Renal: Nephrotic Syndrome: Free MSRA Podcast

⚕️ FREE MSRA PODCAST – Nephrotic Syndrome
🎧 A clear, high-yield breakdown of this renal condition causing massive proteinuria and oedema – perfect for exam prep and real-life clinical scenarios.

🧠 Key Learning Points

📌 Definition
• Nephrotic syndrome is a glomerular disorder marked by:
– Heavy proteinuria >3.5g/24h
– Hypoalbuminaemia <30g/L
– Oedema
– Hyperlipidaemia

📌 Causes & Risk Factors
• Primary renal causes:
– Minimal change disease (esp. in children)
– FSGS (focal segmental glomerulosclerosis)
– Membranous nephropathy
– Membranoproliferative GN
• Secondary causes:
– Diabetes, SLE, amyloidosis
– Infections: Hep B/C, HIV, malaria
– Malignancy: myeloma, lymphoma
– Drugs: NSAIDs, captopril
– Pregnancy (pre-eclampsia), transplant rejection
🧠 Mnemonic: “HOPED” – Heavy proteinuria, Oedema, low Protein (albumin), Elevated lipids, Differential causes

📌 Pathophysiology
• Glomerular damage → increased permeability
• Albumin leaks → ↓ oncotic pressure → fluid shifts → oedema
• Liver compensates → ↑ lipoprotein synthesis → hyperlipidaemia
• Immunoglobulin & antithrombin loss → infection + clot risk

📌 Symptoms
• Generalised oedema: ankles, periorbital, ascites
• Foamy urine (from proteinuria)
• Fatigue, weight gain
• SOB (pleural effusion), oliguria
• In children: delayed growth/puberty
🧠 Pearl: Look for “Muehrcke’s lines” – transverse white nail bands in hypoalbuminaemia

📌 Differential Diagnosis
• Acute glomerulonephritis
• CKD
• Diabetic nephropathy
• Cardiac/liver failure (causing oedema)
• Protein-losing enteropathy

📌 Diagnosis
• Urine:
– Dipstick: +++ protein
– PCR or ACR (spot or 24h)
– Urine microscopy: fatty casts
• Bloods:
– ↓ Albumin, ↑ lipids
– U&Es, LFTs, immunology (ANA, complement, serum light chains)
• Imaging:
– Renal US
– CXR (pleural effusion)
• Renal biopsy:
– Essential in adults to define glomerular disease
– Often not needed in typical paediatric minimal change disease

📌 Management
• Treat underlying cause
• Corticosteroids – 1st line for minimal change
• Other immunosuppressants: cyclophosphamide, mycophenolate, tacrolimus
• ACEi/ARBs: reduce proteinuria + control BP
• Diuretics: loop diuretics ± thiazides for oedema
• Statins for hyperlipidaemia
• Anticoagulation if VTE or high clot risk
• IV albumin: only for severe hypoalbuminaemia
• Vaccination: pneumococcal, varicella
• Diet: salt restriction, fluid restriction, weight monitoring
• Daily weights + leg elevation helpful in oedema control
• Urgent nephrology referral always indicated

📌 Complications
• Thromboembolism (DVT, renal vein thrombosis)
• Infections (due to immunoglobulin loss + immunosuppression)
• Acute kidney injury
• Chronic kidney disease/ESRD
• Hypocalcaemia, bone disease, hypothyroidism, anaemia

📌 Prognosis
• Minimal change disease: excellent

Episode Transcript

(00:00):
All right, let's crack open someserious knowledge here.
You've given us your revision notes on nephrotic syndrome and
consider this our mission, really to take this, you know,
stack of information and just distil the absolute most
important insights. Yeah.
Get right to the core of it. Exactly.
We're going on a deep dive, pullout the crucial details, make
sense of the connections, and hopefully help you get a really

(00:23):
clear picture of this condition fast.
Absolutely. And having these structured
notes, it's, well, it's gold, isn't it?
It gives us a clear path, and our goal is just to walk that
path with you kind of highlighting the landmarks,
giving some context. We're going to cover everything
laid out right here, sticking strictly to this material to
really understand nephrotic syndrome from definition right

(00:44):
through to the complication. OK, perfect.
So let's jump right in then. At its core, what exactly is
nephrotic syndrome? What are the, you know, the
defining features we absolutely need to know?
So it's fundamentally a kidney disorder specifically affecting
the kidneys filtering units. The glamorally.
Precisely, and the notes, they pinpoint 4 key characteristics

