This MCQ tests your knowledge of the physiological and pathophysiological principles behind the GFR.
Reviewed by Jonathan Loomes-Vrdoljak
Glomerular filtration and assessment of renal function
What is glomerular filtration rate (GFR)?
The concentration of metabolites that are filtered by one kidney / unit time
The volume of water reabsorbed by the kidneys/ unit time
The total volume of filtrate formed by all nephrons in both kidneys/ unit time
The volume of filtrate that is reabsorbed by the kidneys/ unit time
How is glomerular filtration rate (GFR) altered by acute kidney injury?
Only reabsorption is altered
How is GFR calculated?
GFR = ClX = (UX)
GFR = Kf x NFP
GFR = PG – PB – πG + πB
GFR = Urinary excretion rate = Filtration rate + Secretion rate – Reabsorption rate
Which parameter of the GFR equation does diabetic nephropathy most likely alter?
Kf, as the surface area available for filtration is reduced
Kf, as membrane permeability is increased
NFP as the oncotic pressure if the blood is increased
NFP as the oncotic pressure if the filtrate is increased
What is Net Filtration Pressure (NFP)?
NFP = PG + PB – πG + πB
NFP = PG – PB + πG + πB
NFP = PG – PB – πG - πB
NFP = PG – PB – πG + πB
Your patient has liver failure and is unable to produce albumin. How does this affect the net filtration pressure (NFP)?
The Bowman’s capsule colloid pressure increases, reducing NFP
Blood plasma oncotic pressure decreases, increasing NFP
Blood plasma oncotic pressure increases, increasing NFP
Blood plasma hydrostatic pressure increases, increasing NFP
For a more comprehensive discussion of the relationship between liver disease and GFR see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552961/.
What is the main way the body regulates GFR with reference to the equation GFR = Kf x NFP?
By altering net filtration pressure, specifically by altering PG
By altering net filtration pressure, specifically by altering PB
By altering blood plasma oncotic pressure, πG
By altering filtrate oncotic pressure, πB
Which of the following is false?
Dilation of the afferent arteriole or constriction of the efferent arteriole increases GFR
Angiotensin 2 constricts the efferent arteriole, increasing GFR
Prostoglandins and atrial natriuretic peptide dilate the afferent arteriole, increasing GFR
Noradrenaline, adenosine and endothelin dilate the afferent arteriole increasing GFR
A patient takes NSAIDs for their backache. What effect can we expect this drug to have on that patient’s GFR?
The kidney maintains a constant renal blood flow rate between 80 and 180 mmHg. The kidney can partly autoregulate this pressure by responding to changes detected by stretch receptors. What name is the given to this mechanism?
If sodium and chloride transport in the early DCT was blocked, how would this impact the kidneys' ability to maintain a constant renal flow rate?
The myogenic response is impaired as depolarisation and subsequent muscle contraction is started by sodium influx into the cell
The tubuloglomerular response would not be activated by the macula densa cells
The juxtaglomerular cells are unable to release renin
There would be no impact on the renal flow rate as these transporters are present in the late DCT
Describe the cascade of events that result from the detection of low blood pressure by the kidney
Renin is released by juxtaglomerular cells —> Renin converts angiotensinogen to angiotensin I —> angiotensin I is converted to angiotensin II by angiotensin converting enzyme
ADH is released by juxtaglomerular cells —> ADH converts angiotensinogen to angiotensin I —> angiotensin I is converted to angiotensin II by angiotensin converting enzyme
Renin is released by juxtaglomerular cells —> dilates the afferent arteriole
Renin is released by juxtaglomerular cells —> constricts the efferent arteriole
Why is ramipril prescribed for patients with hypertension?
Pharmaceutical companies are peddling a useless drug
It blocks the conversion of angiotensin I to angiotensin II reducing blood pressure
It blocks the conversion of angiotensinogen to angiotensin I reducing blood pressure
It catalyses the conversion of angiotensinogen to angiotensin I reducing blood pressure
Which investigations are not helpful in identifying kidney abnormalities?
Peak flow rate
What is the best overall indicator of kidney function?
Your patient has a urine production rate of 2 ml/min, excretes your metabolite of interest at 2 mg/ml, and is present in their blood plasma at 4 mg/ml. Calculate the patient’s renal clearance.
What is the relationship between the renal clearance of creatinine and GFR?
Creatinine is not filtered or secreted
Creatinine is filtered and secreted and thus overestimates GFR
Creatinine is filtered and reabsorbed, so it underestimates GFR
Creatinine is completely reabsorbed, and thus is of no value as a marker for GFR
One of your patients is a body builder. You take a urine sample and find that their urine creatinine is equal to the GFR of someone fitting their demographic, how do you interpret this result?
This is a normal result. Their GFR is better than that of the normal population because they are fit.
This is an abnormal result. Their GFR is reduced as creatinine normally overestimates GFR and they are a body builder.
This is a normal result. Creatinine is involved in the production of muscle so you would expect that body builders would excrete less.
This is a normal result. Serum creatinine underestimates GFR.
What is a limitation of estimating GFR using serum creatinine?
You can lose 50% of your kidney function and still have normal creatinine levels
The sample is expensive to process
The sample is difficult to obtain
There are no limitations
Which variable does not alter serum creatinine concentrations?
A patient with an amputation presents to clinic. How do you expect their actual GFR to be related to the eGFR that you have calculated?
The patient’s eGFR will underestimate the patient's true GFR
They will both be the same
The patient’s eGFR will overestimate the patient's true GFR
The amputation has nothing to do with their GFR