The treatment of renal disease includes drug therapy and nutritional therapy. To prevent renal insufficiency from deteriorating further, the treatment is designed to control hypertension with antihypertensive drugs and sodium and fluid restrictions.
Usually, a physician will prescribe an ACE inhibitor or a calcium channel blocker to control your patient’s hypertension. He also may prescribe a diuretic to reduce your patient’s fluid overload.
If your patient’s phosphate level is elevated, the physician may limit his phosphate intake to 700 to 1,200 mg per day. He also may prescribe an antacid that contains aluminum hydroxide, aluminum carbonate, or a calcium-based phosphate binder. Because high aluminum levels can induce neurologic symptoms, a calcium-based phosphate binder may be preferable. Antacids that contain magnesium are contraindicated because magnesium is excreted by the kidneys.
If your patient is anemic, the physician may prescribe iron supplements and folic acid to increase RBC production. He also may order erythropoietin to be administered I.V. or subcutaneously. However, your patient will need his blood pressure monitored closely, because erythropoietin may worsen his hypertension.
Nutritional therapy may include protein, sodium, potassium, and fluid restrictions. A protein restriction may slow the deterioration of kidney function. Usually, if the physician orders a protein restriction, your patient’s daily protein intake will be reduced to 0.6 to 0.8 g/kg of body weight.
A sodium restriction may vary from 1 to 3 grams per day, depending on the ability of the patient’s kidneys to excrete sodium as well as the amount of edema and the severity of the hypertension. If the physician orders a potassium restriction, your patient’s potassium intake will be reduced to between 2 and 3 grams per day. Because most salt substitutes contain potassium, avoid giving them to your patient with renal disease.
If the physician orders a fluid restriction, your patient usually will be limited to an intake equal to his urine output plus 500 to 600 ml.
Your patient may have a low serum sodium level because of his kidneys’ inability to reabsorb sodium. He also may have a low serum calcium level caused by reduced renal absorption. And his serum potassium and phosphate levels may be elevated because of reduced renal excretion of potassium and phosphate.
If he has elevated blood urea nitrogen (BUN) and creatinine levels, his renal disease may result in azotemia. If his kidneys lose their ability to produce erythropoietin, he may become anemic.
Your patient’s renal disease also may cause signs in other body systems. He may have jugular vein distention, a full and bounding pulse, peripheral edema, pulmonary edema, and heart failure. He may show signs of metabolic acidosis, including Kussmaul’s respirations. And he may develop anorexia, nausea, vomiting, diarrhea, lethargy, and difficulty concentrating.
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