Acute Renal Failure

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Chapter 42 Acute Renal Failure

Dinkar Kaw, MD , Joseph I. Shapiro, MD

1 How is acute renal failure (ARF) diagnosed?

ARF is a rapid loss of glomerular filtration rate (GFR) over a period of hours to a few days. This is usually determined by a sudden rise in plasma creatinine and blood urea nitrogen (BUN) levels. Until the patient achieves a steady state, the level of renal function cannot be assessed by the serum creatinine concentration. If a patient with previously normal renal function suddenly loses all renal function, serum creatinine will rise by only 1 to 2 mg/dL/day. However, patients with muscle wasting who make less creatinine may show smaller increases even with complete cessation of GFR. BUN is another indicator of decreasing glomerular filtration. Although a dramatic rise in BUN compared with creatinine may suggest a prerenal or obstructive (postrenal) cause, one must also consider the possibility that creatinine production by the patient is limited. Measurement of timed creatinine and urea excretion rates allowing for calculation of creatinine and urea clearance is sometimes indicated to clarify this point. In critically ill patients, decrease in urine output can be an indication of decreasing GFR. Increase in serum creatinine or decrease in urine output can be used to assess the risk, injury, and failure stages of ARF.

2 What features distinguish ARF from chronic renal failure?

When a patient is seen some time after the onset of ARF, this distinction may not be easy. Chronic renal failure is more likely than ARF to be associated with anemia, hypocalcemia, normal urine output, and small shrunken kidneys on ultrasound examination. A kidney biopsy may be warranted if the kidneys are of normal size. It has been reported that chronic, but not acute, renal failure may be associated with an increase in the serum osmolal gap (i.e., the difference between measured and calculated serum osmolality).

3 How is ARF classified?

The main categories are prerenal, intrarenal or parenchymal, and postrenal or obstructive (Table 42-1).

Table 42-1 Differential diagnosis of acute renal failure

Prerenal Postrenal Parenchymal
Dehydration Ureter Glomerular
Impaired cardiac function Bladder Interstitial
Vasodilation Urethra Allergic interstitial nephritis
Renal vascular obstruction   Vascular
Hepatorenal syndrome   ATN

ATN, Acute tubular necrosis.

4 How does examination of the urine help in the differential diagnosis of ARF?

Laboratory evaluation begins with careful examination of the urine. Concentrated urine points more to prerenal causes, whereas isotonic urine suggests parenchymal or obstructive causes. Typically, the urine sediment of patients with prerenal azotemia demonstrates occasional hyaline casts or finely granular casts. In contrast, the presence of renal tubular epithelial cells with muddy and granular casts strongly suggests acute tubular necrosis (ATN), microhematuria and red blood cell casts suggest glomerulonephritis, and white cell casts containing eosinophils suggest acute interstitial nephritis. Benign urine sediment is quite compatible with urinary obstruction.

5 What are the implications of urinary electrolytes in the differential diagnosis of ARF?

The determination of urine electrolyte and creatinine concentrations may be helpful in the differential diagnosis of ARF. When used with serum values, urinary diagnostic indexes can be generated. Understanding the concepts behind the interpretation of these indexes is easier and better than trying to remember specific numbers. Quite simply, if the tubule is working well in the setting of decreased GFR, tubular reabsorption of sodium and water is avid, and the relative clearance of sodium to creatinine is low. Conversely, if the tubule is injured and cannot reabsorb sodium well, the relative clearance of sodium to creatinine is not low. Therefore, with prerenal azotemia, the ratio of the clearance of sodium to the clearance of creatinine, which is also called the fractional excretion of sodium (FENa) (FENa = [Urinary sodium]/[Urinary creatinine] × [Plasma creatinine]/[Plasma sodium] × 100), is typically less than 1.0, whereas with parenchymal or obstructive causes of ARF, the FENa is generally greater than 2.0 (Fig. 42-1).

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Figure 42-1 FENa, which measures the percentage of filtered sodium that is excreted in the urine, helps to differentiate between prerenal causes of renal failure and both parenchymal renal diseases (e.g., ATN, allergic interstitial nephritis) and urinary obstruction. Under specific conditions, the predictive value of a low FENa (to diagnose prerenal azotemia) or a high FENa (to exclude prerenal azotemia) is limited.

The FENa test is much less useful when patients do not have oliguria. In this setting, the specificity of a low FENa for prerenal azotemia is markedly diminished. In addition to nonoliguria, several causes of ATN, specifically dye-induced ATN or ATN associated with hemolysis or rhabdomyolysis, may typically be associated with a low FENa. Patients who have prerenal azotemia but have either persistent diuretic effect, chronic tubulointerstitial injury, or bicarbonaturia may have a relatively high FENa. In the last case, the fractional excretion of chloride, which is calculated in an analogous way, will be appropriately low (< 1%). Finally, the early stages of ARF from glomerulonephritis, transplant allograft rejection, or urinary obstruction may be associated with a low FENa.

