When Diabetes Patients Are Referred to a Nephrologist: The Test Results That Trigger It

The three-month diabetes review usually ends the same way: a glance at the A1C, a nod, a new prescription printout. This time the nurse circled two numbers on the lab sheet instead, and the doctor said a sentence that lands harder than it should: “I’d like you to see a kidney specialist.” Nothing hurts. Nothing has changed. And yet the word nephrologist is now sitting on the kitchen table next to the glucose meter.

If you are trying to work out when to see a nephrologist with diabetes, the honest answer is that the referral is almost never about how you feel. It is about what two ordinary tests have been doing over months, and whether the trend has crossed lines that kidney guidelines drew long before your appointment.

This explainer walks through those lines, what the specialist actually does, and why an early referral is far more often a planning conversation than an emergency.

Why does diabetes care sometimes lead to a nephrologist?

A nephrologist is a physician who specializes in the kidneys: how they filter blood, how they fail, and how to slow that failure. Diabetes teams lean on them because the kidney is one of the organs diabetes damages most quietly. The CDC estimates that roughly 1 in 3 adults with diabetes has chronic kidney disease, and diabetes remains the leading cause of kidney failure in the United States.

Those figures sound alarming, so it helps to hold two facts at once. Most people with diabetes never reach kidney failure. And the people who do reach it rarely felt anything until late. The kidneys have enormous spare capacity; you can lose a large share of filtering ability before urine output, energy or appetite change at all. That is precisely why referral decisions run on lab numbers rather than symptoms.

The referral itself is a handover of part of your care, not a verdict. Primary care physicians and endocrinologists manage early kidney changes every day. A nephrologist enters when the numbers suggest the disease is advancing faster than expected, when the picture does not quite fit diabetes alone, or when decisions become more specialized: managing potassium, adjusting medicines that depend on kidney function, or planning years ahead for a kidney that may eventually need support.

If there is one idea worth carrying through this article, it is this: a single lab value matters less than its direction. A stable estimated GFR of 48 for five years and an estimated GFR that has slid from 70 to 48 in eighteen months are entirely different situations, even though the number on today’s sheet is identical. Good referral decisions are built on the graph, not the snapshot.

How does diabetes actually damage the kidney filters?

Each kidney contains about a million tiny filtering units called nephrons, according to the NIH’s kidney institute. Inside every nephron sits a glomerulus: a knot of very fine blood vessels wrapped in a membrane that lets water and waste through while holding back protein and blood cells. Think of it as a colander with holes sized precisely to keep the pasta in.

High blood glucose changes that colander. Sugar attaches to proteins in the vessel walls, the walls thicken, and the supporting tissue slowly scars. Early on, the kidneys often overwork; blood flow through the filters rises, a state called hyperfiltration, which can make the estimated GFR look normal or even high while damage is beginning underneath.

As the membrane loosens, albumin, the most abundant protein in blood, starts slipping into the urine. This is the first measurable footprint of diabetic kidney disease, and it usually appears years before filtering capacity falls. High blood pressure, which travels with diabetes far more often than not, adds mechanical strain to the same vessels. The two conditions feed each other: damaged kidneys hold onto salt and water and push blood pressure up, and higher pressure damages more filters.

Over time, scarred nephrons stop working and the healthy ones take on more load. The Mayo Clinic describes this progression as typically slow, unfolding over many years, which is the encouraging part of the story. Slow processes give clinicians time to intervene. Controlling glucose and blood pressure, and using medicine classes that lower pressure inside the glomerulus itself, can flatten the downward slope. The nephrologist’s job is largely to read that slope early and steepen the interventions before spare capacity runs out.

Which kidney function test for diabetics do doctors watch most closely?

Two tests carry almost all of the weight, and neither requires anything more than a blood draw and a urine sample. The NIH’s kidney institute recommends both as the standard kidney check for people with diabetes.

The first is estimated glomerular filtration rate, or eGFR: a number calculated from blood creatinine (a muscle waste product), along with age and sex, that estimates how many milliliters of blood the kidneys filter each minute. Higher is better. The second is the urine albumin-to-creatinine ratio, or uACR: a spot urine test that measures how much albumin is leaking relative to creatinine, which corrects for how dilute the sample is. Lower is better.

