How Kidney Amyloidosis Is Treated: Controlling Amyloid Production and Protecting the Filters

The ankles came first. Then the shoes that no longer fit by evening, the foamy urine she assumed was nothing, and finally a kidney biopsy report with a word she had to read twice: amyloid. Most people who arrive at this point have never heard of it, and the nephrologist across the desk is about to explain that the problem did not start in the kidneys at all.

That is the strange logic of kidney amyloidosis treatment. The organ that is failing is rarely the organ that is treated first. A protein made somewhere else, in the bone marrow, the liver or a gene inherited decades ago, has folded the wrong way and settled into the kidney’s filters. Rescue the filters and you buy time. Turn off the supply and you change the direction of the disease.

This explainer walks through both jobs in plain language: how the damage happens, why the exact type of amyloid decides everything, what the first months usually look like, and what the evidence honestly says about the road ahead.

How kidney amyloidosis treatment works: stop the supply, shield the filter

Amyloid is a protein that has folded the wrong way and then stacked into stiff, thread-like fibrils the body cannot easily break down. In the kidney, those fibrils lodge in the glomeruli, the microscopic tufts of blood vessels that filter waste out of blood, and in the small vessels and tubules around them. A healthy glomerulus holds on to albumin, the main protein in blood. An amyloid-clogged one lets it pour through, which is why the first clue is so often foamy urine, swollen ankles and a lab report showing heavy protein loss. When that loss climbs above roughly 3.5 grams a day, doctors call it nephrotic syndrome (NIDDK).

Treatment pulls two levers at once, and it helps to keep them separate in your mind.

The first lever is supply. Every form of amyloidosis has a precursor, a normal or variant protein that keeps arriving and misfolding. Cut the supply and deposits stop growing. The body then begins, slowly, to clear what is already there. No standard therapy dissolves existing deposits on demand; improvement in kidney function, when it happens, follows the fall in new protein and lags behind it by months rather than weeks (NHS, Mayo Clinic).

The second lever is protection. While the supply is being shut off, the kidney still has to cope with protein leak, fluid overload, unstable blood pressure and the higher risk of clots and infections that comes with nephrotic syndrome. Kidney-directed care manages those pressures so the filters survive long enough to benefit from the first lever.

Which lever matters most depends on the type of amyloid. That is why the most consequential step in kidney amyloidosis treatment happens before a single medicine is prescribed: finding out precisely which protein is doing the damage.

Which type of amyloidosis is in your kidneys? Why typing comes first

Under the microscope, all amyloid looks alike. A dye called Congo red binds to it and glows apple-green under polarized light, which is how a pathologist confirms the diagnosis on a kidney, fat pad or bone marrow sample (Mayo Clinic). What Congo red cannot tell you is which protein built the fibrils, and that single fact determines whether the right treatment is chemotherapy, an anti-inflammatory biologic, a change in dialysis technique or simply careful monitoring.

Typing is done with antibody stains on the biopsy or, increasingly, with mass spectrometry, a laboratory method that identifies proteins by weight. Blood and urine tests for free light chains, inflammatory markers and, where the history suggests it, genetic testing complete the picture. Getting this wrong is not a small error: a hereditary form mistaken for AL amyloidosis could lead to chemotherapy that cannot help.

Type	Protein that misfolds	Where it comes from	Main treatment target	What is tracked
AL (light chain)	Immunoglobulin light chains	Abnormal plasma cells in bone marrow	The plasma-cell clone	Serum free light chains, urine protein
AA (inflammatory)	Serum amyloid A	Liver, in response to long-standing inflammation or infection	The underlying inflammatory disease	CRP or serum amyloid A, urine protein
Hereditary	Inherited variant proteins (for example fibrinogen or apolipoprotein variants)	A gene change, usually made in the liver	Genetic counseling, organ-specific care, sometimes transplant	Kidney function, family screening
Dialysis-related	Beta-2 microglobulin	Poor clearance during years of dialysis	Dialysis technique, kidney transplant	Joint and bone symptoms
ALECT2	Leukocyte chemotactic factor 2	Not fully understood	Supportive kidney care	Kidney function

AL is the most common form seen in the kidney in the United States, and AA the most common worldwide where chronic infections remain frequent (NIDDK, Mayo Clinic). The sections that follow take each pathway in turn.