6 What is the pathophysiology of ATN?

Renal ischemia, toxic injury to the kidney, or a combination of these insults can cause prolonged loss of renal function. Physiologically, decreased GFR must result from an alteration in glomerular hemodynamic factors, such as a decrease in the effective surface area or permeability of the glomerulus (Kf), a decrease in glomerular blood flow, or an abnormality in tubular integrity, including obstruction of tubular flow by cellular debris or back leak of ultrafiltrate through a porous tubule. In fact, each of these pathogenic features can be shown to be operant in some experimental models of ARF.

7 How does ATN evolve?

The major mechanism by which renal failure is induced may be different from the primary mechanism by which it is maintained. For example, in ischemic ARF, decreases in renal and glomerular blood flow may cause the initial loss of renal function. However, tubular necrosis, with its attendant obstructing debris and back leak of ultrafiltrate, maintains the low GFR. The tubular mechanisms are usually important in the maintenance of ARF from most causes seen clinically. Therefore pharmacologic efforts to improve renal blood flow are not, by themselves, generally effective in shortening the duration of ARF. Interestingly, modern ATN appears to recover much less quickly than when the syndrome was first described. This slow recovery may be related to repeated bouts of renal ischemia, which can be attributed to altered renal vasodilation related to the initial ATN insult. Therefore even mild degrees of hypotension should be avoided when treating patients with ATN.

8 How is ARF prevented?

ATN usually occurs after surgery or preexisting dehydration. In these settings, nephrotoxic drugs, such as radiocontrast dye, aminoglycosides, amphotericin B, nonsteroidal antiinflammatory agents, and some cancer chemotherapeutic agents (e.g., cisplatin, methotrexate), are far more potent in causing ARF. Optimizing volume status and establishing a relatively high rate of urine flow minimize the risk of ARF. In specific situations, such as administration of radiocontrast dye or cisplatin and relatively high-risk surgery (e.g., open heart or biliary tract surgery), mannitol (12.5-25 g administered as an intravenous [IV] infusion) was thought to be a useful adjunct in preventing ARF. However, subsequent studies showed that mannitol actually potentiates ARF after the administration of radiocontrast. Some later studies suggest that administration of N-acetylcysteine or sodium bicarbonate infusions may prevent contrast nephropathy in high-risk patients, but the most accepted prophylaxis consists of isosmotic contrast media and cautious hydration before contrast administration.

9 What are the treatment options in ATN?

ATN is best treated, as previously discussed, by prevention. Because nonoliguric ATN is associated with lower mortality and morbidity rates than oliguric ATN, some excitement exists about the administration of high-dose loop diuretics (1-3 g/24 h given as an IV infusion or as repeated boluses) in concert with renal doses of dopamine (1-3 mcg/kg/min). This therapy, which converts oliguric ATN in some patients to a nonoliguric state, certainly facilitates management of volume and nutritional status. However, it is not clear whether these pharmacologic interventions actually improve the prognosis. Optimizations of fluid status and avoidance of and/or therapy for electrolyte disorders are the mainstays of conservative management of ARF.

10 Which critical electrolyte disorders accompany ARF?

The most common electrolyte disorders that accompany ARF include hyperkalemia, hypermagnesemia, hyperphosphatemia, hypocalcemia, and acidosis (Table 42-2). Of these disorders, hyperkalemia is the most common and probably the one that is usually most serious.

Table 42-2 Electrolyte disturbances in acute renal failure

image

Hyperkalemia most commonly occurs with oliguric ATN or urinary obstruction. It is truly a medical emergency. A serum potassium level above 6.0 mandates electrocardiography, searching for peaked T waves, diminished P-wave amplitude, or prolonged QRS complex. Any of these findings warrants the use of immediate measures to correct hyperkalemia.

11 What immediate measures are used to treat hyperkalemia?

The quickest-acting parenteral therapy is calcium, administered as chloride or gluconate salts. This therapy does not affect the serum potassium level but does antagonize the effects of hyperkalemia on the membrane potential of the heart and prevents, or reverses, the cardiac effects of hyperkalemia. Another rapidly effective approach is the administration of insulin, which drives potassium into cells and lowers the serum potassium level. In patients who have a normal serum glucose level, insulin (10 units IV) is generally administered with dextrose (one ampule of 50% dextrose in water [D50W] or an infusion of D10W). The effects of insulin last somewhat longer than those of calcium and can be prolonged by a constant infusion of insulin, usually administered with glucose to prevent hypoglycemia. Bicarbonate may also be used to raise arterial pH and to shift potassium into cells. Complications include potentially adverse hemodynamic effects of IV bicarbonate and volume expansion from sodium load.

12 What is the uremic syndrome?

The uremic syndrome is a symptom complex associated with renal failure. It may occur with chronic and acute renal failure and involves virtually all organs of the body. Major manifestations are nausea and vomiting, pruritus, bleeding disorder, encephalopathy, and pericarditis. The syndrome generally mandates initiation of nonconservative therapy for ARF such as hemodialysis, peritoneal dialysis, or continuous arteriovenous hemofiltration. The pathogenesis of the uremic syndrome is still poorly understood; however, neither urea nor creatinine produces any of the known manifestations of uremia.

