Does this patient have chronic kidney disease related to diabetes mellitus?

The patient has had diabetes mellitus (DM) (type 1 or type 2) for at least 5 years. S/he has needed changes in therapy to include increasing doses of insulin or additional therapies to keep the blood sugars in control. S/he may have retinopathy, neuropathy and cardiovascular disease. S/he has been evaluated for the presence of chronic kidney disease (CKD) and has been diagnosed with diabetic nephropathy. Medication therapy appropriate for the level of CKD needs to be addressed in order to attain appropriate target glucose control.

What tests to perform?

Microvascular complications such as kidney disease typically develop over 5-10 years, which reflects the accumulation of excessive glucose exposure. Screening and diagnosis for diabetic kidney disease are covered in the chapter on Diabetic Kidney Disease: General Management.

In brief, for patients with type 1 diabetes, screening should start 5 years after diagnosis (Table I). In patients with type 2 diabetes, screening should begin at initial diagnosis since the exact onset of diabetes is often unknown. Up to one-third of patients with newly diagnosed type 2 diabetes already have evidence of kidney disease, which in part can also be attributed to hypertension and additional risk factors. Patients with diabetes should be screened annually for kidney disease with a urine albumin to creatinine ratio and a serum creatinine.

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Table I.

Screening Care for the Eyes and Feet in Diabetes

A hemoglobin A1c should be measured every 3 months if therapy is changed or if the A1c is not at goal; it can otherwise be followed every 6 months if at goal and glucose control is stable. There can be some inaccuracy of the A1c in patients with advanced CKD (eGFR < 30 ml/min/1.73 m2). This is, in part, related to the presence of anemia (from hemolysis, reduced lifespan of the red blood cell, and iron deficiency). Fructosamine, which represents glycation of multiple proteins, and glycated albumin can give an idea of glucose control from the prior 2 weeks. They are additional means of following glucose control but it is not clearly known whether they offer any advantage over A1c measurement in patients with CKD. In those undergoing dialysis, glycated albumin may be a better measure compared to A1c but the difference is modest at most. However, neither test is currently available in the United States for routine clinical use.

Patients should be encouraged to check their blood glucose levels frequently. The intensity of blood glucose monitoring is dependent on the severity of diabetes and intensity of treatment. For example, a patient taking insulin injections four times daily should check blood glucose levels about four times per day or more. Conversely, a patient with mild diabetes controlled with lifestyle management may only need to check blood sugars several times per week. Goal fasting and premeal blood sugars are 80 to 130 mg/dl and goal post-prandial glucoses checked 1 to 2 hours after the meal are <180 mg/dl. However, if the patient is experiencing frequent hypoglycemic reactions, these goals should be adjusted upwards.

How should patients with diabetes mellitus in chronic kidney disease be managed?

Hyperglycemia is a prime cause of vascular complications, including kidney disease. Glycemic control is essential to delay the progression of diabetes-related kidney disease. Multiple factors must be taken into consideration when determining the appropriate level of glycemic control.

The Diabetes Control and Complications Trial (DCCT) compared intensive insulin treatment with conventional treatment in subjects with type 1 diabetes, with A1c levels of 7.2% vs. 9.1%, respectively. After a mean of 9 years, intensive therapy reduced the occurrence of microalbuminuria, albuminuria and falls in glomerular filtration rate (GFR).

Many of these subjects were then followed in the observational Epidemiology of Diabetes Interventions and Complications (EDIC) Study, where they were followed for several years after the end of the DCCT. This follow-up study showed risk reduction of diabetic nephropathy persists long-term, even after glycemic control equalized between the two groups, with a mean A1c of 8% for both groups for several years after the DCCT.

Studies in type 2 diabetes show similar results. The UK Prospective Diabetes Study (UKPDS) demonstrated a reduction in development of microalbuminuria by 24% in subjects in the intensive management group achieving an A1c of 7.0% vs. 7.9% in the conventional treatment group. These subjects also had significantly reduced rates of rises in creatinine.

Similar findings were shown in the Veteran Affairs Cooperative Study on Glycemic Control and Complications in Type 2 Diabetes Feasibility Trial, where subjects had significantly lower rates of microalbuminuria and albuminuria. These results were also found in the Kumamoto study and ADVANCE trial.