Treating AL amyloidosis: turning down the light-chain factory

In AL amyloidosis, a small population of plasma cells in the bone marrow, the same cells that normally make antibodies, produces an excess of one fragment called a light chain. Most people with AL do not have full multiple myeloma, a cancer of those cells, but the treatment logic borrows from it: shrink the abnormal clone, and the light chains that feed the deposits fall away. The NHS describes the medicines as similar to those used for myeloma.

Modern regimens typically combine several classes. A proteasome inhibitor blocks the cell’s waste-disposal machinery, which plasma cells depend on because they manufacture so much protein. An anti-CD38 monoclonal antibody flags the cells for destruction by the immune system. An alkylating agent damages the DNA of dividing cells, and a corticosteroid dampens both the clone and inflammation. Which combination, in what order and for how long is a decision for the hematologist, who weighs heart involvement, kidney function, nerve symptoms and general fitness.

Progress is judged in two stages. The hematologic response is the drop in the abnormal free light chain in blood, usually measured every treatment cycle. The organ response is the later fall in urine protein and stabilization of kidney function. The first can appear within weeks; the second is counted in months (NHS, Mayo Clinic). A deep hematologic response gives the kidneys their best chance, which is why teams often push for it even when someone feels well.

For selected people, an autologous stem cell transplant is an option: intensive chemotherapy followed by return of the person’s own previously collected stem cells to rebuild the marrow (Mayo Clinic). It is demanding, and eligibility is discussed in a later section.

Treating AA amyloidosis: putting out the fire upstream

AA amyloidosis is the body’s inflammation signal turned into a structural problem. Serum amyloid A is a protein the liver releases in large amounts whenever inflammation is active, whether from rheumatoid arthritis, inflammatory bowel disease, a chronic infection such as tuberculosis or bronchiectasis, a long-standing skin or bone infection, or an inherited autoinflammatory condition like familial Mediterranean fever. Keep the level high for years and fragments of it begin to deposit, with the kidney as the usual first casualty (NIDDK).

Treatment therefore has no amyloid-specific drug at its center. It has a diagnosis at its center. The question for the team is: what has kept this person inflamed, and how firmly can it be controlled?

• For rheumatic and autoinflammatory diseases, that usually means the biologic classes that block specific inflammatory messengers, such as TNF, interleukin-6 or interleukin-1, chosen by the rheumatologist for the underlying condition.
• For familial Mediterranean fever, colchicine has been the long-standing preventive mainstay; genetic confirmation guides its use.
• For chronic infection, the treatment is the treatment of that infection, which can include prolonged antibiotics or surgery to remove an infected focus.

The marker to watch is C-reactive protein or serum amyloid A itself. When these stay low over time, new deposition slows and kidney function can stabilize; when they stay high, protein loss tends to progress. Because AA sometimes develops in people who did not know they had an inflammatory disease, part of the work-up is a careful hunt for hidden infection or unrecognized autoimmune activity.

Kidney protection runs alongside exactly as it does in AL, and if the source cannot be controlled, dialysis and transplant remain on the table.

Hereditary, dialysis-related and other rarer forms

A minority of kidney amyloidosis cases fit neither AL nor AA, and these are where a second opinion on typing earns its keep.

Hereditary amyloidoses come from a gene change that produces a slightly altered protein. Several variants, including those affecting fibrinogen A alpha chain, apolipoproteins and lysozyme, favor the kidney. Transthyretin variants, the best-known hereditary form, mainly affect the heart and nerves and involve the kidney less often (Mayo Clinic, Cleveland Clinic). The practical steps are genetic counseling, testing of relatives who wish to know, and planning around the organ that is failing. Because the variant protein is often made by the liver, liver transplantation has been used for some forms, and kidney transplantation is an option for others; the choice is highly individual.

Dialysis-related amyloidosis is built from beta-2 microglobulin, a small protein that healthy kidneys remove but older dialysis techniques cleared poorly. It settles in joints, tendons and bone more than in the kidney itself. Modern high-flux dialysis membranes clear it better, and a successful kidney transplant halts accumulation (NIDDK).

ALECT2 amyloidosis, named for leukocyte chemotactic factor 2, has been recognized more often as mass spectrometry typing has spread. It tends to cause slowly declining kidney function with less dramatic protein loss, has no specific therapy yet, and is managed with standard kidney-protective care.

Two rules apply across all of these. First, no chemotherapy is given unless a plasma-cell clone is proven to be the source. Second, a family history of kidney disease, unexplained neuropathy or heart failure in relatives should prompt the question of genetic testing before treatment is chosen.

