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As the ninth leading cause of death in the United States, avoidance or early detection of kidney disease, and providing proper treatment when it is diagnosed, are crucial.1 Early intervention, such as diet therapy, can slow down the progression of the disease and help minimize complications. Estimates are that more than 10% of adults (which equates to more than 20 million people in the United States) may already have chronic kidney disease (CKD), thus it is important to be diligent in screening for those who have risk factors for its leading causes. These primary causes include having diabetes and/or high blood pressure; other risk factors include cardiovascular disease, obesity, high cholesterol, lupus, and a family history of CKD.2
CKD is generally asymptomatic until its later stages. Stages 1-3 are defined as having a GFR of >30mL/min/1.73m2. Patients with stages 4-5 have a GFR of <30mL/min/1.73m2. Stage 5 CKD is categorized as kidney failure, also referred to as end-stage renal disease (ESRD).1 As the GFR declines, complications occur more often, and may include malnutrition, metabolic acidosis, hyperkalemia, mineral imbalance and bone disorder (calcium, phosphorous, and vitamin D), anemia, and cardiovascular disease (dyslipidemia).3
CKD can be treated in its early stages with pharmacotherapy and lifestyle changes (such as diet and exercise). When CKD leads to ESRD, the only options for patient survival are dialysis treatments or a kidney transplant.2 It is therefore imperative to provide effective therapy to CKD patients who do not yet require dialysis. Medical and nutrition therapy are valuable approaches to managing the condition(s) causing CKD, thereby helping to slow its progression. For example, controlling blood pressure and reducing albuminuria are possible through dietary intervention. Since sodium intake plays a large role in blood pressure control in CKD, recommendations include limiting a patient’s sodium intake to ≤1500mg, monitoring serum potassium in patients on renin angiotensin aldosterone system (RAAS) antagonists, and limiting dietary potassium intake when serum potassium >5mEq/L. By limiting a patient’s intake of dietary protein (0.8g protein/kg/day in nondiabetic patients, and 0.8-1.0g protein/kg/day in diabetic patients), it is possible to reduce albuminuria and improve blood glucose control, hyperlipidemia, blood pressure, renal bone disease, and metabolic acidosis.3
Patients with hypertension may require multiple medications, including RAAS antagonists such as angiotensin converting enzyme inhibitors (eg, Vasotec [enalapril], Altace [ramipril], Zestril [lisinopril]) or angiotensin receptor blockers (eg, Cozaar [losartan], Diovan [valsartan], Benicar [olmesartan]), which are often used to control blood pressure, delay disease progression, reduce albuminuria, and protect against heart disease. Slower progression of CKD is also possible by decreasing albuminuria, particularly in diabetics. Diabetes management through blood glucose control may help also slow progression of CKD, and it is appropriate to individualize the A1C/estimated average glucose goal by patient.3
If a patient progresses to later stages of CKD, complications and comorbidities increase in occurrence and severity. For example, CKD patients have an increased risk of cardiovascular disease (CVD). In fact, most patients who have CKD die of CVD-related complications before they progress to ESRD. Preventive strategies for CVD and CKD do overlap, and include blood pressure, glucose, and even possibly lipid control. CKD patients are also at risk for development or worsening of anemia, due to inadequate synthesis of erythropoietin by the kidneys. Therapy may include erythropoiesis-stimulating agents (ESAs) to increase red blood cell production and prevent the need for transfusion.4 Because of data that showed increased risks of cardiovascular events with ESAs in patients with CKD, the FDA issued a drug safety communication with recommended label changes to improve safety. Drugs in the ESA class are epoetin alfa (marketed as Epogen and Procrit) and darbepoetin alfa (marketed as Aranesp). ESA labels now recommend that for patients with CKD, to consider starting ESA treatment when the hemoglobin is <10g/dL and to individualize dosing, using the lowest dose of ESA sufficient to reduce the need for red blood cell transfusions, adjusting as appropriate.5
Advances in pharmacotherapy for CKD and its related conditions continue. Most recently, Velphoro received FDA approval for the control of hyperphosphatemia in patients with CKD on dialysis.6 PDR Network is a valuable resource for this drug and thousands of other available products, offering alerts and specific product labeling. Keep current by using PDR.net and by keeping your contact information up to date with us. If you use an electronic health record (EHR), please ask for it to include the PDR drug data feeds, including PDR BRIEF. Updated drug information, full labeling, and safety warnings will be integrated into your electronic prescribing system automatically, and at no cost to you. Drug information in EHRs is often months out of date, which is why PDR BRIEF is available at no cost to providers and EHR vendors.
PDR Network can also help you meet certain reporting requirements under Meaningful Use Stage 2 (MU2). One of the core MU2 objectives, “use certified EHR technology to identify patient-specific education resources,” requires that physicians provide more than 10% of their unique patients with education resources specific to their needs.7 PDR+ for Patients drug education guides are an excellent resource that you can provide patients to help you meet this objective. When PDR+ for Patients drug education guides are integrated into your EHR, you can use them to help you fulfill this objective and help your patients start and stay on therapy. Click here to see a sample. If you do not have PDR+ in your EHR, send an email to EHR@pdr.net and tell us the name of your EHR vendor, and we will convey to them that you want PDR included.
Salvatore Volpe, MD, FAAP, FACP, CHCQM
Chief Medical Officer