Diabetic nephropathy, more broadly referred to as diabetes-associated chronic kidney disease (CKD), is one of the most important long-term complications of diabetes mellitus. It is a major cause of chronic kidney failure and substantially increases the risk of cardiovascular disease, hospitalization, and premature mortality.

The good news is that diabetic kidney disease is preventable or its progression can be substantially slowed when it is detected early and treated appropriately.

Modern management has moved beyond simply controlling blood glucose. Current treatment focuses on a cardio-kidney-metabolic approach, combining blood pressure control, renin–angiotensin system blockade when indicated, SGLT2 inhibitors, GLP-1–based therapies, finerenone in appropriate patients, lipid management, lifestyle intervention, and regular monitoring.

The following approach is based primarily on the American Diabetes Association (ADA) Standards of Care 2026, KDIGO CKD guidance, and the 2026 ADA/EASD consensus report on type 2 diabetes.

What Is Diabetic Nephropathy?

Diabetic nephropathy is kidney damage associated with diabetes. Clinically, it is generally recognized by:

Increased urinary albumin excretion
Reduced estimated glomerular filtration rate (eGFR)
Or both

The term diabetic kidney disease (DKD) is increasingly preferred because not every person with diabetes and CKD has classic pathological diabetic nephropathy.

CKD is generally diagnosed when kidney abnormalities persist for at least 3 months.

In people with diabetes, CKD is defined by persistent:

UACR ≥30 mg/g, and/or
eGFR <60 mL/min/1.73 m²

Other markers of kidney damage may also establish CKD.

The ADA recommends measuring both urinary albumin-to-creatinine ratio (UACR) and eGFR because each provides important prognostic information.

Why Is Diabetic Kidney Disease Important?

Diabetes can damage the kidneys through several mechanisms, including:

Chronic hyperglycemia
Glomerular hypertension
Increased intraglomerular pressure
Endothelial dysfunction
Oxidative stress
Inflammation
Activation of the renin–angiotensin–aldosterone system
Progressive glomerular and tubular injury

Initially, kidney damage may be clinically silent.

Albuminuria may develop before a substantial fall in eGFR. As the disease progresses, patients may develop:

Progressive loss of kidney function
Hypertension
Edema
Hyperkalemia
Metabolic acidosis
Anemia
Mineral and bone abnormalities
Cardiovascular disease
Kidney failure requiring dialysis or transplantation

Importantly, CKD itself substantially increases cardiovascular risk.

Who Should Be Screened?

According to the ADA Standards of Care 2026:

Type 1 diabetes

Screening should begin after approximately 5 years of diabetes duration.

Type 2 diabetes

Screening should begin at the time of diagnosis, regardless of treatment.

Screening consists of:

Spot urine UACR
Serum creatinine with eGFR

The ADA recommends at least annual assessment in these populations. Once CKD is established, UACR and eGFR should generally be monitored 1–4 times per year, depending on CKD stage and risk. (Diabetes Journals)

Understanding UACR

Urinary albumin-to-creatinine ratio is one of the most important tests for diabetic kidney disease.

UACR	Category
<30 mg/g	Normal to mildly increased
30–299 mg/g	Moderately increased albuminuria
≥300 mg/g	Severely increased albuminuria

A single abnormal UACR does not necessarily establish persistent albuminuria.

Because UACR has considerable biological variability, two of three abnormal specimens collected over approximately 3–6 months are generally recommended to confirm persistent albuminuria.

UACR may temporarily increase with:

Recent vigorous exercise
Urinary tract infection
Fever
Heart failure
Severe hyperglycemia
Menstruation
Marked hypertension

Therefore, abnormal results should be interpreted in clinical context. (Diabetes Journals)

Assessing eGFR

eGFR should be calculated from serum creatinine using a validated equation.

The 2021 CKD-EPI creatinine equation is recommended by the ADA.

When creatinine-based eGFR may be unreliable—for example in people with very low muscle mass, frailty, amputation, or certain liver disorders—cystatin C can provide additional information. Combining creatinine and cystatin C can improve estimation of GFR in appropriate patients. (Diabetes Journals)

CKD Risk: Think in Both eGFR and Albuminuria

Kidney risk should not be assessed using eGFR alone.

