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Flashcards in Renal & Urology Overview Deck (118)
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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 


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 


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 


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


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


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 




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


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


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 


500ml of 0.9% saline over 15 minutes 


  • this looks like a pre-renal AKI


  • need to give an IV fluid bolus and maintenance fluids


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


What mnemonic can be used to remember the nephrotoxic drugs?



  • D - diuretics


  • A - ACEi / ARBs


  • M - metformin (can predispose to lactic acidosis)


  • N - NSAIDs


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 


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


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


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)


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 




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 


What are the risk factors for AKI?


What mnemonic can be used?



  • 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 


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 


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 


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


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

  • cardiorenal syndrome


  • hepatorenal syndrome


  • renal artery stenosis


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 


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


What is involved in investigations for pre-renal AKI?

Urine dipstick:

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



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



  • 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 


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


Which class of antibiotics are known to be nephrotoxic?



(e.g. amikacin, gentamicin)


these can cause acute tubular necrosis 


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 


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