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The Urinary System · Chapter 6 of 7
A renal biopsy in the summer of 2026: Congo red, apple-green under polarizedA resting neuron’s membrane with a more negative charge inside than outside. light, AA-type amyloid in the glomeruli. This chapter follows serum amyloid A from a liverA large organ that produces bile, detoxifies blood, and stores nutrients. that never switched off to a filtrationThe process by which fluid moves out of capillaries into surrounding tissues due to hydrostatic pres barrier that could no longer hold albuminA plasma protein that helps maintain osmotic pressure and transport substances., reads glomerular against tubular proteinuria, follows the leak into the blood and the ankles — and shows why the drug that once controlled her attacks is now the drug that protects her kidneys.
The question you will answer
Years of high SAA, a filter that leaks albumin, a tubule that works. What is physically in the glomerulusA network of capillaries in the nephron where blood filtration occurs. — and can anything stop it?
Opener · How Amyloid Lands · about 2 minutes
The opener is the same narrated animation you will watch in Scene 1.
Watch the opener first. It sets the question; the chapter answers it.
1
Read the chart
Patient chart · Stina
Summer 2026 · age 51
When
Summer 2026, age 51 — eight weeks after the FMF diagnosis (11 May 2026).
Test
Ultrasound-guided renal biopsy. Congo red: positive, amorphous deposits in the mesangium and capillary walls of the glomeruli. Polarized light: apple-green birefringence. Immunostain: AA-type.
Alongside
24-hour urineThe liquid waste excreted by the kidneys. protein in the nephrotic range, albumin-rich. Serum albumin low. Total calcium “low”. Estimated GFR still normal. Serum EPO high.
Read as
Renal AA amyloidosis — the defining complication of untreated FMF.
Plan
Colchicine, taken every day, now for the kidneys rather than the pain.
Chart clues this module: 1 · A little protein · 2 · Normal scan · 3 · The barrier · 4 · The tubule · 5 · Sterile pyuria · 6 · this chapter
Before you go on · your prediction
What has been breaking the filter, and what will the biopsy most likely show?
Open the one you lean toward. Nothing is recorded and nothing is revealed — you come back to it at the end.
Scarring — decades of inflammation have simply hardened the glomeruli, the way scars form anywhere
Ask whether inflammation alone leaves something a special stain can bind, and whether her tubules and her GFR look like a kidney that has scarred.
A deposit — a protein the liver overmade, misfolded and settled in the filter
Ask which protein, made where, and why the kidney is where it lands first. Then ask whether a deposit can be starved.
An immune attack — antibodies against the glomerulus, like the site’s other cases of nephritis
Ask what an immune glomerulonephritis leaves in the urine that her dipsticks never showed, and whether her disease is autoimmune or autoinflammatory.
From Stina’s diary
May 2026 · age 51 · “Every page” — the doctor who read the binder
2
The story
Three short movements: the case, the anatomyThe study of the structure of the human body. and physiologyThe study of how the body functions., then the tie back to Stina. Each links to the scene where you’ll see it move.
I · The needle and the red stain
Eight weeks after the diagnosis, a needle went into her left kidney under ultrasound. Routine stains showed glomeruli with pale, amorphous material spreading through the mesangium and into the capillary walls. Congo red bound it. Under a polarizer it turned apple-green. The immunostain typed it AA — the kind built from serum amyloid A. No crescents, no immune deposits, no scarred tubules; the tubules were the ones she had already proven intact. The kidney that had looked normal on a scan was, at the level of the filter, packed with something that did not belong.