A patient with:

eGFR 90 but UACR 500 mg/g

may have substantially greater kidney and cardiovascular risk than someone with:

eGFR 90 and UACR <30 mg/g.

Therefore, modern diabetic kidney disease management uses the GFR category + albuminuria category to estimate risk.

When Should You Suspect Another Kidney Disease?

Not every patient with diabetes and CKD has diabetic nephropathy.

Consider another or additional kidney disease when there is:

Rapid decline in eGFR
Active urine sediment
Hematuria
Cellular casts
Rapidly increasing proteinuria
Nephrotic syndrome
Very high or rapidly increasing UACR
CKD developing unusually early
Absence of diabetic retinopathy, particularly in type 1 diabetes
Features suggesting systemic autoimmune, infectious, or other renal disease

In such patients, nephrology referral and sometimes kidney biopsy should be considered. (Diabetes Journals)

Major Goals of Treatment

The modern approach to diabetic kidney disease has several simultaneous goals:

Control blood glucose
Control blood pressure
Reduce albuminuria
Slow eGFR decline
Prevent kidney failure
Reduce cardiovascular events
Reduce heart failure risk
Avoid hypoglycemia
Manage CKD complications
Address lifestyle and cardiovascular risk factors

1. Optimize Blood Glucose

Good glycemic control remains fundamental.

For many adults with diabetes, an HbA1c target around 7% is appropriate, but targets should be individualized according to:

Age
Duration of diabetes
Hypoglycemia risk
Comorbidities
CKD severity
Life expectancy
Treatment burden
Patient preferences

Advanced CKD can increase the risk of hypoglycemia, and HbA1c may become less reliable in advanced kidney disease, particularly in the presence of anemia or altered red-cell survival. Alternative markers such as glycated albumin or fructosamine may sometimes be useful. (Diabetes Journals)

Importantly, glucose lowering alone is no longer considered sufficient kidney-protective therapy.

2. Control Blood Pressure

Blood pressure control is one of the most important interventions for slowing diabetic kidney disease.

The ADA 2026 recommends an on-treatment blood pressure goal of:

<130/80 mmHg, when it can be safely achieved.

A lower systolic target, such as <120 mmHg, may be appropriate for selected patients after considering benefits, adverse effects, frailty, orthostatic symptoms, and overall cardiovascular risk. (Diabetes Journals)

Blood pressure treatment should be individualized.

3. ACE Inhibitor or ARB When Albuminuria Is Present

For people with diabetes, hypertension, and CKD, an ACE inhibitor or ARB is particularly important when albuminuria is present.

The ADA recommends:

ACE inhibitor or ARB for UACR 30–299 mg/g in appropriate patients
Strong recommendation for UACR ≥300 mg/g and/or eGFR <60 mL/min/1.73 m²
Use the maximum tolerated dose

ACE inhibitors and ARBs should not be combined because dual renin–angiotensin system blockade increases adverse events without providing additional kidney benefit. (Diabetes Journals)

Important point

ACE inhibitors and ARBs are not recommended solely to prevent CKD in a patient who has:

Normal blood pressure
Normal UACR
Normal eGFR

(Diabetes Journals)

Monitoring ACE Inhibitors and ARBs

After initiation or dose escalation, monitor:

Serum creatinine
eGFR
Serum potassium
Blood pressure
Volume status

A moderate rise in creatinine does not automatically require discontinuation.

The ADA recommends continuing renin–angiotensin system blockade when the creatinine rise is ≤30%, provided there is no evidence of extracellular volume depletion. (Diabetes Journals)

4. SGLT2 Inhibitors: A Major Advance in Diabetic Kidney Disease

SGLT2 inhibitors have fundamentally changed the treatment of diabetic CKD.

For people with type 2 diabetes and CKD, the ADA 2026 recommends an SGLT2 inhibitor with demonstrated kidney and cardiovascular benefit.

An SGLT2 inhibitor can be initiated when:

eGFR ≥20 mL/min/1.73 m²

and, when tolerated, can generally be continued until kidney failure. (Diabetes Journals)

The kidney benefits are not simply due to lowering blood glucose.

SGLT2 inhibitors can:

Reduce intraglomerular pressure
Reduce albuminuria
Slow eGFR decline
Reduce CKD progression
Reduce heart failure hospitalization
Provide cardiovascular protection

The glucose-lowering effect becomes less pronounced as eGFR falls, but kidney and cardiovascular benefits persist.

