Percutaneous needle biopsy can be helpful for making a diagnosis, assessing prognosis, monitoring disease progression, and choosing among therapeutic options. Indications include acute renal failure which is unresolving and for which a cause is not evident; nephrotic syndrome if one suspects a primary glomerular disease (see discussion of renal biopsy in the section on nephrotic syndrome);proteinuria of 2 g/24 h/1.73 m2 along with an abnormal urine sediment with or without functional deterioration; hematuria associated with an abnormal urine sediment or proteinuria; systemic diseases associated with kidney dysfunction, such as systemic lupus erythematosus, Goodpasture's syndrome, and Wegener's syndrome, to confirm the extent of renal involvement and to guide management and suspected transplant rejection, to differentiate it from other causes of acute renal failure and to guide management. Contraindications include a solitary or ectopic kidney (exception: transplant allografts), horseshoe kidney, uncorrected bleeding disorder, severe uncontrolled hypertension, renal infection, renal neoplasm, hydronephrosis, end-stage kidneys, congenital anomalies, or an uncooperative patient.
When a percutaneous needle biopsy is technically not feasible and renal tissue is necessary for a diagnosis, open renal biopsy under general anesthesia can be done.
Acute renal failure is defined as a sudden decrease in renal function resulting in the retention of urea nitrogen and creatinine in the blood. As creatinine is primarily eliminated by glomerular filtration, it is the most convenient laboratory value for assessing renal function. In the absence of kidney function, the serum creatinine concentration will increase by 1-1.5 mg/dL/d. BUN is also used as a marker for acute renal failure. However, since urea nitrogen synthesis in the liver is protein-dependent, both large quantities of exogenous protein (high-protein diet) and endogenous protein (catabolism) can elevate the BUN concentration independently of renal function. Reduced urine flow rates that occur in obstructive uropathy or congestive heart failure result in increased tubular reabsorption of urea, causing a markedly elevated BUN with only a mildly reduced GFR. Therefore, a rise in BUN is a less reliable marker for acute renal failure than a rise in serum creatinine concentration.
A. Symptoms and Signs: The symptoms of acute renal failure include those related to azotemia generally and those due to the underlying cause. Azotemic patients often complain of anorexia, nausea, and malaise but may be entirely asymptomatic. Complaints relevant to pre- and postrenal as well as intrarenal disease processes are discussed under the specific entities. Physical examination is similar; patients with acute renal failure may demonstrate pericardial friction rub or asterixis or may have no abnormal signs. Hypertension may or may not be noted. Otherwise, the findings are those of the causative problem.
B. Laboratory Findings: There are no abnormalities in the blood that allow separation of acute from chronic renal failure. Both may exhibit elevated BUN and creatinine, hypocalcemia, and hyperphosphatemia.
The clinical course of acute parenchymal renal failure (acute tubular necrosis) depends to a large extent on the underlying cause. Prerenal and postrenal causes, if diagnosed and treated expeditiously, can be corrected, resulting in a return of renal function to normal or to the patient's previous level of function. Depending on the cause of the acute parenchymal (intrinsic) disorder, treatment may be more prolonged (eg, corticosteroids for glomerulonephritis, vasculitides), and renal function may not return to normal. The diagnosis of acute tubular necrosis is made only after all prerenal, postrenal, and other acute parenchymal disorders have been eliminated.
The clinical course of acute renal failure can usually be divided into oliguric, diuretic, and recovery phases. The oliguric phase usually begins within a day after the inciting event but may be delayed up to a week following a nephrotoxic injury. It lasts from a few hours to 3-4 weeks and is followed by the diuretic phase, during which urine volume will increase until it reaches several liters per day. Once the BUN and creatinine stop rising and begin to fall toward normal, the recovery phase has begun. In some individuals with severe oliguric acute tubular necrosis, there may be no diuretic or recovery phase, and dialysis will be required permanently. In others, the initiating event is followed by a nonoliguric phase and then by recovery. Most patients recover renal function within 6 weeks after developing acute tubular necrosis.
All patients with acute tubular necrosis develop complications resulting from the accumulation of nitrogenous wastes, disordered handling of water and electrolytes, and an inability to excrete acid metabolites. These disturbances develop more rapidly and are more severe in patients who are oliguric and hypercatabolic. Life-threatening complications include hypervolemia, causing hypertension and congestive heart failure; hyperkalemia; metabolic acidosis; hyponatremia, leading to central nervous system dysfunction; uremia, with neurologic dysfunction; gastrointestinal bleeding; platelet dysfunction; pericarditis; and infections, which are the leading cause of death. Less serious but common complications include hyperphosphatemia, hypocalcemia, hypermagnesemia, and anemia.
