uremia(redirected from prerenal uremia)
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Related to prerenal uremia: uremic, prerenal azotemia
uremia(yo͝orē`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 ibuprofenibuprofen
, nonsteroidal anti-inflammatory drug (NSAID) that reduces pain, fever, and inflammation. Along with naproxen and ketoprofen, ibuprofen belongs to the propionic acid class of NSAIDs. It was first made available in 1967.
..... Click the link for more information. 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 nephritisnephritis
, inflammation of the kidney. The earliest finding is within the renal capillaries (glomeruli); interstitial edema is typically followed by interstitial infiltration of lymphocytes, plasma cells, eosinophils, and a small number of polymorphonuclear leukocytes.
..... Click the link for more information. ; nephrosisnephrosis
, kidney disease characterized by lesions of the epithelial lining of the renal tubules, resulting in marked disturbance in the filtration function and the consequent appearance of large amounts of protein (albumin) in the urine (see urinary system).
..... Click the link for more information. .
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.
REFERENCEOsnovy nefrologii, vol. 1. Edited by E. M. Tareev. Moscow, 1972. Pages 164–234.
N. R. PALEEV