The major hematologic concern in patients with chronic renal insufficiency is the increased incidence of bleeding. These bleeding problems are secondary to abnormal bleeding times and, in particular, disorders of platelet function related to a decreased amount of factor VIII and von Willebrand antigen in the serum of uremic patients. Anemia, which is common in patients with renal insufficiency, can contribute to prolonged bleeding times (250). Abnormalities in arachidonic acid metabolism, acquired platelet storage pool deficiency, and disturbed regulation of platelet calcium content all contribute to an increased tendency for uremic patients to have significant bleeding during surgery (251). The bleeding time should be routinely checked preoperatively in these patients, and abnormalities should be corrected before surgery. Options for the correction of bleeding time in uremic patients include infusion of desmopressin or cryoprecipitate, both of which act to increase plasma levels of factor VIII and von Willebrand antigen (252,253).
Normal renal function is essential for maintenance of acid-base balance in the body. Patients with renal insufficiency can have a normal anion gap or an elevated anion gap acidosis. When mild renal insufficiency develops, a normal anion gap is present, whereas in more significant and severe renal dysfunction, an elevated anion gap acidosis occurs. Hemodialysis corrects metabolic acidosis. If a patient is severely acidotic (pH <7.15) and emergency surgery is planned, correction of the blood pH to 7.25 using intravenous sodium bicarbonate is indicated. However, correction of metabolic acidosis should be carried out slowly, because in patients with hypocalcemia, seizures may be precipitated (254). It is important to exclude other causes of elevated anion gap acidosis, such as ketoacidosis secondary to diabetes, lactic acidosis secondary to infection, or in rare instances, poisoning with ethylene glycol, methanol, or aspirin.
Impaired kidney function causes phosphate retention by the kidney and impaired vitamin D metabolism. Therefore, hypocalcemia is common in patients with renal insufficiency, but tetany and other signs of hypocalcemia are relatively uncommon because metabolic acidosis increases the level of ionized calcium. Oral phosphate binders, such as aluminum hydroxide (1 to 2 g per meal), and dietary phosphate restriction (1 g per day) is the usual treatment for hypocalcemia– hyperphosphatemia in patients with renal insufficiency. In chronic situations, because of central nervous system toxicity associated with elevated aluminum levels, it is preferable to treat hypocalcemia–hyperphosphatemia with large doses of calcium carbonate (6 to 12 g per day) rather than with the standard aluminum-containing antacids (255).
Approximately 20% of patients with renal insufficiency exhibit clinical evidence of protein calorie malnutrition. Vitamin deficiencies, most notably with water-soluble vitamins, occur with dialysis. Nutritional disturbances in patients with chronic renal insufficiency arise secondary to deficiencies in protein intake, and studies show that, in patients with chronic renal insufficiency, their kidneys are hyperfiltrating (256). Postoperatively, both protein and caloric intake may need to be increased dramatically to meet catabolic demands in surgical patients. As much as 1.5 g/kg of protein and 45 kcal/kg of calories may be needed (256).