Prerenal renal or postrenal kidney failure

In general, several conditions affecting the kidneys typically present with ARF. Others do so only occasionally ( Table 1). In the ICU, by far the most common cause of acute renal failure is diminished renal blood flow (so-called prerenal ARF). This type of ARF can be induced by a variety of insults ranging from hemorrhage to septic shock, and from severe diarrhea to cardiogenic shock. However, the final common pathway appears to be outer medullary ischemia and hypoxia ( Heymanefa/

1995). The clinical circumstances and severity of the insult vary greatly and need to be profound if normal kidneys are to develop severe oliguria or anuria, but less profound if one is already dealing with a patient who has prior renal impairment, is elderly, or has significant renal artery atheroma. There may be functional failure of the kidney following mild to moderate renal ischemia. Cell death is absent or minimal. However, if the injury is severe enough, cell death will occur and the influx of inflammatory cells will establish and maintain ARF (Jo.b.Ds.o.D aD.d R.oka.w 1995). In many of these patients, ARF is one of the manifestations of multiorgan failure. This type of ARF accounts for more than 90 per cent of cases seen in our ICU. Thus, while one should always keep an open mind, other causes of ARF are only considered if there are atypical clinical features as previously described.

Table 1 Disorders causing ARF

In all cases of ARF it is advisable to perform several screening diagnostic investigations to exclude parenchymal (renal) or obstructive (postrenal) causes of ARF.

A very accurate drug-intake history should be taken to assess the possibility of nephrotoxic ARF. Attention should be paid to the use of angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs, and antibiotics. The finding of eosinophils in the urine suggests a drug-induced allergic nephropathy. A full blood examination, including a blood film, and standard biochemical tests for electrolytes and liver function are mandatory.

The urine should always be tested by dipstick for blood and protein, and sent to the microbiology laboratory for culture to exclude urinary tract infection. Urine microscopy, looking for evidence of possible glomerular disease (red cell casts, white cell casts, fragmented red cells), is mandatory if blood is present in the urine.

In a number of centers, renal ultrasonography is also considered a mandatory component of the work-up in a patient with ARF. If the patient presents to hospital with suspected ARF, this approach is warranted as many patients will be found to have urinary tract obstruction. If the patient is known to produce normal amounts of urine and develops ARF in the hospital or in the ICU in association with a clear hypovolemic, hypotensive, or hypoxic insult, we do not routinely perform renal ultrasonography.

If obstruction is suspected (history and symptoms of prostatism, history and symptoms of urolithiasis, no clear hypovolemic or hypotensive insult) and demonstrated on ultrasonography, a number of investigations are available and may be needed to diagnose the site of obstruction. They include cystoscopy, retrograde pyelography, nephrostomy followed by instillation of radiocontrast into the renal pelvis, and radionuclide excretion studies.

It is important to realize that obstructive uropathy can occur without ultrasound evidence of hydronephrosis. Therefore, if clinical suspicion is strong, further investigations (as outlined above) are needed. Intravenous pyelography may occasionally become necessary, but it is generally not needed for diagnostic purposes in severe ARF of the critically ill and is generally contraindicated in these patients.

If there are clinical and laboratory features suggesting that ARF is due to parenchymal renal disease, several other investigations may become necessary. A markedly elevated sedimentation rate, an elevated or abnormally low white cell count in the absence of infection or the presence of eosinophilia, a blood film suggesting hemolysis, serological studies positive for antineutrophil cytoplasmic antibodies, the presence of anti-DNA autoantibodies, the detection of cryoglobulins, the detection of antiglomerular basement membrane antibodies, and so on are all important diagnostic clues to parenchymal renal failure in the appropriate clinical context. Uncommonly, the final diagnosis rests upon the performance of a renal biopsy which can safely be performed in mechanically ventilated patients under ultrasound guidance.

Rarely, ARF may be due to vascular disease (large-vessel vasculitis, severe bilateral atheroma, renal vein thrombosis, cholesterol embolism, etc.). In this situation, renal vein thrombosis may be detected by contrast CT of the abdomen or it may require venography.

Arterial disease can now be reliably detected by the peripheral intravenous infusion of radiocontrast and the use of spiral CT technology ( Olbricht..et..a/ 1995).

A working algorithm for the assessment of the etiology of ARF in the ICU is summarized in Fig 1.

Fig. 1 Illustration of a recommended diagnostic approach in critically ill patients with suspected ARF.

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