Medical Care:
" Prerenal azotemia
o Volume depletion due to blood loss requires IV saline and transfusion to maintain blood pressure (as well as interventions to halt further blood loss). The amount of fluid replacement in liters (free water deficit) can be estimated from serum sodium (patients Na-140/140 X 0.5 X weight in kg) and the rate of decrease in serum sodium should be 0.7 mEq/h (17 mEq/24 h).
o Decreased cardiac output requires optimizing cardiac performance by careful use of diuretics, an angiotensin-converting enzyme inhibitor (ACEI), beta-blockers, nitrates, positive inotropic agents (including dobutamine) and, when indicated, specific therapy for the cause of impaired cardiac function. When ACEIs are contraindicated because of hyperkalemia, the combination of nitrates and hydralazine offers an alternative. As these patients tend to have risk factors for macrovascular disease, the diagnosis of ischemic nephropathy or atheroembolic disease should be entertained when renal function continues to worsen despite optimization of cardiac function.
o Decreased effective arterial volume due to systemic shunting can result from sepsis or liver failure (hepatorenal syndrome [HRS]). These patients often pose a management problem because of severe edema, hyponatremia, and hypoalbuminemia. Decreased oncotic pressure and increased vascular permeability, as well as exaggerated salt and water retention, shifts the Starling forces toward formation of interstitial fluid. Effective treatment of sepsis with the appropriate antibiotics and hypotension with dopamine and norepinephrine is mandated. Crystalloid replacement can be tried, but it often leads to more edema.
o For the severely hypoalbuminemic patient, salt-poor albumin infusion can be undertaken, but there is no conclusive evidence of benefit. Adequate nutrition and effective treatment of sepsis may improve oncotic pressure and normalize vascular permeability, thereby decreasing the systemic shunting. The net result is improved renal perfusion, decreased salt and water retention, improved urine output, and edema. In the HRS, the average survival is 1-2 weeks; however, there is evidence that the kidneys will recover with early liver transplantation. Occasionally, renal function is advanced, requiring replacement therapy.
" Intrarenal azotemia
o Acute renal failure
" Ischemic or nephrotoxic ATN: The initial approach is to restore blood pressure (with fluid replacement) and withdraw nephrotoxic drugs. If oliguria persists, albumin in combination with high-dose furosemide should be tried once. Other approaches that have no conclusive benefit include renal dose dopamine and synthetic atrial natriuretic peptide. The renal failure phase usually lasts 7-21 days if the primary insult can be corrected. Postischemic polyuria can be seen in the recovery phase and represents an attempt to excrete excess water and solute. Saline may be given as maintenance fluid because of salt wasting during this phase. Hypokalemia may result from the saline diuresis. However, matching the hourly urine output with intravenous replacement is not recommended. Recovery is marked by the return of BUN and creatinine to near-baseline values.
" Acute interstitial nephritis: Management is by withdrawal of the offending nephrotoxin, avoidance of further nephrotoxic exposure, and dehydration. The creatinine level begins to improve within 3-5 days. Renal biopsy may be indicated if renal failure is severe or azotemia is not improving. Once the diagnosis is confirmed, a trial of oral prednisone (starting at 1 mg/kg/d and tapering over 6 wk) or intravenous pulse methylprednisolone (1 g for 3 d) in severe cases can be considered. If the patient is a poor candidate for biopsy but the diagnosis is strongly suspected, therapy should be started.
" Radiocontrast-induced azotemia: This becomes evident 3-5 days after exposure. It is best prevented with adequate hydration with half-normal saline at 1 mL/kg/h 12 hours prior to administration of contrast and the use of smaller amounts of contrast. Clearly explain the risks of such procedures to the patient. Administration of N-acetylcysteine recently was found to help prevent contrast nephropathy in a small randomized trial.
o Chronic kidney disease: It is important that patients with CKD be referred early to a nephrologist for the management of complications and for the transition to renal replacement therapy (ie, hemodialysis, peritoneal dialysis, renal transplantation). There is some evidence that early referral of patients with CKD improves short-term outcome. Disease progression can be slowed by a variety of maneuvers, such as aggressive control of diabetes, hypertension, and proteinuria, and dietary protein and phosphate restriction, as well as specific therapies for some of the glomerular diseases, such as lupus. Anemia, hyperphosphatemia, acidosis, and hypocalcemia should be aggressively managed prior to renal replacement therapy.
" Postrenal: Relief of the obstruction is the mainstay of therapy. In anuria, bladder catheterization is mandatory to rule out bladder neck obstruction, whereas in progressive azotemia, catheterization should be done after the patient has voided in order to determine the postvoid residual volume. A postvoid residual volume of 100 mL or more is suggestive of obstructive uropathy, and the cause should be further investigated.
Surgical Care:
" Unilateral or bilateral percutaneous nephrostomy
o If hydronephrosis is due to ureteral obstruction, unilateral or bilateral stents or percutaneous nephrostomy is performed. Recovery of renal function takes 7-10 days, but renal function may be severely impaired, requiring dialysis until such time that partial recovery is adequate for withdrawal of dialysis.
o Up to 500-1000 mL/min of postobstructive polyuria can be seen with relief of obstruction, which is appropriate and represents an attempt to excrete the excess fluid during the period of obstruction.
o Because of salt wasting during this phase, dehydration and hypokalemia are likely. Thus, two thirds of the urine output should be replaced with half-normal saline and potassium chloride if hypokalemic. Close monitoring is indicated to prevent hypotension and prerenal azotemia.
o Matching the hourly urine output with intravenous fluids is not recommended since excess water retention during the period of obstruction cannot be lost if hourly urine output is matched.