All pts with AKI manifest some degree of azotemia (increased blood urea nitrogen [BUN] and Cr). Other clinical features depend on the etiology of renal disease. Pts with prerenal azotemia due to volume depletion usually demonstrate orthostatic hypotension, tachycardia, low jugular venous pressure, and dry mucous membranes. Pts with prerenal azotemia and CHF (“cardiorenal syndrome”) may show jugular venous distention, an S3 gallop, and peripheral and pulmonary edema. Therefore, the physical examination is critical in the workup of pts with prerenal AKI. In general, the BUN/Cr ratio tends to be high (>20:1), more so with volume depletion and CHF than with cirrhosis. The uric acid may also be disproportionately elevated in noncirrhotic prerenal states (due to increased proximal tubular absorption). Urine chemistries tend to show low urine [Na+] (<10-20 mmol/L, <10 with hepatorenal syndrome) and a fractional excretion of sodium (FENa) of <1% (Table 138-2). The urinalysis (UA) typically shows hyaline and a few granular casts, without cells or cellular casts. Renal ultrasonography is usually normal.
Pts with intrinsic renal disease present with varying complaints. Glomerulonephritis (GN) is often accompanied by hypertension and mild to moderate edema (associated with Na retention and proteinuria, and sometimes with gross hematuria). An antecedent prodromal illness and/or prominent extrarenal symptoms and signs may occur if GN occurs in the context of a systemic illness, e.g., vasculitis or SLE; these may include hemoptysis or pulmonary hemorrhage (vasculitis and Goodpasture's syndrome), arthralgias/arthritis (vasculitis or SLE), serositis (SLE), and unexplained sinusitis (vasculitis). The urine chemistries may be indistinguishable from those in pts with prerenal failure; in fact, some pts with GN have renal hypoperfusion (due to glomerular inflammation and ischemia) with resultant hyperreninemia leading to acute volume expansion and hypertension. The urine sediment can be very helpful in these cases. Red blood cell (RBC), white blood cell (WBC), and cellular casts are characteristic of GN; RBC casts are rarely seen in other conditions (i.e., they are highly specific). In the setting of inflammatory nephritis (GN or interstitial nephritis, see below), there may be increased renal echogenicity on ultrasonography. Unlike pts with GN, pts with interstitial diseases are less likely to have hypertension or proteinuria; a notable exception is NSAID-associated acute interstitial nephritis, which can be accompanied by proteinuria due to an associated minimal-change glomerular lesion. Hematuria and pyuria may present on UA. The classic sediment finding in allergic interstitial nephritis is a predominance (>10%) of urinary eosinophils with Wright's or Hansel's stain; however, urinary eosinophils can be increased in several other causes of AKI, such that measurement of urine eosinophils has no diagnostic utility in renal disease. WBC casts may also be seen, particularly in cases of pyelonephritis.
The urinary sediment of pts with ischemic or toxic ATN will characteristically contain pigmented “muddy-brown” granular casts and casts containing tubular epithelial cells; free tubular epithelial cells can also be seen. The FENa is typically >1% in ATN, but may be <1% in pts with milder, nonoliguric ATN (e.g., from rhabdomyolysis) and in pts with underlying “prerenal” disorders, such as CHF or cirrhosis.
Pts with postrenal AKI due to urinary tract obstruction are usually less severely ill than pts with prerenal or intrinsic renal disease, and their presentation may be delayed until azotemia is markedly advanced (BUN >54 µmol/L [150 mg/dL], Cr >1060-1325 µmol/L [12-15 mg/dL]). An associated impairment of urinary concentrating ability often “protects” the pt from complications of volume overload. Urinary electrolytes typically show an FENa >1%, and microscopic examination of the urinary sediment is usually bland. Ultrasonography is the key initial diagnostic tool. More than 90% of pts with postrenal AKI show obstruction of the urinary collection system on ultrasound (e.g., dilated ureter, calyces); false negatives include hyperacute obstruction and encasement of the ureter and/or kidney by tumor or of the ureter by retroperitoneal fibrosis, functionally obstructing urinary outflow without structural dilation. Other imaging techniques, such as a furosemide renogram (MAG3 nuclear medicine study), may be required to define better the presence or absence of obstructive uropathy.
Treatment: Acute Renal Failure Treatment should focus on providing etiology-specific supportive care. For example, pts with prerenal failure due to GI fluid loss may experience relatively rapid correction of AKI after the administration of IV fluid to expand volume. The same treatment in prerenal pts with CHF would be counterproductive; in this case, treatment of the underlying disease with vasodilators and/or inotropic agents would more likely be of benefit. There are relatively few intrinsic renal causes of AKI for which there is safe and effective therapy. GN associated with vasculitis or SLE may respond to high-dose glucocorticoids and cytotoxic agents (e.g., cyclophosphamide); plasmapheresis and plasma exchange may be useful in other selected circumstances (e.g., Goodpasture's syndrome and HUS/TTP, respectively). Antibiotic therapy may be sufficient for the treatment of AKI associated with pyelonephritis or endocarditis. There are conflicting data regarding the utility of glucocorticoids in allergic interstitial nephritis. Many practitioners advocate their use with clinical evidence of progressive renal insufficiency despite discontinuation of the offending drug, or with biopsy evidence of potentially reversible, severe disease. The treatment of urinary tract obstruction often involves consultation with a urologist. Interventions as simple as Foley catheter placement or as complicated as multiple ureteral stents and/or nephrostomy tubes may be required. Dialysis for AKI and Recovery of Renal Function Most cases of community- and hospital-acquired AKI resolve with conservative supportive measures, time, and patience. If nonprerenal AKI continues to progress, dialysis must be considered. The traditional indications for dialysis—volume overload refractory to diuretic agents; hyperkalemia; encephalopathy not otherwise explained; pericarditis, pleuritis, or other inflammatory serositis; and severe metabolic acidosis, compromising respiratory or circulatory function—can seriously compromise recovery from acute nonrenal illness. Therefore, dialysis should generally be provided in advance of these complications. The inability to provide requisite fluids for antibiotics, inotropes and other drugs, and/or nutrition should also be considered an indication for acute dialysis. Dialytic options for AKI include (1) intermittent hemodialysis (IHD), (2) peritoneal dialysis (PD), and (3) continuous renal replacement therapy (CRRT, i.e., continuous arteriovenous or venovenous hemodiafiltration). Most pts are treated with IHD. It is unknown whether conventional thrice-weekly hemodialysis is sufficient or more frequent treatments are required. Few centers rely on PD for management of AKI (risks include infection associated with intraperitoneal catheter insertion and respiratory compromise due to abdominal distention). At some centers, CRRT is prescribed only in pts intolerant of IHD, usually because of hypotension; other centers use it as the modality of choice for pts in intensive care units. Hybrid hemodialysis techniques, such as slow low-efficiency dialysis (SLED), are equally effective and may be used in centers in which CRRT is not employed. |
For a more detailed discussion, see Liu KD, Chertow GM: Dialysis in the Treatment of Acute Renal Failure, Chap. 336, p. 1822, in HPIM-19. |