Protecting the filters: kidney-directed care that runs alongside

While the source is being treated, the kidney needs day-to-day defense. None of the measures below removes amyloid; each one reduces the strain on filters that are already under attack.

• Reducing protein leak. Medicines from the ACE inhibitor and angiotensin receptor blocker classes lower pressure inside the glomerulus and can reduce protein loss. In amyloidosis they are used cautiously, because many people already run a low blood pressure, particularly if nerves or the heart are involved.
• Controlling fluid. Loop diuretics and a lower-salt diet are the mainstays for swelling. Too aggressive a fluid shift can drop blood pressure and starve the kidney of flow, so dosing is adjusted at each visit by the prescriber.
• Avoiding avoidable insults. Non-steroidal anti-inflammatory painkillers, some herbal products and iodinated contrast dye can tip a struggling kidney over. Teams usually ask patients to check before taking anything new.
• Clot prevention. Nephrotic syndrome raises the risk of blood clots because clotting-control proteins leak out with albumin (NIDDK). Whether to use preventive anticoagulation is an individual decision based on albumin level and other risks.
• Infection protection. Antibody loss and immune-suppressing therapy combine to raise infection risk; vaccinations and prompt attention to fevers are part of the plan.

Cholesterol tends to rise with heavy protein loss, blood pressure needs a target that suits the person rather than a textbook, and anemia and bone health are monitored as kidney function changes. The nephrologist and the hematologist or rheumatologist share these decisions, and small adjustments happen often. If a medicine on this list is changed, it is because the numbers moved, not because something has gone wrong.

Who is usually offered intensive treatment, and who is asked to wait

Not everyone with kidney amyloidosis is placed on the most powerful therapy on day one, and being asked to wait is not the same as being left untreated.

For AL amyloidosis, the most intensive option is autologous stem cell transplant. Selection is strict because the procedure stresses the heart, kidneys and gut. Teams look at the degree of heart involvement, the level of kidney function, age and overall fitness, blood pressure stability and the number of organs affected (Mayo Clinic). Someone with significant cardiac amyloid or advanced kidney failure is more likely to be offered combination drug therapy without transplant. Many people who are not initially eligible become candidates later, once a first line of treatment has improved their organ function.

A different group is asked to monitor rather than start. Examples include small amounts of amyloid found incidentally on a biopsy done for another reason, with normal kidney function and no measurable light-chain excess; AA amyloidosis in a person whose inflammatory disease is already quiet; or ALECT2, where no source-directed therapy exists. Monitoring here is active: urine protein, kidney function, blood markers and symptoms checked on a schedule, with a low threshold to act.

A third group sits in between. People already on dialysis with AL amyloidosis are still treated, because the same light chains threaten the heart and nerves and because a future kidney transplant depends on the clone being controlled. Older adults or those with frailty may receive gentler regimens with the same aim reached more gradually.

The honest summary is that eligibility is a moving target reviewed at each stage, and the treating team owns that call.

What the first weeks and months of kidney amyloidosis treatment usually look like

The opening stretch is more about measurement than most people expect. Before therapy begins, teams establish a baseline: kidney function, 24-hour urine protein, free light chains or inflammatory markers, heart markers and imaging, nerve assessment and a bone marrow sample where AL is suspected. Everything later is compared with these numbers.

For AL amyloidosis, drug therapy is organized in cycles, with blood tests and clinic visits often weekly at the start (NHS). Side effects vary by class: tingling or numbness in hands and feet with some proteasome inhibitors, fluid retention and mood or sleep changes with steroids, infusion reactions with antibody therapy, and a higher infection risk with all of them. Reporting new symptoms early lets the team adjust rather than stop.

For AA amyloidosis, the early weeks are about establishing the anti-inflammatory regimen and confirming that inflammatory markers are falling. For hereditary and rarer forms, this period is mostly genetic counseling and kidney-protective adjustments.

Kidney improvement, if it comes, is slow. Blood markers respond first, sometimes within the first cycles; urine protein usually declines over months, and kidney function often stabilizes before it improves (NHS, Mayo Clinic). Swelling can take a while to settle, and some people feel more tired during treatment than before it, which is common and worth saying out loud to the team.

