Renal Workshop

Question 1

Stages of AKI

Answer 1

Stage 1:
Serum Creatinine - increase by greater than or equal to 26 micromol/L within 48h or 1.5-1.9 times baseline

Urine output: Less than 0.5/ml/kg/hr for 6-12h

Stage 2:
Serum Creatinine - 2-2.9 times baseline

Urine output: Less than 0.5/ml/kg/hr for 12h or more

Stage 3:
Serum Creatinine - 3 times baseline or increase to >354 micromol/L or decrease in eGFR to <35ml/min/1.73 in children and young people or initiation of renal replacement therapy

Urine output: Less than 0.3/ml/kg/hr for 24h or more or no urine for 12h or more

Question 2

Risk Factors of AKI

Answer 2

• Previous AKI
• Pre-existing CKD
• over 65 years
• congestive cardiac failure
• atherosclerotic peripheral vascular disease
• diabetes
• liver disease

Question 3

Causes of AKI

Answer 3

Triggers include:

• Sepsis
• Hypovolaemia
• Hypotension
• Certain meds

Causes include:

• Pre renal issues that cause reduced blood flow to kidneys including acute tubular necrosis, sepsis, infections, hypovolaemia and hypotension may all reduce renal blood flow
• Post renal due to obstruction to urine flow from kidneys
• Intrinsic renal causes due to damage to the functional tissues of the kidney

Question 4

Medicines Management in AKI

Answer 4

• Avoid use of nephrotoxic medication (NSAIDs in CKD patients)
• Monitor renal function (ACE inhibitors, ARBS and diuretics can alter renal function)
• Reviewing medicines that may exacerbate AKI (e.g. temporarily withholding ACE inhibitors, ARBs and NSAIDs if patients become acutely unwell)

Question 5

Sick Day Rules

Answer 5

• If vomiting (can’t keep fluid down)
• Diarrhoea (can’t replace volume)
• Fever/feverish illness
• STOP
• ACEi/ARBs
• Metformin and it’s combinations
• NSAIDs
• Diuretics

Question 6

Drug Induced Nephrotoxicity

Answer 6

• Pre-renal – drugs affecting blood flow to the
kidneys
– Diuretics → hypovoleamia
– β blockers → ↓ cardiac output
– ACEI → ↓ renal blood flow
• Intrinsic
– Gentamicin, amphotericin → acute tubular necrosis
(ATN)
– NSAIDs, penicillins, sulphonamides → TIN
– Penicillamine → glomerulonephritis
• Post-renal – drugs causing obstruction
– Ergotamine, bromocriptine

Question 7

Care in the community

Answer 7

• Rx’s
• Why sodium bicarb
• Right kind of vitamin D
• Phosphate binders
• Iron folate Vit B12

Question 8

Chronic Kidney Disease (CKD)

Answer 8

• Long – standing progressive impairment
– Rate of progression depends on cause
– One suggested pathway – glomerular
hyperfiltration
• Reversible in some circumstances
– Removal of urinary tract obstruction
– Correction of arterial narrowing

Question 9

Symptoms of CKD

Answer 9

• Symptoms of underlying cause
• Uraemia
– When >40mmol/L
• N&V, diarrhoea, malaise, anaemia
• ↓ appetite, insomnia, restless legs, paraesthesiae
• Oedema, nocturia/polyuria, bone pain
– When >50 – 60mmol/L
• More severe
• Serious CNS symptoms
• Oliguria
– AKI
– End stage renal failure (ESRF)

Question 10

CKD - complications

Answer 10

• Cardiovascular disease
– 16 fold increase in incidence
– Large number of risk factors
• Anaemia
– Due to erythropoietin deficiency
• Bone disease (renal osteodystrophy)
– Active Vitamin D ↓ and calcium ↓
– Hyperparathyroidism
• Skin disease
• GI complications
• Metabolic abnormalities
• Endocrine abnormalities
• Uraemic effects

Question 11

Management of CKD

Answer 11

• Treat underlying cause of CKD
• Renoprotection
– Control hypertension
– ↓ proteinuria
• Control of CV risk factors
• Correction of anaemia
• Management of calcium, phosphate &
potassium levels
• Suppression of PTH
• Transplant

Question 12

Drug Handling in Renal Impairment

Answer 12

• Absorption
– Unpredictable in uraemia
• Distribution
– ↓ protein binding
– affected by fluid overload / depletion
• Metabolism
– ↓ catabolism – eg insulin
– ↓ conversion of precursor to active metabolite
• Elimination
– ↓ especially in renally excreted drugs
• End organ sensitivity
– Renal response may be ↓ eg thiazide diuretics