8 Meq/L PH 7.2) May Require Iv Therapy (See Chap. 51) .: Evaluation of Therapeutic Outcomes

prevent
volume overload from excessive sodium intake. After the serum

bicarbonate has normalized, a maintenance regimen of bicarbonate
to neutralize daily acid production may be all that is necessary (12 to
20 mEq/day in divided doses). Doses are subsequently titrated to
maintain normal plasma bicarbonate concentrations. Patients with renal
tubular acidosis may require higher doses of alkalinizing agents
(see Chap. 51). Fluid balance should be monitored carefully because
of the sodium content of these agents. Citrate-containing solutions
should not be used in combination with aluminum-containing compounds
because they can enhance aluminum absorption and increase
the risk of aluminum intoxication. Excessive doses of alkalinizing
agents may cause metabolic alkalosis, as well as lethargy or cardiac
depression secondary to a decrease in ionized serum calcium
concentration. Gastrointestinal distress characterized by gastric distention
and flatulence is relatively common with high doses of oral
sodium bicarbonate. Patients with severe acidosis (serum bicarbonate
<8 mEq/L; pH <7.2) may require IV therapy (see Chap. 51).
Metabolic acidosis in both adult and pediatric patients undergoing
dialysis can often be managed by using higher concentrations of
bicarbonate or acetate in the dialysate (>38 mEq/L bicarbonate is safe
and effective). Administration of oral bicarbonate salts as described
above may also be necessary for some patients.
Tromethamine (tris-hydroxymethyl aminomethane) and Carbicarb
(sodium carbonate and sodium bicarbonate) are alternative
alkalinizing agents that have been evaluated for treatment of more
severe acidemia. There are extremely limited data regarding their use
in patients with CKD, which precludes their use in this population. 108
_ EVALUATION OF THERAPEUTIC OUTCOMES
Regular monitoring of arterial blood gases and serum electrolytes are

necessary to determine the effectiveness of therapy. A gradual correction
is appropriate to avoid overcorrection and subsequent complications
such as alkalosis and other electrolyte abnormalities (see
Chap. 51). Laboratory measurement of serum bicarbonate is associated
with several technical problems. Blood collection techniques,
transportation, and assay methodology can affect the measured concentrations.
Blood samples should not have contact with air; process
delays should be avoided; and consistent analytical methods should
be used with serial measurements to improve accuracy. 16
_ TREATMENT OF CARDIOVASCULAR DISEASE IN CKD
Mortality secondary to cardiovascular disease is 10 to 30 times

greater in dialysis patients than in the general population. 9 In addition
to traditional cardiac risk factors such as diabetes, hypertension,
hyperlipidemia, tobacco use, and physical inactivity, patients with
kidney disease have other unique risk factors. Among these are hyperhomocysteinemia,
elevated levels of C-reactive protein, increased oxidant
stress, and hemodynamic overload. 109 Complications previously
discussed such as anemia and metabolic disorders of CKD are also
contributory. In particular, arterial vascular disease (i.e., atherosclerosis)
and cardiomyopathy are the primary types of cardiovascular
disorders present in the CKD population. 9 These disorders lead to development
of ischemic heart disease and its manifestations including
myocardial infarction. As a predominant comorbidity, cardiovascular
disorders and their sequela are the leading cause of death in the ESKD
population.3,5
_ ETIOLOGY AND EPIDEMIOLOGY

_ Hypertension
As a primary cause or a consequence of progressive loss of kidney

function, hypertension is prevalent in the majority of patients with
Stage 3 or 4 CKD (see Chap. 43). Approximately 80% to 90% of
patients initiating dialysis are hypertensive. 110 The pathogenesis of

hypertension in CKD is multifactorial, but in many hypertensive dialysis
patients, fluid retention is a major contributor. 110 In addition to
the general pathophysiologic mechanisms responsible for the development
of hypertension, patients with ESKD may also have increased
sympathetic activity, the presence of an endogenous digitalis-like
substance, elevated levels of endothelin-1, erythropoietin use, hyperparathyroidism,
and structural changes in the arteries (e.g., metastatic
calcification) as contributing factors.110
Patients withESKDalso display an abnormal diurnal blood pressure
rhythm as evidenced by the fact that their blood pressure does not
decrease during the nighttime hours.110 It is unclear what causes this
disturbance in the diurnal rhythm, but this nondipping phenomenon
indicates sustained elevations in blood pressure are present over a prolonged
period of time when compared to the general population.
_ Hyperlipidemia
CKD with or without nephrotic syndrome is frequently accompanied

by abnormalities in lipoprotein metabolism. It is well established
that dyslipidemias cause atherosclerotic cardiovascular disease
and there are many compelling reasons to aggressively treat these
disorders.111 A clear association between hypercholesterolemia, hypertriglyceridemia,
or other lipoprotein changes in patients with CKD
and the high incidence of cardiovascular disease has not been demonstrated
in large prospective studies. However, it is likely that the same
lipoprotein abnormalities that confer increased risk of cardiovascular
disease in the general population would also be harmful to patients
with kidney disease. A low or declining serum cholesterol in patients
with ESKD is also indicative of malnutrition and is associated with
increased mortality.16 Thus a fine balance must be struck to optimize
patient outcomes.
The few epidemiologic studies in CKD patients with nephrotic
syndrome suggest that their relative risk of coronary death or myocardial
infarction is higher than that of matched controls. 112 Similar
analyses have been done in CKD patients without nephrotic syndrome
and in patients on dialysis; low HDL, high triglycerides, high
apolipoprotein B, and high lipoprotein (a) were all associated with
a higher risk of cardiovascular disease. 112 The findings are not uniform,
as hypertriglyceridemia alone has not been shown to be a strong
independent risk factor for coronary heart disease in patients with normal
kidney function.111 However, hypertriglyceridemia may reduce
levels of protective HDL, which is now classified as a major risk
factor for coronary heart disease. Based on these findings and the high
prevalence of atherosclerotic cardiovascular disease in patients with
CKD, this population is considered to be in the highest-risk group
for such cardiovascular conditions (i.e., equivalent to that of patients

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prevent

volume overload from excessive sodium intake. After the serum

_ EVALUATION OF THERAPEUTIC OUTCOMES

Regular monitoring of arterial blood gases and serum electrolytes are

_ TREATMENT OF CARDIOVASCULAR DISEASE IN CKD

Mortality secondary to cardiovascular disease is 10 to 30 times

_ ETIOLOGY AND EPIDEMIOLOGY

As a primary cause or a consequence of progressive loss of kidney

patients initiating dialysis are hypertensive. 110 The pathogenesis of

CKD with or without nephrotic syndrome is frequently accompanied

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