Acute Renal Failure
Acute renal failure (ARF) has no unifying definition. Most criteria include a combination of absolute serum creatinine (Scr) value with change in either Scr or daily urine output.
A popular definition is an increase in Scr of 0.5 mg/dL in patients with previously normal renal function or an increase of more than 1.0 mg/dL in patients with chronic renal disease. Unfortunately, Scr is not a sensitive test; its use can delay recognition of ARF.
Alterations to any of the basic kidney components (vasculature, glomeruli, tubules, and interstitium) can cause ARF. The manifestations of ARF depend on which components are involved.
ARF can be categorized as prerenal (resulting from decreased renal perfusion), intrinsic (resulting from structural damage to the kidney), postrenal (resulting from obstruction of urine flow from the kidney out of the body), and functional (resulting from hemodynamic changes at the glomerular level) .
The presentation can be subtle and depends on the setting. Outpatients often are not in acute distress; hospitalized patients may develop ARF after a catastrophic event.
Symptoms in the outpatient setting include change in urinary habits, weight gain, or flank pain. Clinicians typically notice symptoms of ARF before they are detected by inpatients.
Signs include edema, colored or foamy urine, and, in volume-depleted patients, orthostatic hypotension.
Rapid diagnosis of ARF is essential; delayed recognition can worsen nephrologic injury.
Physical examination should include assessment of the patient's volume and hemodynamic status.
Monitoring changes in urine output can help diagnose the type of ARF. Acute anuria (less than 50 mL urine/24 h) is secondary to complete urinary obstruction or a catastrophic event (e.g., shock). Oliguria (450 mL urine/24 h, or less) suggests prerenal azotemia, functional ARF, or acute intrinsic renal failure. Nonoliguric renal failure (more than 450 mL urine/24 h) usually results from acute intrinsic renal failure or incomplete urinary obstruction.
Urinalysis can help clarify the cause of ARF. High urinary specific gravity, in the absence of glucosuria or mannitol administration, suggests prerenal azotemia or functional ARF. Proteinuria and hematuria suggest glomerular injury. Glucosuria, aminoaciduria, and phosphaturia suggest acute proximal tubular dysfunction. Benign urine sediment suggests prerenal azotemia, functional ARF, or urinary obstruction. Red blood cells and red blood cell casts
indicate glomerular injury. White blood cells and white blood cell casts result from interstitial inflammation (i.e., interstitial nephritis), secondary to an allergic, granulomatous, or infectious process
Simultaneous measurement of plasma and urinary chemistries and calculation of the fractional excretion of sodium (FENa) can help determine the etiology of ARF (). The FENa is calculated as
where UNa = urine sodium, PCr = plasma creatinine, UCr = urine creatinine, and PNa= plasma sodium.
Creatinine and blood urea nitrogen (BUN) are easy to measure, but they are insensitive to rapid changes in glomerular filtration rate (GFR).
Diagnostic procedures include inserting a urinary catheter into the bladder (exclude postrenal obstruction); plain film radiograph (document the presence of two kidneys or renal stones); radioisotope scan, renal angiography, renal ultrasound, or cystoscopy with retrograde pyelography (document obstruction); and renal biopsy.
The primary goal of therapy is to prevent ARF. If ARF develops, the goals are to avoid or minimize further renal insults that would delay recovery and to provide supportive measures until kidney function returns.
PREVENTION OF ACUTE RENAL FAILURE
Nephrotoxin administration (e.g., radiocontrast dye) should be avoided whenever possible.
When patients require contrast dye and are at risk of ARF because of diabetes mellitus, chronic kidney disease, or old age, renal perfusion should be
maximized. For example, hydration with normal saline can be started at 1 mL/kg on the morning of contrast dye administration. Additional preventive strategies include oral acetylcysteine 600 mg twice daily on the day before and the day of contrast dye administration in patients with chronic renal disease, glycemic control in diabetics, and calcium channel blockers in patients with kidney transplants.