See it move: Scene 1 · How Amyloid Lands · Scene 2 · Reading the Biopsy
II · From a liver that never switched off
Serum amyloid A is an acute-phase protein: the liver makes it in a burst when IL-1β and its downstream cytokines say so, and stops when the fire is out. In untreated FMF the fire never went out, and for decades the liver made SAA without pause. Kept high, its fragments misfold into insoluble β-sheet fibrils — AA amyloid — and settle in tissues. The kidney is the favorite landing site: a fifth of the cardiac output through a fenestrated capillaryCapillaries with pores (fenestrations) that allow rapid exchange of fluids and small solutes (found bed with a delicate basement membrane and podocytesSpecialized cells in the glomerulus that form filtration slits, preventing large molecules from ente whose slit diaphragms are the finest sieve in the body. Fibrils pack the mesangium, thicken and split the basement membrane, and efface the foot processes, until the barrier that was built around albumin’s size and charge can no longer hold it. That is glomerular proteinuria: a heavy leak of albumin and larger proteinsLarge molecules made of amino acids with various functions in the body. through a broken filter, climbing to the nephrotic range. Tubular proteinuria is a different thing — a small leak of the low-molecular-weight proteins a healthy filter always passes and a damaged PCT fails to reclaim. Hers is heavy, albumin-rich and biopsy-confirmed: glomerular, unmistakably. And what leaves through the filter leaves the blood: serum albumin falls, the colloid osmotic pressureThe pressure exerted by proteins (mainly albumin) in the blood that pulls water into the capillaries that held waterThe universal solvent essential for life. in the capillariesThe smallest blood vessels where gas, nutrient, and waste exchange occurs between blood and tissues. falls with it, fluid moves to the interstitium and the ankles pit. Albumin is also what carries nearly half of the calcium in the plasmaThe liquid component of blood., so the “low” total calcium on her labs is, in part, albumin’s absence written a second way — Module 20 will read the rest of it. Meanwhile the filter’s net filtration pressure(NFP): The difference between hydrostatic and colloid osmotic pressures, determining whether fluid m changes: a lower plasma colloidA mixture where small particles are dispersed but not dissolved in a liquid. osmotic pressureThe force exerted by water moving across a membrane due to osmosis. means less pull back into the glomerulus, so the kidney, sensing volume slipping away, leans on reninAn enzyme secreted by the juxtaglomerular cells that helps regulate blood pressure by triggering the, angiotensin and aldosteroneA hormone that increases sodium and water reabsorption in the kidneys, helping regulate blood pressu to hold on to salt — and the edemaExcess fluid in interstitial spaces. worsens.
See it move: Scene 1 · How Amyloid Lands · Scene 3 · Glomerular versus Tubular · Scene 4 · The Nephrotic Cascade
III · Treatable at the root
This is the part that makes the chapter a teaching triumph rather than only a tragedy. Amyloid is fed by SAA, and SAA is fed by inflammation. Colchicine, taken faithfully, suppresses the attacks, drops SAA toward normal, and starves the deposit of its raw material; the literature shows it prevents amyloidosis in FMF and can stabilize an established amyloid nephropathy. Adherence is no longer about pain. For Stina it is about whether her kidneys survive.
See it move: Scene 5 · Treatable at the Root
3
Watch · explore · think · check
5 scenes. Each one has a short animation or a slide, something to explore, a true/false spot-check of your thinking, and a quick check. Every scene gives you an evidence card for your board.
How to read the scenes
- Animation (dark teal) — a short animated explainer, one idea each
- Slide (dark teal) — a still to study: a micrograph, a diagram or a map
- Explore (purple) — something to push on while you watch
- Game (purple) — a quick challenge
- Think (gold) — reason it out, then spot-check yourself with a few true/false questions; not graded
- Check (gold) — a quick H5P that scores itself
Scene 1 of 5
How Amyloid Lands
A protein that does not clear; it deposits.
Animation · narrated, with captions
How Amyloid Lands
Module 19 · 19.6 · Opener and Scene 1 · 6 scenes · 2 minutes · narrated. Press Play to start; the words appear in the caption box under the picture.
Scene 1
Paused
Keyboard: when the picture has focus, Space plays or pauses, the left/right arrow keys move between scenes, and M mutes or unmutes.
Text description and full narration
Six-scene narrated animation with captions, built from BioRender parts: a white blood cell, the liver, misfolding strands, a β-sheet fibril stack and an amyloid tangle, a heart and kidney, the filtration barrier, a glomerulus, and the filtration-barrier kit (endothelium, basement membrane, podocyte feet, slit diaphragms) with albumin; the graph and dipstick are drawn.
Scene 1 · A burst, then stop (0:00–0:21)
On screen: A white blood cell sends out IL-1β; it travels to the liver, which answers with serum amyloid A. On a graph of SAA in the blood over time, the line jumps up with the inflammation and drops back down when it ends. Labels: “serum amyloid A: an acute-phase protein”, “inflammation → a burst”, “inflammation ends → it stops”. Chip: “that’s the design”.
