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Flashcards in Renal & Urology Overview Deck (118)
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1

What are the functions of the kidney?

  • regulation of blood pressure & volume via RAAS
     
  • acid-base balance

 

  • electrolyte balance

 

  • production of new RBCs stimulated by Epo

 

  • contains 1-alpha-hydroxylase, which is needed to produce the active form of vitamin D

 

  • acts as a filter for the excretion of water-soluble waste products 

2

How is the kidney involved in bone metabolism?

  • the prohormone, 25(OH)D is produced in the liver 

 

  • the kidney contains 1-alpha-hydroxylase, which will hydroxylate the prohormone to produce the active hormone

 

  • active vitamin D leads to increased calcium absorption in the gut and the bone 

3

How is renal function measured?

renal function = flow rate from the glomerulus into the Bowman's capsule

 

  • this is the glomerular filtration rate (GFR)
    • it is a measure of the volume of blood being filtered by the glomerulus each minute

 

  • any value of GFR > 90 ml/min is considered normal
    • this means that the glomerulus is filtering 90ml of blood each minute

 

  • GFR typically reduces at a rate of 1 ml/min/year 

4

What is the gold standard measurement of GFR?

  • the only way that GFR can be measured is with inulin clearance

 

  • inulin is freely filtered by the glomerulus, not secreted or reabsorbed in the tubules and is not synthesised or metabolised by the kidney

 

  • calculations involve concentrations of inulin in the urine and serum

5

How can blood urea be used as an endogenous marker of GFR?

 

  • urea is a by-product of protein metabolism that is freely filtered at the glomerulus

 

  • it has variable reabsorption (30-60%) depending on nutritional state, hepatic function and GI bleeding 
    • e.g. GI bleed can raise serum urea 

 

  • raised serum urea can indicate poor kidney function

6

How can serum creatinine be used to estimate GFR (eGFR)?

 

What equation is used to work this out and what factors does it take into account?

  • creatinine is derived from muscle cells, freely filtered at the glomerulus and not reabsorbed

 

  • the Cockcroft-Gault equation is used to estimate creatinine clearance and eGFR
    • this estimates how much creatinine is being cleared from the blood

 

  • creatinine clearance is affected by age, sex, ethnicity and weight
    • more creatinine is produced when there is more muscle mass 

 

 

7

What would a normal urea : creatinine ratio be?

  • urea is reabsorbed by the tubules, but creatinine is not

 

  • normal urea to creatinine ratio is 40:1 to 100:1

 

  • this ratio is used when looking at different types of kidney injury

8

What is the problem with the Cockroft-Gault equation?

  • it is used to measure creatinine clearance as a measure of eGFR

 

  • it often overestimates the true GFR, especially when < 30 ml/min

9

If both of these people have a serum creatinine of 100, why is it important to measure eGFR?

  • creatinine clearance (eGFR) is important to measure when giving drugs that are renally cleared

 

  • if the drugs are not being cleared sufficiently, it can lead to renal toxicity 

10

500ml of 0.9% saline over 15 minutes 

11

  • this looks like a pre-renal AKI

 

  • need to give an IV fluid bolus and maintenance fluids

 

  • hold nephrotoxic medications
    • metformin
    • NSAIDs
    • ACE-inhibitors

12

What mnemonic can be used to remember the nephrotoxic drugs?

DAMN

 

  • D - diuretics

 

  • A - ACEi / ARBs

 

  • M - metformin (can predispose to lactic acidosis)

 

  • N - NSAIDs

13

What is meant by acute kidney injury?

 

Why does it occur and how is it measured?

  • a rapid decline in renal function over hours to days

 

there is failure to maintain homeostasis of:

 

  • fluid - leading to oliguria or volume overload

 

  • electrolytes - leading to hyperkalaemia

 

  • acid-base balance - leading to metabolic acidosis 

 

  • it is measured by looking at urea and creatinine 

14

What are 2 easy ways to spot an AKI?

 

Is it reversible?

  • the easiest way to recognise AKI is that the patient stops peeing

 

  • look at creatinine as this will be acutely raised

 

  • it is potentially reversible

15

What is meant by chronic kidney disease?

 

How is it diagnosed?

 

 

  • this is a chronic and irreversible process with 5 stages

 

  • there must be impaired renal function for > 3 months based on:
    • abnormal structure or function
    • or GFR < 60 ml/min for > 3 months
    • +/- evidence of kidney damage 

 

  • this is progressive and irreversible, ending in end-stage renal failure

 

  • it is monitored by looking at eGFR

16

What symptoms may someone with an AKI present with?

symptoms depend on underlying cause, but typically:

 

  • oliguria / anuria
    • abrupt anuria suggests a post-renal cause 

 

  • nausea & vomiting

 

  • dehydration

 

  • shortness of breath

 

  • confusion
    • encephalopathy from uraemia (build-up of urea in the brain)

17

What signs might someone with AKI present with?