Amphotericin B nephrotoxicity can be reduced by slowing the infusion rate to 24 hours or, in at-risk patients, substituting liposomal amphotericin B.
Many other strategies are popular but lack supportive evidence, including mannitol, loop diuretics, dopamine, and fenoldopam.
TREATMENT OF ESTABLISHED ACUTE RENAL FAILURE
No drugs have been found to accelerate ARF recovery. Therefore, patients with established ARF should be supported with nonpharmacologic and pharmacologic approaches through the period of ARF.
Supportive care goals include aggressive fluid management to maintain eu- volemia, tissue perfusion, and electrolyte balance.
Avoidance of nephrotoxins is essential in the management of patients with ARF.
Renal replacement therapy, the most popular nonpharmacologic therapy, is indicated for some patients with ARF (Table 73-3). Intermittent and continuous options have different advantages (and disadvantages) but, after correcting for severity of illness, have similar outcomes. Consequently, hybrid approaches (e.g., sustained low-efficiency dialysis and extended daily dialysis) are being developed to provide the advantages of both. The hybrid approach, however, makes drug dosing difficult to manage. DressAfford mother of the bride or groom dresses with jackets
Intermittent renal replacement therapy (e.g., hemodialysis) has the advantage of widespread availability and the convenience of lasting only 3 to 4 hours. Disadvantages include difficult venous dialysis access in hypotensive patients and hypotension due to rapid removal of large amounts of fluid.
Of the continuous renal replacement therapies (CRRTs), peritoneal dialysis is usually not suitable except for children. CRRT, performed as continuous hemodialysis, continuous hemofiltration, or both, is becoming increasingly popular. CRRT gradually removes solute resulting in better tolerability by critically ill patients. Disadvantages include limited availability, need for 24-hour nursing care, high expense, and incomplete guidelines for drug dosing
Loop diuretics have not been shown to accelerate ARF recovery or improve patient outcome; however, diuretics can facilitate management of fluid overload (Figure 73-1). The most effective diuretics are mannitol and loop diuretics.
Mannitol 20% is typically started at a dose of 12.5 to 25 g intravenously (IV) over 3 to 5 minutes. Disadvantages include IV administration, hyperosmolality risk, and need for monitoring because mannitol can contribute to ARF.
Equipotent doses of loop diuretics (furosemide, bumetanide, torsemide, ethacrynic acid) have similar efficacy. Ethacrynic acid is reserved for sulfa-allergic patients. Continuous infusions of loop diuretics appear to be more effective and to have fewer adverse effects than intermittent boluses. An initial
IV loading dose (equivalent to furosemide 40 to 80 mg) should be administered before starting a continuous infusion (equivalent to furosemide 10 to 20 mg/h).
Strategies are available to overcome diuretic resistance (Table 73-4), a common problem in patients with ARF. Agents from different pharmacologic classes, such as diuretics that work at the distal convoluted tubule (thiazides) or the collecting duct (amiloride, triamterene, spironolactone), may be synergistic when combined with loop diuretics. Metolazone is commonly used because, unlike other thiazides, it produces effective diuresis at GFR less than 20 mL/min.
Enteral (see Chapter 56), but not parenteral, nutrition has been shown to improve patient outcomes.
The most common interventions are management of fluid and electrolyte balance (see Chapter 76).
Hyperkalemia is the most common and serious electrolyte abnormality in ARF. Typically, potassium must be restricted to less than 3 g/day and monitored daily.
Additional electrolytes (and restrictions) that should be monitored include sodium (less than 3 g/day), magnesium, and phosphorus. The choice of treatment for hyperphosphatemia depends on whether the calcium-phosphate product is more than 55 (treat with sevelamer or oral aluminum-containing phosphate-binding antacids) or less than 55 (treat with calcium-containing antacids).
EVALUATION OF THERAPEUTIC OUTCOMES
Close monitoring of patient status is essential .
Drug concentrations should be monitored frequently because of changing volume status, changing renal function, and renal replacement therapies in patients with ARF