Major evidence comes from trials including:

CREDENCE
DAPA-CKD
EMPA-KIDNEY

(Diabetes Journals)

SGLT2 Inhibitor Safety

Important adverse effects and precautions include:

Genital mycotic infections
Volume depletion
Hypotension
Rare diabetic ketoacidosis
Euglycemic DKA
Rare urinary infection complications
Rare Fournier gangrene

Patients should receive sick-day guidance.

SGLT2 inhibitors should generally be withheld during situations such as:

Prolonged fasting
Severe acute illness
Major surgery
Significant dehydration

They should also be stopped and evaluated promptly if DKA is suspected. (Diabetes Journals)

5. GLP-1 Receptor Agonists

GLP-1 receptor agonists are increasingly important in patients with type 2 diabetes and CKD.

The ADA 2026 recommends a GLP-1 receptor agonist with demonstrated benefit to reduce cardiovascular risk and kidney disease progression in appropriate patients with type 2 diabetes and CKD. (Diabetes Journals)

Potential benefits include:

Improved glycemic control
Weight reduction
Cardiovascular risk reduction
Reduction in albuminuria
Favorable kidney outcomes
Low intrinsic risk of hypoglycemia when used without insulin or insulin secretagogues

Semaglutide has particularly important contemporary kidney-outcome evidence.

GLP-1–based therapy is especially useful when:

Obesity or overweight is present
ASCVD risk is high
Additional glucose lowering is needed
SGLT2 inhibitor therapy is contraindicated or insufficient
Cardiovascular risk reduction is a major treatment objective

The 2026 ADA/EASD consensus also emphasizes earlier use of SGLT2 inhibitors and/or GLP-1-based therapies for organ protection, with combination therapy considered in people with concomitant CKD, cardiovascular disease, or heart failure. (Diabetes Journals)

6. Finerenone: Kidney and Cardiovascular Protection

Finerenone is a nonsteroidal mineralocorticoid receptor antagonist (nsMRA).

It is an important option for selected patients with:

Type 2 diabetes
CKD
Albuminuria
Adequate eGFR
Appropriate serum potassium

The ADA 2026 recommends an nsMRA with demonstrated clinical benefit in people with diabetic CKD and albuminuria when eGFR ≥25 mL/min/1.73 m², with potassium monitoring after initiation. (Diabetes Journals)

Evidence from FIDELIO-DKD and FIGARO-DKD demonstrated reductions in important kidney and cardiovascular outcomes.

Why finerenone is different

Finerenone is not simply another blood-pressure drug.

It targets mineralocorticoid receptor–mediated inflammation and fibrosis and provides additional cardiorenal protection in appropriate patients.

Key safety issue

The major concern is:

Hyperkalemia

Therefore, serum potassium should be checked before treatment and monitored after initiation and dose adjustment.

7. Combining Kidney-Protective Therapies

Modern treatment increasingly recognizes that different therapies act through different pathways.

In appropriate patients, treatment may include:

ACE inhibitor/ARB + SGLT2 inhibitor + finerenone ± GLP-1 receptor agonist

rather than relying on one medication.

The ADA 2026 states that simultaneous initiation of an SGLT2 inhibitor and finerenone can be considered in selected adults with type 2 diabetes, UACR ≥100 mg/g and eGFR 30–90 mL/min/1.73 m² who are receiving renin–angiotensin system blockade. (Diabetes Journals)

The CONFIDENCE trial provides evidence that combined finerenone and empagliflozin produces a greater reduction in albuminuria than either treatment alone in appropriately selected patients. (Diabetes Journals)

8. Metformin in CKD

Metformin remains useful in appropriate patients with type 2 diabetes.

However:

It is contraindicated when eGFR <30 mL/min/1.73 m²
Treatment should be reassessed when eGFR falls below 45
Dose and monitoring should be individualized according to kidney function and clinical circumstances

In advanced CKD, GLP-1-based therapy may be preferred for glycemic management because of its cardiovascular benefits and lower hypoglycemia risk. (Diabetes Journals)

9. Nutrition and Lifestyle

Lifestyle treatment remains essential even when modern medications are used.

