Medical Aspects of Long-Term Renal Replacement Therapy

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 sodium intake should be limited to 2 g (88 mEq [88 mmol]), potassium to 2.3 g (60 mEq [60 mmol]), and phosphate to 800 to 1000 mg. Fluid intake, inclusive of the fluids contained in food, is limited to 1000 to 1500 mL/day and monitored by measuring 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 (35 g/L); serum albumin is the best predictor of survival in these patients.

Clinical Calculators

Ideal Body Weight

The anemia that occurs in renal failure should be treated with erythropoiesis-stimulating agents (ESAs) and iron supplementation (see Anemia of Renal Disease and Anemia and coagulation disorderserythropoietin therapy and thereafter every 2 to 3 months (1). Iron deficiency is the most common reason for erythropoietin resistance. However, some dialysis patients who have received multiple blood transfusions have iron overload and should not be given iron supplements.

Risk factors for coronary artery disease must be managed aggressively because many patients who require RRT have hypertension, dyslipidemia, or diabetes; smoke cigarettes; and ultimately die of cardiovascular disease (2). Continuous peritoneal dialysis is more effective than hemodialysis in removing fluid. As a result, hypertensive patients require fewer antihypertensive medications. Hypertension can also be controlled in many hemodialysis patients by filtration alone. Antihypertensive medications are required in the remainder. Treatment of dyslipidemia, diabetes management, and smoking cessation are very important.

Hyperphosphatemia, a consequence of phosphate retention due to low glomerular filtration rate (GFR), increases risk of soft-tissue calcification, especially in coronary arteries and heart valves. It also stimulates development of secondary hyperparathyroidism. Patients with hyperphosphatemia should avoid foods high in phosphorus. Pharmacologic treatment options include calcium-based phosphorus binders, non-calcium–based phosphorus binders, or inhibition of phosphorus absorption.

hypercalcemia.

3). Some patients (eg, those hospitalized with acute kidney injury and very high serum phosphate concentrations) require the addition of aluminum-based phosphate binders, but these should be used as short-term medications only (eg, 1 to 2 weeks as needed) to prevent aluminum toxicity (4).

5). Diarrhea is a potential adverse effect.

hypophosphatemia. Treatment of hypocalcemia4

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.

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 electroencephalogram [EEG]).

≥ 50 mcg/L suggests toxicity. Aluminum-related osteomalacia can also be diagnosed by needle biopsy of bone (requires special stains for aluminum).

Renal osteodystrophy is abnormal bone mineralization. It has multiple causes, including , elevated serum phosphate, secondary hyperparathyroidism, chronic metabolic acidosis, and aluminum toxicity. Treatment is of the cause.

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× PO4 product has resulted in considerable improvement (6, 7). A recent clinical trial also suggests that vitamin K supplementation may be beneficial (8).

Calciphylaxis (Trunk)

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This image shows early skin changes of ischemia and necrosis in localized areas resulting from calciphylaxis.

Image courtesy of Karen McKoy, MD.

Constipation

1. 1. KDIGO Clinical Practice Guideline for Anemia in Chronic Kidney Disease: Diagnosis and evaluation of anemia in CKD. Kidney Int Suppl 2:288-291, 2012. doi:10.1038/kisup.2012.33

2. 2. U.S. Renal Data System (USRDS), National Institute of Diabetes and Digestive and Kidney Diseases: End Stage Renal Disease. Accessed May 14, 2024.

3. 3. Jamal SA, Vandermeer B, Raggi P, et al: Effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease: an updated systematic review and meta-analysis. Lancet 382(9900):1268-1277, 2013. doi: 10.1016/S0140-6736(13)60897-1

4. 4. KDIGO Executive Committee: KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease—Mineral and bone disorder (CKD-MBD). Kidney Int Suppl 7(1):1-159.

5. 5. Pergola PE, Rosenbaum DP, Yang Y, et alJ Am Soc Nephrol 32(6):1465-1473, 2021. doi: 10.1681/ASN.2020101398

6. 6. Zitt E, König M, Vychytil A, et al: Use of sodium thiosulphate in a multi-interventional setting for the treatment of calciphylaxis in dialysis patients. Nephrol Dial Transplant 28(5):1232–1240, 2013. https://doi.org/10.1093/ndt/gfs548

7. 7. Nigwekar SU, Brunelli SM, Meade D, et alClin J Am Soc Nephrol 8(7):p 1162-1170, 2013. doi:10.2215/CJN.09880912

8. 8. Nigwekar SU