Utility of untimed urinary albumin measurements in assessing albuminuria in black NIDDM subjects. Clinical identification Green tea polyphenols nondiabetic Coenzyme Q and liver health patieht in Diabetiic patients with Diabetic nephropathy patient support I and type II disease presenting with renal dysfunction. Effects of pentoxifylline on inflammatory parameters in chronic kidney disease patients: a randomized trial. Mann JF, Green D, Jamerson K, et al. Staging of patients who meet the definition of CKD. Find a doctor. Mayo Clinic Alumni Association.

Diabetic nephropathy patient support -

These wastes can build up in your body and cause damage to other organs. The causes of diabetic kidney disease are complex and most likely related to many factors.

Some experts feel that changes in the circulation of blood within the filtering units of the kidney glomeruli may play an important role.

The following risk factors have been linked to increased risk of developing this disease: high blood pressure, poor glucose sugar control and diet. In the early stages, there may not be any symptoms. As kidney function decreases further, toxic wastes build up, and patients often feel sick to their stomachs and throw up, lose their appetites, have hiccups and gain weight due to fluid retention.

If left untreated, patients can also develop heart failure and fluid in their lungs. Join our email list for useful tips on living with diabetes and kidney disease. The diagnosis is based on the presence of abnormal amounts of protein in the urine.

A variety of tests can be done to tell if a person has kidney disease, such as serum creatinine and BUN blood area nitrogen. The most widely used are serum creatinine and BUN blood urea nitrogen. These are not very sensitive tests because they do not begin to change until the patient develops more severe disease.

Other more sensitive tests are: creatinine clearance, glomerular filtration rate GFR and urine albumin. Estimated of glomerular filtration rate eGFR is considered a better measure of kidney function compared to creatinine.

Urinary albumin-to-creatinine ration UACR is also used to check for high protein in the urine albuminuria , which is a sign of kidney disease. In patients with Type I juvenile-onset or insulin-dependent diabetes, a diagnosis of early kidney disease can be based on the presence of very small amounts of protein in the urine microalbuminuria.

Special methods are needed to measure these small amounts of protein. When the amount of protein in the urine becomes large enough to be detected by standard tests, the patient is said to have "clinical" diabetic kidney disease. Almost all patients with Type I diabetes develop some evidence of functional change in the kidneys within two to five years of the diagnosis.

About 30 to 40 percent progress to more serious kidney disease, usually within about 10 to 30 years. The course of Type II adult-onset or non-insulin-dependent diabetes is less well defined, but it is believed to follow a similar course, except that it occurs at an older age. Careful control of glucose sugar can help slow the progression, or perhaps prevent, kidney disease in people with diabetes.

You should follow the advice of your doctor and other members of your healthcare team regarding diet and medicines to help control your glucose levels. Aside from SGLT2 inhibitors, the glucose-lowering drugs with the strongest evidence of benefit on cardiovascular and kidney outcomes in patients with preexisting cardiovascular or kidney disease are the GLP-1 receptor agonists [ 31 ].

Thus, in patients with type 2 diabetes and DKD who have not achieved glycemic control despite initial glucose-lowering therapy which is typically metformin and an SGLT2 inhibitor, a GLP-1 receptor agonist can improve glycemic control and may provide additional benefit [ ]. GLP-1 receptor agonists are discussed below and in other topics.

See "Initial management of hyperglycemia in adults with type 2 diabetes mellitus" and "Management of persistent hyperglycemia in type 2 diabetes mellitus" and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus". Our recommendations outlined above are consistent with guidelines from the American Diabetes Association ADA and the Kidney Disease Improving Global Outcomes KDIGO on the treatment of patients with DKD [ 37,38 ].

The glycosuria is dependent upon kidney function, and therefore the magnitude of glycosuria and lowering of blood glucose is smaller among individuals with reduced kidney function. SGLT2 inhibitors have additional effects on the kidney, and, given their weak glucose-lowering effect, these effects are likely independent of glycemic control.

By blocking the cotransporter, they reduce sodium reabsorption, which is usually increased in patients with diabetes due to the excess tubular glucose load.

The resulting natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa.

Increased sodium delivery to the macula densa normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure ie, reduces glomerular hyperfiltration through constriction of the abnormally dilated afferent arteriole [ 39 ]. This decrease in glomerular hyperfiltration can, hypothetically, slow the rate of progression of kidney disease see "Diabetic kidney disease: Pathogenesis and epidemiology", section on 'Glomerular hyperfiltration'.

A range of additional mechanisms may explain the benefits of SGLT2 inhibitors on kidney disease progression [ 40 ]. SGLT2 inhibitors reduce the risk of kidney disease progression among patients with DKD who are already taking ACE inhibitors or ARBs [ 33, ], as well as the incidence of cardiovascular disease [ 33 ].

