Start with a phone call. Your doctor’s office has a triage line and a nurse will talk it through with you. They are genuinely good at this, they do it all day, and it costs nothing. Most practices have a phone line where a nurse takes calls about whether something needs to be seen, and how soon. It is often not advertised — you ring the main number and ask to speak to the triage nurse. There is no charge and you do not need an appointment to use it.
If it feels more serious than that, go to urgent care. You will usually be seen faster than at a hospital, and the care is good.
If it feels life-threatening, call 911 or go to the emergency room. Do not wait until you are sure.
Which one is yours to decide, not ours. But our advice is to assume it is worse than it looks and take the more cautious road. And trust your body — if it is telling you something is wrong, it is probably right. The best possible outcome of a trip to the emergency room is walking out saying well, that was a waste of an evening — but I feel a lot better knowing it is nothing serious.
Before you call, have these ready. They are what the nurse will ask, and the call goes better when you are not working them out on the phone.
You are not diagnosing yourself by having this ready. You are handing them the things they would otherwise spend the call extracting — and the decision stays entirely theirs.
Writing to the portal instead of calling? The same list works, in that order, in one message. Put the direction it is going and the immune-system line near the top — portal messages get read quickly, and those two change how the rest is read.
One of the things people type into Google most is foam in my urine, should I be worried
.
Sometimes it is nothing. Sometimes it is protein leaving through a kidney that is letting it through. This room is about telling which, and what to ask for.
Tick the ones that are true right now. Then read the line underneath them — it is there, and not at the bottom of the page, because that is where you need it.
What we would do, as a friend rather than as your doctor. This is our opinion and we stand behind it. It is not medical advice and we are not examining you.
And it is not a one-time reading. If you start feeling worse while you are deciding, move up a level. Nobody has ever been criticised for turning up and being sent home. A false alarm is the best possible outcome here.
None of them ticked? Then nothing below this is an emergency, and you can read the rest at your own pace. Kidney trouble is usually slow. That is exactly why the sudden version needs a list of its own.
The short answer, before anything else.
Foam that is still there when you come back to look is protein. Your kidneys
filter blood through membranes with holes small enough to hold protein back. Foam means
protein is getting through anyway. That is a finding. It is not a diagnosis, and it is
not nothing — it has to be explained rather than noted and forgotten.
→ where this is explained: What brought you here today?
C3G is one reason that happens. Part of your immune system switches on to
attack something and does not switch off again. What it leaves behind clogs the filters.
→ where this is explained: What it is, in plain words
It gets missed because it falls between two specialists. The kidney doctor watches the kidney. The blood doctor watches the blood. Nobody is given the job of looking at both at once.
The one thing to do next: ask for a protein-to-creatinine ratio, not a dipstick — and ask what it was last time. Two numbers and a date are worth more than any single result.
Everything below explains each of those, in whatever order suits you. Nothing below is urgent if none of the boxes above are ticked.
Or tell me what is going on, and I will keep track. Four questions, in any order, and you can change any answer. Nothing you type leaves your machine.
There is no wrong door into this, and no right order. Whichever one sounds like you is the one to open — the others will still be here on the day one of them starts sounding like you too.
People reach this page from completely different places. One noticed foam. One was handed a biopsy report with three words on it she had never seen. One had a creatinine that jumped and nobody could say why. One was told her bicarbonate was low and nothing more was said about it.
Pick whichever sounds like you. There is no wrong door and no right order. These are not steps. Each one drives the next, and the last one drives the first — it is a loop, not a line. Which is why what started it so often goes nowhere, and why it is a poor use of a fifteen-minute appointment.
You noticed it, and noticing it was the right call. People are far better observers of their own bodies than they are given credit for. You have watched the same thing every day for years, so you see a change in the pattern. No test does that, and no appointment is long enough to find it.
What it means. Your kidneys filter the blood through membranes with holes small enough to hold protein back. Foam means protein is getting through anyway. The practical test is time: foam that vanishes in a few seconds is usually nothing, and foam still sitting there when you come back to look is protein. Protein in the urine is a finding — not a diagnosis, but something that has to be explained rather than noted and forgotten.
deposits clog the filters → protein leaks into the urine → less protein in the blood → fluid leaves the vessels → swelling
“Has my protein been measured properly — a protein-to-creatinine ratio, not a dipstick? And what was it last time?”