Narration: Serum amyloid A is an acute phase protein. When interleukin-1β and the cytokines downstream of it signal inflammation, the liver makes serum amyloid A in this burst, and when the inflammation ends, it stops making it. That's the design.
Scene 2 · Inflammation that never ended (0:21–0:39)
On screen: The graph again, now over years: the SAA line climbs and never comes back down, attack after attack. Chips: “untreated familial Mediterranean fever: the inflammation never truly ended”, “for decades, Stina’s liver made SAA without pause”, “kept high for years, SAA does something it was never meant to do”.
Narration: So, in untreated Mediterranean fever, the inflammation never truly ended, and for decades, Stina's liver made SAA without pausing, so it was kept high for years, and SAA does something it's never really meant to do.
Scene 3 · Misfold, stack, deposit (0:39–0:55)
On screen: Twisted green strands (“fragments of SAA misfold”) → a straight blue stack (“they stack into straight β-pleated-sheet fibrils”, “no longer soluble”) → a brown tangle (“AA amyloid: it does not clear — it deposits”).
Narration: Fragments of it misfold, and they stack into straight beta-pleated sheet fibrils, and they stop being soluble. So, now they've become amyloid A, and amyloid does not clear. It deposits.
Scene 4 · Why the kidney (0:55–1:22)
On screen: A heart sends an arrow to a kidney: “a fifth of the cardiac output”. Beside it, the filtration barrier: “fenestrated capillaries”, “a thin basement membrane”, “podocyte slits: the finest sieve in the body”. Chip: “all of it exposed, minute after minute, to whatever is in the blood”.
Narration: The kidney is a favorite landing site for amyloid, and the reasons are the ones this module has already built. A fifth of your cardiac output passes through the kidney. Its capillaries are fenestrated. The basement membrane is really thin, and the podocyte slits are the finest sieve in the body, so all of it is exposed minute after minute to whatever is in the blood.
Scene 5 · Mesangium, membrane, feet (1:22–1:41)
On screen: A glomerulus: brown amyloid clumps appear between its capillary loops (“the mesangium: the supporting tissue between the loops”) and then in the loop walls. The view changes to the barrier drawn flat: amyloid settles in the basement membrane, which thickens and then splits along its middle; the podocyte feet flatten and spread until the slits between them are gone.
Narration: Fibrils settle first in the mesangium, the supporting tissue between the capillary loops, and then they creep into the capillary walls. The basement membrane thickens, and then it starts to split. The podocyte feet, they flatten, and they lose the filtration slits between them.
Scene 6 · The cutoff has moved (1:41–1:58)
On screen: On the damaged barrier, albumin rises from the blood and passes through into the capsular space. Chips: “three layers, one cutoff”, “now the cutoff has moved”. A dipstick card: the protein pad has changed color: “protein +”.
Narration: So, these three layers have one cutoff, albumin, right? Yeah, now the cutoff has moved. Now, albumin is able to pass into the urine, and on a dipstick, that's a plus sign.
Prefer the full lecture? Renal Corpuscle Anatomy (original video on the site) · histology page: Renal Corpuscles
Explore
Twenty years in twenty seconds
Mark your two predictions on the timeline first. Then drag one glomerulus through twenty years.
Text description of this explore
A time slider from 2006 to 2026 over a drawing of one glomerulus. This is a teaching model of how AA amyloid typically builds, set against Stina’s chart; nobody measured her urine albumin before 2024. Step 1: before dragging, mark the years you think albumin first crossed the filter and the year a dipstick would first read a plus sign. Step 2: move the slider, predict the dipstick reading for that year, then run it; pale purple deposits gather between the capillary loops and the loop walls thicken, and a readout gives urine albumin, the dipstick pad and serum albumin. Step 3: compare your marks with the model and with the note “recheck it sometime” in 2024.
Think · not graded
SAA is meant to rise with inflammation and fall when it ends. What single factA statement based on direct observation that is repeatedly confirmed. about Stina’s disease turns a protective protein into a deposit — and which module first put that fact on her chart?
Spot-check your thinking: true or false?
Check · Single Choice
Why is the kidney amyloid’s favorite target?
Evidence card 1
Add it to your evidence board
Years of SAA misfolded into fibrils that settled in the one capillary bed built to be a sieve.
Scene 2 of 5
Reading the Biopsy
Congo red, a polarizer, apple-green.