The general goal A1c in patients with diabetes is about 7% or less to prevent or slow progression of kidney disease. The American Diabetes Association recommends this general target but also advises stricter (A1c <6.5%) and looser (A1c <8%) depending on the balance between benefit and harm in individuals. In 2012, the updated Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines also recommended a target A1c of ~7.0%. This overall glycemic goal is strongly supported by substantial data from multiple trials showing a reduction in microalbuminuria with tighter glycemic control. The data clearly demonstrates decreased rates of development of microalbuminuria. The number of subjects who then develop albuminuria and declines in GFR are generally reduced as well, albeit some of this is related to fewer patients developing microalbuminuria.

Additionally, any improvement in glycemic control even to A1c levels above 7% results in improvement in nephropathy, as well as retinopathy and neuropathy, when compared to a higher A1c. This supports the concept that the best A1c attainable should be achieved when possible, even if cannot be 7%.

Achieving an A1c of 7% can be difficult. It requires vigilance on the part of the patient and physician and is accompanied by higher rates of hypoglycemia. Thus, the target A1c should be based on the individual. Higher target A1c levels should be considered in children and patients with a prior history of severe hypoglycemia or hypoglycemia unawareness, shortened life expectancy, presence of comorbidities such as seizures, or a long (>25 years) history of diabetes with development of only minimal complications.

The ACCORD study showed higher rates of hypoglycemia and mortality in the intensive treatment group attaining an A1c of 6.4% compared to the conventional group achieving a target A1c of 7.5%; the increased mortality could not be attributed to hypoglycemia. In the ADVANCE trial, the intensive treatment group did not have higher rates of mortality. Neither ACCORD, ADVANCE, nor VADT demonstrated improved cardiovascular outcomes with lower A1c levels; therefore, the target A1c is considered ~7% rather than 6.5% or lower.

In patients at risk of hypoglycemia, a higher target A1c should be strongly considered. The risk of hypoglycemia is greater in patients with Stages 4-5 CKD and the consequences of hypoglycemia may be greater as well. The presence of advanced CKD in an elderly patient who has multiple co-morbidities is particularly risky. Thus, A1c targets in such patients should be increased to closer to 8% rather than 7%.

Patients on chronic dialysis no longer need to achieve good glycemic control to prevent deterioration of kidney function. However, good control may still have benefits in delaying the progression of retinopathy, neuropathy and potentially macrovascular disease such as cardiovascular complications. Survival is also superior with lowering of A1c for patients on dialysis, no matter what the final level attained.

Blood pressure control, lipid management and weight control are vitally important. Please refer to chapters on Diabetic Kidney Disease: General Management and Blood Pressure Management.

Medications for treatment of diabetes

There are multiple therapies available to attain glucose control in diabetes in CKD.


All available insulin preparations can be used in CKD, however the insulin type, dose and administration must be tailored to each individual patient to achieve goal glycemic levels but limit hypoglycemia. There are multiple insulin preparations now available.

The rapid-acting insulin analogs aspart (Novolog), lispro (Humalog, U100 and U200) and glulisine (Apidra) are absorbed the quickest and are ideal for quick correction of elevated blood sugars or for prandial insulin needs. These insulins have an onset of action at 5 to 15 minutes, peak action at 30-90 minutes and an average duration of about 5 hours. Some studies have shown the duration of action of glulisine to be slightly longer than the other two rapid-acting insulins. These insulins should be given at most 15 minutes prior to a meal.

Patients with Stage 4-5 CKD and those on dialysis often have some degree of delayed gastric emptying; giving rapid-acting insulin after the meal may be helpful for matching the insulin peak with the time of the postprandial blood glucose peak. In patients with nausea who may not know ahead of time how much they will be able to eat, postprandial rapid-acting insulin dosing may be worth trying. Similarly, patients on peritoneal dialysis obtain large amounts of calories from their dialysis fluid and often eat less than they might expect so that postprandial dosing may be helpful for them as well.

The only short-acting insulin available is regular crystalline insulin, which has an onset of action at 30 to 60 minutes, peak action at 2 to 3 hours and duration up to 5 to 8 hours. Regular insulin should ideally be given about 30 minutes prior to a meal.

The available intermediate-acting insulin is isophane, or NPH (neutral protamine Hagedorn). It has an onset of action at 2 to 4 hours, peak concentration at 4 to 10 hours and duration up to 10 to 18 hours. In order to achieve adequate basal coverage, it is typically dosed twice daily. Its use can be limited by its highly variable absorption. In patients getting overnight peritoneal dialysis using a cycler, sometimes the time duration of NPH or premixed insulins (see below) may be useful to cover the glucose absorption that occurs from the dialysis fluid.

