Fractional excretion of sodium

The percentage of filtered Na+ load excreted in the final urine is a measure of renal function, as is also the clearance of Na+ expresses as a percentage of GFR FEn, (%) = x V) / x GFR) x 100. 

Theoretically, if drug-induced damage of the medullopapillary portion of the nephron, decreases in reabsorption of Na+ and water lead to increase in FE a- 

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Obtain blood urea nitrogen (BUN), serum creatinine (SCr), calculated fractional excretion of sodium (FeNa), serum electrolytes, and arterial blood gases. 

While some clinical and laboratory findings assist in the general diagnosis of ARF, others are used to differentiate between prerenal, intrinsic, and postrenal ARF. For example, patients with prerenal ARF typically demonstrate enhanced sodium reabsorption, which is reflected by a low urine sodium concentration and a low fractional excretion of sodium. Urine is typically more concentrated with prerenal ARF and there is a higher urine osmolality and urine plasma creatinine ratio compared to intrinsic and postrenal ARF. 

Sodium and water balance can be maintained despite wide variations in intake with normal kidney function. The fractional excretion of sodium (FENa) is approximately 1% to 3%... 

ARF, acute renal failure BUN, blood urea nitrogen FEft a, fractional excretion of sodium Sa, serum creatinine RBC, red blood cell WBC, white blood cell. 

Simultaneous measurement of urine and serum chemistries and calculation of the fractional excretion of sodium (FENa) can help determine the etiology of ARF (see Table 75-2). The FENa is calculated as ... 

Calculate measured creatinine clearance Calculate fractional excretion of sodium Plans for renal replacement... 

Serum sodium concentration is generally maintained by an increase in fractional excretion of sodium, resulting in a volume-expanded state. The most common manifestation of increased intravascular volume is systemic hypertension. 

In general, the sediment in the urine is normal. Proteinuria or erythrocyturia are not characteristic of hepatorenal syndrome. The excretion of sodium in the urine is lower than 10 mmol/day, with a fractional excretion of sodium of < 1%. For this reason, there is likewise increased renal retention of water. The urine osmolality is greater than the plasma osmolality, which results in a quotient of >1.3. With increasing severity of hepatorenal syndrome and transition of the penultimate phase, the urine becomes iso-osmotic with an osmolality quotient of 1 or < 1. (19, 43,52,53, 60) (s. tab. 17.4)... 

A 43-year-old woman with rheumatoid arthritis developed dizziness having taken celecoxib 200 mg/day for 2 weeks. At the start of treatment she had normal renal function (104). Her serum creatinine was 670 pmol/l (7.4 mg/dl) and blood urea nitrogen 30 mmol/1 (90 mg/dl). Creatinine clearance was 16 ml/minute. Urinalysis was normal and casts were not present. Urinary chemical analysis showed a sodium concentration of 18 mmol/1, a fractional excretion of sodium of 0.3, and a renal failure index of 0.493, consistent with prerenal acute renal insufficiency. Celecoxib was withdrawn. Although her renal function then improved, her serum creatinine was still abnormal (4.7 mg/dl) 1 month later. 

Corwin HL, Schreiber MJ, Fang LS. Low fractional excretion of sodium. Occurrence with hemoglobinuric and myoglobinuric-induced acute renal failure. Arch Intern Med 1984 144 981-982. 

Renal toxicity has been attributed to sequelae from the development of the capillary leak syndrome. Vascular leak resulted in significant extravascular fluid accumulation (ascites, pleural effusions, peripheral edema) and weight gains of as much as 17 kg in 3 weeks [11]. As in sepsis syndrome, hypotension, oliguria and reduced fractional excretion of sodium accompanied the capillary leak. 

FENa fractional excretion of sodium lAKI ischemic acute kidney injury... 

Renal hypoperfusion without systemic hypotension most commonly results from bilateral renal artery occlusion, or unilateral occlusion in a patient with a single functioning kidney. In these conditions, the sodium-retentive hormones are activated by the decline in renal parenchymal perfusion. However, systemic arterial blood pressure is usually elevated, leading to an inhibition of antidiuretic hormone release. Consequently, the urinary indices will reflect enhanced sodium reabsorption (i.e., a low fractional excretion of sodium), but the urinary solutes may not be maximally concentrated. 

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-... 

Vigilant monitoring of patients with ARF is essential, particularly in those who are critically ill (Table 42-8). Once the laboratory-based tests (urinalysis, fractional excretion of sodium calculations, etc.) have been conducted to diagnose the cause of ARF, they usually do not have to be repeated. In established ARF, daily measurements... 

In persons with normal kidney function, sodium balance is maintained at a sodium intake of 120 to 150 mEq/day. The fractional excretion of sodium (FENa) is approximately 1% to 3%. Water balance is also maintained, with a normal range of urinary osmolality of 50 to 1200 mOsm/L. In patients with severe CKD (Stages 4 and 5), sodium balance is achieved, but results in a volume-expanded state. FENa may increase to as much as 10% to 20%, possibly due to increased concentrations of atrial natriuretic peptide. An osmotic diuresis occurs with an increase in FENa leading to obligatory water losses and impairment in the kidney s ability to dilute or concentrate urine (urinary osmolality is often fixed at that of plasma or approximately 300 mOsm/L). Nocturia is present relatively early in the course of CKD (Stage 3) secondary to the defect in urinary concentrating ability. Total renal sodium excretion decreases despite an increase in sodium excretion by remaining nephrons. Volume overload with pulmonary edema can result, but the most common manifestation of increased intravascular volume is systemic hypertension. ... 

Ca X P calcium phosphorus product serum calcium multiplied by serum phosphorus CKD chronic kidney disease CPK creatine phosphokinase DEO deferoxamine EPO erythropoietin ESKD end-stage kidney disease ESRD end-stage renal disease FEk fractional excretion of potassium FEn fractional excretion of sodium GFR glomerular filtration rate Hct hematocrit HDL high-density fipoprotein Hgb hemoglobin... 

Loop diuretics are the most potent diuretics, as evidenced by the fact that they increase peak fractional excretion of sodium (EeNa) to 20% to 25%. Thiazide- and potassium-sparing diuretics are less potent and increase peak FeNa to 3% to 5% and 1% to 2%, respectively. Although a large portion of the filtered sodium is reabsorbed in the proximal nephron, the efficacy of proximal-acting diuretics such as acetazolamide are limited by reabsorption of the excess fluid and sodium in the loop of Henle. 

After 20-30 min for equilibration, perfusate samples are collected to coincide with the start of urine collections at 5 to 15 min intervals. The urine volume depends on both perfusion pressure and oncotic pressure [102]. Perfusion pressure and flow are monitored continuously. Renal function is assessed from renal vascular resistance, urine flow, the ratio of l C-inulin in urine to plasma (U/Pinulin), glomerular filtration rate (GFR as inulin clearance UV/P) and the fractional excretion of sodium (FEjvja) potassium (FEj ). Inulin measurement can also be performed chemically. In some situations GFR is misleading as an index of "good function" in this model. For example, in the absence of an oncotic agent, a "reasonable" GFR is over 1 ml/ g/ min, however U/Pinulin is rarely more than 2, FENa is over 0.1 and histological examination shows extensive proximal necrosis within 20-40 min of initiating perfusion. It appears that in this situation the massive... 

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