Healthcare Consideration: In patients with progressive CKD, providers must be vigilant in determining the presence of clin- ical indicators that dialysis is necessary. Patients should also be educated on the symptoms of uremia and to contact their pro- viders appropriately if symptoms develop (Rosenberg, 2021).
Self-Assessment Quiz Question #6 Sally read that her diagnosis of chronic kidney disease can increase her risk of cardiovascular disease, and she wants to do what she can to prevent it. She does not want a heart at- tack or stroke to affect her ability to spend more time with her grandkids. Since Sally is 75 years old and has a GFR of 44 mL/ min/1.73m 2 , which of the following are recommended to reduce
her cardiovascular risk? a. Fish oil supplements. b. Statins. c. Fenofibrate. d. Ibuprofen. TREATMENT OF CHRONIC KIDNEY DISEASE COMPLICATIONS:
Medication usage A reduction in kidney function can affect the body’s ability to re- move medications from the bloodstream. This reduced function can cause differing effects depending on the medication in ques- tion. Some medications may require dosage adjustments based on the patient’s estimated GFR, while others are contraindicated in moderate or severe renal impairment due to accumulation of Treatment of hyperphosphatemia The KDIGO Work Group guidelines recommend maintaining se- rum phosphate levels within the normal range of 2.5 to 4.5 mg/ dL in CKD patients who are not on dialysis. Dialysis patients have a higher target phosphate goal between 3.5 to 5.5 mg/dL due to the difficulty in maintaining lower levels and unclear benefit on outcomes in these patients. Phosphate levels can be reduced through dietary phosphate restriction as well as the use of phos- phate binders. Dietary phosphate can be restricted to approxi- mately 900 mg/day, and processed foods such as cola should be restricted over high biologic value foods such as meat and eggs (Berkoben & Quarles, 2021). Patients with persistently high phosphate levels over 5.5 mg/ dL despite one to two months of dietary phosphate restriction may require the use of phosphate binders. Phosphate binders Calcium-containing phosphate binders Calcium-containing phosphate binders include calcium acetate and calcium carbonate. Calcium acetate may be a more efficient phosphate binder than calcium carbonate. Their calcium content can potentially lead to hypercalcemia, and when combined with high phosphate levels, can lead to extraskeletal calcium–phos- phate deposits. Vascular calcification and adynamic bone disease can also be seen in patients taking calcium-containing phosphate binders, leading to increased morbidity. Calcium levels should be monitored in patients on calcium-containing phosphate binders, Non-calcium-containing phosphate binders Non-calcium-containing phosphate binders include sevelamer and lanthanum. It appears both products are equally effective in lowering phosphate levels, though more long-term safety data is available for sevelamer (Berkoben & Quarles, 2021). Sevelamer is available in two forms: sevelamer hydrochloride, sold under the name Renagel, and sevelamer carbonate, sold un- der the name Renvela. Sevelamer works by binding phosphate through ion exchange. It is typically administered three times dai- ly, at a dose of 800 mg TID for phosphate levels between 5.6 and 7.4 mg/dL, or 1,600 mg TID for phosphate levels greater than 7.5 mg/dL. The cost of sevelamer is significantly more than calci - um-containing phosphate binders, a factor that may need to be considered when choosing a phosphate management regimen for chronic kidney disease patients (Berkoben & Quarles, 2021; DiPiro et al., 2019). Lanthanum is a rare earth element that has effectiveness in re- ducing phosphate levels in chronic kidney disease patients. It is sold under the brand name Fosrenol. It appears to cause reduced
the medication or its metabolites. Whenever a new medication is added in a patient with chronic kidney disease, appropriate references should be consulted to determine if any dosage ad- justments are necessary. Dosages may need to be lowered, or administered at extended intervals, to prevent accumulation and adverse effects (DiPiro et al., 2019). work by binding dietary phosphate in the gastrointestinal tract to reduce the amount of phosphate available for absorption. Phosphate binders can be divided into several categories: cal- cium- containing phosphate binders, non-calcium-containing phosphate binders, iron-based phosphate binders, and alumi- num-based phosphate binders. Most patients are recommended to use non- calcium-containing phosphate binders, with excep- tions when serum calcium is low and parathyroid hormone is high, or if non-calcium-containing phosphate binders are not affordable or available. This is due to the risk of side effects seen with calci- um-containing phosphate binders, and potential mortality ben- efits with the use of non-calcium containing phosphate binders (Berkoben & Quarles, 2021). and these medications should be reduced or discontinued if hy- percalcemia develops (Berkoben & Quarles, 2021). Calcium acetate (PhosLo) is the most commonly used calci- um-containing phosphate binder. It is typically started at a dos- age of 1,334 mg three times daily with each meal and can be increased every two to three weeks until phosphate levels are in target range. Side effects associated with calcium acetate include hypercalcemia, nausea, vomiting, and constipation (Berkoben & Quarles, 2021; DiPiro et al., 2019). rates of hypercalcemia and parathyroid hormone oversuppression when compared with calcium carbonate. Lanthanum tablets are chewable rather than swallowed whole, which may be a bene- fit over sevelamer to some patients. It is typically initiated at a dose of 500 mg three times daily and is increased by 750 mg per day every two to three weeks until target phosphate levels are achieved (Berkoben & Quarles, 2021; DiPiro et al., 2019). Short-term safety studies of up to two years have not uncovered any severe adverse effects with lanthanum treatment. Gastroin- testinal effects were the principal adverse effects that developed, and no evidence of hepatic toxicity was found. Long-term effects on bone and other organs remain unclear; since lanthanum ac- cumulated in several organs in animal studies, such as the liv- er, further research may be needed to evaluate this possibility. Short-term use appears to be unlikely to cause lanthanum toxicity (Berkoben & Quarles, 2021; DiPiro et al., 2019).
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