Test	What it measures	Range considered normal	Level that raises concern	Level that commonly prompts nephrology referral
eGFR (blood)	Filtering capacity of the kidneys	60 or above, with no other kidney damage markers	Below 60 on repeat testing over 3 months	Below 30, or a fast, sustained decline
uACR (urine)	Albumin leaking into urine	Below 30 mg/g	30 to 300 mg/g on 2 of 3 samples	Above 300 mg/g on repeat testing

The thresholds in the table follow the staging used by the NIH’s kidney institute and international kidney guidelines. They work as a pair. A person can have a perfectly normal eGFR with a high uACR, which is early diabetic kidney disease. Another can have a reduced eGFR with almost no albumin, which prompts the question of whether something other than diabetes is at work. Read together, the two tests locate you on a grid that predicts risk far better than either alone, and that grid is what your doctor is actually consulting when the word referral comes up.

What eGFR levels prompt a nephrologist referral?

The eGFR ladder has well-known rungs. The NIH’s kidney institute describes stage 1 as 90 or above, stage 2 as 60 to 89, stage 3a as 45 to 59, stage 3b as 30 to 44, stage 4 as 15 to 29, and stage 5 as below 15. Stages 1 and 2 only count as kidney disease if there is another marker of damage, most often albumin in the urine.

The clearest single trigger is an eGFR that has fallen below 30 and stayed there. The NIH’s kidney institute advises that people at this level talk with their team about seeing a nephrologist, because stage 4 is when planning for the possibility of dialysis or transplant, adjusting medicines cleared by the kidney, and managing bone and blood chemistry become specialized work. Referral here is about starting those conversations years before they are needed.

Many people are referred earlier than 30, and reasonably so. A common pattern that worries clinicians is speed: an eGFR that drops by a noticeable margin year after year rather than drifting down slowly with age. Kidney guidelines generally treat a sustained rapid fall as a referral reason in its own right, whatever the current value, because the trajectory predicts where you will be in five years better than the starting point does.

One caution about the number itself. Because eGFR is estimated from creatinine, it is affected by muscle mass, recent heavy exercise, hydration, certain medicines and a large meat meal the night before. A very muscular person may test low without kidney trouble; a frail older adult may test deceptively high. Newer equations no longer use race as an input. When the estimate seems out of step with the rest of the picture, laboratories can measure a second marker, cystatin C, which is less influenced by muscle. Your team may repeat the test before acting on it; that is good practice, not indecision.

How much albumin in the urine is too much?

Albumin is the earlier and, in diabetes, often the more important signal. The staging used by the NIH’s kidney institute labels a uACR below 30 mg/g as normal to mildly increased, 30 to 300 mg/g as moderately increased (the range once called microalbuminuria), and above 300 mg/g as severely increased.

A single high reading proves little. Vigorous exercise within the previous day, a fever, a urinary infection, menstrual bleeding, very high blood glucose, or simply being dehydrated can push albumin up for a day or two. That is why kidney guidance asks for confirmation: an abnormal result on at least two of three samples collected over three to six months before it is treated as persistent. If your doctor asked for a second or third urine sample, they were following the rules, not hedging.

Once albumin is confirmed in the moderate range, most people stay with their primary or diabetes team, who tighten glucose and blood pressure targets and typically consider medicines that reduce pressure inside the filters. The referral conversation usually begins when albumin sits persistently above 300 mg/g, especially if eGFR is also slipping. Heavy albumin loss signals a more damaged membrane, tends to progress faster, and raises cardiovascular risk enough that specialists want to be involved in the plan.

The two numbers should always be read together. International kidney guidelines arrange eGFR and uACR on a grid where risk climbs toward the bottom right corner: low filtration plus heavy albumin. Someone with an eGFR of 50 and normal albumin sits in a different part of that grid from someone with an eGFR of 50 and albumin above 300 mg/g, and the second person is far more likely to be referred. Ask your team to show you where you sit on that grid; it turns an abstract number into a map.

Diabetic nephropathy referral criteria beyond eGFR and albumin

Not every referral is driven by the two headline tests. Several other findings send diabetes care toward a nephrologist, and they matter because they often mean the kidney problem is not straightforward diabetic damage.

Blood in the urine is the first. Diabetic kidney disease does not usually cause visible or microscopic bleeding. When a urine test picks up red cells with no infection or stone to explain them, clinicians consider other kidney conditions, such as inflammation of the glomeruli, that need different treatment and sometimes a biopsy. A specialist’s review of the urine under a microscope can be revealing here.