Slide · a still to study
The Renal Biopsy
Reading the biopsy
- H&E: pale, glassy, structureless material in the mesangium and the capillary walls. The tubules are intact.
- Congo red: the deposits stain salmon-pink.
- Polarized light: the Congo red deposits glow apple-green.
- Immunostain: positive for AA, the amyloid made from serum amyloid A.
The left panel is a normal glomerulus from the site’s slide 209, for comparison.
Prefer the full lecture? Renal Corpuscle Anatomy (original video on the site) · histology page: Renal Corpuscles
Explore
The polarizer
Four unlabelled glomeruli, three stains. Predict which stain sets each apart, then switch and read the report you would write.
Text description of this explore
A microscope with four unlabelled glomeruli, drawn: glomerulus 1 has clean open loops; glomerulus 2 has pale glassy material between the loops; glomerulus 3 is pale, shrunken and solid; glomerulus 4 is crowded with cells and studded with tiny dark deposits. Step 1: predict which stain or method will set each apart: Congo red under a polarizer, H&E alone, immunofluorescence, or none because it is normal. Step 2: choose a glomerulus and a stain (H&E, Congo red, or Congo red with a polarizer), predict whether it will glow apple-green, then switch; a readout gives the report line you would write. Step 3: decide which glomerulus’s tubules would also be damaged, and why Stina’s are not.
Think · not graded
Her 2015 gut biopsy (Module 17) and her 2026 kidney biopsy show the same deposit in different organs. What does that tell you about the disease — and about how many other organs a stain would find it in?
Spot-check your thinking: true or false?
Check · Drag the Words
Trace SAA → amyloid → leak, and colchicine’s point of action.
Evidence card 2
Add it to your evidence board
Congo red, apple-green, AA-typed: the deposit is named and the filter is where it sits.
Scene 3 of 5
Glomerular versus Tubular
The kind of leak names the broken station.
Animation · narrated, with captions
Glomerular versus Tubular
Module 19 · 19.6 · Scene 3 · 6 scenes · 2 minutes · narrated. Press Play to start; the words appear in the caption box under the picture.
Scene 1
Paused
Keyboard: when the picture has focus, Space plays or pauses, the left/right arrow keys move between scenes, and M mutes or unmutes.
Text description and full narration
Six-scene narrated animation with captions, built on two copies of BioRender’s stretched-out nephron, with amyloid deposits, albumin and small and large protein shapes; the gauges and dipsticks are drawn.
Scene 1 · Left: a packed barrier (0:00–0:29)
On screen: Two stretched-out nephrons side by side, each with a urine-protein gauge and a serum-albumin gauge beneath it. Top chip: “Protein in the urine names the broken station — if you read what kind of protein it is.” On the left nephron, brown deposits pack the glomerulus: “left: the barrier is packed with deposit”. Albumin and a larger protein travel the whole tubule: “albumin and larger proteins pass — the very things it was built to hold”, “and a lot of them: nothing else held them”.
Narration: Protein in the urine names kind of like the broken station. If you read what kind of protein it is, put two nephrons side by side, and in the one on the left, the filtration barrier is packed with deposit. It lets through albumin, and it lets proteins larger than albumin through, the very things it was kind of like built to not let through. And it does let a lot of other things through, because the barrier is the only thing that ever held them back.
Scene 2 · Glomerular proteinuria (0:29–0:47)
On screen: More albumin passes the proximal tubule untouched: “the tubule can’t help: no station for albumin”. The left urine-protein gauge fills high and the serum-albumin gauge drops: “glomerular proteinuria — heavy · albumin-rich · into the nephrotic range”, “serum albumin falls as it goes”.
Narration: The tubule, it can't help. It doesn't have a trading station for albumin. This is glomerular proteinuria, heavy, albumin-rich, climbing into the nephrotic range, with serum albumin falling as it goes.
Scene 3 · Right: a damaged tubule (0:47–1:01)
On screen: The right nephron’s glomerulus is ringed in green: “right: the barrier is fine”. Small proteins pass it and travel on, while a red dashed box marks the proximal tubule: “it passes only the smallest proteins, as a healthy filter always does”, “but the damaged PCT fails to reclaim them”. The right urine-protein gauge rises a little; serum albumin stays steady.
Narration: In the nephron on the right, the barrier is perfectly fine. It passes only the smallest proteins, it's a healthy filter, always passes. But the proximal tubule is damaged, so it fails to reclaim them.
