The term acute renal failure (ARF), like acute respiratory failure and congestive cardiac failure, simply and broadly defines a clinical syndrome. This syndrome is characterized by an abrupt decrease in glomerular filtration rate, a rapid deterioration in renal function, and the accumulation in blood of nitrogenous waste products.
Unfortunately, unlike other syndromes seen in the intensive care unit (ICU), such as the acute respiratory distress syndrome and the sepsis syndrome, there are no consensus criteria for the diagnosis of ARF let alone the assessment of its severity. Such lack of consensus results in great variability in epidemiology and in diagnostic and therapeutic information. This is because the diagnosis, incidence, causes, and effects of therapy of ARF will clearly depend on how this syndrome is defined (Bellomo... and... .Ronco...1995).
Despite these very serious nosological concerns, ARF is currently diagnosed in practice when the urea and creatinine concentrations in the blood rise above normal in the setting of a suspected renal insult. Such a rise is frequently, although not always, associated with decreased urinary output. It also has a characteristic clinical course: the glomerular filtration rate remains fixed at low levels until recovery, the serum creatinine rises steadily at a rate of approximately 50 to 100 mol/l each day, and urinary output remains relatively fixed until recovery starts. Such recovery often takes place after 1 to 2 weeks, but will take longer if the patient remains critically ill. However, recovery may take a shorter time (3-5 days) if the insult has been moderate in severity and the patient has promptly recovered from the initial injury.
Such recovery is typically characterized by a plateau in the serum urea and creatinine levels, a daily increase in urinary output, and later a progressive decrease in nitrogenous waste products. This syndrome is frequent in the ICU (Gioeneveld eL§L 1991).
Despite the usual straightforward nature of the diagnosis of ARF, critical care physicians often have to deal with several clinical questions.
1. Does this patient presenting with an elevated plasma urea and serum creatinine concentration have acute, rapidly progressive, or chronic renal failure?
2. What is the etiology of this patient's acute renal failure?
3. What investigations should be performed to confirm the diagnosis and establish an etiology? Acute, rapidly progressive, or chronic renal failure?
The differentiation of acute from rapidly progressive or chronic renal failure is important because it helps in the etiological diagnosis and can usually be made on history alone. In most cases seen in the ICU, one is dealing with patients with known near-normal or moderately impaired renal function who may have been in hospital for some time and experience a serious ischemic injury to the kidney secondary to hypotension, decreased cardiac output, severe blood loss, severe sepsis, or a combination of these factors. Such patients rapidly develop a rising serum creatinine and plasma urea concentration, commonly with, but occasionally without, concomitant oliguria.
In some cases, however, the clinical presentation does not provide clear information regarding the course and rapidity of onset of renal dysfunction. In these patients, history and physical examination may point to a subacute illness (particularly of a vasculitic type) which may have caused a rapidly progressive loss of renal function. Clues to a vasculitic disorder include weeks of recurrent fevers and sweats, myalgias, a syndrome consistent with sinusitis, hemoptysis, dyspnea, arthralgias, pleuritic chest pain, a rash, evidence of synovitis, and the like.
In other patients, the presentation may be one of severe hypertension with renal failure. In these patients, it may be unclear whether the hypertension has caused renal failure or whether it is a manifestation of an as yet undiagnosed chronic renal failure. A number of clinical findings may be helpful in the diagnosis (see below). Other patients may present with an acute illness and a possible mild to moderate ischemic injury to the kidney, and be found to have blood levels of urea and creatinine which are markedly higher than would be expected given the nature and severity of the insult. In such patients, one may be dealing with true ARF and a misassessment of the severity of the insult or with previously unrecognized chronic renal failure with a small acute component. A history of nocturia, difficulties with micturition, previous renal disease, diabetes, chronic analgesic ingestion, kidney stones, and a family history of kidney disease all suggest pre-existent chronic renal failure. Physical examination may display the sallow skin coloration of uremia, pruritic excoriations, palpably enlarged kidneys, a full bladder, and an enlarged prostate, which are all clues to chronic renal disease.
Very few laboratory studies are helpful in distinguishing chronic from acute renal failure. However, an unexplained normochromic normocytic anemia is suggestive of chronic renal failure. An abdominal radiograph or ultrasound may assist in the diagnosis by showing the presence of either small scarred kidneys or large polycystic kidneys. The presence of nephrocalcinosis or dilatation of the pelvicaliceal system are also useful diagnostic clues. Finally, radiographic studies of the outer clavicle or hands can document the presence of renal osteodystrophy or osteomalacia, findings not seen in acute renal failure.
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