening on light microscopy.
  • Subepithelial spikes on sliver stain.
  • Positive immunohistochemistry for PLA2.
158
Q

What is the commonest causes of glomerulonephritis in adults worldwide?

A

IgA nephropathy

159
Q

Histology of granulomatosis with polyangiitis (GPA)?

A

Crescentic glomerulonephritis

160
Q

Positive ANA indicates which type of nephritis?

A

Lupus nephritis

161
Q

Treatment for acute blood clot urinary retention?

A

Continuous bladder irrigation via urethral catheter.

162
Q

Outline the features of ADPKD

A
  • Hypertension
  • Recurrent UTIs
  • Flank pain
  • Haematuria
  • Palpable kidneys
  • Renal impairment
  • Renal stones
163
Q

What is the favoured route of administration of calcium resonium?

A

Enema, so potassium is secreted by the rectum.

164
Q

How can potassium be removed from the body?

A
  • Calcium resonium
  • Loop diuretics
  • Dialysis
165
Q

Triad of features associated with renal cell carcinoma

A
  • Flank pain
  • Flank mass
  • Haematuria
166
Q

What ECG pattern would be indicative of severe hyperkalaemia?

A

Sinusoidal waves

167
Q

Normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness

A

HUS

168
Q

Name a non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease

A

Sevelamer

169
Q

What is a complication of rapid correction of hypernatraemia?

A

Cerebral oedema

170
Q

List the causes of hyperkalaemia

A
  • AKI
  • Drugs: potassium sparing diuretics, ACEi, ARBs, spironolactone, ciclosporin, heparin
  • Metabolic acidosis
  • Addison’s disease
  • Rhabdomyolysis
  • Massive blood transfusion

Metabolic (6 decks)

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