Fatigue management is practical: pacing activity, treating anemia, correcting low blood pressure on standing and keeping protein intake adequate. Many people work through treatment with adjustments; others need a period away. Neither is a sign of how well the treatment is going.

Dialysis and kidney transplant: when the filters cannot be rescued

Some people are diagnosed only after the kidneys have lost most of their function, and others progress despite good control of the source. For them the conversation turns to replacing the filter rather than protecting it.

Dialysis in amyloidosis follows the same options as in other kidney diseases: hemodialysis through a vascular access or peritoneal dialysis through the abdominal lining (Mayo Clinic, NIDDK). Two features shape the choice. Low or unstable blood pressure, common when amyloid affects the heart or autonomic nerves, can make the fluid shifts of hemodialysis harder to tolerate, so peritoneal dialysis is sometimes preferred. Heavy ongoing protein loss can continue even on dialysis, keeping albumin low. Treatment of the underlying amyloid source does not stop when dialysis starts; if anything it becomes more important, because heart and nerve involvement continue regardless of the kidneys.

Kidney transplantation is possible and is offered to selected people. The central condition is that the source of new amyloid must be under durable control first, because deposits can form in the new kidney just as they did in the old one. In AL, transplant teams look for a deep, sustained hematologic response; in AA, for inflammatory markers held low over time; in hereditary forms, for a plan that addresses the protein’s origin. Heart function is assessed closely because it determines whether the person can safely undergo surgery and immunosuppression (Cleveland Clinic).

Timing, donor options and the order of any combined procedures are among the most individualized decisions in the whole pathway, and they involve nephrology, hematology or rheumatology, transplant surgery and cardiology together.

What kind of diet is recommended for people with amyloidosis?

There is no diet that removes amyloid, and no supplement with credible evidence that it does. What food can do is make the kidney’s job easier and keep the body strong enough for treatment. A renal dietitian, if one is available to you, tailors the following principles to your test results.

• Salt. Sodium drives fluid retention, so a lower-salt pattern is the single most useful change for swelling and blood pressure in nephrotic syndrome (NIDDK). Most sodium in a typical diet comes from processed and restaurant food rather than the salt shaker.
• Protein. Losing albumin in urine tempts people to eat large amounts of protein to compensate. That can increase the load on the glomeruli. The usual advice is moderate, steady protein intake, adjusted if kidney function falls, rather than either extreme.
• Potassium and phosphorus. These are not restricted for everyone. They become relevant when kidney function declines or specific medicines raise their levels; the dietitian will say if and when.
• Fluids. Free fluid is usually not limited unless swelling or heart involvement requires it.
• Gut involvement. If amyloid affects the digestive tract, smaller frequent meals and attention to unintentional weight loss matter more than any single food rule.

Alcohol is worth discussing openly, since it interacts with several treatments and with blood pressure. Herbal products and high-dose vitamin regimens should be cleared with the team, because some are hard on the kidneys or interfere with medicines.

A practical target for most people is simply this: enough calories and protein to maintain muscle through treatment, less sodium than before, and no unproven additions.

Renal amyloidosis prognosis: what the evidence actually shows

People ask two questions in this room: will my kidneys recover, and how long do I have. Both deserve straight answers, and the straight answer is that no single figure applies to an individual, because outcomes hinge on a handful of variables that differ from person to person.

The first is type. AA amyloidosis in a person whose inflammation can be controlled behaves very differently from AL amyloidosis with heart involvement. The second is the heart. Across forms of amyloidosis, cardiac involvement is the strongest driver of how the disease behaves, which is why heart markers are checked even when the kidney is the presenting organ (Mayo Clinic, Cleveland Clinic). The third is how much kidney function remains at diagnosis and how much protein is being lost; both influence the chance that function stabilizes rather than declines. The fourth, and the one treatment can change, is depth of response: how far and how durably the source protein is suppressed.

What the mainstream evidence supports is this. AL amyloidosis was once a rapidly fatal disease when untreated, and the NHS notes that treatment can now control it for many people for years, although it can return and require further treatment. Earlier diagnosis and modern combination therapy have improved the outlook compared with earlier eras. Kidney function does improve in a proportion of people who achieve a deep response, more often when treatment starts before advanced damage.

What the evidence does not support is a life-expectancy number pulled from a website and applied to you. Staging systems exist, and your hematologist or nephrologist can explain where you sit within one and what that meant for people in similar situations, with the caveats that come with any statistic.

