In the ED, the goals are to identify patients at risk for acute kidney injury who aren't obviously ill and for those with diagnosed kidney injury to correct metabolic effects, decrease ongoing renal injury, and prevent iatrogenic injury. Determine if kidney injury is prerenal, postrenal, or intrinsic.
Obtain CBC, electrolyte levels including magnesium and phosphorus, and hepatic function tests and blood cultures if clinically appropriate. Obtain urinalysis, urine osmolality, and urine culture.
ECG is often the fastest screening test for hyperkalemia, but sensitivity for a level over 6.5 mmol/L ranges from 14% to 60%.9,10 Although ECGs were read as "abnormal" in 83% of patients in one study, peaked T waves were only seen in 34%, which led to delayed therapy for most patients for whom peaked T waves were not evident11 (see chapter 17, "Fluids and Electrolytes"). Chest radiography helps evaluate for increased volume, effusions, and pneumonia, all of which can result from or precipitate renal failure.
Obtain bedside US to assess urinary bladder volume. A large postvoid bladder residual volume (>125 mL) suggests bladder outlet obstruction for which you would place a urethral catheter. See chapter 92, "Acute Urinary Retention" for further discussion. Anuria is 100 mL urine per day and can be present with prerenal, postrenal, or intrinsic kidney disease. Alternating oliguria and polyuria is virtually pathognomonic of obstruction.
Creatinine and Glomerular Filtration Rate
Creatinine (Cr) is the mainstay for measuring renal function; it is a breakdown product of the skeletal muscle protein creatine, and its level is thus linked to muscle mass. In patients with no renal function (GFR = 0), serum Cr level increases 1 to 3 milligrams/dL a day. Lesser increases in Cr indicate residual renal function, whereas faster increases suggest rhabdomyolysis. Elevation of serum Cr may take 48 hours to accumulate after onset of decreased function, and a patient with a very low baseline Cr level can lose more than half of the functioning nephrons before serum Cr elevates to an abnormal level.
Cr clearance is used to estimate GFR, and although it is not perfect, it is a useful measure in the ED. Patients with lower muscle mass (e.g., older patients and women) have lower actual GFRs for any given Cr level. Glomerulonephritis increases tubular secretion of Cr, but trimethoprim, cimetidine, and salicylates decrease tubular secretion of Cr, thus altering the Cr level independently of the GFR.
GFR calculations are provided online, for hand-held devices, and in electronic medical record systems, and there are several formulas for GFR calculation. Normal kidney function is a GFR >90 mL/min/1.73 m2, where 1.73 m2 is used as the average body surface area. Stages of kidney disease are characterized by GFR: stage 1, GFR 90 mL/min/1.73 m2; stage 2, GFR 60 to 89 mL/min/1.73 m2; stage 3, GFR 30 to 59 mL/min/1.73 m2; stage 4, GFR 15 to 29 mL/min/1.73 m2; and stage 5, GFR <15 mL/min/1.73 m2 (dialysis or transplant needed).
The ratio of BUN to Cr can suggest hypovolemia because of differences in the way each is handled in the nephron. Both substances are passively filtered at the glomerulus, but whereas Cr remains within the tubule, the renal tubule is highly permeable to urea, which is passively reabsorbed with sodium. Therefore, in the setting of avid sodium retention, urea clearance is as low as 30% of GFR, whereas in the setting of adequate volume and sodium, urea clearance can increase to 70% to 100% of GFR. Thus, if the patient has normal concentrating ability, in the setting of prerenal failure, the serum ratio of BUN to Cr is typically >10. BUN level is depressed in patients with malnutrition and hepatic synthetic dysfunction and can be increased in the setting of protein loading, GI hemorrhage, or trauma. Although an elevated ratio of BUN to Cr had been assumed to suggest more reversible prerenal physiology, recent evidence has called that into question.12
Fractional Excretion of Sodium
The fractional excretion of sodium (FeNa = UNa/PNa ÷ UCr/PCr, where U = urine and P = plasma) is another indicator that is commonly used to identify hypovolemia, but it has important limitations. For example, in the setting of intrinsic renal failure in which tubular concentrating capacity is retained, as in the case of glomerulonephritis, the fractional excretion of sodium may be depressed if there is concomitant volume depletion. With tubular injury such as ischemic acute tubular necrosis, the loss of concentrating ability results in a dilute urine, with a fractional excretion of sodium >1%, even if the patient is volume depleted (Table 88-4).