Among patients with DKD and severely increased albuminuria, the best data come from three large trials:. Approximately two-thirds of enrolled patients had type 2 diabetes; 98 percent were taking an ACE inhibitor or ARB.

The beneficial effect of dapagliflozin was similar in patients with DKD and in patients with other forms of kidney disease, reinforcing the concept that beneficial effects are independent of glycemic control.

There were no differences between the treatment groups with respect to major adverse effects. Less than half 46 percent of participants had diabetes. At two years, empagliflozin reduced the incidence of ESKD 3. The risks of all-cause mortality 4. Effects were similar in patients with and without diabetes and regardless of the eGFR at the start of the study.

Numerous other large trials of SGLT2 inhibitors in patients with type 2 diabetes enrolled subsets of patients with mostly nonalbuminuric DKD [ 45, ].

Compared with placebo, SGLT2 inhibitors reduced the rate of kidney disease progression among patients with diabetes regardless of preexisting DKD 1.

The relative benefits from SGLT2 inhibitors were similar among patients with different baseline levels of albumin excretion. However, given that the rate of kidney disease progression is substantially higher in patients with severely increased albuminuria, the absolute benefits of SGLT2 inhibitor therapy are greater among those with higher levels of albuminuria, despite similar relative risks.

SLGT2 inhibitors also reduced the rates of major cardiovascular events among patients with established atherosclerotic cardiovascular disease regardless of whether patients had DKD [ 31,33,45,51,56,59 ]. These drugs also prevent heart failure hospitalization and death in patients who have heart failure with reduced ejection fraction.

See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Clinical outcomes'. SGLT2 inhibitors increase the risk of genital infections by two- to fourfold; such infections primarily include vulvovaginal candidiasis, which occur in 10 to 15 percent of women taking these drugs.

SGLT2 inhibitors are also associated with Fournier's gangrene in rare cases [ 62 ]. In addition, SGLT2 inhibitors can produce "euglycemic" diabetic ketoacidosis in type 1 diabetes and more rarely in type 2 diabetes.

Thus, patients with a prior history of or risk factors for genital infections may reasonably choose to not take an SGLT2 inhibitor. In patients with DKD who have a lower absolute risk for progression of kidney disease, and who also do not have established atherosclerotic cardiovascular disease or heart failure, the benefits and harms of taking an SGLT2 inhibitor may be more closely balanced.

See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Adverse effects'. Activation of the mineralocorticoid receptor is associated with cardiovascular and kidney disease, putatively by stimulating inflammatory and fibrotic cascades [ 63 ].

Steroidal MRAs, such as spironolactone , reduce albuminuria in patients with DKD but often cause hyperkalemia in patients with reduced eGFR, particularly when ACE inhibitors or ARBs are also used.

The nonsteroidal MRA finerenone also reduces albuminuria and has a smaller effect on the serum potassium [ 64,65 ]. The effects of finerenone on kidney disease progression were examined in two large trials:. All patients were taking a maximal, or maximally tolerated, dose of an ACE inhibitor or ARB at baseline.

Hyperkalemia occurred more frequently with finerenone Compared with placebo, finerenone reduced the risk of heart failure hospitalization 3.

Hyperkalemia was more common with finerenone In a pooled analysis of these two trials, finerenone lowered the risk of kidney failure 3. The great majority of patients enrolled in these two trials were not simultaneously treated with an SGLT2 inhibitor, and the subgroup of patients who were was too small to determine with certainty whether or not finerenone provided additional benefit.

Another nonsteroidal MRA, esaxerenone, also reduces albuminuria in patients with DKD [ 69 ]. However, trials of esaxerenone report higher rates of hyperkalemia than those examining finerenone [ ], and the effects of esaxerenone on mortality and ESKD are unknown.

However, the effect was predominantly due to a reduction in new-onset albuminuria. Similarly, another GLP-1 receptor agonist dulaglutide slowed the rate of decline in eGFR and prevented worsening of albuminuria in trials of patients with type 2 diabetes with and without CKD [ 73,74 ].

Thus, if additional glucose-lowering therapy is required in a patient with DKD despite initial glucose-lowering therapy and an SGLT2 inhibitor, then we would prefer starting a GLP-1 receptor agonist. GLP-1 receptor agonists also reduce the rates of cardiovascular disease [ 31 ].

See "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Microvascular outcomes' and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects'.

By inhibiting dipeptidyl peptidase DPP 4, DPP-4 inhibitors prevent the deactivation of a variety of bioactive peptides, including GLP-1, thereby modestly increasing GLP-1 levels. However, unlike GLP-1 receptor agonists, DPP-4 inhibitors have not prevented the development or progression of kidney disease in patients with diabetes, nor do they have any cardiovascular benefits [ 75,76 ].