What people often get wrong about kidney amyloidosis

Misunderstandings cluster around this diagnosis, partly because the same word covers very different diseases.

It is not Alzheimer’s disease. Brain amyloid in dementia is a different protein behaving in a different organ. Systemic amyloidosis does not spread to the brain in this way.

It is not automatically cancer. AL amyloidosis arises from an abnormal plasma-cell clone, and a minority of people also meet criteria for multiple myeloma, but most do not (NHS). Chemotherapy is used because those cells respond to it, not because a tumor is present. AA, hereditary and dialysis-related forms have nothing to do with cancer.

Less swelling does not mean the disease is controlled. Diuretics reduce fluid quickly. Deposits and protein loss change slowly. The blood and urine markers, not the ankles, tell the team whether the source is under control.

A normal creatinine does not mean healthy kidneys. Heavy protein loss can be present for a long time before the standard blood measure of filtering moves, which is why urine testing carries so much weight.

Diet or supplements cannot dissolve amyloid. No food, herb or vitamin has been shown to clear deposits. Claims to the contrary are marketing.

It is not contagious, and it is not usually inherited. Only the hereditary forms carry a genetic risk to relatives, and genetic testing can settle the question.

Treatment is not a single course with a finish line. Even after a good response, monitoring continues for years because light chains or inflammation can return, and early detection of relapse protects the kidneys a second time.

Being on dialysis does not end amyloid treatment. The heart and nerves remain at risk, and future transplant depends on the source staying quiet.

Questions to ask your care team

Bringing a written list to appointments is not a sign of distrust; it is how experienced patients keep a complex plan straight. These are the questions that tend to move care forward.

• Which type of amyloid was found, and how was the typing confirmed? Was mass spectrometry or genetic testing used, and is any further testing needed before treatment starts?
• Where is the protein coming from in my case, and what is the plan to reduce its supply?
• Which other organs have been checked, particularly the heart and nerves, and what did those tests show?
• How much kidney function do I have now, how much protein am I losing, and what change in those numbers would count as a response?
• Am I a candidate for intensive treatment such as stem cell transplant, and if not now, what would need to change?
• What side effects should I expect from each medicine, which ones should make me call the same day, and who do I call outside clinic hours?
• Which of my current medicines, supplements or over-the-counter products should I stop or avoid because of my kidneys?
• What is my personal blood pressure target, given that amyloidosis can lower it?
• Should I be taking anything to prevent blood clots while my albumin is low?
• How often will I be tested during and after treatment, and what would prompt a change of plan?
• If my kidneys continue to decline, when would dialysis or transplant be discussed, and which option suits my situation?
• Is there a dietitian, social worker or specialist nurse I can talk to about eating, work and daily life during treatment?
• Should my relatives be tested for anything?

Answers will differ from person to person, and some will change over time. Asking again at the next visit is entirely reasonable.

When to call your doctor

Kidney amyloidosis and its treatments both carry risks that are easier to handle early. Call your care team the same day, or seek urgent care, if any of the following happen.

• Sudden or worsening breathlessness, breathlessness lying flat, or new chest pain or pressure. These can signal fluid overload, a heart rhythm problem or a clot in the lung.
• Fainting, near-fainting or severe dizziness on standing. Low blood pressure from autonomic nerve involvement, diuretics or infection can be dangerous.
• Fever or chills during treatment, especially with chemotherapy or biologic therapy. Infection risk is raised and delays matter.
• A swollen, warm or painful calf or arm, particularly on one side, which may indicate a blood clot.
• Passing much less urine than usual, rapid weight gain over a few days, or swelling that suddenly worsens.
• Confusion, unusual drowsiness or new severe headache.
• Bleeding that does not stop, black stools or vomiting blood.
• Severe or persistent diarrhea or vomiting, which can quickly dehydrate someone with fragile kidney function and unstable blood pressure.
• Rapidly worsening numbness, weakness or pain in the hands or feet, or a new tingling that appears after a treatment change.

Between emergencies, a slower list is also worth reporting at the next contact rather than waiting for a scheduled visit: increasing foaminess of the urine, gradual return of ankle swelling, a persistent drop in appetite or weight, or a new symptom that has no obvious explanation. These are the signs teams use to catch a change in the disease or a side effect while adjustment is still simple. Every decision about what to do next rests with the clinicians who know your case, and they would rather hear from you early than late.

Frequently asked questions

What is the life expectancy for someone with AL amyloidosis with treatment?