(01:06):
that really define it. You need this specific pattern.
OK, lay them on us, the four. 1st and probably most central is
heavy protein area. We're talking about losing a lot
of protein in the urine. How?
Much is a lot. The notes specify more than 3.5
grammes over 24 hours. Wow.
OK. That level of protein loss is

(01:27):
significant. And clinically thinking about
symptoms, this is where that phoney urine thing comes in,
right? Exactly.
That's often a visual clue for patients.
So second is hypoalbuminemia. Low Albumin.
Yeah, low albumin, it's a key protein in the blood.
The threshold here typically less than 30 grammes per litre.
Sometimes the notes say even under 25.
Right. And losing all that protein from
the blood, especially albumin that has big knock on effects.

(01:50):
Which leads us to #3. Edoema.
Swelling. Swelling.
Yeah. Usually starting where the legs,
ankles, peripheral edoema. That's the typical starting
point. It's because albumin, it sort of
helps hold fluid within your blood vessels, right?
When it's low, that fluid just well leaks out into the
surrounding tissues. OK.
And the fourth key characteristic.

(02:11):
Hyperlipidemia, so elevated levels of fats like cholesterol
in the blood. OK, so let's recap.
The picture is a kidney problem.Glomerular damage.
Causing massive protein loss in the urine.
Proteinuria. Leading to low protein in the
blood. Hypoalbuminemia.
Which causes the swelling. Edoema.
And you often see high fats alongside it.

(02:32):
Hyperlipidemia. You got it.
That's the tetrad. And the underlying issue driving
all of this, as the notes describe, is damage to those
kidney philtres, the glomeruli, the.
Linky sieve. That's a great analogy.
They're supposed to keep big things like protein in the
blood, but when they're damaged,the holes get too big.
So proteins, especially albumin,just slip right through.

(02:52):
Exactly into the urine in excessive amount.
The notes also add that along with these core features, you
often see other consequences or associations, things like
coagulation abnormalities. Clotting problem.
Yeah, a reduction in overall kidney function and sometimes
immunological issues too. That makes perfect sense.
It's like a cascade effect from that initial kidney damage.

(03:13):
Now, a really crucial point thatwas raised early on in the notes
is that while often the exact reason, it isn't clear, it's
idiopathic. Right, right.
Often is. The causes that we can identify
differ quite a bit depending on a person's age.
That feels like a really high yield piece of info for anyone
listening. It absolutely is huge point.
And that takes us neatly into the aetiology.

(03:36):
You know what causes this glomerular damage in the first
place? The sources break this down
neatly into primary and secondary causes.
OK. So primary means the problem
starts in the kidney itself likeit's a kidney specific disease,
correct? Problems with the glomeruli
themselves. The key primary causes
highlighted are minimal change glomerular disease.
The one common in children. Exactly noted as very common in

(03:58):
kids. Then in adults, the more common
primary culprits are focal segmental glomerulosclerosis,
FSGS, and membranous nephropathy.
Membrano proliferative glomerulonephritis is also
mentioned, affecting both children and young adults.
Right. And then the secondary causes,
this is where it connects to other stuff going on in the body
that ends up affecting the kidneys.

(04:19):
The lists look pretty long. It is, and it's important
because it shows nephrotic syndrome isn't always just about
the kidney in isolation. So what are some big categories
here? Well, the notes group them
nicely. You've got systemic problems
like infections. Bacterial, viral, parasitic are
listed OK. Immunological or inflammatory
conditions are key. Think lupus, rheumatoid
arthritis, prime examples. Right, autoimmune stuff.

(04:42):
Exactly. Metabolic diseases are
significant too, notably diabetes and amyloidosis.
Then there are inherited causes like Alport syndrome, certain
malignant diseases like multiplemyeloma.
Myeloma, OK. And even specific drugs.
The notes list nsides and captopril.
Wow, Nsis are so common. That's really worth remembering.

(05:03):
And I saw insect stings on that list too.
That seems random. It just shows how diverse the
triggers can potentially be. Also on that secondary list are
pregnancy related issues, specifically preeclampsia and
even transplant rejection. So it really underscores that
this can be a sign of something much bigger happening
systemically. Absolutely, which leads nicely
into risk factors. Thinking about susceptibility,

(05:25):
are there specific things mentioned that makes someone
more likely to develop this? Yeah, what makes someone more at
risk? Well, unsurprisingly, the risk
factors described really mirror the causes we just talked about.
Makes sense. So a personal or family history
of kidney disease is a risk thatlinks to inherited causes or
just underlying kidney vulnerabilities.