The use of DPP-4 inhibitors in patients with type 2 diabetes, including their safety and need for dose adjustments in the setting of CKD, is discussed separately. See "Dipeptidyl peptidase 4 DPP-4 inhibitors for the treatment of type 2 diabetes mellitus". A large trial of more than individuals with type 2 diabetes treated with metformin monotherapy directly compared the kidney effects of the GLP-1 receptor agonist liraglutide with a DDP-4 inhibitor, insulin, and glimepiride [ 77 ].

There were no significant differences among the groups at five years in terms of eGFR decline or development of CKD in this low-risk group. The patients enrolled had normal kidney function and well controlled blood pressure at baseline, and the number of events was small.

This study does not support the use of expensive GLP-1 receptor agonists for kidney protection in patients at low risk.

Therapies of limited use — Various other approaches have been studied as methods to slow the progression of DKD. However, there are insufficient data to advocate their use:. Data are conflicting as to whether protein restriction can slow the progression of kidney disease [ ]. In addition, it is uncertain whether a low-protein diet is significantly additive to other measures aimed at preserving kidney function, such as ACE inhibition and aggressive control of blood pressure and blood glucose [ 78 ].

Other aspects of monitoring should be based upon the clinical situation. See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers".

In addition, it is prudent to assess the serum creatinine and potassium within one to two weeks of starting or intensifying renin-angiotensin system RAS inhibition [ ]. Blood pressure should be assessed within one to two weeks of initiating or intensifying these agents.

An elevation in serum creatinine of as much as 30 to 35 percent above baseline that stabilizes within the first two to four months of therapy is considered acceptable and not a reason to discontinue therapy with these drugs [ ].

Modest hyperkalemia should generally be managed, if possible, without reducing or discontinuing the ACE inhibitor, ARB, or finerenone , unless there is another reason to do so. If discontinued for hyperkalemia, the ACE inhibitor or ARB should be resumed as soon as it is safe to do so.

See "Treatment and prevention of hyperkalemia in adults", section on 'Patients who can have the serum potassium lowered slowly'. Similarly, the serum creatinine, serum potassium, and blood pressure, plus the patient's volume status, should generally be ascertained within a few weeks of commencing a sodium-glucose cotransporter 2 SGLT2 inhibitor.

See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Hypotension'. Both RAS inhibition and SGLT2 inhibitors may increase the risk of symptomatic hypotension, and other antihypertensive therapies should be withdrawn first if possible before considering cessation of these evidence-based therapies.

Similarly, SGLT2 inhibitors may cause volume depletion, and withdrawal or reduction of thiazide or loop diuretics should be attempted before discontinuing the SGLT2 inhibitor.

See "Definition and staging of chronic kidney disease in adults", section on 'Referral to a specialist'. PROGNOSIS — A substantial proportion of people with diabetic kidney disease DKD will have progressive loss of kidney function and will develop end-stage kidney disease ESKD.

The strongest risk factor for risk of progression is the presence of increased albuminuria, while people with reduced estimated glomerular filtration rate eGFR or anemia are also at increased risk. With available protective therapies, a dramatic stabilization of kidney function is likely to be achievable.

See "Diabetic kidney disease: Manifestations, evaluation, and diagnosis", section on 'Natural history'. Of note, people with DKD are at particularly high risk of cardiovascular events, and most have a higher risk of death mostly cardiovascular than developing kidney failure.

Cardiovascular protective therapies are therefore also critical. See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Reducing the risk of macrovascular disease'. SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.

See "Society guideline links: Glomerular disease in adults" and "Society guideline links: Chronic kidney disease in adults" and "Society guideline links: Diabetic kidney disease". These articles are best for patients who want a general overview and who prefer short, easy-to-read materials.

Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients.

You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword s of interest. The evidence supporting our recommendation is presented separately. See "Goal blood pressure in adults with hypertension", section on 'Patients with chronic kidney disease' and "Goal blood pressure in adults with hypertension", section on 'Patients with diabetes mellitus' and 'Blood pressure control' above.

However, glycemic targets in type 1 diabetes have not been well studied in patients with advanced chronic kidney disease CKD. The approach to target an A1C of 7 percent or less, if tolerated is similar in patients with type 2 diabetes, although fewer supportive data are available than for type 1 diabetes.

The evidence for these approaches is presented elsewhere. See "Glycemic control and vascular complications in type 1 diabetes mellitus" and "Glycemic control and vascular complications in type 2 diabetes mellitus" and 'Glycemic control' above. See 'Other' above.

