Prerenal azotemia

Azotemia (prerenal) Urine Concentrated urine odor... 

Assess patient for prerenal azotemia and hold diuretic therapy o Fluid resuscitate if evidence of volume depletion... 

Monitoring changes in UOP can help diagnose the cause of ARF. Acute anuria (less than 50 mL urine/day) is secondary to complete urinary obstruction or a catastrophic event (e.g., shock). Oliguria (400 to 500 mL urine/day) suggests prerenal azotemia. Nonoliguric renal failure (more... 

Common laboratory tests are used to classify the cause of ARF. Functional ARF, which is not included in this table, would have laboratory values similar to those seen in prerenal azotemia. However, the urine osmolality-to-plasma osmolality ratios may not exceed 1.5, depending on the circulating levels of antidiuretic hormone. The laboratory results listed under acute intrinsic renal failure are those seen in acute tubular necrosis, the most common cause of acute intrinsic renal failure. 

Hypoxic states Cardiovascular collapse (shock), acute CHF, acute Ml, and other conditions characterized by hypoxemia have been associated with lactic acidosis and may cause prerenal azotemia. If such events occur, discontinue metformin. Surgicai procedures Temporarily suspend metformin for surgical procedures (unless minor and not associated with restricted intake of food and fluids). Do not restart until the patient s oral intake has resumed and renal function is normal. 

Toxicity Aminoglycosides are associated with significant nephrotoxicity or ototoxicity. These agents are excreted primarily by glomerular filtration thus, the serum half-life will be prolonged and significant accumulation will occur in patients with impaired renal function. Toxicity may develop even with conventional doses, particularly in prerenal azotemia or impaired renal function. 

The risk of severe neurotoxic reactions is sharply increased in patients with impaired renal function or prerenal azotemia. These include disturbances of vestibular and cochlear function, optic nerve dysfunction, peripheral neuritis, arachnoiditis, and encephalopathy. The incidence of clinically detectable, irreversible vestibular damage is particularly high in patients treated with streptomycin. 

Lactic acidosis occurs rarely but is a fatal complication in 50% of cases. Lacfic acidosis is characterized by an increase in blood lactate levels (greater than 5 mmol/L), a decrease in blood pH, and electrolyte disturbances. Signs and symptoms of lacf ic acidosis include unexplained hypervenf ilaf ion, myalgia, malaise, and somnolence, which may advance to cardiovascular collapse (shock), acute CHF, acute Ml, and prerenal azotemia. 

Renal damage is the most significant toxic reaction. Renal impairment occurs in nearly all patients treated with clinically significant doses of amphotericin. The degree of azotemia is variable and often stabilizes during therapy, but can be serious enough to necessitate dialysis. A reversible component is associated with decreased renal perfusion and represents a form of prerenal renal failure. An irreversible component results from renal tubular injury and subsequent dysfunction. 

Patients with nephrotic syndrome can develop acute renal failure as a consequence of intravascular hypovolemia and/or sepsis with subsequent prerenal azotemia or acute tubular necrosis. Renal hypoperfusion in these patients can be potentiated by the administration of diuretics, inhibitors of angiotensin-converting... 

FE of urea has been recently shown to be more useful than the FE of sodium in distinguishing between prerenal and renal azotemia in humans (Carvounis et al. 2002) and thus may also be useful in making this distinction in animal models. Changes in the FE of urea also reflect changes in urine flow rates (in general, these values move parallel to each other) and can be used as an estimate of this parameter (Finco 1997). The methods used to detect urea in urine are the same as those used in serum (Newmann and Price 1999). 

The findings are entirely compatible with prerenal azotemia associated with diminished fluid intake during a drug-induced psychosis (81). 

A 77-year-old woman who had taken lithium for 10 years developed delirium, hypernatremia, prerenal azotemia, and a serum lithium concentration of 1.4 mmol/1 her condition was attributed to dehydration related to partial nephrogenic diabetes insipidus (381). 

Laboratory Test Prerenal Azotemia Acute Intrinsic Renal Faihiie Postrenal Obstruction... 

A wide range of aldesleukin-induced adverse effects is associated with the capillary leak syndrome, which is characterized by an increase in vascular permeability with subsequent leakage of fluids and proteins into the extravascular space (4). This results in a third-space clinical syndrome, generalized or peripheral edema, weight gain, cardiovascular and pulmonary comphcations with hypotension, pericardial, and pleural effusions, ascites, oliguria, and prerenal azotemia. Symptoms usually resolve in a few days after aldesleukin withdrawal. Studies on the mechanism have raised a number of hypotheses, such as damage to the endothehal cells, release of secondary cytokines, and activation of the complement cascade (15). 

Clinically, volume depletion manifests itself in one of two patterns related to alterations in serum chemistry values either there is an elevation in the blood urea nitrogen (BUN) with no increase in serum creatinine, or both are elevated but the BUN proportionately more so than the creatinine. This phenomenon, which has been termed prerenal azotemia", results from reduced flow through the nephron and increased contact time between the tubular contents and the epithehum of the collecting duct. Urea is a small, non-charged moiety, which is transported much more easily than is creatinine (a much larger, usually charged molecule). Ordinarily, prerenal azotemia and reductions in GFR... 

OKT3, an immunosuppressive monoclonal antibody, can induce systemic vascular changes (leaky syndrome) and prerenal azotemia, presumably by stimulating the release of cytokines (e.g., tumor necrosis factor). These effects are seen more often in poorly hydrated patients. There is also evidence that OKT3 may induce a direct tubular toxicity, since significant numbers of patients developing renal insufficiency also exhibit enzymuria. 

Diuretic drugs often cause a mild reduction of the plasma potassium concentration hyponatremia may be observed. Hypercalcemia may occur with hemoconcentration, but occasionally the free-ionized and the protein-bound fraction is increased. Thiazides cause hyperglycemia and reduce glucose tolerance, especially in diabetics. Thiazides may cause prerenal azotemia with hyperuricemia as a result of decreased renal blood flow and GFR as a result of reduced blood volume. Thiazides, like other diuretics, by causing hemoconcentration increase the plasma concentration of lipids. Many thiazides induce microsomal enzymes and thus affect lipoprotein concentrations. 

Smaller vessels may be obstructed with cholesterol emboli, vascular lesions, or platelet plugs, all of which will present as isolated decreased perfusion of the glomeruli. The serum creatinine frequently is increased since the lesions are usually diffuse. However, the urinalysis most commonly will be normal since the kidney itself is not ischemic and the glomeruli are not involved. The urinary indices suggest prerenal azotemia (i.e., a low urine sodium concentration and a low fractional excretion of sodium) in the absence of systemic hypotension or a decrease in effective blood volume. The urine volume may or may not be diminished. However, the onset of oliguria sec-... 

Orthostatic hypotension Volume depletion Prerenal azotemia... 

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