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B Acid Base Disorders
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Damaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins The resultant metabolic acidosis is primarily due to loss of renal mass This limits production of ammonia (NH3) and limits buffering of H+ in the urine (Other causes include decreased filtration of titratable acids such as sulfates and phosphates, decreased proximal tubular bicarbonate resorption, and decreased renal tubular hydrogen ion secretion) Although patients with chronic renal failure are in positive hydrogen ion balance, the arterial blood pH is maintained at 733 737 and serum bicarbonate concentration rarely falls below 15 mEq/L The excess hydrogen ions are buffered by the large calcium carbonate and calcium phosphate stores in bone This contributes to the renal osteodystrophy of chronic renal failure described below The serum bicarbonate level should be maintained at greater than 21 mEq/L according to recently published national guidelines Alkali supplements include sodium bicarbonate, calcium bicarbonate, and sodium citrate Citrate salts increase the absorption of dietary aluminum and should be avoided in patients exposed to aluminum Administration should begin with 20 30 mmol/d of alkali divided into two doses per day and titrated as needed
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C Cardiovascular Complications
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Long-term complications of chronic kidney disease include a high risk of morbidity and mortality of cardiovascular disease in comparison to the general population Mortality due to a cardiovascular cause accounts for 45% of all deaths of patients receiving dialysis The precise biologic mechanisms for this are unclear but may have to do with the uremic milieu, underlying coexistent comorbidities, and a hesitancy to perform investigative procedures in patients with chronic kidney disease 1 Hypertension As renal failure progresses, hypertension due to salt and water retention usually develops Hyperreninemic states and exogenous erythropoietin administration can also exacerbate hypertension Hypertension is the most common complication of ESRD and must be meticulously controlled Failure to do so can accelerate the progression of renal damage Control of hypertension can be achieved with salt and water restriction, weight loss if indicated, and pharmacologic therapy The ability of the kidney to adjust to variations in sodium and water intake becomes limited as renal failure progresses An elevated sodium chloride intake leads to congestive heart failure, edema, and hypertension, whereas low salt intake leads to volume contraction and hypotension A mildly decreased salt diet (4 g/d) can be started, and salt intake
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1 Anemia The anemia of chronic renal failure is characteristically normochromic and normocytic It is due primarily to decreased erythropoietin production, which becomes clinically significant when GFR falls below 20 25 mL/min Many patients are iron deficient as well Low-grade hemolysis and blood loss from platelet dysfunction or hemodialysis play an additional role
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Recombinant erythropoietin or darbepoetin is used in patients whose hematocrits are less than 33% if no other causes are present The effective dose can vary; the starting dose of erythropoietin is 50 units/kg (3000 4000 units/dose) once or twice a week Darbepoetin is started at 045 mcg/kg once weekly and can be administered every 2 4 weeks Both medications should be titrated to a hemoglobin of 11 13 g/ dL according to national guidelines, but studies suggested that an upper limit of 12 g/dL might be more appropriate for optimal safety These agents can be given intravenously (eg, in the hemodialysis patient) or subcutaneously (eg, in any predialysis or dialysis patient) Subcutaneous administration is preferable to intravenous administration because it requires a 33% lower dose for the same effect Iron stores must be adequate to ensure response Hemodialysis patients typically require 50 200 mg intravenous iron each month due to expected blood loss at dialysis Other patients with serum ferritin less than 100 ng/mL or iron saturation less than 20% should also receive iron supplementation Depending on the clinical situation, iron therapy should be withheld if the serum ferritin is greater than 800 ng/mL Oral therapy with ferrous sulfate, 325 mg once daily to three times daily, is adequate but not always well tolerated, and gut absorption of iron is impaired in uremic patients Ferrous fumarate is the best-accepted formulation, and intravenous iron may be used in dialysis patients Hypertension is a complication of epoetin alfa therapy in about 20% of patients It develops more abruptly in the patients with the lowest hematocrit values at initiation of therapy, and in those with the greatest rate of rise in hemoglobin The dosage may require adjustment, or antihypertensive drugs may need to given Hemoglobin levels should rise no more than 1 g/dL every 3 4 weeks 2 Coagulopathy The coagulopathy of chronic kidney disease is mainly caused by platelet dysfunction Platelet counts are only mildly decreased, but the bleeding time is prolonged Platelets show abnormal adhesiveness and aggregation Clinically, patients can have petechiae, purpura, and an increased tendency for bleeding during surgery Treatment is required only in patients who are symptomatic Raising the hematocrit to 30% can reduce bleeding time in many patients Desmopressin (25 mcg intravenously every 8 12 hours for two doses) is effective and often used in preparation for surgery It causes release of factor VIII bound to von Willebrand s factor from endothelial cells Conjugated estrogens, 06 mg/kg diluted in 50 mL of 09% sodium chloride infused over 30 40 minutes daily, or 25 5 mg orally for 5 7 days, have an effect for several weeks Dialysis improves the bleeding time but does not normalize it Peritoneal dialysis is preferable to hemodialysis because the latter requires heparin to prevent clotting in the dialyzer Cryoprecipitate (10 15 bags) is rarely used and lasts less than 24 hours
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