However, while these drugs are more beneficial than other antihypertensive agents in patients with albuminuric DKD, they do not have clear advantages over calcium channel blockers or diuretics among those without albuminuria.

See 'Severely increased albuminuria: Treat with angiotensin inhibition' above. We also suggest use of an SGLT2 inhibitor in patients with DKD who have lower levels of urine albumin excretion Grade 2B. The SGLT2 inhibitor is typically added to the patient's existing glucose-lowering regimen since these drugs have weak glucose-lowering effects in patients with reduced kidney function.

See 'Type 2 diabetes: Treat with additional kidney-protective therapy' above. SGLT2 inhibitors increase the risk of genital infections by two- to fourfold primarily vulvovaginal candidiasis and have been associated with Fournier's gangrene in rare cases.

SGLT2 inhibitors are not appropriate for use in patients with type 1 diabetes and kidney disease. See 'Monitoring during therapy' above. Why UpToDate? Product Editorial Subscription Options Subscribe Sign in. Learn how UpToDate can help you. Select the option that best describes you.

View Topic. Font Size Small Normal Large. Treatment of diabetic kidney disease. Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Authors: Vlado Perkovic, MBBS, PhD Sunil V Badve, MD, PhD George L Bakris, MD Section Editors: Richard J Glassock, MD, MACP David M Nathan, MD Deputy Editor: John P Forman, MD, MSc Contributor Disclosures.

All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jan This topic last updated: Jul 17, aspx Accessed on March 05, Jamerson K, Weber MA, Bakris GL, et al.

Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med ; Intensive diabetes therapy and glomerular filtration rate in type 1 diabetes.

Fullerton B, Jeitler K, Seitz M, et al. Intensive glucose control versus conventional glucose control for type 1 diabetes mellitus. Cochrane Database Syst Rev ; :CD Fioretto P, Steffes MW, Sutherland DE, et al. Reversal of lesions of diabetic nephropathy after pancreas transplantation.

Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. The Diabetes Control and Complications DCCT Research Group. Kidney Int ; Hemmingsen B, Lund SS, Gluud C, et al.

Targeting intensive glycaemic control versus targeting conventional glycaemic control for type 2 diabetes mellitus.

Amod A, Buse JB, McGuire DK, et al. Glomerular Filtration Rate and Associated Risks of Cardiovascular Events, Mortality, and Severe Hypoglycemia in Patients with Type 2 Diabetes: Secondary Analysis DEVOTE Diabetes Ther ; Davis TM, Brown SG, Jacobs IG, et al.

Determinants of severe hypoglycemia complicating type 2 diabetes: the Fremantle diabetes study. J Clin Endocrinol Metab ; Alsahli M, Gerich JE. Hypoglycemia, chronic kidney disease, and diabetes mellitus. Mayo Clin Proc ; Flynn C, Bakris GL. Noninsulin glucose-lowering agents for the treatment of patients on dialysis.

Nat Rev Nephrol ; Lewis EJ, Hunsicker LG, Bain RP, Rohde RD. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The Collaborative Study Group. Diabetes mellitus. In: Goldman-Cecil Medicine. Elsevier; Elsevier Point of Care. Clinical Overview: Diabetic nephropathy.

De Boer IH, et al. Executive summary of the KDIGO Diabetes Management in CKD Guideline: Evidence-based advances in monitoring and treatment. Kidney International. Office of Patient Education. Chronic kidney disease treatment options.

Coping effectively: A guide for patients and their families. National Kidney Foundation. Robertson RP. Pancreas and islet cell transplantation in diabetes mellitus. Accessed May 25, Ami T. Allscripts EPSi. Mayo Clinic. June 27, Castro MR expert opinion.

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Oatient of Potassium and Nnephropathy During nephropaathy Use of Angiotensin Converting Enzyme ACE nepjropathy or Angiotensin II Receptor Blocker Diabetic nephropathy patient support or Dizbetic Renin Patifnt DRI Therapy. Diseases of the kidney are a common finding in Circadian rhythm sleep aids with diabetes, Coenzyme Q and liver health up to one-half demonstrating signs of renal damage in nepbropathy lifetime Diabetic nephropathy patient support. Diabetes is the leading cause nephropayhy kidney disease in Canada 4. Kidney disease can be a devastating complication, as it is associated with significant reductions in both length and quality of life 5,6. A variety of forms of chronic kidney disease CKD in diabetes can be seen, including diabetic nephropathy, ischemic nephropathy related to vascular disease, hypertensive nephrosclerosis, as well as other renal diseases that are unrelated to diabetes 7,8 Figure 1. This chapter discusses how to screen for and diagnose CKD in people with diabetes, how to slow its progression, and the impact of CKD on other aspects of diabetes management. Figure 2 Level of urinary albumin by various test methods and stage of CKD in diabetes.