The main object to increase renal perfusion and to maintain urine output. Azotemia is an elevation of blood urea nitrogen (BUN) and serum creatinine levels. In a condition when abnormally high levels of nitrogen containing compounds such as urea, creatinine, various body waste compounds, and other nitrogen rich compounds in blood, normally happens when kidneys insufficient or dysfunctional filtering of blood. Perturbation of any of these processes impairs the kidney’s excretory function, resulting in azotemia.
- Asterixis, flapping tremor
- Decreased alertness
- Edema, anasarca
- Oliguria or anuria mainly decreased or absent urine output
- Orthostatic blood pressure, fluctuates depending on body position
- Pale skin
- Uremic frost, a condition that occurs when urea and urea derivatives are secreted through the skin in sweat, which evaporates away to leave solid uric compounds, resembling a frost.
Prerenal azotemia occurs because of impaired renal blood flow or decreased perfusion resulting from decreased blood volume, decreased cardiac output (congestive heart failure), decreased systemic vascular resistance, decreased effective arterial volume from sepsis or hepato renal syndrome, or renal artery abnormalities. It may be superimposed on a background of chronic renal failure. Iatrogenic factors, such as excessive diuresis and treatment with ACE inhibitors, should be ruled out.
Intrarenal azotemia occurs because of injury to the glomeruli, tubules, interstitium, or small vessels. It may be acute oliguric, acute nonoliguric, or chronic. Systemic disease, nocturia, proteinuria, loss of urinary concentrating ability (low urine specific gravity), anemia, and hypocalcemia are suggestive of chronic intrarenal azotemia.
Post renal azotemia occurs when an obstruction to urine flow is present. It is observed in bilateral ureteral obstruction from tumors or stones, retroperitoneal fibrosis, neurogenic bladder, and bladder neck obstruction from prostatic hypertrophy or carcinoma and posterior urethral valves. It may be superimposed on a background of chronic renal failure.
In congestive heart failure or any other condition that causes poor perfusion of kidneys, the sluggish flow of glomerular filtrate results in excessive absorption of BUN and elevation of its value in blood. Creatinine, however, is not absorbable and therefore does not rise significantly.
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