Prerenal azotemia is a condition in which urea nitrogen and creatinine accumulate in the blood. This is a common cause of acute kidney failure, especially in hospital settings.
Patients with cardiac or hepatic failure will present with their own signs and symptoms as well.
Evaluation of the patient includes a full history, physical exam, and laboratory studies. When evaluating azotemia, the clinician should evaluate the onset, and whether the cause is prerenal, intrarenal, or postrenal.
A complete blood count (CBC) will show increased hematocrit, which is indicative of the hemoconcentration typically observed in prerenal azotemia. Moreover, a complete metabolic panel (CMP) reveals elevated sodium, calcium, total protein, uric acid and albumin.
Urine studies demonstrate low output (<500mL/day) in addition to a low fractional excretion of sodium (FENa]), which is less than 1%. In fact, the FENa distinguishes prerenal etiology from acute tubular necrosis (>2%). Furthermore, fractional excretion of urea (FEUrea) and fractional excretion of uric acid (FEUA) may be used as well. Specifically, prerenal causes are associated with levels of FEUrea less than 35% or FEUA below 9% to 10% .
In ill patients with heart failure, the sodium and albumin levels are low.
Imaging techniques are used to identify the presence of renal vein thrombosis, renal artery stenosis, renal malignancy, or vasculitis. Doppler ultrasonography of the kidneys can assess renal blood flow and reveal any thrombosis or stenosis present in the vasculature. CT scan may also be useful. If findings from ultrasonography and CT are inconclusive, MRI or MRA can be performed.
The therapeutic approach of prerenal azotemia is geared towards treating the underlying cause and managing the decreased fluid status.
Fluid replacement in free water loss
The amount of fluid replacement in cases with free water loss can be determined by the following equation: [(Na/140) – 1] × 0.5 × weight. The result of this calculated volume is the free water deficit. The sum of the free water deficit and the daily maintenance fluids (1.5 to 2L per day) equals the total volume. Half of this resultant volume is given in the first 24 hours, after which a new volume is determined using the new laboratory results. An alternative to this fluid regimen forgoes the maintenance fluids, and the total free water deficit is administered in 24 hours.
The type of fluid used in patients with free water loss is the hypotonic form, which includes 0.5% saline or 5% dextrose in water (D5W).
Alert patients are encouraged to drink water. Patients with hemorrhage are given IV saline as well as other indicated treatments.
This electrolyte should be monitored every 6 to 8 hours. Additionally, the medical team should be careful when adjusting fluids and electrolytes to avoid complications such as cerebral edema.
Isotonic fluid loss
Fluid replacement in patients with diarrhea requires normal saline. If the volume depletion is accompanied by normal–anion-gap metabolic acidosis, the treatment of choice is 0.5% normal saline with bicarbonate.
Fluid loss due to diuretic use
This occurs particularly in the elderly population. The patient develops dehydration, hyponatremia  and possibly hypokalemia. Therefore, therapy consists of normal saline and potassium replacement.
Treatment of heart failure
Diminished cardiac output, or heart failure, should be treated with drugs that improve cardiac function. These include beta blockers, ACE inhibitors, diuretics, nitrates, and other medications as well.
Treatment of decreased effective arterial volume
In patients with shunting due to hepatic failure or sepsis, therapy is complicated by low serum sodium and albumin. Sepsis is treated with antibiotics, norepinephrine, and dobutamine. Additionally, adequate nutrition is very important in these patients.
Diminished renal blood flow or hypoperfusion lead to prerenal azotemia. Specifically, this condition occurs when the following parameters are decreased: extracellular volume, cardiac outptut, systemic vascular resistance, or effective arterial volume (from sepsis or hepatorenal syndrome) .
Volume depletion is the most frequent renal cause of acute renal failure . Diuretic use was implicated in 25% to 40% of cases with prerenal AKI in the elderly population . Other medications that contribute to prerenal azotemia are nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors.
In patients with underlying disease, renal structural changes disrupt compensatory mechanisms and, hence, cause decreased renal perfusion. This can occur in a background of low blood pressure .
In case of a recent onset of heart failure, diminished cardiac output results in reduced glomerular filtration.
Arterial vasodilation and hypotension in sepsis cause the activation of several important mechanisms, including the activation of the renin-angiotensin system, sympathetic nervous system, and ADH release. These cause vasoconstriction of the afferent arterioles and enhanced reabsorption of sodium.