The long-acting insulin analogs glargine (Lantus, Basaglar; U100) and detemir (Levemir) are readily available. Glargine has an onset of action at 2 to 4 hours, with minimal peak and lasts approximately 20 to 24 hours. It is usually dosed once daily. Detemir has an onset of action at 1 to 3 hours, with a small peak at 6 to 8 hours and approximate duration of action of 18 to 22 hours. Detemir is typically dosed twice daily to give adequate basal coverage in those with type 1 diabetes; in type 2 diabetes, it can often be dosed only once daily. Recently, a more concentrated version of glargine U300 (Toujeo) has become available, in pen-form only; it has an even smaller peak and less day-to-day variability. Degludec (Tresiba) is a newly available very long-acting insulin that is available in U100 and U200 pen forms. It has a half-life of about 25 hours, a minimal peak, and low day-to-day variability.

There are various premixed preparations of insulin available that include a fixed percentage of an intermediate-acting insulin and a rapid- or short-acting insulin. One such example is “70/30” which is 70% NPH and 30% regular insulin. Because they contain a combination of 2 different insulin types, they have two separate peaks in insulin. These preparations can offer convenience for the patient with twice daily dosing but offer less flexibility and restrictions in ability to titrate insulin doses. The insulin must be taken at fixed times and the patient must have regular meal times and size. As noted above, sometimes these premixed insulins are useful to cover the glucose absorption that occurs with overnight peritoneal dialysis.

The majority of insulin is U100, defined as 100 units of insulin per 1 mL. U500 contains 500 units per 1 mL and is available only as regular insulin. The high concentration of U500 alters its kinetics, making it act more like NPH insulin when used subcutaneously. U500, the U300 form of Glargine (Toujeo), and the U-200 form of degludec are concentrated forms of insulin useful for patients with severe insulin resistance who require large doses of insulin as well as patients with minimal fat depots. The U200 form of Humalog offers the advantage of the same amount of insulin delivered in a smaller volume. It is also useful for those with high insulin requirement and will allow the pens to last longer (each pen contains 600 units per pen instead of the standard 300 units).

Oral medications

Metformin (a biguanide) increases insulin sensitivity and decreases hepatic gluconeogenesis. Metformin does not cause hypoglycemia when used by itself. B12 deficiency has been reported with long-term use. Lactic acidosis is a rare and serious side effect of metformin use, which can occur when toxic levels of metformin accumulate. Metformin is cleared by the kidney, thus its use in CKD is restricted. The FDA guidelines were revised so that metformin should not be given to patients with an eGFR < 30 mL/min/1.73 m2 (FDA); it is prudent to reduce the maximum dose to 1000 mg/day with an eGFR <45 mL/min/1.73 m2. Metformin should not be used with eGFR <30 ml/min/1.73 m2. Metformin should be held in situations that are associated with hypoxia or acute kidney injury (AKI) such as sepsis/shock, hypotension, acute myocardial infarction, and use of radiographic contrast or other nephrotoxic agents.

Second-generation sulfonylureas (glipizide, glyburide, glimepiride and gliclazide) bind to a sulfonylurea receptor on pancreatic beta-cells and therefore increase insulin secretion. They can lead to hypoglycemia. Glipizide and gliclazide may be used in CKD stage 3 or worse. It is best to avoid the use of glyburide in CKD stage 3 since it has a long half-life and can cause hypoglycemia in patients with decreased GFR. Glimepiride can be used starting at the lowest dose (1 mg) and titrated with caution. Gliclazide is not available in the US.

Glinides (nateglinide, repaglinide) work in a glucose-dependent mechanism and result in quick insulin release through an ATP-dependent potassium channel on beta-cells of the pancreas. Their ideal use is for control of post-prandial hyperglycemia; they can also lead to hypoglycemia. The active metabolite of nateglinide will accumulate in renal disease, thus it should not be used with a GFR <60 ml/min/1.73m2. Repaglinide appears to be generally safe in those with CKD.

Thiazolidinediones (pioglitazone, rosiglitazone) increase insulin sensitivity by acting as peroxisome proliferator-activated receptor gamma agonists. They do not lead to hypoglycemia. They are metabolized by the liver and thus can be used in CKD. However, fluid retention is a major limiting side effect and they should not be used in advanced heart failure and other fluid-retaining states. This also makes their use in CKD, particularly patients on dialysis, limiting. They have been linked with increased fracture rates and bone loss, thus the appropriate use in patients with underlying bone disease (such as renal osteodystrophy) needs to be considered. Although there was a concern several years ago about an increased risk of ischemic heart disease with rosiglitazone, subsequent analyses did not support this conclusion and a prior warning from the FDA was lifted.