(05:46):
Having autoimmune diseases like lupus or RA obviously increases
risk because they are listed secondary causes, certain
infections, same logic and the use of specific drugs like those
NS 80s we mentioned. It all ties back to that list of
secondary causes. So if someone listening has,
say, a history of uncontrolled diabetes or they're on certain

(06:07):
long term meds, a clinician would be sort of more attuned to
the possibility of nephrotic syndrome if they show up with
swelling or, you know, other symptoms.
Precisely knowing these potential triggers and risk
factors helps guide that initialsuspicion and points you towards
the right investigations. OK, let's maybe just quickly

(06:28):
revisit the path of Physiology. How does this actually play out
inside the body? We use the leaky flicker
analogy, but what's the core mechanism?
Yeah. The central problem, as we
touched on, is that glomerular damage leading to increased
permeability, the philtre gets leaky, right?
So the kidneys, philtres are meant to be selective sieves,
right? Let's small waste out, keep the

(06:48):
big important stuff like proteins in the blood.
But when the philtre is damaged,the holes get bigger.
Essentially, yes. Larger pores or actual breaks in
that filtration barrier. This allows those larger
proteins, especially albumin, tojust escape from the bloodstream
and spill out into the urine waytoo much.
And that massive protein loss, that's the defining event.

(07:08):
It is losing so much protein, especially albumin directly
causes the low blood protein level, the hypoalbuminemia.
Which then causes the swelling, the edoema.
Yes, because there isn't enough protein, specifically albumin,
in the blood vessels to exert oncotic pressure and hold fluid
inside them, so it leaks out into tissues causing edoema

(07:29):
sites pleural effusions. OK.
And the high fats? The hyperlipidemia.
That's a more complex consequence, thought to be
related to the liver trying to compensate for the protein loss,
but it's part of that cascade. It's all a chain reaction,
starting with that damaged philtre.
And the notes stressed that the specific way the damage happens,
the exact pathophysiology can vary depending on the underlying

(07:51):
'cause right? Which is why finding in the
cause is so vital for treatment.Exactly right.
The mechanism in minimal change disease is very different from
say diabetic nephropathy, even though both can lead to
nephrotic syndrome. OK.
So given these hallmark features, yeah, heavy protein
loss, swelling, what other conditions might, you know, look
similar? What else could be on the

(08:11):
differential diagnosis list? Yeah, differentials are crucial.
You need to rule out mimics. The notes mention key conditions
like acute glomerulonephritis, chronic kidney disease and
diabetic nephropathy. And these can also involve
protein in the urine or some swelling.
They absolutely can, yes, but the distinguishing factor which
the notes emphasise is often thespecific combination and

(08:33):
crucially, the severity of the features.
Wow, right? Nephrotic syndrome is defined by
that heavy proteinuria, the significant hypoalbuminemia plus
the edoema and hyperlipidemia. Other conditions might have some
protein loss or some swelling, but the whole package and the
sheer magnitude of these findings often points more
definitively towards nephrotic syndrome.

(08:53):
Got it. So it's not just a bit of
protein, it's a really pronounced pattern.
OK, let's get a sense of scale. How common is this condition?
What's the epidemiology look like?
Well, the numbers give some context, though the notes do
mention specific UK data can be a bit limited.
The estimated annual incidence for adults in the UK is
somewhere around two to seven cases per 100,000 people.
Relatively uncommon overall. Relatively, yeah.

(09:16):
Globally, it's estimated around 3 per 100,000 for adults.
For children globally, the incidence seems to vary a bit
more, maybe 2 to almost 17 casesper 100,000.
But the really crucial take awayfrom the epidemiology section
again reinforces that point we made earlier about age and
'cause. That huge difference between
kids and adults. Exactly.

