William Aird Profile picture
Feb 1, 2023 4 tweets 2 min read Read on X
1/4

#GI #GIbleed #urea

Elevated BUN: creatinine ratio favors UPPER over lower GI bleed.

Why?

1) Hb in stomach --> amino acids (aa).
2) aa absorbed by small intestine.
3) aa transported and taken up by liver.
4) In the liver, aa undergo deamination, leading to release of NH3. Image
2/4

5) NH3 (aka ammonia) is converted to urea by the urea cycle, leading to elevated blood urea levels.
6) Meantime, creatinine is not influenced by the protein/aa bolus.
7) Thus, BUN/creatinine ratio is increased.
3/4

So why does blood cause this bump in urea and increase in BUN/creatinine ratio, whereas a steak dinner does not?

Because blood has poor BIOLOGICAL VALIUE (the protein is poorly utilized by the body).

The LOWER the biological value of a protein, the HIGHER the urea.
4/4

For more information see:

thebloodproject.com/cases-archive/…

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More from @WilliamAird4

Feb 13
1/9

I’ve long taught a simple framework for hypoproliferative normocytic anemia that I still love:

• nutritional deficiency
• inflammation
• organ dysfunction (kidney, liver, endocrine, marrow)

Clinically useful. Memorable. Teachable.

And it still holds up. Image
2/9

But conceptually, something interesting is happening.

These categories aren’t actually the same kind of explanation.

Nutritional deficiency and inflammation are mechanisms.
Organ dysfunction is different.

And even within organs, not all behave the same way.
3/9

Take kidney disease.

We often say “anemia from CKD” as if that explains it.

And in a way, it almost does.

Because kidney disease sits very close to mechanism:
↓ EPO → ↓ erythropoiesis

It’s only one step away.
Read 9 tweets
Feb 13
1/11

I posted a poll:

A woman with ferritin 10 and Hb 12.2 (baseline 14). How should this be described?

Here’s how you answered:

• non-anemic Fe deficiency: 35%
• Fe deficiency anemia: 32%
• Fe deficiency with relative anemia: 27%
• none: 6%

Really interesting spread! Image
2/11

This tells us something important: clinicians sense a mismatch between definition-based language and physiology-based thinking, even if we disagree on terminology.
3/11

By strict WHO criteria, she is not anemic.
Hb ≥12 in women = normal.

So formally the correct label is: iron deficiency without anemia.
Read 11 tweets
Feb 10
RETICS IN PV

I recently ran a poll asking whether polycythemia vera (PV) is associated with:

• ↑ absolute reticulocyte count
• ↑ % reticulocytes
• both
• neither

The most popular answer was also the best answer: ↑ absolute reticulocyte count. Image
2/10

At first glance, that can feel counterintuitive.

PV is a disease of excessive red cell production, so why wouldn’t the reticulocyte percentage also be increased?

The answer depends on what reticulocytes actually measure.
3/10

Two metrics that are often conflated:

• Absolute reticulocyte count = how many reticulocytes are circulating

• Reticulocyte percentage = reticulocytes ÷ total red cell mass

They answer different physiologic questions.
Read 11 tweets
Feb 2
1/13

I posted a poll asking:

In acute GI bleed anemia, would you give 1 g IV iron regardless of ferritin?

Results:

• 27% yes — anticipate iron debt
• 12% sometimes
• 21% only if ferritin is low
• 41% no
2/13

First, an important acknowledgment:
There is no right answer here.

There are no firm guidelines that tell us what to do in this situation. Reasonable clinicians land in different places.

This is a gray zone where physiology, timing, and judgment matter.
3/13

So rather than argue what we should do, I want to walk through the numbers and biology and explain why some clinicians anticipate iron debt even when ferritin is normal.

Let’s take a concrete example.
Read 13 tweets
Jan 23
1/9

Yesterday I posted a CBC + reticulocyte count and asked for your diagnostic thoughts. Many of you offered great reasoning. The correct diagnosis was hemoglobin C disease.

Let’s unpack why this case is such a good learning example. 👇 Image
2/9

Microcytosis often triggers a reflex binary:
iron deficiency vs thalassemia trait.

That’s a useful starting point. But it’s incomplete. Structural hemoglobin variants (like HbC and HbE) also belong on that list.
3/9

Several people calculated the Mentzer index (MCV/RBC):

75 / 4.0 ≈ 18 → “suggests iron deficiency (ID).”

Important teaching point:

The Mentzer index was designed to distinguish thal trait vs ID. It is not validated for structural hemoglobinopathies like HbC or HbE.
Read 9 tweets
Oct 21, 2025
1/7

A STRUCTURED APPROACH TO NORMOCYTIC ANEMIA

A practical, population, and molecular look at how we reason through normocytic hypoproliferative anemia at the bedside.

(Full TBP tutorial linked below ⬇️)
2/7

1️⃣ The ABC Spine – A Bedside Framework

A: substrate supply (nutritional)
B: regulatory signaling (inflammatory)
C: organ dysfunction (kidney, liver, endocrine, marrow)

We focus here on the hypoproliferative end of the spectrum, where the marrow is not keeping up. Image
3/7

2️⃣ Anemia of the Elderly – A Population Perspective

In older adults, causes divide roughly:

1/3 nutritional 
1/3 inflammatory
1/3 unexplained

Each slice maps back to A, B, or C of the spine. Image
Read 7 tweets

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