Important measures include:

Healthy eating

Encourage a dietary pattern emphasizing:

Vegetables
Fruits in appropriate portions
Whole grains
Legumes
High-quality protein
Unsaturated fats
Reduced refined carbohydrates
Reduced highly processed foods

Sodium

For CKD, reducing dietary sodium to approximately:

<2,300 mg/day

may help control blood pressure and reduce cardiovascular risk, with individualization according to kidney function, medications, and comorbidities. (Diabetes Journals)

Protein

For adults with CKD stage G3 or higher who are not on dialysis, the ADA recommends approximately:

0.8 g/kg/day

Higher protein intake, particularly >1.3 g/kg/day, should generally be avoided in non-dialysis CKD. (Diabetes Journals)

Protein recommendations should be individualized, particularly in older adults, people with frailty, malnutrition, or advanced CKD.

Physical activity

Regular physical activity should be encouraged according to cardiovascular status, functional capacity, age, and comorbidities.

Smoking cessation

Smoking cessation is strongly recommended because smoking increases cardiovascular and kidney risk.

Weight management

For people with overweight or obesity, clinically meaningful weight reduction can improve:

Glycemic control
Blood pressure
Cardiovascular risk
Metabolic health

GLP-1-based therapies can be particularly useful when pharmacologic weight management is appropriate.

10. Lipid Management

People with diabetes and CKD have increased cardiovascular risk.

Statin therapy should therefore be considered according to:

Age
ASCVD risk
Existing cardiovascular disease
CKD severity
Diabetes duration
Other risk factors

In patients with established ASCVD or high cardiovascular risk, additional lipid-lowering therapies may be appropriate.

The treatment goal is not simply to “treat cholesterol”; it is to reduce the very high cardiovascular burden associated with diabetes and CKD.

11. Avoid Nephrotoxins

Patients with diabetic CKD should be educated about medications and exposures that can worsen kidney function.

Particular caution is required with:

NSAIDs
Unnecessary nephrotoxic medications
Dehydration
Unmonitored herbal preparations
Certain contrast-related situations
Inappropriate medication combinations

Medication doses should be reviewed whenever eGFR declines.

People with diabetes and CKD have an increased risk of acute kidney injury, so prevention of AKI is an important component of long-term kidney protection. (Diabetes Journals)

12. Monitor for CKD Complications

Once eGFR falls below 60 mL/min/1.73 m², clinicians should actively assess for CKD complications.

These may include:

Anemia
Hyperkalemia
Metabolic acidosis
Mineral and bone disorders
Hyperphosphatemia
Secondary hyperparathyroidism
Vitamin D abnormalities
Fluid overload
Resistant hypertension

The frequency of laboratory monitoring should increase as CKD advances. (Diabetes Journals)

13. When Should a Patient Be Referred to a Nephrologist?

Nephrology referral should be considered for:

eGFR <30 mL/min/1.73 m²
Rapidly declining eGFR
Persistent or rapidly increasing albuminuria
Nephrotic-range proteinuria
Active urinary sediment
Hematuria suggesting another renal disease
Resistant hypertension
Persistent hyperkalemia
Difficult electrolyte abnormalities
Significant metabolic acidosis
Unexplained CKD
Suspected non-diabetic kidney disease
Progressive CKD approaching kidney failure

Early nephrology involvement can facilitate preparation for kidney replacement therapy and management of complications. (Diabetes Journals)

Practical Clinical Algorithm

Step 1 — Screen

For people with diabetes:

UACR + eGFR

at recommended intervals.

Step 2 — Confirm

If UACR is elevated, repeat testing and confirm persistent albuminuria.

Step 3 — Stage

Classify using:

eGFR + albuminuria

Step 4 — Look for atypical features

Consider alternative kidney disease if there is:

Hematuria
Active sediment
Rapid eGFR decline
Rapidly increasing proteinuria
Nephrotic syndrome

Step 5 — Control blood pressure

Target approximately:

<130/80 mmHg when safely achievable

Step 6 — Use ACE inhibitor/ARB when indicated

Particularly with hypertension and albuminuria.

Titrate to the maximum tolerated dose.

Step 7 — Add SGLT2 inhibitor

For appropriate patients with type 2 diabetes and CKD:

eGFR ≥20 mL/min/1.73 m²

Step 8 — Consider GLP-1-based therapy

Especially when cardiovascular risk, obesity, or additional glycemic control is important.