Additionally, when large blood vessels develop thrombosis, emboli, or dissection, the kidneys become hypoperfused.
The United States Renal Data System (USRDS) reported in 2008 that azotemia was the most prevalent (44%) in the age range of 45 to 64 years old. Ages 65 and above demonstrated a frequency of approximately 16% to 20%. Furthermore, there was a mild gender preference towards males (56%).
Prerenal azotemia is defined by an increase in BUN and creatinine, secondary to the pathogenic changes in the systemic circulation that cause low renal hypoperfusion. The following 3 mechanisms culminate in water and salt retention in addition to lower urine production.
Hypovolemia stimulates the baroreceptor reflexes on the aortic arch and carotid sinus, which in turn activate the sympathetic nervous branch that leads to renal afferent arteriolar vasoconstriction and the release of renin.
When the afferent arterioles constrict, the glomerular pressure and GFR are reduced. Therefore, renin mediates the conversion of angiotensin I to angiotensin II. The latter stimulates the release of aldosterone, which causes the reabsorption of water and salt in the distal collecting tubule.
Impairment of the vasodilatory response
The normal regulatory mechanisms that maintain perfusion and renal blood flow are compromised by kidney diseases that interrupt blood flow, filtration fraction, and reabsorption.
Note that afferent arteriolar dilation maintains the perfusion of the kidneys, but once systemic blood pressure decreases below 80mmHg, perfusion is disrupted.
Certain medications that affect the release of prostaglandin or angiotensin influence the arterioles and can also have an impact on the vasodilatory response.
Prevention of AKI can be achieved by several methods. Patients suffering from severe hemorrhage, trauma, burns, or other stressful events should be managed carefully with fluids and blood.
When considering imaging with dye contrasts, precaution should be applied especially in the elderly and those with renal diseases, hypovolemia, heart failure, or diabetes. In cases where IV contrasts are necessary, avoidance of NSAIDs is recommended and normal saline or sodium bicarbonate can be used to dilute the contrast.
Since endothelin plays a role in renal damage, drugs that target its receptor have demonstrated success in slowing down and stopping the disease in experiments.
Prerenal azotemia is a dynamic process that develops when renal hypoperfusion and the resultant reduction in glomerular filtration occurs. Moreover, this condition is a predominant cause of acute kidney injury (AKI)   . By definition, prerenal azotemia is associated with an increase in blood urea nitrogen (BUN) and serum creatinine levels.
The body has built-in physiological mechanisms to maintain glomerular filtration rate (GFR). Impairment of these functions leads to volume depletion and prerenal AKI. Additionally, the latter may be caused by other prerenal events such as congestive heart failure, and hepatic diseases. When any of these problems occur in previously healthy kidneys, the body activates adaptive responses to enhance the retention of sodium and water.
Renal damage associated with prerenal conditions may be reversible. However, tubular ischemia as a consequence of severe hypoperfusion is permanent.
Evaluation of the patient involves a history, physical exam, laboratory tests, and, possibly, imaging. Once prerenal azotemia is diagnosed, the etiology should be determined. Furthermore, therapy depends on the underlying cause, especially when replacing fluids and managing the complications.
Prerenal azotemia is a common condition in which nitrogen waste products accumulate in the blood. The kidneys filter blood and remove waste products. However, they lose some of their function when the blood flow in the kidney is decreased or absent. Since the waste products are not filtered properly, they remain in the body.
This condition is seen frequently in the hospital setting. The following includes the causes of azotemia:
The symptoms that emerge are often related to the causes of prerenal azotemia. For example, in cases of dehydration, the symptoms include dry mouth, confusion, little urine output, fast heart rate, fatigue, pale colored skin, and thirst.
In cases of heart failure, there is shortness of breath while laying down, shortness of breath with physical activity, shortness of breath while sleeping, fast breathing, swelling of the legs and a variety of other symptoms.
The medical team will thoroughly assess the patient to diagnose and find the cause of prerenal azotemia. A thorough history, physical exam, laboratory (blood and urine) studies, and possibly imaging are all performed.
Treatment consists of treating the underlying cause of prerenal azotemia and managing the decreased fluid status. Intravenous fluid and blood transfusion may be used to restore the blood volume.
In patients with heart failure, medications to improve the pumping function of the heart are important.
Since sodium, potassium, and other substances may be decreased, their correction is important.