Scene 4 · Tubular proteinuria (1:01–1:19)
On screen: Right panel: “tubular proteinuria — light · low-molecular-weight · never alone”, “glucose, bicarbonate spill; K⁺ not secreted”, “the same cells do all of those jobs”.
Narration: This is tubular proteinuria. It's light, made of low molecular weight proteins, and it never comes alone. Glucose usually spills with it, bicarbonate spills with it, potassium is not secreted because the same cells do all of those jobs.
Scene 5 · What a dipstick reads (1:19–1:35)
On screen: A dipstick under each nephron. Left: the protein pad has turned: “protein: positive” — “the dipstick reads albumin: it reads the left nephron clearly”. Right: the pad is unchanged: “protein: negative” — “it can miss the right one entirely”, “a chemistry panel catches it”.
Narration: The dipstick will read albumin, that's it, that's all it reads, so it reads the left nephron very clearly, and it completely misses what's going on with the nephron on the right. The right one is caught by a chemistry panel.
Scene 6 · Stina is the left (1:35–1:55)
On screen: A gold frame around the left nephron: “Stina: heavy, albumin-rich, every tubular lab normal → the nephron on the left”. Right: “her leak was localized to the filter before a biopsy ever went in”.
Narration: Stina, she's got heavy, albumin-rich, with every tubular lab normal, is the nephron on the left, left, that's her. Her leaking was localized to the filter before a biopsy ever went in and found it.
Prefer the full lecture? Urine Formation 3: Reabsorption and Secretion (original video on the site)
Game
Which station broke?
Six urine reports. Assign each a broken station and a weight before the reports grade.
Text description of this game
A sorting desk with six urine reports, each listing total protein, the kind of protein (albumin or small proteins), glucose, bicarbonate and serum albumin. For each, choose the broken station (glomerulus or PCT) and the weight (light or nephrotic). After you commit, each report shows its answer. Step 2: two reports with the same total protein, 1.4 grams a day, point to opposite stations; choose the single line that separates them.
Think · not graded
A dipstick mostly reads albumin. Which kind of proteinuria could it miss entirely — and in which patient on the site’s pages would that matter?
Spot-check your thinking: true or false?
Check · Summary
Distinguish glomerular from tubular proteinuria.
Evidence card 3
Add it to your evidence board
Heavy, albumin-rich, biopsy-confirmed: glomerular, and localized to the filter before the biopsy ever went in.
Scene 4 of 5
The Nephrotic Cascade
What leaves the filter leaves the blood.
Slide · a still to study
From a Leak to an Ankle
The cascade
- Albumin leaves in the urine.
- Serum albumin falls.
- Plasma colloid osmotic pressureThe force exerted by gases in the respiratory system, affecting airflow and gas exchange. falls.
- Net filtration at every systemic capillary tips outward.
- Fluid gathers in the interstitium: pitting edema.
- Effective blood volume falls.
- RAAS and ADH hold on to salt and water, and the edema grows.
Side branches
- About half of plasma calcium rides on albumin, so total calcium reads “low” (Module 20).
- A lower plasma colloid osmotic pressure also changes the glomerulus’s own net filtration pressure (the BCOP in the GFR Game).
One leak sets off a loop that feeds itself. The swelling at her ankles is the filter’s failure, read at the far end.
Prefer the full lecture? Urine Formation 1: Glomerular Filtration (original video on the site)
Explore
The pressure ledger
Lower serum albumin and predict what happens to filtration in two capillaries. Then switch on RAAS.
Text description of this explore
A two-capillary pressure ledger: a glomerular capillary and an ankle capillary. A slider sets serum albumin from 4.2 down to 1.8 g/dL and a selector switches RAAS on or off. Before each run, predict what happens to net outward pressure in each capillary; then arrows redraw and a readout gives colloid osmotic pressure, glomerular net filtration pressure, the ankle’s net outward pressure and RAAS. Step 2 asks whether RAAS helps or hurts the ankle. Step 3 applies the GFR formula to a leaking patient.
Think · not graded
RAAS is doing exactly what it evolved to do: defend volume. Why does the right response to a falling effective volume make a nephrotic patient worse — and what would you give, or block, first?
Spot-check your thinking: true or false?
Check · Mark the Words
Mark the history that turns a benign trace into an alarm.