(09:36):
In adults, something like 8090% of cases are idiopathic, meaning
the cause isn't obvious or the known.
Preliminary causes are typicallyFSGS and membranous nephropathy,
and secondary causes like type 2diabetes and SLE are also common
in adults. But in kids?
But in children, minimal change,disease just dominates, accounts

(09:57):
for a massive 7090% of cases. Wow, that is a dramatic
difference. Minimal change is still seen in
adults, Yeah. It is, but only accounts for
maybe 1025% of adult cases. So this age distinction is
clearly a defining epidemiological feature.
And that obviously has big implications for how you'd
approach diagnosis and treatmentbased on age.
Absolutely. It significantly influences the

(10:19):
likely diagnosis and that initial management approach,
especially the question of whether you need a biopsy
upfront. Right.
So putting ourselves in the shoes, is someone actually
experiencing this? Yeah.
What does it look and feel like?What are the clinical features
listed in the notes? OK.
So the most obvious, the most common presentation is that new
onset swelling usually starts inthe lower extremities, legs,

(10:41):
ankles. Peripheral edoema.
Right, and the notes detail how this edoema can become much more
widespread as things get more severe.
Spreading up the body to the abdomen maybe?
Yeah, potentially leading to a site's fluid in the abdomen and
also periorbital edoema that's swelling around the eyes.
OK. And all that fluid buildup
obviously means. Significant weight gain, often

(11:02):
quite rapid. Other symptoms people frequently
report are fatigue, just feelingwiped out, sometimes decreased
urine output, Alleguria and shortness of breath, especially
with exertion. Exertional Dyspenoia.
And that's due to fluid around the lungs, pleural effusion,
that's. Often the cause, yeah.
Other symptoms listed include hypertension, which can develop
discomfort just from the swelling itself, abdominal or

(11:25):
genital discomfort, dizziness, abdominal cramps.
The notes also mentioned signs pointing towards complications
like infections or clots. Yes, exactly.
So things like fever, nausea, vomiting could suggest an
infection. Pain, swelling, redness in a
limb might point towards a DVTA blood clot, and in children

(11:45):
specifically, growth issues or delayed puberty can be features.
OK. And what about on physical
examination? What would a clinician be
looking for? Well, obviously the edoema
itself checking its extent, listening to the chest for signs
of pleural effusion causing breathlessness.
But interestingly, despite all that swelling, someone can
actually show signs of hypovolemia, low blood volume

(12:06):
within the vessels. The paradox we mentioned
earlier, fluids in the tissues not circulating properly, How
would that manifest? The notes list things like a
fast heart rate, tachycardia, cold hands and feet, cold
peripheries, and that low urine output oliguria which we already
mentioned as a symptom. So fast heart rate, cold
extremities, low urine output despite being swollen elsewhere.

(12:27):
That's a key clinical Pearl feels kind of intuitive at
first. It does.
Other signs can include those related to the hyperlipidemia,
the high fats. Sometimes you might see
xanthomata or xanthelasmata, which are these visible fatty
deposits under the skin. And of course you'd be looking
for any signs pointing to a potential secondary cause, like
a rash or joint swelling suggesting lupus for instance.

(12:50):
And there was that one really specific kind of memorable sign
mentioned in the notes. Oh yes, the fingernails.
Mirakis Lines. Mirakis lines those transverse
white lines across the nails. They're highly associated with
significant hypoalbuminemia. A classic textbook sign, really.
OK, so you see this pattern of symptoms, these signs, how do
you actually confirm the diagnosis and figure out the

(13:14):
underlying cause? What investigations are key?
Right. The investigations are crucial.
They aim to one, confirm those core diagnostic criteria we
talked about and two, search forthe underlying cause and any
complications. Urine tests are absolutely
foundational. Makes sense.
You need to quantify that protein loss.
Exactly, so a 24 hour urine collection or more commonly now

(13:37):
a spot urine protein to creatinine ratio tells you how
much protein is being lost. Confirms the heavy protein area.
OK, Anything else in the urine? The notes also mentioned looking
at the urine sediment under a microscope for cellular casts
like fatty casts or red blood cell casts.
These can sometimes give clues about the specific type of
kidney damage happening. Right.

(13:57):
And then blood tests to check the other core features.
Absolutely. Serum albumin obviously to
confirm the low blood protein, Urea and electrolytes to check
overall kidney function, lipid levels to assess the
hyperlipidemia. Standard stuff like liver
function tests too. What about tests to hunt for
those secondary causes? Yeah, that's key.
The notes list things like serumlight chains and protein

(14:20):
electrophoresis, especially if you're suspecting something like
multiple myeloma, tests for infections like HIV complement
levels, and auto antibodies likeAna antinuclear antibody if
you're thinking about autoimmuneconditions like lupus.
And imaging, I saw a chest X-rayand ultrasound mentioned, Yeah.
Chest X-ray, mainly to look for pleural effusion and a renal or