First, what the words mean. Your immune system has a part called complement — a chain of proteins in the blood that switches on to attack something that should not be there, and then switches itself off again. C3 is the protein at the middle of that chain. A kidney biopsy is read by looking at what has been left behind in the filters.
So “C3 dominant” means: the pathologist found C3 in your filters and very little else alongside it. That is not a hint pointing towards C3G. It is the definition of it. The chain has been switching on and failing to switch off — burning C3 out of your blood and leaving the debris in the filters, day after day.
Which is also why it is worth knowing: a switch that will not turn off is a different problem from an attack that will not stop, and it is treated differently.
something jams the switch → complement runs on → C3 consumed and deposited → filters clog → damage → which feeds back and switches complement on harder
“Has the cause been established — genetic, antibody, or M-protein? If not, what would it take?”
What a light chain is. An antibody is built from two large pieces and two small ones. The small ones are called light chains. A healthy antibody-making cell produces them in matched pairs and uses them all up.
What has happened here. One of those cells has copied itself into a small colony — a clone — all making the same antibody over and over. A clone makes far more light chains than it can use, and the spares circulate loose in the blood. They are small enough to pass into the kidney, which larger proteins cannot do.
What they do there varies, and this matters. They can clog the small tubes, they can build up in the filter walls, and some of them act against the very protein whose job is to switch complement off. Different routes, different damage, sometimes different treatment — which is why “an abnormal protein was found” is the beginning of a question, not the end of one.
This is the node that most changes what gets done, and the one place on this page where being older matters. Blocking complement protects the kidney and does nothing whatever about the clone.
a clone of plasma cells → free light chains → deposition in the kidney → complement activation → everything downstream
“Has anyone looked for an abnormal protein in my blood? I have read there is a blood test that finds the small ones the older test can miss.”
If they ask which test you mean, it is the serum free light chain assay. You do not need to say that to be taken seriously — but it is here in case you want it.
Kidney numbers do not move only because the disease moved. Blood flow to the kidney can fall for reasons that have nothing to do with the filters, and creatinine follows within days. A spike read as the disease is progressing can lead to treatment being escalated for something that was never the disease advancing.
GRADE U The specific route — a bile-and-vagus-nerve reflex tightening the small arteries of the kidney — is this project’s own reading of the pattern and is not established practice. The general point beneath it is not controversial: one number is an event, two numbers are a direction.
“Was this repeated? Was I dehydrated, unwell, or on anything new that week? Is this a trend or a spike?”
Damaged kidneys are worse at clearing acid. The nephrons still working make more ammonia to shift the load, and ammonia concentrated in the kidney can itself switch on the same complement pathway. More complement, more damage, less bicarbonate, deeper acidosis — the loop closing on itself.
damage → acid builds → surviving nephrons make more ammonia → ammonia activates the alternative pathway → more complement → more damage → and round again
GRADE B The mechanism is carried from this project’s own work rather than re-checked against the primary literature today. The practical part stands on its own feet: bicarbonate is cheap, oral, measurable, and among the most reachable things on this whole page.
“What is my bicarbonate, and is it low enough to be worth treating?”
Bacteria in the gut make short-chain fatty acids — butyrate above all — and those act as anti-inflammatory signals. Lose them and complement regulation loses a brake. Complement trouble also damages the microbiome, so this is a second loop feeding the first from a different door.
dysbiosis → fewer short-chain fatty acids → a brake comes off complement → the same loop, entered somewhere else → which damages the microbiome further
GRADE U Nobody has run the trial. U is not a failing grade — it means the evidence does not settle it either way, which is different from evidence of no effect.
“Is there any reason not to pay attention to my gut while the rest is being sorted out?”
While you are here — two things worth pinning down
When did you first notice it? Not the date you started looking into it — the first time you thought that is new. A month, a season, or “around when we moved” is a perfectly good answer.
Is it every time, or only sometimes? First urine of the morning, or all day. Every day, or a few days a week. Patterns carry information that a single observation cannot.
Write the answers down somewhere you will find them again. You are not diagnosing yourself — you are keeping the two facts that get asked for first and are hardest to reconstruct later.
One branch of your body’s alarm system is stuck on, and the debris it makes clogs the kidney’s filters. If you are ever told your protein is up or your kidney numbers have drifted, this paragraph is the reason why. The system underneath it →
Your body has a defence system called complement. Think of it as an alarm that can fire on its own, without waiting to be told — useful when something needs killing quickly, dangerous when it will not switch off.
