Merck & Co., Inc.

The Merck Manual of Geriatrics logo
red line
click here to go to the Contents page of The Merck Manual of Geriatrics
click here to go to the title page of The Merck Manual of Geriatrics
click here to search The Merck Manual of Geriatrics
click here to go to the Index of The Merck Manual of Geriatrics
red line
Section 12. Kidney and Urinary Tract Disorders
Chapter 98. Renal Disorders
Topics:    Introduction | Nephrotic Syndrome | Glomerulonephritis | Renal Artery Stenosis, Thrombosis, and Embolism | Acute Renal Failure | Chronic Renal Failure

red line

Chronic Renal Failure

The clinical condition resulting from various pathologic processes that lead to insufficiency of renal excretory and regulatory function.

Chronic renal failure is much more common in the elderly than in younger persons. Although the causes are myriad, some chronic illnesses common in the elderly (eg, diabetes mellitus, hypertension, urinary tract obstruction and hydronephrosis secondary to prostatic hypertrophy or cancer, arterial obstruction secondary to atherosclerosis) can cause or predispose the elderly to chronic renal failure. Long-term use of drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain analgesics (especially in combination) can cause chronic interstitial nephritis and papillary necrosis, resulting in chronic renal failure.

Treatment

Progression of chronic renal failure can sometimes be slowed by dietary modification, antihypertensive therapy, and other renoprotective measures.

Dietary modification: The rate of decrease in renal function in patients with progressing renal disease can be slowed slightly by protein restriction. The benefits of delaying progression of renal disease with a low-protein intake must be weighed against the small declines in various indexes of nutritional status. Protein intake should initially be reduced to 0.7 g/kg of body weight; ultimately, protein intake may need to be reduced to as low as 0.3 g/kg of body weight. Keto acid-amino acid supplementation may be necessary to prevent protein depletion. Salt restriction also may be needed to suppress volume expansion. Restriction of fat intake and lowering of serum cholesterol and triglyceride levels also appear to slow renal deterioration. Reduction of phosphate absorption with the addition of antacids at mealtimes is often necessary to avoid hyperphosphatemia.

Antihypertensive therapy: Patients with diabetic nephropathy benefit from lowering of blood pressure into the normal range. Moreover, angiotensin-converting enzyme inhibitors used not only to control hypertension but also to create lower-than-usual blood pressures have been shown to retard the rate of progression of nondiabetic renal disease.

Dialysis: Long-term maintenance dialysis (hemodialysis or long-term ambulatory peritoneal dialysis) is the mainstay of treatment for patients with chronic renal failure. More than half of all patients receiving chronic dialysis are > 60 years. Most elderly patients do well with dialysis; complications are related more to extrarenal diseases than to age alone. Psychologically, elderly patients often are better able to adapt to chronic dialysis than are younger patients. As soon as a patient is identified as needing hemodialysis, an arteriovenous fistula should be created, because such fistulas tend to mature more slowly in elderly persons.

Renal transplantation: Renal transplantation is increasingly used in persons > 60. Selection criteria should consider the patient's overall health status and severity of extrarenal disease (comorbidity) rather than age. Renal transplantation in elderly persons remains controversial, largely because of a reluctance to allocate a scarce resource (the donor kidney) to an elderly person with a limited life expectancy. Elderly transplant patients matched with dialysis patients by age, underlying diagnosis leading to renal failure, and number of comorbidities have 5-year survival rates of 81% vs. 51%, respectively. Because elderly persons have reduced immunity (immune incompetence), they require less aggressive immunosuppressant therapy, which should make them less susceptible to serious infections.

Treatment of complications: Complications of chronic renal failure, including anemia, hyperphosphatemia, hypocalcemia, hyperparathyroidism, and pruritus, must be treated.

Anemia resulting from chronic renal failure often requires more aggressive treatment in elderly patients than in younger patients because of coexisting heart disease. Red blood cell indices do not provide a reliable estimate of iron deficiency in uremia. Iron deficiency should be excluded by evaluation of serum iron and ferritin levels, and oral iron supplements should be given only if indicated. The management of non-iron deficiency anemia has changed radically with the use of recombinant human erythropoietin. Correction of the anemia results in improved cardiac function, exercise tolerance, central nervous system function, appetite, and sexual function. Erythropoietin (epoetin alfa) usually is started at a dose of 50 to 100 U/kg sc 3 times a week (or IV if the patient is already on hemodialysis) and adjusted downward as necessary to maintain the Hct between 30 and 35%.

Hyperphosphatemia, hypocalcemia, and hyperparathyroidism become problems because phosphate retention begins early in chronic renal insufficiency; phosphate retention stimulates parathyroid hormone hypersecretion and in turn helps to lower the serum phosphate concentrations back within the normal range. Therefore, control of serum phosphate levels is essential for the prevention and treatment of secondary hyperparathyroidism. Calcium carbonate and acetate antacids are the phosphate binders of choice, because toxicity may result from aluminum-containing (bone demineralization, dementia, anemia) and magnesium-containing (respiratory depression) antacids in renal failure patients. More dietary calcium is often needed. When the serum phosphate becomes elevated in the presence of increased parathyroid hormone, phosphate precipitates out with calcium, producing widespread soft tissue calcification and enhanced hypocalcemia.

Hypocalcemia also can result from inadequate vitamin D activity, causing decreased GI absorption of calcium, which in turn stimulates parathyroid hormone release and glandular hypertrophy. Hypocalcemia results from insufficient activity of the 1alpha-hydroxylase enzyme, which is produced in the proximal tubule of the kidney and is responsible for converting the carrier form of vitamin D3 (25-OH cholecalciferol) to the metabolically active form of vitamin D3 (1,25(OH)2 cholecalciferol). The hypocalcemia generally can be corrected by giving 1,25(OH)2 cholecalciferol orally (calcitriol 0.25 to 0.50 µg daily) and ingesting adequate amounts of calcium.

Pruritus can be a major problem in elderly uremic patients, especially if xerosis coexists. In addition to skin moisturizers, ultraviolet treatments are effective and safe. Antipruritic agents (eg, antihistamines, ataractics) are rarely helpful; they also are toxic in the elderly, causing sedation, other central nervous system adverse effects, and anticholinergic adverse effects.

Copyright © 2009 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Whitehouse Station, N.J., U.S.A.  Privacy  Terms of Use  Sitemap