Evidence card 4
Add it to your evidence board
Low albumin, low colloid osmotic pressure, edema, a “low” calcium — one leak read four ways.
Scene 5 of 5
Treatable at the Root
Starve the deposit.
Animation · narrated, with captions
Treatable at the Root
Module 19 · 19.6 · Scene 5 · 6 scenes · 1¾ minutes · narrated. Press Play to start; the words appear in the caption box under the picture.
Scene 1
Paused
Keyboard: when the picture has focus, Space plays or pauses, the left/right arrow keys move between scenes, and M mutes or unmutes.
Text description and full narration
Six-scene narrated animation with captions, built from BioRender parts: a white blood cell, the liver, a glomerulus (and a greyed copy for a scarred one) and amyloid clumps; the fire, the conveyor, the SAA gauge and the tablet are drawn.
Scene 1 · A supply chain: fire and factory (0:00–0:25)
On screen: Three stations in a row. On the left a fire with a white blood cell beside it: “the fire: IL-1β-driven attacks of familial Mediterranean fever”. An arrow carries IL-1β to the middle station, the liver: “the factory: the liver makes serum amyloid A (SAA) as long as the fire burns”. A gauge under the liver reads SAA high. Top chip: “the part that turns this chapter from a tragedy into something you can act on”.
Narration: This is the part that turns the chapter from a tragedy into something you can act on. If you draw the disease as a supply chain, at one end you have the fire, the interleukin-1β-driven attacks of Mediterranean fever. In the middle you have the factory, the liver, making serum amyloid A as long as the fire burns.
Scene 2 · The filter at the far end (0:25–0:33)
On screen: The third station appears, a glomerulus: “the filter: the glomerulus collects amyloid built from SAA”. A conveyor belt runs from the liver to the glomerulus carrying SAA chips, and brown amyloid clumps pile up on the glomerulus.
Narration: At the far end is the filter, the glomerulus, collecting that amyloid built.
Scene 3 · Colchicine works at the fire (0:33–0:53)
On screen: A colchicine tablet appears: “colchicine does not touch the amyloid”. It moves to the fire: “it works at the fire”. The fire shrinks to an ember, the SAA gauge falls toward normal, and the conveyor slows: “taken faithfully, every day: the attacks are suppressed, SAA falls toward normal, the conveyor slows to a trickle”.
Narration: Colchicine does not touch the amyloid. It works at the fire and if you take it faithfully every day it suppresses the attacks and with the inflammation quiet the liver's amyloid falls toward normal. The conveyor slows to a trickle.
Scene 4 · No new fibrils arrive (0:53–1:14)
On screen: No new chips reach the filter: “new fibrils stop arriving”. Two of the clumps fade: “the deposit stops growing — it can stabilize and even partly regress”. Chip: “colchicine has been shown to prevent amyloidosis in FMF”.
Narration: New fibrils stop arriving at the filter. The deposits already there, growing there — there's evidence that says that they can stabilize and even partly regress. Colchicine has been shown to prevent amyloidosis in Mediterranean fever.
Scene 5 · What it cannot do (1:14–1:29)
On screen: A grey, collapsed glomerulus beside the card: “what colchicine cannot do: rebuild a glomerulus that has already scarred and collapsed”. Chip: “that is why timing is everything”.
Narration: What it cannot do is rebuild a glomerulus that has already scarred and collapsed. That's why timing is everything and that's why for Stina adherence is no longer about pain.
Scene 6 · Adherence is kidney survival (1:29–1:38)
On screen: Final chips: “for Stina, adherence is no longer about pain” and “the drug that controlled her attacks now decides whether her kidneys survive”.
Narration: The drug that controlled her attacks is now the drug that decides whether or not her kidneys survive.
Prefer the full lecture? Urine Formation 2: Control of Filtration (original video on the site)
Game
The supply chain
Three stations, three dials. After a decade with no treatment, which single dial changes the 24-hour protein most?
Text description of this game
A supply chain of three stations: the fire (IL-1β-driven attacks), the factory (the liver making serum amyloid A) and the filter (amyloid in the glomeruli). Each has a dial: an IL-1β blocker, colchicine, and a hypothetical “amyloid remover”. After a decade of no treatment, choose one dial, predict how much it changes the 24-hour protein over the next two years, then run it; a readout gives SAA, new fibrils and the 24-hour protein. Step 2 is the honest card: which dial does not exist, and what the deposit already in the filter will and will not do.