Potassium is the second. Damaged kidneys and several kidney-protective medicines can both raise blood potassium, and a level that keeps creeping up despite adjustments is a common reason for specialist input, because potassium outside its narrow range affects heart rhythm.

Blood pressure that stays high on three or more medicines is a third. Resistant hypertension and kidney disease are so intertwined that nephrologists manage it routinely, and they look for narrowed kidney arteries or hormonal causes that primary care may not routinely screen for.

An unusual story is a fourth. Kidney disease appearing within a few years of a type 1 diagnosis, kidney changes without any diabetic eye disease, a sudden rather than gradual decline, or a strong family history of kidney disease all raise the question of a second diagnosis. The Mayo Clinic notes that eye and kidney damage in diabetes usually travel together, so their absence is informative.

Finally, recurrent kidney stones, a persistently low blood count attributed to kidney disease, or repeated episodes of acute kidney injury during illness each justify a specialist’s opinion. None of these is a symptom you can feel; all of them are visible in routine results, which is why the annual check carries so much weight.

When to see a nephrologist with diabetes: who is referred and who is asked to wait

Deciding when to see a nephrologist with diabetes is a judgment call, but the typical pattern is fairly consistent across guidelines and health systems.

Referral is usual for people with an eGFR persistently below 30, albumin persistently above 300 mg/g, a rapid year-on-year decline in filtration, unexplained blood in the urine, potassium or blood pressure that will not settle, or any picture where the cause is uncertain. It is also common when someone has already had one or more episodes of acute kidney injury, or when a clinician simply feels the case has outgrown general management. Age, other illnesses and the person’s own wishes all shape the timing.

Many people are asked to wait, and this is not neglect. Someone with type 2 diabetes, an eGFR of 65, a uACR of 40 mg/g on two samples, well-controlled blood pressure and a stable trend is in a group that primary care and diabetes teams are well equipped to manage. The interventions at this stage are the same ones a nephrologist would recommend: tighter glucose and blood pressure control, medicine classes that protect the filters, attention to salt and smoking, and a repeat of both tests within a year or sooner. Referring everyone at this stage would swamp specialist clinics without changing the plan.

There is a middle group where practice varies. Stage 3a with moderate albumin, or stage 3b with a slow decline, may be co-managed: the nephrologist sees the person once, sets a plan, and hands routine monitoring back with clear triggers for re-referral. If you are in this zone and feel unsettled, it is entirely reasonable to ask for that single consultation. The decision sits with your treating team, but they will usually welcome the question, because uncertainty about a kidney trend is itself a recognized reason to ask a specialist.

What are the earliest signs of diabetic kidney disease?

The uncomfortable truth is that the earliest sign is a lab result, not a feeling. The NHS notes that chronic kidney disease often causes no symptoms until it is advanced, and the Mayo Clinic describes the same pattern specifically for diabetic kidney disease. Albumin appearing in the urine is the first detectable change, and it is invisible.

Symptoms tend to arrive when a large share of filtering capacity has gone. Swelling around the ankles, feet or eyes reflects salt and water the kidneys can no longer clear. Urine that looks unusually foamy can reflect heavy protein loss. Fatigue, poor appetite, nausea, itching, difficulty concentrating and trouble sleeping appear as waste products accumulate. Blood pressure that becomes harder to control is another late signal. Needing to urinate more at night can occur, but it also happens with high blood glucose, prostate changes and simple aging, so it is a poor guide on its own.

This is not a checklist to diagnose yourself from. Every one of those symptoms is more commonly caused by something else, and their absence tells you nothing reassuring about your kidneys. The practical lesson is the opposite of vigilance for symptoms: it is trust in the routine test. A person who has a uACR and eGFR every year will learn about kidney disease five to fifteen years earlier than a person waiting to feel unwell.

If early signs of diabetic kidney disease do show up on paper, they arrive with a genuine advantage. The changes at the moderate albumin stage are the ones most responsive to blood pressure control and to the kidney-protective medicine classes discussed later, and some people see albumin fall back toward normal. That window is why the annual check exists, and why it should not be skipped in a year when everything feels fine.

How often should kidney function be checked with diabetes?

The NIH’s kidney institute recommends that people with type 2 diabetes have both eGFR and uACR checked when diabetes is first diagnosed and then every year. For type 1 diabetes, the same guidance recommends starting the annual checks five years after diagnosis, because kidney changes rarely appear earlier. Those are the minimum intervals for someone whose results are normal.