  • hypertension

 

  • distended bladder
    • typically seen with an obstructive cause

 

  • postural hypotension due to dehydration

 

  • if they have fluid overload - raised JVP, peripheral / pulmonary oedema
    • i.e. in cirrhosis, heart failure, nephrotic syndrome

 

  • if they have vascular disease - bruising, rash, pallor 

 

 

18

What classification system is used for AKI?

KDIGO classification system

 

  • need to check the patient's baseline creatinine to determine whether a rise is significant 

 

Stage 1:

  • 1.5x rise in creatinine compared to baseline 
  • OR urine output <0.5 ml/kg/hr for > 6 hours

 

Stage 2:

  • 2x rise in creatinine compared to baseline 
  • OR urine output <0.5 ml/kg/hr for > 12 hours 

 

Stage 3:

  • 3x rise in creatinine compared to baseline
  • OR urine output < 0.3 ml/kg/hr for > 24 hours
  • OR anuria for > 12 hours 

19

What are the risk factors for AKI?

 

What mnemonic can be used?

CHARD CH

 

  • C - chronic kidney disease 
  • H - hypovolaemia
    • this is the most common cause of AKI
  • A - age > 75
  • R - renal transplant
  • D - diabetes

 

  • C - contrast administration
  • H - heart ailure 

20

What is meant by a pre-renal cause of AKI?

 

What 4 states can lead to pre-renal AKI?

there is inadequate perfusion to the kidney

 

when there is decreased blood flow to the glomerulus, there is decreased blood filtration

 

  • this is most commonly due to hypovolaemia

 

  • systemic vasodilatation (e.g. in sepsis)

 

  • decreased cardiac output

 

  • intrarenal vasoconstriction 

21

What is meant by renal and extrarenal losses leading to hypovolaemia and pre-renal AKI?

Renal loss:

  • loss of fluid from diuretic overuse

 

  • osmotic diuresis (e.g. diabetic ketoacidosis)

 

Extrarenal loss:

  • vomiting and/or diarrhoea

 

  • burns

 

  • sweating

 

  • blood loss 

22

What can cause systemic vasodilatation or decreased cardiac output leading to pre-renal AKI?

Systemic vasodilatation:

  • sepsis
  • neurogenic shock

 

Decreased cardiac output:

  • heart failure
  • myocardial infarction

23

What can cause intra-renal vasoconstriction leading to pre-renal AKI?

  • cardiorenal syndrome

 

  • hepatorenal syndrome

 

  • renal artery stenosis

24

What are the consequences of pre-renal AKI?

 

What will happen to the urea:creatinine ratio and why?

  • reduced urine output
    • if there is no bloodflow to the kidney, urine cannot be produced

 

  • urea is raised much higher than creatinine so urea:creatinine > 100:1

 

  • this is due to dehydration and urea resabsorption by the kidneys
    • urea is still being reabsorbed as the kidneys themselves are not damaged 

25

What is involved in the inital management of pre-renal AKI?

 

What factors need to be monitored?

  • start with NEWS monitoring and observe for life-threatening complication
    • should be able to identify hyperkalaemia / hypovolaemia 

 

  • need to treat hypovolaemia 

 

  • catheterise the patient to monitor fluid balance

 

  • need to monitor K+, lactate (for signs of sepsis) and daily creatinine

26

What is involved in investigations for pre-renal AKI?

Urine dipstick:

  • proteinuria and/or haematuria could be a sign of glomerulonephritis 

 

USS:

  • should be performed within 24 hours unless there is an obvious cause 

 

VBG:

  • check electrolytes, glucose & lactate
  • check platelets to rule out thrombotic cause like HUS or TTP

 

  • if AKI does not improve, consider investigations for intrinsic renal disease 

27

What is involved in the management of pre-renal AKI?

  • bolus fluid and maintenance fluid

 

  • treat the underlying cause e.g. sepsis

 

  • stop nephrotoxic medications

 

  • stop / change medications that are heavily renally excreted
    • e.g. LMWH
    • if eGFR < 30 then use another form of prophylactic VTE 

 

  • avoid radiological contrast

28

Which class of antibiotics are known to be nephrotoxic?

aminoglycosides

 

(e.g. amikacin, gentamicin)

 

these can cause acute tubular necrosis 

29

What causes a renal AKI?

 

What are the 4 different types?

  • this is caused by cellular / intrinsic damage to the kidney

 

  • the different types depend on where the damage is located
    • tubular
    • glomerular
    • interstitial
    • vascular 

30

What is the main tubular cause of renal AKI?

 

What causes this?

acute tubular necrosis

 

  • ischaemia

 

  • drugs
    • NSAIDs
    • paracetamol
    • ACE inhibitors

 

  • toxins
    • contrast
    • myoglobulinuria in rhabdomyolysis 

 

  • these cause death of the tubular epithelial cells than form the renal tubules of the kidneys