Alpha-glucosidase inhibitors (acarbose, miglitol) inhibit absorption of carbohydrates and thus slow glucose elevation post-prandially. These agents are not associated with hypoglycemia but side effects of bloating, flatulence and abdominal cramping can be limiting. Acarbose is only minimally absorbed, but with reduced renal function, serum levels of the drug and its metabolites increase significantly. Although no adverse effects have been reported, its use in patients with a GFR <26 mL/min/1.73 m2 is not advised. Miglitol has greater systemic absorption and undergoes renal excretion, and it should not be used in patients with decreased GFR.

Dipeptidyl peptidase 4 (DPP 4) inhibitors decrease the breakdown of incretin hormones such as GLP-1 and include the oral medications sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), and alogliptin (Nesina). They do not cause hypoglycemia. Sitagliptin can be used at the full dose of 100 mg if the GFR is >50. If the GFR is 30 to <50 ml/min/1.73m2, 50 mg daily is recommended and for a GFR <30, 25 mg daily is recommended. For saxagliptin, with a GFR >50, 5 mg daily can be used; for GFR 50 or less, the recommended dose is 2.5 mg daily. Linagliptin does not need to be adjusted in kidney disease since only a fraction is renally cleared. The dose of alogliptin should be reduced from 25 mg to 12.5 mg daily if the eGFR is <60 ml/min/1.73m2; 6.25 mg daily is advised if the eGFR is <30 ml/min/1.73m2.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors (canagliflozin [Invokana], dapagliflozin [Farxiga], and empagliflozin [Jardiance]) reduce glucose absorption in the proximal tubule leading to increased glucose excretion into the urine, weight loss, and an A1c reduction of ~0.8%; they do not cause hypoglycemia. The EmpaReg study recently demonstrated significant benefits in reduction of cardiovascular outcomes and mortality and worsening of eGFR with empagliflozin use. A recent article (CANVAS trials) showed patients receiving canagliflozin also had a decreased risk of cardiovascular disease but also an increased risk of amputations. Genital yeast infections occur in up to 10% or women and older patients may experience symptoms due to volume contraction. In addition, there are reports of “euglycemic” diabetic ketoacidosis, primarily in those with type 1 diabetes (in whom they are used “off-label”) but also in very rare patients with type 2 diabetes.

These medications are not considered to be effective if the eGFR is <45 ml/min/1.73m2. It is recommended that no more than 100 mg daily of canagliflozin should be used with an eGFR of 45 to < 60 ml/min/1.73m2 due to a small increase in adverse events related to intravascular volume contraction; it should not be used if the eGFR is <45 ml/min/1.73m2. Empagliflozin should be stopped if the eGFR is <45 ml/min/1.73m2 and dapagliflozin should not be used with an eGFR of <60 ml/min/1.73m2 primarily due to a lack of efficacy.

Non-insulin subcutaneous medications

Glucagon-like peptide-1 (GLP-1) receptor agonists (exenatide [Byetta], exenatide extended-release [Bydureon], liraglutide [Victoza], albiglutide [Tanzeum], dulaglutide [Trulicity] and lixisenatide [Adlyxin]) are injectable medications that mimic gut hormones known as incretins, leading to insulin release, delayed glucagon secretion, and delayed gastric emptying. They are approved for use in type 2 diabetes along with sulfonyureas and metformin although, in practice, they are used with insulin as well. There are now fixed dose combinations of insulin degludec/liraglutide (IDegLira) and insulin glargine/lixisenatide (IGlarLixi). The GLP-1 receptor agonists also decrease appetite by increasing satiety, which leads to weight loss in many patients. Both agents have been associated with pancreatitis, and nausea is a common side effect that can limit its use. In addition, liraglutide has been associated with the development of thyroid C-cell tumors in animal studies and thus should not be given to patients with or at risk for medullary thyroid cancer. Exenatide is given twice daily whereas liraglutide is given once daily; exenatide extended-release, albiglutide and dulaglutide are dosed once weekly. The LEADER study recently demonstrated significant reductions in cardiovascular mortality and the rate of loss of GFR with liraglutide.