Step 9 — Consider finerenone

For appropriate patients with type 2 diabetes, CKD, and albuminuria, with adequate eGFR and potassium.

Step 10 — Reduce cardiovascular risk

Address:

Lipids
Smoking
Weight
Physical activity
Diet
ASCVD risk

Step 11 — Monitor

Follow:

UACR
eGFR
Potassium
Blood pressure
HbA1c
CKD complications

Can Diabetic Kidney Disease Be Reversed?

Early kidney abnormalities may improve substantially, particularly when albuminuria is identified and treated early.

However, established structural kidney damage may not be completely reversible.

The main objective is therefore:

Prevent progression and preserve kidney function for as long as possible.

A reduction in albuminuria is generally a favorable sign. The ADA recommends aiming for at least a 30% reduction in urinary albumin in people with CKD and UACR ≥300 mg/g when appropriate treatment is instituted. (Diabetes Journals)

Key Take-Home Messages

Diabetic kidney disease is common but potentially modifiable.
Screen type 2 diabetes with UACR and eGFR from diagnosis.
Screen type 1 diabetes beginning approximately 5 years after diagnosis.
Confirm persistent albuminuria rather than relying on one abnormal UACR.
Assess kidney risk using both eGFR and albuminuria.
Aim for individualized blood pressure control, generally <130/80 mmHg when safely achievable.
Use an ACE inhibitor or ARB in appropriate patients with diabetes, hypertension, and albuminuria.
Do not combine ACE inhibitors and ARBs.
SGLT2 inhibitors are now a cornerstone of kidney protection in type 2 diabetes with CKD and can generally be initiated at eGFR ≥20.
GLP-1-based therapy provides important cardiovascular and kidney benefits.
Finerenone provides additional kidney and cardiovascular protection in selected patients with albuminuric diabetic CKD.
Nutrition, exercise, weight management, smoking cessation, and avoidance of nephrotoxins remain essential.
Refer patients with advanced, rapidly progressive, or atypical CKD to nephrology.
Modern diabetic kidney disease treatment is increasingly multidrug, risk-based, and cardio-kidney focused, rather than simply glucose-centered.

Frequently Asked Questions

1. What is the earliest sign of diabetic nephropathy?

One of the earliest clinically detectable abnormalities is increased urinary albumin excretion, measured using the urine albumin-to-creatinine ratio (UACR).

However, albuminuria is not present in every person with diabetic CKD, so eGFR should also be assessed.

2. Can diabetic nephropathy occur with a normal eGFR?

Yes.

A patient may have:

eGFR ≥60 mL/min/1.73 m²

but still have CKD if persistent albuminuria or another marker of kidney damage is present.

Therefore, a normal serum creatinine does not necessarily mean the kidneys are normal.

3. Can diabetic kidney disease occur without albuminuria?

Yes.

Some patients develop a progressive reduction in eGFR without significant albuminuria. This is sometimes called nonalbuminuric diabetic kidney disease.

Therefore, both UACR and eGFR are necessary for screening.

4. Does every patient with diabetes need an ACE inhibitor?

No.

ACE inhibitors or ARBs are particularly indicated when diabetes is accompanied by hypertension and albuminuria or CKD.

They are not recommended solely for primary prevention in patients with normal blood pressure, normal UACR, and normal eGFR. (Diabetes Journals)

5. Can SGLT2 inhibitors be used when eGFR is low?

Yes, in appropriate patients.

Current ADA guidance recommends initiating SGLT2 inhibitors for type 2 diabetes with CKD when eGFR is ≥20 mL/min/1.73 m².

The glucose-lowering effect becomes weaker at lower eGFR, but kidney and cardiovascular benefits remain important. (Diabetes Journals)

6. Should an SGLT2 inhibitor be stopped when eGFR falls below 20?

Not necessarily.

The ADA 2026 notes that in selected patients who tolerate therapy, an SGLT2 inhibitor may be continued even when eGFR falls below 20 until kidney failure develops, primarily for cardiovascular and kidney protection. (Diabetes Journals)

7. Can metformin be used in CKD?

Yes, within appropriate eGFR limits.

Metformin is contraindicated when eGFR is <30 mL/min/1.73 m². Treatment should be reassessed as eGFR declines, and dosing should follow current prescribing recommendations. (Diabetes Journals)

8. Is finerenone safe in diabetic kidney disease?

Finerenone can provide substantial kidney and cardiovascular benefit in appropriately selected patients.

