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Transcript
Management of CKD
Reference: Brosnahan G, Fraer M.
Management of Chronic Kidney
Disease: What is the Evidence?
Southern Med J. 2010;103(3):222–230.
• Chronic kidney disease (CKD) is a strong risk
factor for cardiovascular events and death.
• Hypertension, dyslipidemia, anemia, vascular
calcifi cation and secondary
hyperparathyroidism have all been implicated
in the pathogenesis of cardiovascular disease
associated with CKD.
• Therefore early intervention on CKD helps
reduce the progression of CHF,
hospitalizations and mortality.
Hypertension in CKD
• Hypertension is associated with more rapid progression of CKD and
is usually systolic in almost 70–80% of patients with CKD.
• Besides, it is more severe in CKD patients than in non-CKD patients.
• Even small changes in blood pressure (BP) can signifi cantly affect
the rate of CKD progression, and lowering BP markedly reduces
proteinuria, even when agents other than renin-angiotensin system
(RAS) blockers are used.
• Patients with CKD are a high-risk group and a BP goal of <130/80
mmHg is recommended.
• Several studies have revealed that the lowest risk for CKD
progression was achieving and maintaining a systolic BP of 110–129
mmHg.
Effective Antihypertensive Agents in CKD
• The treatment of choice to delay progression
of renal disease is either an angiotensinconverting enzyme inhibitor (ACEI) or
angiotension receptor blocker (ARB),
particularly if protei-nuria (>1 g/day). Most
patients with CKD require more than one drug
to control their BP, and the second agent is
usually a diuretic since reduced GFR is
associated with volume expansion (see Fig. 1).
Dyslipidemia and Its Treatment in CKD
• Dyslipidemia in patients with CKD is associated with high
cardiovascular morbidity and mortality rate.
• In the absence of defi nitive evidence, the KDOQI (Kidney
Disease Outcomes Quality Initiative) guidelines follow closely
the National Cholesterol Education Program Adult Treatment
Panel (ATP) III guidelines for the general population.
• A summary of the medical treatment of dyslipidemia in CKD is
depicted in Fig. 2.
• The doses of fi brates need to be reduced in patients with
reduced renal function; besides the combinations of statins
and fi brates are not recommended for patients with stages 4
and 5 CKD due to the increased risk of rhabdomyolysis.
Treatment of Anemia in CKD
• The KDOQI guidelines and the European guidelines
recommend assessing iron stores and vitamin B12 and
folate levels before considering therapy with
erythropoiesisstimulating agents (ESA).
• Iron stores are considered adequate if serum ferritin levels
are >100 ng/mL and the transferrin saturation (TSAT) is
>20% in predialysis patients with CKD.
• Based on several trials, the KDOQI guidelines were updated
in 2007; and stated that the ideal Hb levels should be
between 11 and 12 g/dL.
• The Food and Drug Administration also recommends to
maintain Hb between 10 and 12 g/dL, and to start
treatment with ESA only if Hb is <10 g/dL (see Fig. 3).
Treatment of Metabolic Acidosis
• Decline in renal function is associated with reduced ability to
excrete the daily acid load, which is derived from protein intake and
catabolism.
• The resultant metabolic acidosis increases protein catabolism,
leading to bone and muscle loss, and malnutrition.
• Metabolic acidosis also stimulates ammonia production in the
remnant nephrons, which in turn increases interstitial infl
ammation and fi brosis, accelerating the decline in renal function.
• Treatment of metabolic acidosis with bicarbonate supplementation
(to achieve serum bicarbonate levels of ≥23 mmol/L) can slow the
progression of CKD and improve the nutritional status.
• Nutritional parameters such as dietary protein intake, lean body
mass, and serum albumin level can also be improved signifi cantly
when metabolic acidosis is corrected.
Comprehensive Basket
in Anemia Management