Once either test is abnormal, frequency rises, and the exact rhythm becomes a decision for your team. People with moderately increased albumin or an eGFR in the 45 to 59 range are often tested twice a year. Those with heavier albumin loss, an eGFR below 45, or a recent rapid decline may be checked every three to four months, sometimes aligning with the routine diabetes visit so no extra trip is needed. After a change in kidney-protective medicine, a blood test within a few weeks is standard to check creatinine and potassium.

Illness changes the schedule too. Vomiting, diarrhea, a high fever or any episode of dehydration can drop filtering temporarily, and many clinicians will re-check kidney function after recovery, particularly for people already in stage 3 or beyond. Some also give written sick-day guidance about which medicines to pause during such episodes; that guidance is individualized and should come from your prescriber, not from a general article.

A practical tip: ask for your actual numbers each time, not just “your kidneys are fine.” Write down the eGFR and uACR with the date. Over three or four years, that handwritten list becomes the trend line clinicians most want to see, and it lets you notice a drift long before anyone uses the word referral. Many patient portals now plot these values automatically; if yours does, look at the graph rather than the latest value.

What happens at the first nephrologist visit and in the weeks after?

The first appointment is mostly conversation and review. Expect questions about how long you have had diabetes, your blood pressure history, eye exams, family kidney problems, past episodes of dehydration or acute kidney injury, and every medicine and supplement you take, including over-the-counter pain relievers, because some of them strain kidneys. Bring a list, or the bottles themselves.

The specialist will look at every kidney result you have ever had, plotted over time, and will usually repeat both eGFR and uACR along with a fuller blood panel: potassium, bicarbonate, calcium, phosphate, hemoglobin and sometimes parathyroid hormone, which shift as kidney function declines. A urine sample examined under a microscope is common, to look for blood cells or casts that would point away from diabetes. Blood pressure is measured carefully, sometimes with a request for home readings or a 24-hour monitor.

An ultrasound of the kidneys is often ordered to check size, shape and drainage. A kidney biopsy, in which a needle removes a tiny sample of tissue for examination, is uncommon in typical diabetic kidney disease; the Mayo Clinic notes it is reserved for cases where the diagnosis is unclear.

The following weeks usually look like this. Repeat labs return within days. If a medicine is started or adjusted, a blood test one to several weeks later checks that creatinine and potassium have settled; a small, early rise in creatinine after starting certain kidney-protective classes is expected and is not the same as damage. A follow-up visit typically falls within three to six months for stable stage 3 disease and sooner for stage 4 or a fast decline, though your team sets the interval. Between visits, the plan is unglamorous: blood pressure logs, glucose control, hydration, and avoiding medicines your nephrologist has flagged. Most people leave the first visit with a clearer map than they arrived with, and that alone tends to lower the anxiety the referral created.

How do treatments slow diabetic kidney damage?

Treatment aims to protect the filters that remain, and it works on several fronts at once. Glucose control comes first, because less sugar circulating means less chemical damage to vessel walls. Blood pressure control comes a close second, because every point of excess pressure is transmitted straight into the glomeruli. Both are managed by your existing team with targets tailored to you.

Beyond those basics, several medicine classes act directly on the kidney. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers relax the small vessel leaving each glomerulus, which lowers pressure inside the filter and reduces albumin leak; they have been the backbone of diabetic kidney protection for decades. Sodium-glucose cotransporter-2 inhibitors, developed as glucose-lowering drugs, cause the kidney to excrete glucose and sodium, which resets a pressure-sensing mechanism inside the nephron and lowers filter pressure independently of blood sugar. Glucagon-like peptide-1 receptor agonists lower glucose and weight and appear to reduce inflammation in kidney tissue. A newer class, nonsteroidal mineralocorticoid receptor antagonists, blocks a hormone pathway that drives scarring and inflammation in the kidney.

None of these is a recommendation. Whether any class suits you depends on your eGFR, potassium, blood pressure, other conditions and current prescriptions, and every choice belongs to your prescribing clinician. Expect a check of creatinine and potassium within a few weeks of starting some of these medicines, and expect that a modest early rise in creatinine may be accepted rather than treated as a problem.