(14:42):
abdominal ultrasound is important to assess the kidney
size and structure, check for any blockages, and can also help
guide a biopsy if needed. Right, the biopsy.
The notes seem to really emphasise the renal biopsy.
Why is that often so vital? It often is, especially in
adults, Notes state. It's needed if the diagnosis
isn't crystal clear or specifically in adults, because

(15:04):
that range of potential causes, particularly the primary
glomerular diseases, is just so much wider than in children.
OK, the biopsy let's pathologistactually look at the kidney
tissue under a microscope. It allows them to identify the
exact type of glomerular damage.And knowing that specific type
is critical because. Because the specific type of
damage often dictates the specific treatment strategy, it

(15:25):
also helps predict the likely prognosis, how things might go
long term. But there was that exception for
children you mentioned earlier. Yes, exactly.
Because minimal change disease is so so common in children and
it usually responds really well to initial steroid therapy, a
renal biopsy is often not neededinitially in children who
present typically for minimal change disease, you usually try

(15:47):
treatment first. Only if they don't respond or if
the presentation is unusual would you then consider a biopsy
in a child. That's a major difference in
approach based purely on age. Got it.
And the investigations would also cover checking for
potential complications like that clotting risk.
Correct. So a full blood count, checking

(16:08):
for anaemia and a coagulation screen would definitely be part
of the standard work up. OK.
So once it's all diagnosed, cause of identified, hopefully
what's the management plan? What does treatment actually
involve? So management has several key
goals as outlined in the notes. You want to reduce that
proteinuria. Stop the leaks.
Exactly control blood pressure, manage the edoema, the swelling,

(16:29):
and crucially treat the underlying 'cause if you've
identified 1 and if it's treatable.
And the mainstream medications often involve hitting the immune
system right, especially for those primary causes.
That's often the case, yes, particularly corticosteroids.
They're frequently the first line treatment, especially for
things like minimal change disease.
OK. For cases that don't respond or

(16:49):
for specific underlying diagnosis identified on biopsy,
other immunosuppressants come into play.
The notes list examples like cyclophosphamide,
mycophenolimaphetil, calcinirin inhibitors like Hycolimus or
rituximab, and. Managing blood pressure isn't
just about blood pressure. It helps the kidney too.
Absolutely critical hypertensioncontrol is vital, and the notes

(17:11):
specifically highlight using ACEinhibitors or Arb's angiotensin
receptor blockers. Why those specifically?
Because not only do they lower blood pressure, they also have a
direct effect on reducing protein loss in the urine.
That's a really key therapeutic benefit in nephrotic syndrome.
Double whammy. Nice.
And what about tackling those complications?
We talked about the high fats, the clots.

(17:32):
Yep, management includes addressing those directly.
So statins for the hyperlipidemia, for patients at
high risk of blood clots, or obviously if a clot actually
occurs, anticoagulants are necessary.
And what about giving IV albuminback if it's so low?
That's mentioned, intravenous albumin might be considered for
severe hypoalbuminemia, especially if someone is very

(17:54):
volume depleted, but the notes indicate this approach is kind
of variable, maybe more for symptomatic relief in specific
situations rather than routine treatment.
OK, what about things beyond prescribing any lifestyle or
dietary advice? Oh definitely.
Non prescribing management is vital.
Dietary sodium, salt restrictionand often fluid restriction are

(18:14):
key to managing the edoema. Right, less fluid and less
swelling. Exactly.
For milder swelling, just simplethings like elevating the legs
when sitting, maybe using compression stockings can help.
And daily weight cheques are really important.
They help monitor fluid balance and see how well diuretics are
working if they're being used. Any other important points?
Vaccinations. Yes, good point.

(18:35):
Due to the increased risk of infection both from the disease
and potentially the immunosuppressive treatment,
vaccines are advised, particularly the pneumococcal
vaccine and the chicken pox vaccine for children if they
haven't had it or been vaccinated.
And is this typically managed byAGP or do you need a specialist?
The notes are pretty clear on this urgent referral to a

(18:56):
nephrologist. A kidney specialist is essential
for a proper investigation, diagnosis and ongoing
management. Makes sense.
Are there times when someone needs to be admitted to hospital
straight away? Yes.
The notes list indications for acute hospital admission, things
like really severe refractory edoema, developing serious
complications like a blood clot or severe infection, maybe

(19:18):
inability to comply with treatment at home, or if there
are features suggesting nephrotic syndrome alongside the
nephrotic picture. OK, So finally, let's look
ahead. What's the prognosis?
What's the likely outlook for someone diagnosed with nephrotic
syndrome? Well, the notes make it very
clear that the prognosis varies hugely.
It really depends primarily on the underlying cause and how

(19:39):
well the condition responds to the treatment given.
So some causes have a much better outlook than others.
Dramatically so, minimal change.Disease, especially in children,
generally has a very favourable outlook.
Many achieve complete remission,meaning the protein leak stops,
although collapses can definitely happen down the line.
But other types might not be so straightforward.