13 What are the indications for nonconservative therapy for ARF?

Indications for nonconservative therapy, such as dialysis, include uremic signs or symptoms, fluid overload, and/or electrolyte abnormalities that are refractory to conservative management. It has become the standard of care to provide nonconservative therapy when the BUN level exceeds 100 mg/dL or the serum creatinine exceeds 10 mg/dL, especially in the setting of oliguric ATN. These latter guidelines are not absolute and must be interpreted in the light of other clinical features.

14 What are the options for nonconservative therapy of ARF?

The three main options for nonconservative therapy of ARF are hemodialysis, peritoneal dialysis, and continuous renal replacement therapy (CRRT). Each option has advantages and disadvantages (Box 42-1), and, of course, variations exist of each of these modalities.

Box 42-1 Dialysis options in the treatment of acute renal failure

Intermittent Hemodialysis

Advantages

Efficient and intensive dialysis technique

Dialysis staff required for shorter period of time

Disadvantages

May cause hemodynamic instability

Relative need for anticoagulation

Potential for disequilibrium

Need for expensive machinery

Need for personnel to perform hemodialysis

Requirements

Venous access, anticoagulation, skilled staff, and expensive equipment

Peritoneal Dialysis

Advantages

Slow, gentle form of dialysis

Provides better hemodynamic stability than intermittent hemodialysis

No need for anticoagulation

Disadvantages

Electrolyte disorders and volume corrected slowly

Many nursing units unfamiliar with methodology

Risk for leaks and peritoneal infection

Requirements

Peritoneal catheter, sterile peritoneal dialysis solutions, and trained staff

CRRT

Advantages

Slow, continuous form of dialysis

Provides better hemodynamic stability than intermittent hemodialysis

Efficient solute removal and electrolyte balance

Round-the-clock maintenance of volume status

Nutrition and medications given while volume status is maintained

Disadvantages

Patient immobilization

Systemic anticoagulation

Nursing staff intensive

Expensive machinery

Requirements

Round-the-clock skilled nursing staff, vascular access, anticoagulation, and complex equipment

Hemodialysis involves the pumping of blood through an artificial kidney that removes solutes primarily by dialysis along a concentration gradient; water is removed by ultrafiltration driven by a pressure gradient. Central venous access, anticoagulation, a skilled technician, and expensive equipment are mandatory for this process.

Peritoneal dialysis involves the repetitive instillation and removal of fluid into and from the peritoneal cavity, respectively. Solute removal again results primarily by dialysis along a concentration gradient, and fluid removal occurs by ultrafiltration driven by an osmotic pressure gradient. Although this method is less efficient and less rapid than hemodialysis, no central venous access, anticoagulation, skilled technician, or expensive equipment is necessary.

The amount of dialysis that needs to be prescribed is still somewhat controversial. Extrapolations from chronic renal failure prescription guidelines may not be sufficient to prevent the signs and symptoms of uremia in patients with ARF. Earlier study suggested that a more intensive regimen of hemodialysis may actually improve survival in this setting. However, later studies did not confirm the benefits of intensive dialysis treatment.

15 What is CRRT?

CRRT includes a number of treatments characterized by slow, gradual, continuous removal of fluid and electrolytes. Continuous venovenous hemodialysis (CVVHD) is the most widely used method. It involves solute removal by convection and fluid removal by hydrostatic pressure across high-flux membrane. Like conventional dialysis, CVVHD requires central venous access, anticoagulation, skilled staff, and complex equipment. Continuous arteriovenous hemofiltration and dialysis is a technically simple but less-efficient form of CRRT. Although each of these techniques has advantages and disadvantages, in general, the expertise of the professionals working at the center is probably the most important factor. Because of the difficulty in orienting nursing staff to continuous dialysis methods, slow low-efficiency daily dialysis has been developed that provides dialysis over approximately one half of the hours of the day. Of interest, the biocompatibility of the hemodialysis membrane appears to be an important factor in determining outcome, whereas the intensity of the dialysis prescription (i.e., blood flow, dialysate flow) does not appear to be an important factor in determining patient outcomes.

Key Points Acute Renal Failureimage

1. Serum creatinine concentration may be insensitive to the loss of renal function.

2. ARF due to acute tubular necrosis may be initiated by one mechanism and maintained by another different mechanism.

3. Results elicited by measures to prevent ATN are far superior to those yielded by efforts to provide treatment.

4. Urinalysis and urine electrolyte and creatinine estimation can provide important information about the cause of ARF.

5. Hyperkalemia is an important life-threatening complication of ARF requiring urgent management.

6. Renal replacement therapy, in the form of dialysis, may be required for correction of volume status, electrolyte imbalance, and acidosis, if conservative therapy fails.

Bibliography

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