The remaining levers are lifestyle. Stopping smoking, moderating salt, keeping physically active, maintaining a healthy weight and avoiding regular use of certain over-the-counter anti-inflammatory pain relievers all reduce strain. The CDC and the NIH’s kidney institute frame these as core kidney protection in diabetes, not optional extras. None of them reverses scar tissue, but together they can change the slope of the line, which is the whole point.

What people often get wrong about kidney referrals in diabetes

The first misunderstanding is that a referral means dialysis is coming. It usually means the opposite: someone wants a specialist involved while there is still time to slow things down. Stage 3 kidney disease is the most common point of referral, and most people at stage 3 never progress to kidney failure, particularly when blood pressure and glucose are controlled.

The second is that feeling well means the kidneys are fine. As the NHS points out, kidney disease usually causes no symptoms until it is advanced. Normal energy and normal urination are not evidence of healthy kidneys; the uACR and eGFR are.

The third is that a single bad result is a diagnosis. Both tests fluctuate with hydration, exercise, illness and diet. Kidney guidelines require abnormal results to persist for at least three months before chronic kidney disease is diagnosed, and albumin to be confirmed on repeat samples. If your doctor wants a re-test before acting, that is the guideline working as intended.

The fourth is that kidney disease with diabetes must be caused by diabetes. It usually is, but the absence of eye disease, blood in the urine, or a very fast decline can point to a different condition that needs different treatment. Nephrologists exist partly to spot these.

The fifth is that protein in the diet should be cut to near zero the moment albumin appears. Very low protein intake carries its own risks, especially in older adults, and dietary changes in kidney disease are individualized by a dietitian working with your team.

The last, and perhaps most costly, is the belief that nothing can be done. Scar tissue does not regrow, which is true. But the rate of new scarring is highly modifiable, and people who start protective treatment at the moderate albumin stage can hold a stable eGFR for many years. The referral is the beginning of that work, not an admission that it failed.

Questions to ask your care team

A referral appointment goes better when you arrive with questions written down. These are the ones nephrologists say they wish more people asked.

• What are my current eGFR and uACR, and how have they changed over the past two to three years? Can I see the graph?
• Which specific result prompted this referral: the level, the speed of change, or something else in my labs or urine?
• Do my results fit diabetic kidney disease, or is there anything suggesting another cause that needs separate tests?
• What eGFR and uACR would you consider a good outcome for me a year from now?
• Are any of my current medicines, including over-the-counter ones and supplements, harder on the kidneys as function falls?
• Which kidney-protective medicine classes are options for me, what are the trade-offs, and what monitoring would follow a change?
• What blood pressure range are we aiming for, and should I be measuring at home?
• Do I need written sick-day guidance for episodes of vomiting, diarrhea or fever?
• How often should I be tested now, and who orders those tests: you or my primary care team?
• Would a referral to a kidney dietitian help, and what should I not change on my own?
• At what point would we start talking about long-term planning, and what would that conversation cover?

Two habits make these questions useful. Ask for numbers, not adjectives; “mildly reduced” hides a lot. And ask who owns each part of the plan, because kidney care in diabetes is shared between several clinicians, and gaps open in the handovers rather than in the visits themselves. If something is unclear when you get home, the portal message or the nurse line is the right tool; write the question the same day, while the visit is fresh.

When to call your doctor

Most diabetic kidney disease moves slowly and is managed at scheduled visits. A small number of situations should not wait for the next appointment, and knowing them removes the temptation to watch and worry.

Contact your care team the same day if you notice new or rapidly worsening swelling of the legs, feet or face; a sharp drop in how much urine you pass, or none for many hours; visible blood in the urine; shortness of breath, especially when lying flat; a new irregular or racing heartbeat; severe muscle weakness; or persistent nausea and vomiting that stops you keeping fluids or medicines down. Several of these can reflect fluid overload or potassium disturbance, both of which are treatable and both of which are time-sensitive.

Seek emergency care immediately for chest pain, severe breathlessness, confusion, fainting, or a seizure. These can occur when waste products or potassium rise quickly, and they need hospital assessment rather than a phone call.

Call promptly, though not necessarily urgently, if you have vomiting or diarrhea lasting more than a day, a high fever, or any illness that stops you eating and drinking normally, particularly if your eGFR is below 45. Dehydration is one of the commonest triggers of a sudden fall in kidney function, and your prescriber may want to adjust medicines temporarily or check your bloods once you recover. Ask in advance for written sick-day guidance so you know the plan before you need it.

