MANAGING CHRONIC RENAL INSUFFICIENCY: PREVENT AND/OR MANAGE COMPLICATIONS OF CHRONIC RENAL INSUFFICIENCY
Anemia in renal failure results in multisystemic disabling symptoms, excess cardiovascular morbidity (left ventricular hypertrophy, ischemic heart disease, congestive heart failure), worsening of diabetic retinopathy, and possibly accelerated progression renal failure.
Left ventricular hypertrophy in persons with chronic renal failure may reverse after improvement of anemia with erythropoietin—independent of blood pressure control; resorption of hard exudates and reduction in macular edema in diabetic retinopathy may also follow improvement in hematocrit. pharmacy united kingdom
Before treating with recombinant erythropoietin, other causes of anemia such as gastrointestinal blood loss or hemoglobinopathy should be excluded. Oral iron supplements will ensure adequate iron stores (transferrin saturation >20%; ferritin >100 ng/ml). Patients unable to maintain adequate iron stores with oral iron may be given intravenous iron.
The ideal hematocrit at which erythropoietin should be started, as well as the target hematocrit, are not established and remain controversial. Based on retrospective uncontrolled studies, clinical experience and wisdom, it is recommended that erythro poietin treatment be started in patients with progressive chronic renal failure once hematocrit falls below 33%, and target hematocrit should be 36% Starting dose should be 100 to 200 U per kilogram of body weight subcutaneously once or twice a week and adjusted to result in a weekly rise in hematocrit of <2%. The precise starting dose is determined by the severity of anemia and/or amount of residual renal function. Iron deficiency, infection, immunosuppressive drugs, loss of residual renal function and possibly ACE inhibitors may impair response to erythropoietin.
Renal Osteodystrophy and Hyperphosphatemia
Secondary hyperparathyroidism—a consequence of both phosphate retention and deficiency/unresponsiveness, leads to osteitis fibrosa cystica and hypoplastic bone—characterized by decreased bone turnover.
When administration of vitamin D, phosphate binders, and calcium in the treatment of early renal osteodystrophy should be started is undefined. However, it is known that dietary phosphate restriction, early treatment with calcium-containing phosphate binders preempts severe secondary hyperparathyroidism.
Dietary phosphate should be restricted to less than 1 gram daily. Calcium-containing phosphate binders (taken with meals) and vitamin D may prevent development of severe secondary hyperparathyroidism. Intact serum parathyroid hormone levels guides the management of renal osteodystrophy.
With declining glomerular filtration rate (GFR), patients with chronic renal insufficiency are less able to excrete rapid infusions of fluid. Progressive fluid retention may result in severe pulmonary edema especially if the patient is not receiving enough diuretics and/or if ESRD is imminent. This should be treated with increasing doses plus metolazone, but unresponsiveness to medical therapy signals the need to begin renal replacement therapy.
Electrolyte and Acid-Base Derangements
Metabolic acidosis in renal failure worsens renal bone disease, increases skeletal muscle catabolism and inhibits protein synthesis. Treatment consists of oral sodium bicarbonate (0.5 to 1 meq per kilogram of body weight per day), though the benefits have not been proven in a randomized clinical trial.
Hyperkalemia associated with type 4 renal tubular acidosis is common, especially in diabetic patients and/or those receiving ACE inhibitors. If such patients have hypertension, increasing the dose of plus metolazone may control hyperkalemia, as will liberalizing salt intake in those who are normotensive. Should these maneuvers fail, ACE inhibitors should be stopped. Persistent hyperkalemia heralds the incipient need for dialytic therapy. Sodium polystyrene sulfonate titrated to the serum potassium may control hyperkalemia nicely.
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The risk of malnutrition is increased because of anorexia, enhanced catabolism and reduced intestinal absorption of nutrients. Fluid retention may mask weight loss so comprehensive nutritional assessment should be performed routinely. Unfortunately, commonly measured laboratory indices of nutritional status may be affected by renal disease, therefore no single parameter is sufficient.
Nutritional assessment should include history (food intake) and physical examination, serial measurements of serum albumin, cholesterol and blood urea nitrogen. These variables should be complemented by serial anthropometric measurements—skin fold thickness at the triceps to estimate body fat and mid-arm circumference to estimate muscle mass.
A prescribed diet should provide 35 kcal per kilogram of body weight per day with 0.8 to 1 gram per kilogram of body weight of high biologic value protein. viagra soft