(19:59):
Unfortunately, yes. More severe cases or certain
primary diseases like FSGS, particularly if they don't
respond well to steroids, can progress over time to chronic
kidney disease, CKD, or even endstage renal failure.
ESRF. Requiring dialysis or transplant
eventually. Potentially yes, and there was
that specific statistic mentioned for FSGS in adults.

(20:22):
Yeah, I remember seeing that. The notes state that about 50
percent of adults with idiopathic FSGS may progress to
ESRD within 5 to 10 years. That really brings home the
potential seriousness and the variability depending on the
specific type. That's quite sobering, but
treatment has improved things overall.
Oh absolutely. The historical note mentioned
that the introduction of corticosteroids dramatically

(20:43):
improved survival rates comparedto the pre steroid era treatment
makes a huge difference. OK.
And just to quickly recap those potential complications one last
time, what are the main things we need to be aware of and why
do they happen? Sure.
So the complications are really direct consequences of the
syndrome's effects. Infections are common.
That's due to weakened immunity,partly from losing

(21:04):
immunoglobulins in the urine, partly from the
immunosuppressive treatments used, blood clots, venous
thromboembolism, VTE including DVT in the legs, and potentially
renal vein thrombosis clots in the kidney veins.
That's a high risk because the condition causes a
hypercoagulable state. The blood is stickier.

(21:25):
Right clotting risk is a big one.
Huge one acute kidney injury canhappen, especially if volume
depletion gets severe and then the big long term 1 is
progression to chronic kidney disease or ESRF, particularly
with steroid resistant types or certain underlying causes like
amyloidosis or advanced diabeticnephropathy.
And there were also issues with bones and thyroid mentioned.

(21:46):
Yes, less common maybe, but boneconditions like ostatis
fibrosis, cystica or osteomalacia can occur due to
changes in calcium invite of D metabolism partly related to
protein loss, and the syndrome can sometimes trigger or worsen
hyperthyroidism. Anaemia can also occur partly
from losing iron binding proteins or erythropoietin

(22:06):
factors in the urine. Wow.
OK, so we've really taken a deepdive in nephrotic syndrome, all
based on the notes you shared. We've covered what it is that
huge range of potential causes. Primary and secondary, yeah.
How it actually disrupts the body.
The pathophysiology. What symptoms and signs might
make you concerned. The key investigations needed to
pin down the diagnosis and find the cause.

(22:28):
Including that crucial role of biopsy, especially in adults.
Right. And then how it's managed, meds,
diet, the lot, and finally the potential prognosis and those
serious complications to watch out for.
It really is a condition that highlights just how intricate
the kidneys are, doesn't it, andhow their dysfunction can ripple
right through the body. Understanding that specific
underlying cause is just so paramount as it really guides

(22:50):
everything that follows. Absolutely.
Thinking back over everything we've covered, based on your
notes, what's the one thing thatreally stands out to you?
That's a good question. I think considering how much the
prognosis and the specific management hinges on identifying
that precise underlying glomerular disease.
You know the massive difference between treating minimal change

(23:13):
in a child versus managing, say,FSGS in an adult.
It really makes you consider just how vital that initial
diagnostic step can be, sometimes involving an invasive
procedure like the renal biopsy.How critical is getting that
specific pathological diagnosis right at the start to really
shape the entire journey and outcome for a patient?

(23:34):
It's a key decision point. That's a great point to reflect
on. Well, thank you so much for
sharing your notes and allowing us to explore this topic with
you today. My pleasure if you listening are
looking for more high yield information like this, perhaps
as you continue your own learning journey or revision,
you might find some really useful resources over at
pastthemsracom. And don't forget, for additional
free resources, you can always check out freemsracom as well.

(23:57):
Excellent. Well, until our next deep dive.