TABLE 88-4Laboratory Findings in Conditions That Cause Acute Renal Failure |Favorite Table|Download (.pdf) TABLE 88-4 Laboratory Findings in Conditions That Cause Acute Renal Failure
|Category ||Dipstick Test ||Sediment Analysis ||Urine Osmolality (mOsm/kg) ||Fractional Excretion of Sodium (%) |
|Prerenal ||Trace to no proteinuria, SG >1.015 ||A few hyaline casts possible ||>500 ||<1 |
|Renal || || || || |
| Ischemia ||Mild to moderate proteinuria ||Pigmented granular casts, renal tubular epithelial cells ||<350 ||>1 |
| Nephrotoxins ||Mild to moderate proteinuria ||Pigmented granular casts ||<350 ||>1 |
| Acute interstitial nephritis ||Mild to moderate proteinuria; hemoglobin, leukocytes ||White cells, eosinophils, casts, red cells ||<350 ||>1 |
| Acute glomerulonephritis ||Moderate to severe proteinuria; hemoglobin ||Red cells and red cell casts; red cells can be dysmorphic ||>500 ||Depends on volume status |
|Postrenal ||Trace to no proteinuria; hemoglobin and leukocytes possible ||Crystals, red cells, and white cells possible ||<350 ||>1 |
Microscopic examination of urine is useful in establishing the differential diagnosis. In acute glomerulonephritis, red blood cells enter the filtrate at the glomerulus and, on microscopic urinalysis, appear as casts and dysmorphic cells due to the increased tonicity of the renal medulla. In acute tubular necrosis, the tubular epithelium breaks down and allows protein to leak into the filtrate, and tubular epithelial cells may be seen in the sediment.
Hyaline casts are common in prerenal failure and can be a normal finding, but pigmented granular casts are common with ischemic or toxic tubular injury. Brown granular casts are common in hemoglobinuria or myoglobinuria. The finding of hemoglobin on urine dipstick analysis with no red cells on microscopy suggests myoglobinuria. Some crystals may be present in a normal urinalysis. Crystals are best seen with polarized light microscopy. Red cell casts and proteinuria suggest glomerulonephritis or an underlying autoimmune disease.
Renal US is the test of choice for urologic imaging in the setting of acute kidney injury. It has approximately 90% sensitivity and specificity for detecting hydronephrosis due to mechanical obstruction. Figure 88-2 contrasts normal kidney US findings with US findings indicating hydronephrosis. If renal US detects hydronephrosis, a secondary imaging study to define the location of obstruction may be required. Bipolar renal length is easy to assess by US, and kidney dimension of <9 cm suggests chronic renal failure. Renal parenchyma should be isoechoic or hypoechoic compared with that of the liver and spleen. Hyperechogenicity indicates diffuse parenchymal disease. Color flow Doppler US allows assessment of renal perfusion and can allow diagnosis of large-vessel causes of renal failure. Resistive index is the ratio of the difference between systolic and diastolic flow to systolic flow [(Vmax – Vmin)/Vmax] as measured by color flow Doppler. In the vasoconstrictive phase of ischemic renal failure, in which there may be no diastolic flow, the ratio may be as high as 1.0. The normal ratio is <0.7.
US of normal kidney and kidney showing hydronephrosis. A. Normal kidney, capsule margin at arrows. B. Hydronephrosis as would be expected in obstructive uropathy; the dilated kidney fills the majority of the screen, capsule at arrows. [Image used with permission of Michael B. Stone, MD, RDMS.]
In intermittent or partial obstruction, hydronephrosis may not be present, and it may even be absent in complete obstruction in the setting of retroperitoneal fibrosis. Furthermore, functional dilatation can occur in the setting of chronic reflux.
Noncontrast CT has sensitivity for hydronephrosis that is equivalent to that of US and has the added advantage of demonstrating the site and often the cause of obstruction. If functional obstruction is a consideration in the presence of a dilated GU tract, radionuclide scans and magnetic resonance urographs before and after administration of diuretics can be obtained.