Uremia (redirected from urinemia)

uremia (yrē`mēə), condition resulting from advanced stages of kidney failure in which urea and other nitrogen-containing wastes are found in the blood. Uremia can be caused by NSAIDs (nonsteroid anti-inflammatory drugs), especially in older patients treated primarily with ibuprofen for arthritis. Some of the early signs of uremia are lethargy, mental depression, loss of appetite, and edema; later symptoms include diarrhea, anemia, convulsions, coma, and a gray-brown coloration. Treatment of uremia, which is directed at the underlying kidney disease, is usually with dialysis and renal transplantation. Treatments with genetically engineered erythropoietin decrease the complication of anemia. See nephritis; nephrosis.

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uremia

Excess nitrogenous waste products in the blood and their toxic effects. Kidney impairment (see Bright disease; diabetes mellitus; hypertension; kidney failure; nephritis) or disorders that hinder urine excretion (e.g., prostatic disorders) allow urea and other protein waste products to accumulate. Symptoms usually start with fatigue and loss of concentration. They may include itching and muscle twitches; dry, flaky, yellowish skin; dry mouth, metallic taste, and ammonia breath; and nausea, vomiting, diarrhea, and constipation. Advanced stages affect the nervous, cardiovascular, and respiratory systems and can lead to hypertension, seizures, heart failure, and death. If the underlying disorder cannot be treated, dialysis or kidney transplant may be required.

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uremia [yə′rē·mē·ə]

(medicine)

A condition resulting from kidney failure and characterized by azotemia, chronic acidosis, anemia, and a variety of systemic signs and symptoms.

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Uremia 

a toxic condition caused by severe impairment of renal function. It may be acute or chronic.

Acute uremia occurs in acute renal insufficiency during oliguria and is marked by severe impairment as well as by systemic disorders. The concentration of creatinine, urea, indican, ammonia, and other nitrogenous compounds increases markedly in the blood, resulting in azotemia. The content of such electrolytes as potassium, magnesium, calcium, and chlorine becomes altered, the acid-base balance is disturbed, resulting in acidosis, and water is retained in the body. Cardiovascular changes are manifested by tachycardia, arrhythmia, and hypertension. Other symtoms include anemia, digestive disorders, neurological disturbances, and often pulmonary edema. Acute uremia persists for five to ten days and sometimes up to 30 days or longer. The majority of persons affected with the disease return to work in three to 12 months.

Chronic uremia (terminal uremia, or terminal chronic renal insufficiency) is caused by many chronic kidney diseases. Affected persons experience lassitude, become emotionally unstable, and exhibit various types of neuromuscular phenomena. Hearing is impaired and the skin becomes pale yellow in color and is dry, flaccid, and painfully itchy. Other common symptoms are loss of appetite, nausea, vomiting, thirst, convulsions, polyneuritis, and nasal, cutaneous, or intestinal hemorrhages. The process of change in the electrolytes intensifies, and azotemia and acidosis become more marked. The bones decalcify and the joints are affected. Blood pressure rises sharply and pericarditis develops. The specific gravity of the urine remains low.

The treatment of uremia is conservative; methods used include cleansing of the blood by means of an artifical kidney or by peritoneal dialysis. A kidney transplant may be indicated.

REFERENCE

Osnovy nefrologii, vol. 1. Edited by E. M. Tareev. Moscow, 1972. Pages 164–234.

N. R. PALEEV