Lec 4- Acute and Chronic Kidney disease

Question 1

Anatomy

Answer 1

*

Question 2

The kidney

Answer 2

Question 3

What do the kidneys do?

Answer 3

• Removes waste products from the body
  
  • Nitrogenous (Urea), electrolytes
• Acid-base homeostasis- metabolic acidosis/alkalosis
• Fluid balance
  
  • Anti-diuretic hormone (ADH)
• BP regulation
  
  • Renin-Angiotensin-Aldosterone System (RAAS)
• EPO production
• Excrete drugs from the body
• Vitamin D metabolism (to produce active metabolites)
• Insulin metabolism

Question 4

Effects of CKD

Question 5

How do we measure renal function

Answer 5

• Creatinine
• 24-hour urine collection
• 51 chromium (EDTA test)- for patients on chemotherapy or narrow TI drugs
• Cystatin C eGFR
• Prediction equations
  
  • Modification of diet in renal disease (MDRD eGFR)
    
    • Becomes more useful <60mL/min or in stages 3/4
    • Tends to over estimate renal function at a lower level
      
      • Particularly in obesity, muscle mass and fluid overload
  • Cockcroft-Gault (CrCl)
    
    • Useful for bedside calculation and drug dosing
    • Not for diagnosis

Question 6

Cockcroft-Gaultcalculation of creatinine clearance (CrCl)

Answer 6

Question 7

What is acute kidney injury (AKI)

Answer 7

• Replaces the old terminology AFR
• An abrupt decline in renal function over hours or days
• Defined : An acute rise in serum creatinine OR a reduction in urinne output (As compared with CKD)

Question 8

Why is AKI important

Answer 8

• It is estimated there are 350,000 to 750,000 cases of AKI every year
• AKI causes up to 100,000 deaths a year
• The cost to the NHS is estimated to be £500 million each year
• AKI is common, harmful and in many cases preventable
• AKI is a marker of a more seriously unwell patient
• One in five emergency admissions to hospital has AKI
• AKI leads to failure to excrete toxins and regulate electrolytes, acid-base and volume status
• Some patients may require long term dialysis following AKI

Question 9

AKI- different to CKD

Answer 9

• The rapid decline over hours or days
• Can be reversible
• Many patients become oliguric (Low urine output- can be anuric (no output))
• If pre-existing renal impairment the ‘acute on chronic’
• Can be
  
  • Pre-renal (40-80%)- normally drug induces, due to low perfusion to the kidney
  • Intra-renal (10-50%)- autoimmune, drug-induced
  • Post-renal (<10%)- BPH, obstruction

Question 10

Causes of AKI

1) Pre-renal

Answer 10

• Sudden and severe drop in BP
• Interruption of blood flow to the kidneys from severe injury or illness

Question 11

Causes of AKI

2) Intrarenal

Answer 11

• Direct damage to the kidneys by inflammation
• Toxins
• Drugs
• Infection
• Reduced blood supply

Question 12

Causes of AKI

3) Post-renal

Answer 12

• Sudden obstruction of urine flow due to elarged prostate
• Kidney stones
• Bladder tumour
• Injury

Question 13

Staging of AKI

Answer 13

Question 14

Defining AKI

Answer 14

Question 15

Investigations of AKI

Answer 15

• Pharmacological management
  
  • Drug history (review nephrotoxins)
• Clinical examination
  
  • Pre-renal: reduced skin turgor, hypotensive
  • Intra-renal: rash, vasculitic lesions- spots on the skin
  • Post renal: distended bladder, BPH (Begin Prostatic Hyperplasia)
• Urinalysis
  
  • Pre-renal: concentrated urine
  • Intra-renal: isotonic urine
  • Obstructive post renal: Anuria or crystalluria–Glomerularnephritis: proteinuria and haematuria
• Blood examination
  
  • Identify AKI -Cr, Urea, albumin
  • Identify the cause: ESR, WCC, renal biochemistry screen, immunological tests
• Ultrasound of renal tract, biopsy

Question 16

Complications of AKI

Answer 16

• High BP and subsequent damage
• Confusion
• Dehydration, nausea and vomiting
• Serious infection and death (hyperkalaemia)
• Hyperkalaemia- fluid balance changes
  
  • Urinary excretion reduced and intracellular K+ released
  • Rapid rises in extracellular potassium in tissue damage, sepsis, AF
  • Treatment (IV insulin/glucose, calcium gluconate IV, calcium sodium, salbutamol nebulisers, sodium bicarbonate IV)
• Hyperphosphatemia-
  
  • Phosphate excreted by the kidney
  • Phosphate binders with food
• Hypocalcaemia- impairment in vitamin D metabolism
  
  • Malabsorption secondary to disordered vit D metabolism
  • Asymptomatic until <1.6-1.7mmol/L
  • Oral replacement if needed
• Acidosis- metabolic acidosis
  
  • Inability to excrete hydrogen ions
  • Can treat with oral sodium bicarbonate 1-6g/day or IV sodium bicarbonate polyfusor

Question 17

Treating AKI

Answer 17

• The mainstay of treatment is stopping/withholding nephrotoxins
• Further treatment depends on the cause/stage of AKI
• Monitor renal function
• Fluid resuscitation- Normally fluid challange (small amount over 30 minutes to see output if ok then we give them the rest of the bag)
• Appropriate drug dosing (frequency and strength)
• Managing patient acutely
• CANDA pneumonic

Question 18

Drugs to avoid/reduce in renal patients

Answer 18

• Aminoglycosides
• gentamicin
• Contrast Media
• Bisphosphonates
• LMWH- important to watch as most hospital patients on this
• Statins- interstitial AKI
• Aciclovir
• Opioids
• NSAIDs
• ACE inhibitors
• Allopurinol
• Digoxin
• Lithium- Narrow TI

Question 19

Sick day guidance

Answer 19

• When you are unwell with any of the following
  
  • Vomiting or diarrhoea (Unless minor)
  • Fevers, sweats and shaking
• Then stop taking medication listed
• Restart when you are well (After 24-48 hours of eating and drinking normally)