There is no single figure that applies to an individual. Outlook in AL amyloidosis depends mainly on whether and how much the heart is involved, how much kidney function remains, and how deeply and durably the abnormal light chains are suppressed by treatment. The NHS notes that treatment can control the condition for years in many people, though it may return. Ask your hematologist how your stage and response translate into realistic expectations for you.

Is amyloidosis a disability?

It can be, depending on how it affects daily function rather than on the diagnosis alone. Most disability frameworks assess limitations such as fatigue, breathlessness, neuropathy, the demands of dialysis or the effects of ongoing chemotherapy. Some people work throughout treatment with adjustments; others cannot for a period. A social worker or patient advocate can explain the process where you live, and your medical team can document the functional impact needed for an application.

What is the prognosis for patients with amyloidosis in the kidney?

Renal amyloidosis prognosis varies widely by type and stage. AA amyloidosis with well-controlled inflammation often stabilizes; AL amyloidosis depends heavily on cardiac involvement and treatment response; hereditary forms depend on the specific variant. Kidney function at diagnosis and the amount of protein loss also matter. Kidney function can improve in a proportion of people who achieve a deep response, more often when treatment begins before advanced damage. Your nephrologist can place your numbers in context.

What are the main amyloidosis diet recommendations for the kidneys?

The core recommendations are less sodium, moderate rather than very high protein, and adjustments to potassium and phosphorus only if kidney function declines or the dietitian advises it. No diet or supplement removes amyloid, and unproven products can harm fragile kidneys. Adequate calories and protein to maintain muscle through treatment matter as much as any restriction, and gut involvement may call for smaller, frequent meals. A renal dietitian tailors this to your results.

Can kidney amyloidosis be reversed?

Partly, in some people. Once the supply of new amyloid protein is shut off, the body slowly clears existing deposits, and urine protein can fall while kidney function stabilizes or improves over months. Recovery is more likely when treatment starts before advanced scarring and when the source is deeply suppressed. Kidneys that have already lost most of their function usually do not regain it, which is why early typing and treatment carry such weight.

Is kidney amyloidosis a type of cancer?

Usually not. AL amyloidosis comes from an abnormal plasma-cell clone in the bone marrow, and only a minority of people also meet criteria for multiple myeloma, which is a cancer of those cells. Treatment borrows myeloma medicines because the clone responds to them. AA, hereditary, dialysis-related and ALECT2 amyloidosis have no connection to cancer at all, which is one reason correct typing must come before any treatment.

How long does kidney amyloidosis treatment last?

It depends on the type. AL amyloidosis therapy is given in cycles, with response judged over months rather than weeks, and follow-up monitoring continues for years afterward because light chains can return. AA amyloidosis treatment usually lasts as long as the underlying inflammatory disease needs control, which is often indefinitely. Kidney-protective medicines and dietary measures typically continue long term. Your team sets the duration based on your response markers.

Can you have a kidney transplant if you have amyloidosis?

Yes, in selected people. The key requirement is durable control of the amyloid source first, such as a deep, sustained light-chain response in AL or persistently low inflammatory markers in AA, because new deposits can form in the transplanted kidney. Heart function is assessed closely, since it determines how safely someone can undergo surgery and immunosuppression. Timing and donor options are decided jointly by nephrology, transplant surgery, cardiology and the specialist treating the source.

Does everyone with kidney amyloidosis need dialysis?

No. Many people whose amyloid source is controlled early keep enough kidney function to avoid dialysis, and some see their protein loss fall and function stabilize. Dialysis becomes necessary when the filters have already failed at diagnosis or continue to decline despite treatment. If it is needed, treatment of the underlying amyloid continues, because the heart and nerves remain at risk and a future transplant depends on the source staying quiet.

Will I need a kidney biopsy to diagnose amyloidosis?

Often, though not always. Amyloid can sometimes be confirmed on a less invasive sample such as abdominal fat or bone marrow, but a kidney biopsy shows directly that the kidney is the affected organ, how much scarring exists and, with the right laboratory methods, which protein is responsible. The decision weighs bleeding risk, kidney size and whether other samples have already answered the question. Your nephrologist will explain which approach fits your situation.

References

• NHS: Amyloidosis
• NIDDK (NIH): Amyloidosis and kidney disease
• NIDDK (NIH): Nephrotic syndrome in adults
• Cleveland Clinic: Amyloidosis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.