The major concern is hyperkalemia, so potassium must be monitored carefully.

Current ADA recommendations support use of an effective nonsteroidal MRA in albuminuric diabetic CKD when eGFR is ≥25 mL/min/1.73 m². (Diabetes Journals)

9. Should patients with diabetic nephropathy eat a very low-protein diet?

Not routinely.

For CKD stage G3 or higher, the ADA recommends approximately 0.8 g/kg/day for non-dialysis patients.

Very high protein intake should generally be avoided. More restrictive diets should be individualized and supervised by an experienced renal dietitian, particularly because malnutrition can become an important concern in advanced CKD. (Diabetes Journals)

10. Can diabetic nephropathy be prevented?

Risk can be substantially reduced by:

Good glycemic management
Blood pressure control
Appropriate ACE inhibitor/ARB therapy when indicated
SGLT2 inhibitor therapy in appropriate patients
Cardiovascular risk reduction
Healthy diet
Weight management
Exercise
Smoking cessation
Avoidance of nephrotoxins
Regular UACR and eGFR monitoring

Early detection is particularly important because treatment is more effective before substantial irreversible kidney damage occurs.

11. When should I see a kidney specialist?

Consult a nephrologist when kidney function is significantly reduced, particularly eGFR <30, or when there is rapid deterioration, severe albuminuria/proteinuria, hematuria, resistant hypertension, electrolyte abnormalities, or uncertainty about the cause of kidney disease. (Diabetes Journals)

Conclusion

Diabetic nephropathy is no longer managed simply by “controlling sugar.”

The modern approach is a comprehensive cardiorenal protection strategy.

Early screening with UACR and eGFR, intensive but individualized blood pressure control, appropriate use of ACE inhibitors/ARBs, SGLT2 inhibitors, GLP-1-based therapies, and finerenone, together with lifestyle intervention and cardiovascular risk reduction, can substantially slow CKD progression and reduce cardiovascular complications.

The most important principle is simple:

Detect diabetic kidney disease early, quantify both albuminuria and eGFR, and initiate kidney-protective therapy before irreversible kidney failure develops.

This article is for educational purposes and does not replace individualized medical assessment or treatment by a qualified healthcare professional.

References

American Diabetes Association Professional Practice Committee. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1):S246-S260. (Diabetes Journals)
American Diabetes Association Professional Practice Committee. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2026. Diabetes Care. 2026;49(Suppl 1). (Diabetes Journals)
KDIGO. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. 2024. (KDIGO)
KDIGO. KDIGO 2022 Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. KDIGO; current published diabetes-specific guideline, with a 2026 update in development/public review. (KDIGO)
American Diabetes Association & European Association for the Study of Diabetes. Management of Type 2 Diabetes, 2026: A Consensus Report. Diabetes Care. 2026. (Diabetes Journals)
Bakris GL, Agarwal R, Anker SD, et al. Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. N Engl J Med. 2020;383:2219-2229.
Pitt B, Filippatos G, Agarwal R, et al. Cardiovascular events with finerenone in kidney disease and type 2 diabetes. N Engl J Med. 2021;385:2252-2263.
Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in patients with chronic kidney disease. N Engl J Med. 2020;383:1436-1446.
Herrington WG, Staplin N, Wanner C, et al. Empagliflozin in patients with chronic kidney disease. N Engl J Med. 2023;388:117-127.
Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and renal outcomes in type 2 diabetes and nephropathy. N Engl J Med. 2019;380:2295-2306.
Perkovic V, Koitka-Weber A, Cooper ME, et al. Evaluation of the effects of finerenone on albuminuria in diabetic kidney disease. Kidney International.
KDIGO. Clinical Practice Guideline for Diabetes Management in Chronic Kidney Disease. KDIGO; 2022. (KDIGO)

Guideline update note: KDIGO states that its 2022 diabetes-in-CKD guideline remains the current published KDIGO diabetes-specific guideline, while a 2026 update has been released as a draft for public review and is still undergoing revision. Therefore, this article uses the finalized ADA 2026 recommendations alongside the current published KDIGO 2022 diabetes guideline and KDIGO 2024 CKD guideline, rather than presenting the draft KDIGO 2026 update as final. (KDIGO)