 |
All patients undergoing long-term renal replacement therapy (RRT) develop accompanying metabolic and other disorders. These disorders require appropriate attention and adjunctive treatment. Approach varies by patient but typically includes nutritional modifications and management of multiple metabolic abnormalities (see also Chronic Kidney Disease: Nutrition).
Diet:
Diet should be carefully controlled. Generally, hemodialysis patients tend to be anorexic and should be encouraged to eat a daily diet of 35 kcal/kg ideal body weight (in children, 40 to 70 kcal/kg/day depending on age and activity). Daily Na intake should be limited to 2 g (88 mEq), K to 60 mEq, and phosphate (PO4) to 800 to 1000 mg. Fluid intake is limited to 1000 to 1500 mL/day and monitored by weight gain between dialysis treatments. Patients undergoing peritoneal dialysis need a protein intake of 1.25 to 1.5 g/kg/day (compared with 1.0 to 1.2 g/kg/day in hemodialysis patients) to replace peritoneal losses (8.4 +/- 2.2 g/day). Survival is best among patients (both hemodialysis and peritoneal dialysis) who maintain a serum albumin > 3.5 g/dL; serum albumin is the best predictor of survival in these patients.
Anemia of renal failure:
The anemia that occurs in renal failure should be treated with recombinant human erythropoietin and iron supplementation (see Chronic Kidney Disease: Anemia and coagulation disorders). Because the absorption of oral iron is limited, many patients require IV iron during hemodialysis. (Na ferric gluconate and iron sucrose are preferred to iron dextran, which has a higher incidence of anaphylaxis.) Iron stores are assessed using serum iron, total iron-binding capacity, and serum ferritin. Typically, iron stores are assessed before the start of erythropoietin therapy and thereafter every other month. Iron deficiency is the most common reason for erythropoietin resistance. However, some dialysis patients who have received multiple blood transfusions have iron overload (see Iron Overload) and should not be given iron supplements.
Coronary artery disease:
Risk factors must be managed aggressively because many patients who require RRT have hypertension, dyslipidemia, or diabetes; smoke cigarettes; and ultimately die of cardiovascular disease. Continuous peritoneal dialysis is more effective than hemodialysis in removing fluid. As a result, hypertensive patients require fewer antihypertensive drugs. Hypertension can also be controlled in about 80% of hemodialysis patients by filtration alone. Antihypertensives are required in the remaining 20%. Patients given ACE inhibitors or angiotensin II receptor blockers may need closer monitoring of serum K+ to prevent hyperkalemia. For approaches to dyslipidemia, see Lipid Disorders: Treatment; for diabetes management, see Diabetes Mellitus and Disorders of Carbohydrate Metabolism: Diabetes Mellitus (DM); and for smoking cessation, see Smoking Cessation.
Hyperphosphatemia:
Hyperphosphatemia, a consequence of phosphate retention due to low GFR, increases risk of soft-tissue calcification, especially in coronary arteries and heart valves, when Ca × PO4
> 50 to 55. It also stimulates development of secondary hyperparathyroidism. Initial treatment is Ca-based antacids (eg, Ca carbonate 1.25 g po tid, Ca acetate 667 to 2001 mg po tid with meals), which function as phosphate binders and reduce PO4 levels. Constipation and abdominal bloating are complications of chronic use. Patients should be monitored for hypercalcemia. Sevelamer carbonate 800 to 3200 mg or lanthanum carbonate 250 to 1000 mg with each meal is an option for patients who develop hypercalcemia while taking Ca-containing phosphate binders. Some patients (eg, those hospitalized with acute renal failure and very high serum PO4 concentrations) require addition of aluminum-based phosphate binders, but these drugs should be used short-term only (eg, 1 to 2 wk as needed) to prevent aluminum toxicity.
Hypocalcemia and secondary hyperparathyroidism:
These complications often coexist as a result of impaired renal production of vitamin D. Treatment of hypocalcemia is with calcitriol either orally (0.25 to 1.0 μg po once/day) or IV (1 to 3 μg in adults and 0.01 to 0.05 μg/kg in children per dialysis treatment). Treatment can increase serum PO4 level and should be withheld until the level is normalized to avoid soft-tissue calcification. Doses are titrated to suppress parathyroid hormone (PTH) levels, usually to 150 to 300 pg/mL (PTH reflects bone turnover better than serum Ca). Oversuppression decreases bone turnover and leads to adynamic bone disease, which carries a high risk of fracture. The vitamin D analogs doxercalciferol and paricalcitol have less effect on Ca and PO4 absorption from the gut but suppress PTH equally well. Early hints that these drugs may reduce mortality compared with calcitriol require confirmation. Cinacalcet, a calcimimetic drug, increases sensitivity of parathyroid Ca-sensing receptors to Ca and may also be indicated for hyperparathyroidism, but its role in routine practice has yet to be defined. Its ability to decrease PTH levels by as much as 75% may decrease the need for parathyroidectomy in these patients.
Aluminum toxicity:
Toxicity is a risk in hemodialysis patients who are exposed to aluminum-contaminated dialysate (now uncommon) and aluminum-based phosphate binders. Manifestations are osteomalacia, microcytic anemia (iron-resistant), and probably dialysis dementia (a constellation of memory loss, dyspraxia, hallucinations, facial grimaces, myoclonus, seizures, and a characteristic EEG). Aluminum toxicity should be considered in patients receiving renal replacement therapy who develop osteomalacia, iron-resistant microcytic anemia, or neurologic manifestations such as memory loss, dyspraxia, hallucinations, facial grimaces, myoclonus, or seizures. Diagnosis is by measurement of plasma aluminum before and 2 days after IV infusion of deferoxamine 5 mg/kg. Deferoxamine chelates aluminum, releasing it from tissues and increasing the blood level among patients with aluminum toxicity. A rise in aluminum level of ≥ 50 μg/L suggests toxicity. Aluminum-related osteomalacia can also be diagnosed by needle biopsy of bone (requires special stains for aluminum). Treatment is avoidance of aluminum-based binders plus IV or intraperitoneal deferoxamine.
Bone disease:
Renal osteodystrophy is abnormal bone mineralization. It has multiple causes, including vitamin D deficiency, elevated serum PO4, secondary hyperparathyroidism, chronic metabolic acidosis, and aluminum toxicity. Treatment is that of the cause.
Vitamin deficiencies:
Vitamin deficiencies result from dialysis-related loss of water-soluble vitamins (eg, B, C, folate) and can be replenished with daily multivitamin supplements.
Calciphylaxis:
Calciphylaxis is a rare disorder of systemic arterial calcification causing ischemia and necrosis in localized areas of the fat and skin of the trunk, buttocks, and lower extremities. Cause is unknown, though hyperparathyroidism, vitamin D supplementation, and elevated Ca and PO4 levels are thought to contribute. It manifests as painful, violaceous, purpuric plaques and nodules that ulcerate, form eschars, and become infected. It is often fatal. Treatment is usually supportive. Several cases have been reported in which Na thiosulfate given IV at the end of dialysis 3 times/wk along with aggressive efforts to reduce the serum Ca × PO4 product has resulted in considerable improvement.
Constipation:
Constipation is a minor but troubling aspect of long-term RRT and, because of resulting bowel distention, may interfere with catheter drainage in peritoneal dialysis. Many patients require osmotic (eg, sorbitol) or bulk (eg, psyllium) laxatives. Laxatives containing Mg or phosphate should be avoided.
Last full review/revision July 2012 by James I. McMillan, MD
Content last modified November 2012
| |
|