In C3 glomerulopathy, one branch of that alarm is stuck in the on position. The protein it burns through is called C3. It gets consumed in the blood, and the debris settles in the kidney’s filters, which are the finest sieves in the body and do not tolerate being clogged.
Two things follow from that, and they explain most of what people notice first. Protein that should have stayed in the blood leaks into the urine — which is what makes it foam, the way soapy water does. And the filters, working against the clog, get slowly worse at their job.
And two more, while this is fresh
What is it actually like? Foam that vanishes while you watch, or foam still sitting there a minute later. Tea-coloured, pink, cloudy, or normal in colour. The description does work that a yes-or-no answer cannot.
Where does the swelling show up, and when? Face and eyes on waking points somewhere different from ankles at the end of a day. One leg is a different question from both. If there is no swelling at all, that is worth saying too.
A low C3 with a normal C4 is a fingerprint, and it is easy to miss because it only shows when both are measured together. If a doctor ever says your complement was checked, this is the question that tells you whether it was checked usefully. What complement is, in plain words →
GRADE A Complement can be switched on by more than one route. Low C3 with a normal C4 is the fingerprint of one route — the alternative pathway — rather than another. Both low usually points elsewhere.
Standard complement immunology, and the basis on which C3G is defined. This is a pattern in a blood test, not a diagnosis, and it does not tell you what is happening in you. What it does is tell a doctor where to look, which is worth a great deal when nobody has been looking anywhere.
“Have my complement levels been checked — both C3 and C4 together?” That is the question, and the word together is doing the work. One without the other does not show the pattern.
GRADE A A kidney biopsy is the only thing that settles it. C3G is defined by what the biopsy shows: C3 dominant on immunofluorescence, with little or no immunoglobulin alongside it.
Definitional. If your biopsy report says “C3 dominant”, that sentence is why you are reading this page.
The question that decides most things
Which way is it going? Better, worse, or level — and over weeks or over months. This is the single most useful thing you can bring, and the one people least often have an answer to.
You do not have to work it out yourself. Ask for the previous numbers. Creatinine and eGFR from a year ago and two years ago, and the protein measurements alongside them. A number can sit inside the normal range for years while travelling steadily across it, and only the older results show that.
C3G is not one disease with one cause, and what gets done about it depends entirely on which cause you have. If treatment is ever proposed and nobody has said which of the four you are, this is the table to come back to. Why a brake fails three different ways →
C3G is not one disease with one cause. The alarm can be stuck for several different reasons, and what is done about it depends entirely on which. This is the most practical thing on this page.
| Why it is stuck | Roughly how often | What follows |
|---|---|---|
| Why it is stuck Inherited — a gene affecting the brakes or the accelerator. Factor H (CFH) is the commonest. | Roughly how often CFH mutations in about a quarter of cases | What follows The gene does not go away, so blocking the pathway tends to be long-term. Family members may want screening. |
| Why it is stuck An antibody — usually C3 nephritic factor (C3NeF), which jams the switch on. | Roughly how often Around half of C3GN; higher in dense deposit disease | What follows Acquired rather than inherited. If the antibody can be removed, the driver may go with it. |
| Why it is stuck An M-protein — an abnormal antibody from a small clone of plasma cells. | Roughly how often More common with age | What follows The important one. Blocking complement protects the kidney but does nothing about the clone. This needs treatment aimed at the clone itself. |
| Why it is stuck More than one of the above | Roughly how often Common | What follows The gene loads it; something acquired pulls the trigger. Explains why families with the same gene have different outcomes. |
GRADE B The proportions above — CFH in roughly a quarter, C3NeF in about half of C3GN and more in DDD — are carried from this project’s own C3G work rather than re-checked against the primary literature today. Treat them as the right order of magnitude, not as exact figures.
Graded B deliberately. They are good enough to tell you which questions to ask and not good enough to quote.
What else was going on
What changed around the same time? An infection, a new medicine, a stopped medicine, a hospital stay, a vaccination, a bad stretch of something unrelated. Complement is an alarm system, and alarm systems are set off by events.
What else is different about you now? Energy, appetite, weight, blood pressure, how well you sleep, how often you are up in the night. These are not side notes. They are the part nobody is assigned to look at, which is why they go unmentioned and unrecorded.