Exenatide is not recommended for use with a GFR <30 mL/min/1.73 m2. Furthermore, exenatide has been found to cause renal failure in a number of cases. Liraglutide is not cleared by the kidney; no dose adjustment in CKD appears to be needed. There are also no dose restrictions with albiglutide or dulaglutide. Lixisenatide should not be used when the GFR is < 15 ml/min/1.73m2.

The amylin analog pramlintide (Symlin) is also an injectable medication that is used with meals as an adjunct to insulin therapy. Amylin is secreted along with insulin by pancreatic beta-cells and levels are below normal in patients with diabetes. It can be used in type 1 and type 2 diabetes. No dose adjustment appears necessary for CKD; it has not been studied in ESRD.

Glycemic control in Type 1 and Type 2 diabetes mellitus

Glycemic management differs between type 1 and type 2 diabetes. The overall goal to optimize glycemic control in order to reduce micro- and macrovascular complications and minimize hypoglycemia, however, is the same. An individual with type 1 diabetes needs, of course, insulin; there are multiple ways insulin can be administered. A wide range of therapies can be applied to those with type 2 diabetes depending on patient desire, response and co-morbidities.

Type 1 DM

The ideal insulin regimen in individuals with type 1 diabetes reproduces physiologic insulin secretion by the pancreas. This is best accomplished by the use of multiple daily injections (MDI), which combines a long-acting basal insulin and a rapid-acting insulin with meals.

Prior to the development of insulin analogs, conventional treatment for type 1 diabetes combined twice daily NPH and regular insulin, usually given before breakfast and before dinner. This required stable daily regimens with fixed meal times and meal sizes each day, and this regimen does not mimic physiologic insulin secretion.

With the availability of insulin analogs, glargine has surpassed the use of NPH as a basal insulin. It can be given once daily in most individuals and results in more stable glucose control, with improved fasting glucose levels and overall less hypoglycemia compared to NPH. Detemir has also shown promise compared to NPH. It is given twice daily and also results in less hypoglycemia with superior glucose control compared to NPH. Both glargine and detemir show less intra- and interindividual variability with greater predictability and reproducibility in comparison to NPH. The two newer very long-acting basal insulins, insulin glargine U300 and insulin degludec have even less intra- and interindividual variability and less hypoglycemia than insulin glargine U100 and detemir.

The rapid-acting insulin analogs are superior to regular insulin when used for prandial insulin. Studies show less hypoglycemia with better post-prandial glucose levels. These insulins also allow for flexibility in mealtimes and meal sizes, as the insulin can be given immediately before a meal and tailored to the amount of carbohydrates being eaten. Any of the rapid-acting insulins are considered optimal choices for prandial insulin.

An even closer approximation of physiologic insulin secretion can be achieved by using an insulin pump that delivers insulin by continuous subcutaneous insulin infusion (CSII). A rapid-acting insulin is given both basally and as a bolus prior to meals through the pump. The pump can be programmed to deliver different basal rates at different times of the day, so this has an advantage over the injection of a long-acting insulin such as glargine or detemir. Insulin pumps can be used at all stages of CKD. However, adjustment of insulin dosing can be complicated and insulin pump use should be supervised by diabetes clinicians and diabetes educators experienced in their use.

External devices that can measure glucose continuously are now available. Such Continuous Glucose Monitoring Systems (CGMS) involve the insertion of a small catheter into the subcutaneous fat, and glucose is measured every 5 minutes with real time instantaneous as well as computerized downloadable readouts possible. In this way, the patient can detect upward or downward trends in glucose levels in real time and the more detailed evaluation of patterns allows for better adjustment of insulin dosing. The CGMS readouts can be linked to insulin pumps to facilitate insulin dosing. The use of CGMS and its coupling to insulin pumps should be supervised by diabetes clinicians and diabetes educators experienced in their use.

Type 2 DM

Multiple options and combinations of therapies are available for the treatment of type 2 diabetes.

Oral medications are an ideal starting point. Kidney function permitting, metformin is a first-line agent because it does not cause hypoglycemia, is associated with weight loss and is inexpensive. It can cause mild to moderate gastrointestinal upset and the dose should be increased slowly. Dosing with CKD is discussed above. Any of the additional oral agents can be used second-line when lifestyle changes and metformin are not enough to attain goal control. DPP 4 inhibitors can be safely used at the appropriate dose in CKD, though the reduction in A1c and hyperglycemia is modest with an average reduction in A1c between 0.5-1%; however, these are often desirable as they do not cause hypoglycemia.

