Nutrition and Renal Disease
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Nutrition and Renal Disease
Acute Renal Failure
Acute renal failure, manifested by oliguria or anuria, usually occurs suddenly and is often reversible. It is marked by a reduction in the glomerular filtration rate and a modification in the kidneys ability to excrete metabolic wastes.
Its causes can be prerenal, intrinsic, and postrenal. Prerenal causes include severe dehydration and circulatory collapse. Causes intrinsic to the kidney include acute tubular necrosis, nephrotoxicity, vascular disorders, and acute glomerulonephritis. Obstructive (postrenal) causes include benign prostatic hypertrophy and bladder or prostate cancer.1
The most common form of intrinsic renal disease is acute tubular necrosis, accounting for about 75 percent of cases. Acute tubular necrosis may be due to posttraumatic or surgical shock or to the toxic effects of drugs, metals, or organic compounds.
Nutrition strategies in acute tubular necrosis vary depending on its stage. During phase one, oliguria, less than 400 milliliters of urine is produced per day. This phase usually lasts one to three weeks. Signs and symptoms include nausea, vomiting, fluid overload, and elevation of BUN, creatinine, phosphorus, and potassium levels. Dialysis may be needed during this stage to reduce acidosis, control hyperkalemia, and correct uremia.
The diuretic phase of acute tubular necrosis lasts one to two weeks, and is characterized by increased urine output and a return of the ability to eliminate wastes. Fluid and electrolyte balance should be monitored and replacements made as necessary. The convalescent phase occurs over the next two to six months.1,2
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Diet in Acute Renal Failure
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