Also let your team know before starting any new over-the-counter medicine or supplement, and if a pharmacist or another clinician flags a medicine as unsuitable for your kidney function. None of this replaces the scheduled checks, and every decision about treatment rests with your treating team; these are simply the moments when a call is better than waiting.

Frequently asked questions

How do I know if diabetes is affecting my kidneys?

You usually cannot tell by how you feel; only two tests show it. A urine albumin-to-creatinine ratio detects protein leaking from damaged filters, and a blood eGFR estimates filtering capacity. Both are recommended yearly for people with diabetes. An abnormal result should be repeated within three months before anything is concluded, because hydration, exercise and illness can shift both values temporarily.

What are the three warning signs of kidney disease people talk about?

The three most cited are swelling of the ankles or around the eyes, foamy urine from protein loss, and persistent fatigue with poor appetite. All three appear late, when much filtering capacity is already gone, and all three are more often caused by something else. They are not a self-diagnosis tool. The reliable warning sign is a rising urine albumin result on routine testing, which arrives years earlier.

What eGFR levels lead to a nephrologist referral?

An eGFR that stays below 30 is the most consistent trigger, according to NIH kidney guidance, because stage 4 disease involves specialized planning. Many people are referred earlier, particularly when eGFR is falling quickly year over year, when urine albumin is heavily raised, or when something in the picture does not fit typical diabetic kidney disease. Your team weighs the trend, not just the current value.

Does a referral to a nephrologist mean I will need dialysis?

No. Most referrals happen at stage 3 kidney disease, and most people at that stage never reach kidney failure, especially when blood pressure and glucose are controlled. The referral is designed to slow decline while there is still time. Dialysis planning becomes a topic in stage 4 or 5, and even then it is a conversation about options that may unfold over years rather than an imminent event.

What are the diabetic nephropathy referral criteria beyond eGFR?

Persistent urine albumin above 300 mg/g, unexplained blood in the urine, potassium that keeps rising, blood pressure that stays high on several medicines, repeated episodes of acute kidney injury, recurrent kidney stones, or a story that does not fit diabetes, such as kidney changes without eye disease. Uncertainty itself is a valid reason; clinicians often refer simply because the trend is unclear.

Can diabetic kidney disease be reversed?

Scar tissue in the kidney does not regrow, so lost filtering capacity is generally not recovered. What can change is the rate of further loss. At the moderate albumin stage, good blood pressure and glucose control, together with kidney-protective medicine classes chosen by your prescriber, can lower albumin and hold eGFR stable for many years. Treatment is about controlling progression rather than undoing damage.

How long does it take for diabetes to damage the kidneys?

Usually many years. The Mayo Clinic and the NIH’s kidney institute describe diabetic kidney disease as a slow process, which is why type 1 screening is not recommended until five years after diagnosis. Type 2 diabetes is often present for years before it is found, so screening starts at diagnosis. The slow pace is the reason early detection and treatment can make such a difference to the long-term course.

Will my diabetes medicines change after seeing a nephrologist?

Possibly, but that decision belongs to your prescribers working together. Some glucose-lowering medicines are cleared by the kidney and may need review as eGFR falls, while certain classes are chosen partly for their kidney-protective effects. Never stop or adjust a medicine on your own after a referral; bring your full list to the appointment and ask what, if anything, the specialist recommends changing and why.

Which kidney function test for diabetics is more important, blood or urine?

Both, and together. The urine albumin-to-creatinine ratio usually changes first in diabetes and detects damage while eGFR is still normal. The blood eGFR shows how much filtering capacity remains. Kidney guidelines place the two on a grid to estimate risk; a person with normal eGFR and heavy albumin, and a person with low eGFR and no albumin, need different investigations and follow-up.

Will I need a kidney biopsy?

Usually not. A kidney biopsy, where a needle removes a tiny piece of tissue for examination under a microscope, is reserved for cases where the diagnosis is uncertain: blood in the urine, a very rapid decline, kidney disease without diabetic eye changes, or features suggesting another condition. The Mayo Clinic describes it as uncommon in typical diabetic kidney disease. Your nephrologist will explain the reasoning if it is suggested.

References

• NIDDK (NIH): Diabetic Kidney Disease
• NIDDK (NIH): Chronic Kidney Disease Tests & Diagnosis
• CDC: Diabetes and Chronic Kidney Disease
• NHS: Chronic kidney disease

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.