Think · not graded
Colchicine does not touch amyloid. It touches the fire that feeds the factory that makes the deposit. What does that tell you about when treatment had to start to matter most — and which year on her timeline would you pick?
Spot-check your thinking: true or false?
Check · Multiple Choice
What does colchicine do that protects Stina’s kidneys?
Evidence card 5
Add it to your evidence board
The drug that controlled her attacks is now the drug that protects her life; it works upstream of the deposit.
4
Your evidence board
Every scene gave you an evidence card, and the chart adds more. Sort each card into the column it supports: A deposit in the filter, Neither on its own, or Scarring or immune attack. Some cards can honestly go in more than one place — that’s allowed, and the feedback tells you which cards decide the case.
5
Your verdict
Time to decide. Look back at your bet, then build your verdict from statements that hold up — no writing needed.
Look back at your prediction
Years of high SAA, a filter that leaks albumin, a tubule that works — the biopsy shows…
Find the one you chose at the top. Does the evidence support it, refute it, or revise it?
- Scarring — decades of inflammation have simply hardened the glomeruli, the way scars form anywhere
- A deposit — a protein the liver overmade, misfolded and settled in the filter
- An immune attack — antibodies against the glomerulus, like the site’s other cases of nephritis
Build your verdict · no writing
Choose the statement that holds in each set. The ones you keep become your argument.
6
The finding
Finding · biopsy-confirmed renal AA amyloidosis
Biopsy-Confirmed Amyloid in the Glomeruli
Summer 2026, age 51: AA amyloid in the mesangium and capillary walls of the glomeruli, Congo red positive, apple-green under polarized light, with nephrotic-range, albumin-rich glomerular proteinuria, a low serum albumin, pitting edema, and a total calcium that reads “low” partly because the protein that carries it is gone. Tubules intact; GFR still holding. Chart entry: renal AA amyloidosis, the defining, life-threatening complication of untreated FMF — built from decades of serum amyloid A, localized to the filter by the tubule’s own competence, and treatable at its root by colchicine lowering SAA.
Next · Chapter 7
Not a Trace, an Alarm
One line on a lab report in 2024 set all of this in motion and was nearly dismissed. With the mechanism in hand, rewrite that sentence — and log the clue for what it always was.
Reliable information on rare diseases
NORD · NIH GARD · Orphanet · MedlinePlus Genetics: FMF · FMF & AID Global Association · Autoinflammatory Alliance · Global Genes · Amyloidosis Foundation
Stina has one rare disease. In the United States, about 1 in 10 people live with one of the more than 7,000 known rare diseases. These organizations are where patients, families and clinicians go for trustworthy information.
Hop to:
← Familial Mediterranean Fever — case home
All pages for Module 19 — The Urinary System
19.0 Module Overview
19.1 A Little Protein in the Urine
19.2 The Kidney from the Outside In
19.3 The Nephron and the Filtration Barrier
19.4 Reabsorption, Secretion, and How Urine Is Made
19.5 Master Regulator, and the Road Out
19.6 When the Filter Breaks
19.7 Not a Trace, an Alarm
19.8 Conclusion and Assessment
19.9 Evidence Behind the Case
All Modules
- Anatomical Language, Membranes & Homeostasis
- Just Enough Chemistry
- The Cell & Its Transport
- Making Cells & Proteins
- The Integumentary System
- The Skeletal System
- The Muscular System
- Nervous Tissue & the Senses
- The Spinal Cord
- The Brain & the Blood–Brain Barrier
- The Autonomic Nervous System
- Special Senses (in developmentThe process of growth and differentiation.)
- The Endocrine System
- Blood
- The Heart
- Blood Vessels
- The Digestive System
- The Respiratory System
- The Urinary System
- Fluids, Electrolytes & Acid–Base Balance
- The Reproductive System
- The Immune System
List of terms
- polarized
- liver
- filtration
- albumin
- glomerulus
- urine
- anatomy
- physiology
- fenestrated capillary
- podocytes
- proteins
- colloid osmotic pressure
- water
- capillaries
- plasma
- net filtration pressure
- colloid
- osmotic pressure
- renin
- aldosterone
- edema
- fact
- pressure
- development