++
Impairment of the kidney's ability to regulate urine volume and composition produces problems with hemostasis. This is usually associated with a decreased glomerular filtration rate (GFR).
++
The etiology of acute renal failure may be categorized on the basis of the type of renal injury. It may be prerenal (decreased perfusion of the kidney), intrarenal (damage to the actual nephron), or postrenal (downstream obstruction of the urinary tract; Table 87-1).11
++
Prerenal patients have decreased perfusion of the kidney. Dehydration is usually the cause and may be secondary to vomiting, diarrhea, diabetic ketoacidosis, or decreased intravascular volumes associated with nephrotic syndrome, burns, or shock.
++
Intrarenal failure results from direct, intrinsic damage to the nephrons caused by glomerulonephritis (hematuria, proteinuria, edema, and hypertension), HUS, nephrotoxic exposures, crush injuries, sepsis, or disseminated intravascular coagulation.
++
Obstruction leads to postrenal failure and may be accompanied by symptoms, although blockage may be insidious and without symptoms. Causes of postrenal obstruction include posterior urethral valves, ureteropelvic junction abnormalities, renal stones, and trauma. Abdominal pain and an abdominal mass due to hydronephrosis may be noted.
++
The history may reflect the underlying disease and the category of renal failure. The physical examination will help determine the mechanism. It is essential to evaluate for hypovolemia, volume overload, hypertension, or obstruction.
++
Patients may have oliguria with urine output less than 1 mL/kg/h or be nonoliguric with an output excessive for the volume status. Azotemia may be noted.
++
Laboratory evaluation should include electrolytes, studies of renal function, urinalysis and a search for the underlying pathology. The creatinine clearance is a good measure of GFR and is useful in initial assessment and ongoing monitoring. A 24-hour urine is normally needed.
++
A rapid approximation can be made using the formula:
++
P = plasma concentration of creatinine (mg/dL);
++
Normal values are the following:
++
Newborn and premature: 40 to 65 mL/min/1.73 m2
Normal child: Female, 109 mL/min/1.73 m2 or male, 124 mL/min/1.73 m2
Adult: Female, 95 mL/min/1.73 m2 or male, 105 mL/min/1.73 m2
++
A single-voided urine in adults has been of some use in assessing renal function. In patients with stable renal function, a spot protein:creatinine ratio of >3.0 represents nephrotic range proteinuria (a ratio of <0.2 is normal). The fractional excretion of sodium is useful in differentiating between prerenal and acute tubular disease. Ultrasonography is also important in the evaluation of these patients. Combining data from serum, urine, and ultrasonography helps differentiate among prerenal, intrarenal, and postrenal failure (Table 87-1).
++
Initial management must focus on stabilization with correction of fluid imbalance (Fig. 87-3). If the intravascular volume is adequate or overloaded, urine output may be enhanced with furosemide, usually in an initial dose of 1 mg/kg increased up to 6 mg/kg/dose. Mannitol may be administered if there is no response to furosemide. The dose is 0.5 to 0.75 mg/kg/dose IV. Do not use these agents if obstruction is present.
++
++
In oliguric or anuric patients with decreased intravascular volume, fluid may be administered slowly, often in conjunction with monitoring of the central venous pressure. Low-dose dopamine occasionally may be used to increase renal blood flow and GFR. Those with high urine output must receive a significant amount of fluid to avoid hypovolemia.
++
Hypertension may be caused by fluid overload or high renin secretion. Children having acute hypertension with a diastolic pressure more than 100 mm Hg should be treated parenterally because of the risk of seizures, encephalopathy, and other sequelae. Only a mild reduction is needed, usually to the diastolic range of approximately 100 mm Hg. Nitroprusside and nifedipine are useful for reduction of pressure.
++
Hyperkalemia causes membrane excitability with possible cardiac dysrhythmias. A potassium level >6.5 mEq/L can cause elevation of the T wave. Specific and immediate treatment for a potassium level >7.0 mEq/L is required. Treatment may include calcium chloride, 20 to 30 mg/kg slowly; sodium bicarbonate, 1 to 2 mEq/kg/dose; or glucose and insulin infusion of 1 mL/kg of D50W followed by 1 mL/kg of D25W and 0.5 U/kg of regular insulin per hour to keep serum glucose between 120 to 300 mg/dL. Kayexalate at 1 g/kg/dose every 4 to 6 hours mixed with 70% sorbitol, orally or rectally, may be useful after initial stabilization. Other abnormalities that may need specific treatment include anemia, metabolic acidosis, hyponatremia, and hyperphosphatemia.
++
Dialysis may be required for unresponsive fluid overload, severe hyperkalemia, severe hyponatremia or hypernatremia, unresponsive metabolic acidosis, BUN >100 mg/dL, or altered level of consciousness secondary to uremia. Such patients obviously require hospitalization.