Around half of cases still have no cause found even after complete testing — which is a statement about the tests, not about you. If you are ever told “we did not find anything”, that sentence and this one mean different things, and the difference matters.
GRADE B Even after complete testing — genetics, C3NeF, high-sensitivity M-protein screening, full complement panels — around half of cases still have no cause identified.
That is not the same as having no cause. It means the tests are not yet good enough to find it. Being told “we did not find anything” is a statement about the tests, and it is worth hearing it that way.
The tests are also the ones insurers most often resist, because several are expensive and none is routine. That is a fight worth having, and the reason is not curiosity: the cause determines the treatment, whether your family should be screened, and what happens if a transplant is ever discussed.
GRADE U Whether treating the gut changes the course of C3G. The alternative pathway has a large presence in the gut, and complement there is influenced by the bacteria living in it. Nobody has run the trial.
U is not a failing grade. It means the evidence does not settle it either way — which is different from evidence of no effect, and it is a genuinely open question rather than a closed one.
What has already been tried
List what you have taken, and what happened. Including the things that did nothing, and the things you stopped because you could not tolerate them.
What did not work narrows the field as sharply as what did. A treatment aimed at one mechanism that changed nothing is evidence about the mechanism. That information is usually sitting in your memory and nowhere in your record.
And what makes it better or worse day to day? Salt, fluid, standing, heat, a particular time of the month or year.
Trials are recruiting, and some of them are in the United States. If anyone ever tells you there is nothing available, come back and read the count and the date it was read.
GRADE A As of 6 September 2026 there were 22 open C3G trials on ClinicalTrials.gov. Five of them have sites in the United States — four of those recruiting now — carrying 32 United States sites between them, and 349 sites elsewhere: Japan 45, Spain 30, China 29, Germany 29, France 28, Brazil 26, the United Kingdom 23, Italy 18, South Korea 13, Canada 12.
Read directly from the registry on that date and regenerated from the saved data, not retyped. Trial status and site status are different things and they change at different speeds — a trial can be recruiting while the hospital nearest you is closed. Check the registry entry itself before travelling anywhere.
Entry to any trial is arranged by a licensed physician, and nothing here is an endorsement of any particular one. The point is narrower and worth stating plainly: if someone has told you there is nothing available, that was not true on the day this page was written.
The one that gets left out
What have you stopped doing? Not how bad it feels — what it costs you. Stairs you now avoid, the walk you no longer take, the shift you cut back, the evening you sleep through.
This is the pillar most often missing from a record and the one that most changes how urgently anything gets acted on. “I am tired” and “I stopped gardening in June because I could not manage the beds” are read completely differently, and the second one is the true sentence.
These are written to be said out loud, or pasted into a portal message. If an appointment gets moved up and you have ten minutes to prepare, this is the part to print.
These are written to be said out loud, or pasted into a portal message.
Answer the boxes as you read and you end up holding a history — which is worth more at the appointment than anything else on this page. If you ever change doctors, or see a second one, this is the thing that travels with you.
If you answered the boxes as you came down this page, you are holding: when it started · whether it comes and goes · what it is actually like · where it shows up · which way it is going · what changed around it · what you have tried and what happened · and what you have stopped doing.
That is a history. It is the substrate everything else is read against, and it is the reason the work done before the appointment matters more than the appointment. Without it, a doctor is reading one snapshot. With it, they are reading a direction — and on this page direction has come up in almost every box, because on a loop the numbers matter far less than which way they are travelling.
Take it with you. There is a tool on this site that will help you set it out before a visit, and a page about being heard once you are in the room. Neither is required. The eight answers above are the thing that matters; the tools only tidy them.
What is written here, and what is not, said plainly. If something you needed is on the second list, tell us — that is how it gets written.
✓ What C3G is, the C3/C4 pattern, the four causes and why they change the treatment, the testing gap, and the trial counts as of the read date.
→ Treatment detail — which drugs, in what order, and what the newer complement blockers have actually shown — is not written yet. It is the next thing to go on this page, and it needs the grades doing properly rather than quickly.
→ Living with it: what to expect, what to monitor, and the emotional part, which is not a footnote.
Nothing here is a diagnosis, and none of it replaces someone who can examine you. Every claim above carries the grade of the evidence behind it, and the grade travels with the claim.