BP still not at goal


Add long-acting caloum channel blocker (CCB). May also consider adding low-dose ft-blocker instead of CCB at this time if patient has angina, heart failure, or arrhythmia necessitating their use.

I pulse greater than or equal to 84

BP still not at goal


tefine pulse


Add low-dose ^ blocker or «-//3-biocker (if not already being used) NOTE: The use of a |J-bk>cker and a norvJihydtopyridine CCB should be avoided in the elderty and those with conduction abnormalities.


Add other subgroup of calcium channel blocker eg., a <*hydropyri<*ne CCB a i agent is being used). NOTE: The use of a /i-Wocker and a nond-hydro-pyridme CCB should be avo<ded in the elderly and those with conduction abnormalities.

BP still not at goal i


Add long-acting o-blocker, central «-agonist, or vasodilator. NOTE: Central «-agonists (ie.. Clonidine) should not be used with ^-blockers due to the high likaliKuwi of ca»ara hrariurarrf i

FIGURE 26-2. Hypertension management algorithm for patients with CKD. Dosage adjustments should be made every 2 to 4 weeks as needed. The dose of one agent should be maximized before another is added. (ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; B P, blood pressure; CrCl, creatinine clearance; K, potassium; Scr, serum creatinine.) (From Joy MS, Kshirsagar A, Franceschini N. Chronic kidney disease: Progression-modifying therapies. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill; 2008: 752, with permission.)

The nondihydropyridine calcium channel blockers (CCBs) have been shown to

also decrease protein excretion in patients with and without diabetes, but the reduction in proteinuria appears to be related to the reductions in blood pressure. The maximal effect of nondihydropyridine CCBs on proteinuria is seen with a blood pressure reduction to less than 130/80 mm Hg and no additional benefit is seen with increased doses. Dihydropyridine CCBs, however, do not have the same effects on protein excretion. In fact, dihydropyridine CCBs worsen protein excretion, despite similar re-

ductions in blood pressure as nondihydropyridine CCBs. Other Interventions to Limit Progression of CKD Hyperlipidemia Treatment

Hyperlipidemia plays a role in the development of cardiovascular disease (CVD) in patients with CKD. The primary goal of treatment of dyslipidemias is to decrease the risk of atherosclerotic CVD. A secondary goal in patients with CKD is to reduce proteinuria and decline in kidney function. Treatment of hyperlipidemia in patients with CKD has been demonstrated to slow the decline in GFR by 1.9 mL/min per year of treatment with antihyperlipidemic agents.31

The NKF suggests that CKD should be classified as a coronary heart disease (CHD) risk equivalent and the goal LDL-C level should be below 100 mg/dL (2.59

25 32

mmol/L) in all patients with CKD. ' The most frequently used agents for the treatment of dyslipidemias in patients with CKD are the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors ("statins") and the fibric acid derivatives. However, other treatments have been studied in patients with CKD and should be considered if first-line therapies are contraindicated.

Another important consideration in treating lipid disorders in patients with CKD is management of proteinuria. Protein excretion in the nephrotic range (greater than 3 g/day) is associated with an increase in both total and LDL-C levels.3 Triglyceride levels can also be elevated in patients with severe proteinuria. Results from clinical trials suggest that the use of ACEIs to reduce proteinuria can decrease TC levels.34

While the use of ACEIs is unlikely to decrease cholesterol to goal levels, reducing proteinuria can aid in cholesterol reduction, particularly in patients with nephrotic syndrome or severe proteinuria. Conversely, treatment of hyperlipidemia can reduce protein excretion and subsequent progression of CKD.4

Smoking Cessation

While the effects of smoking on the development and progression of CKD are well established, as discussed previously, t he effect of smoking cessation on CKD progression has not been studied. Data are emerging that suggest that smoking cessation may be a practical approach to slow the progression of CKD. Smoking cessation has been shown to reduce the risk of myocardial infarction by 50% to 70%, regardless of previous nicotine exposure.15 However, smoking cessation does not reverse existing kidney dysfunction in former smokers.

Anemia Treatment

Anemia decreases oxygen delivery to the renal tubules, promoting the release of inflammatory and vasoactive cytokines, which contribute to the progression of CKD. Treatment of anemia in patients with CKD reduces the cardiovascular effects of anemia and has been demonstrated to decrease morbidity and mortality by as much as

20%. Studies have demonstrated that treatment of anemia may slow the progression of CKD.36 The management of anemia will be discussed later.

Outcome Evaluation

Monitor SCr and potassium levels and blood pressure within 1 week after initiating ACE-I or ARB therapy. Discontinue the medication and switch to another agent if a sudden increase in SCr greater than 30% occurs, hyperkalemia develops, or the patient becomes hypotensive. Titrate the dose of the ACE-I or ARB every 1 to 3 months to the maximum tolerable dose. If blood pressure is not reduced to less than 130/80 mm Hg, add another agent to the regimen. Refer the patient to a nephrologist to manage complications associated with CKD. As CKD progresses to stage 4, begin discussion to prepare the patient for renal replacement therapy (RRT).

Patient Encounter, Part 1

A 62-year-old obese Caucasian female with a history of diabetes and hypertension presents to clinic for routine follow-up. Her fasting blood sugars have been elevated recently, averaging 180 to 250 mg/dL (10-13.9 mmol/L).

PMH: Diabetes mellitus for 8 years, not currently controlled; hypertension for 5 years, not currently controlled; hyperlipidemia, currently managed by diet therapy

FH: Mother is alive at age 87 with coronary artery disease; father is deceased from diabetes; she has no siblings

SH: She does not work; she smokes one pack of cigarettes per day, but denies alcohol or illicit drug use; she is sedentary

Meds: Furosemide 20 mg orally daily; nifedipine XL 30 mg orally daily; glyburide 10 mg orally daily

ROS: Unremarkable PE:

VS: BP 145/92 mm Hg, P 82 bpm, T 36.9°C (98.4°F), ht 5'4' (163 cm), wt 86.4 kg (190 lb)

CV: RRR, normal S1, S2; no murmurs, rubs or gallops; lungs clear

Abd: Obese; no organomegaly, bruits or tenderness, (+) bowel sounds; heme (-) stool

Exts: Trace pedal edema bilaterally; decreased sensation in feet to light touch; no lesions

Labs (Fasting): Sodium 145 mEq/L (145 mmol/L); potassium 3.2 mEq/L (3.2 mmol/ L); chloride 112 mEq/L (112 mmol/L); carbon dioxide 26 mEq/L (26 mmol/L); blood urea nitrogen (BUN) 20 mg/dL (7.14 mmol/L urea); serum creatinine (SCr) 1.4 mg/ dL (124 ^mol/L); glucose 240 mg/dL (13.32 mmol/L); total cholesterol 196 mg/dL (5.07 mmol/L); low-density lipoprotein cholesterol (LDL-C) 112 mg/dL (2.90 mmol/ L); high-density lipoprotein cholesterol (HDL-C) 28 mg/dL (0.72 mmol/L); triglycerides 280 mg/dL (3.16 mmol/L); hemoglobinA1C (HbA1C) 10% (0.1); urine microalbumin 270 mg/dL (2.7 g/L)

What risk factors does the patient have for the development of CKD? What signs and symptoms are consistent with CKD? How would you classify her CKD? Identify your treatment goals for the patient.

What lifestyle modifications would you recommend for this patient with CKD? What pharmacologic alternatives are available for this patient for treatment of CKD?

What other interventions are appropriate to minimize the progression of CKD?

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