Renal & Urology Overview Flashcards
(118 cards)
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?
DAMN
- 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?
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
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














