Pioglitazone can be considered, though fluid retention and weight gain makes it a less optimal choice. The SGLT2 inhibitors are reasonable choices for a second agent given their proven cardiovascular and CKD benefits if kidney function allows their use. GLP-1 receptor agonists can be added to oral agents such as sulfonylureas (but should not be used concurrently with DPP 4 inhibitors); the potential for reduction in hyperglycemia along with weight loss can be appealing. They can also be used as single agents. Sulfonylureas are inexpensive and effective but they do cause hypoglycemia. In CKD, glipizide (or gliclazide – not available in the U.S.) is advised.

In patients with uncontrolled A1c levels, high levels of insulin resistance or progressive beta-cell failure, insulin should be introduced. Typically, a basal insulin such as once daily glargine or once daily detemir is initiated first. A starting dose of 10 to 15 units can be used, with further escalation based on blood sugars. The insulin dose can be increased by 1-2 units every 3 days to get to a target fasting blood sugar of 100-140 mg/dl.

Some patients may achieve goal glucose control with the combination of basal insulin and oral agents. Insulin may also be combined with GLP-1 receptor agonists. If goal glycemic control cannot be obtained with basal insulin alone, or there is concurrent hypo- and uncontrolled hyperglycemia, then a rapid-acting insulin analog should be started. This may be needed in a patient who has goal fasting blood sugars but daytime hyperglycemia.

What happens to patients with diabetes mellitus and chronic kidney disease?

Diabetes is one of the most common causes of kidney failure worldwide and it is the most common cause of kidney failure in the US. Kidney disease affects 20-40% of patients with diabetes. Kidney pathology is similar in type 1 and type 2 diabetes, as is the natural history, with the exception that hypertension and vascular disease occurs earlier in the course of kidney disease in type 2 diabetes.

Individuals with diabetes have higher rates of cardiovascular disease, and diabetes is considered a risk factor equivalent to coronary artery disease. Cardiovascular disease (CVD) is the leading cause of mortality in CKD stage 5. The presence of CKD in DM is therefore a potent combination putting the patient at great risk for CVD.

Individuals with diabetes carry higher rates of CVD if microalbuminuria is present, and the risk escalates as kidney disease worsens to albuminuria and decreasing GFR. Patients with stage 5 CKD and diabetes have a 40% increased annual mortality compared to those without DM. The risk is further exacerbated by the presence of hypertension (HTN) and dyslipidemia.

In addition to medications to control hyperglycemia and proteinuria, the use of blood pressure medications and lipid lowering agents should be aggressively pursued. Please see additional chapters on Diabetic Kidney Disease: General Management and Blood Pressure Management for further information.

How to utilize team care?

As appropriate, consider referral to an endocrinologist for diabetes management, especially if insulin pump or CGMS use is desired. The patient should also follow with an ophthalmologist or optometrist for an annual dilated exam to examine for retinopathy. The ophthalmologist or optometrist will determine whether more frequent visits are necessary.

Referral to a podiatrist should be considered in the presence of neuropathy or foot ulcers. The use of a cardiologist or vascular surgeon is as indicated by the presence of coronary artery disease or peripheral vascular disease. Referral to a weight-loss specialist can also be considered, particularly in the presence of morbid obesity.

The use of a certified diabetes educator is helpful to help the patient understand the treatment and management of diabetes, glucose meter use, and insulin teaching. Lifestyle modification is vitally important. Weight loss helps reduce insulin resistance and, in general, a body mass index <25 kg/m2 is the goal. Nutrition in patients with diabetes and CKD needs particular attention as it is a complicated balance of carbohydrate, protein, potassium, phosphorus, sodium and fluid intake. A dietitian can be helpful to counsel the patient in regards to appropriate dietary considerations. Physical or occupational therapy may be indicated, particularly in the presence of severe neuropathy.

Are there clinical practice guidelines to inform decision making?

  • Kidney Disease Outcomes Quality Initiative (KDOQI): Clinical Practice Guidelines and Clinical Practice recommendations for Diabetes and Chronic Kidney Disease.

  • American Diabetes Association: Standards of Medical Care in Diabetes

Other considerations

Additional diagnoses that are common in diabetes and CKD: retinopathy, neuropathy, HTN, hyperlipidemia, foot ulcers, cardiovascular disease including coronary artery disease, peripheral vascular disease, cerebrovascular disease.