TREATMENT FOR ACUTE KIDNEY FAILURE

• Other important management of patients with acute kidney failure

Indications for kidney biopsy

Most cases of acute kidney failure are due to prerenal failure or to the clinical syndrome of acute tubular necrosis. They occur in an appropriate clinical setting and follow a typical time course, with recovery of kidney function over a few weeks. In such instances kidney biopsy should not be performed, since the information gained is exceedingly unlikely to influence management, and the risks of the procedure are therefore not warranted. There are, however, circumstances in which kidney biopsy is essential to establish a correct diagnosis, with important implications for both management and prognosis. Biopsy should be considered when:

1. The history, examination, or laboratory tests suggest a systemic disorder that could cause acute kidney failure and could be diagnosed by kidney biopsy;
2. The urine sediment contains red cell casts;
3. The case history is atypical; and
4. Kidney failure is unusually prolonged (say beyond 6 weeks), although in this context cortical necrosis is better diagnosed by computed tomography (CT) scanning or angiography.

Nutrition

Patients with acute kidney failure are invariably catabolic and derive a larger fraction of their energy expenditure from protein breakdown than normal. Insulin resistance, metabolic acidosis, the release of proteinases into the circulation, and changes in the metabolism of branched-chain amino acids have all been suggested as possible reasons. If nutrition is neglected, patients with acute kidney failure lose weight very rapidly, and those that lose most have the highest mortality. However, it has not been proven in controlled trials that any form of nutritional support can generate a positive nitrogen balance, improve nutritional status, or alter the mortality rate in patients with acute kidney failure.

Nevertheless, there is a consensus that early institution of nutritional support probably improves prognosis. Despite this, and almost certainly to the patient's detriment, action is frequently delayed or not taken at all, particularly if it is thought that the extra fluid load required will mandate the institution of dialysis or the need for additional dialysis sessions in an already busy unit.

Typical recommended daily adult requirements are total energy 35 kcal/kg body weight, protein 1 g/kg but and nitrogen 0.16 g/kg but there is no good evidence on which to base stipulations and some would advocate more calories and more protein for those who are catabolic. If patients with acute kidney failure are oliguric, the nutritional support should be given in a restricted fluid volume, with reduced amounts of sodium, potassium, and phosphate. For practical purposes it is sensible to have enteral and parenteral fluids that satisfy these needs available routinely (a variety of commercial preparations are available): extra water and electrolytes can always be added when required. In the many patients who are too unwell to take adequate food by mouth, commonly those who need it most, tube feeding or parenteral nutrition should be started early. Protein restriction, aimed at moderating the rise of plasma urea, is not appropriate management for the patient with acute kidney failure.

Bleeding

In uraemia the bleeding time is prolonged, and in acute kidney failure this summates with any abnormality of haemostasis that might be simultaneously induced by the precipitating condition. Better control of uraemia and the routine use of H2-receptor antagonists have been associated with a greatly reduced risk of upper gastrointestinal bleeding, a previously frequent and grave occurrence. Impairment of haemostasis is not a cause of great clinical concern in most patients, but there are some who bleed—from anywhere and everywhere.

Sepsis

Overwhelming septicaemia is a common cause of acute kidney failure, and in such instances the diagnosis is often straightforward. However, in many more cases the role of sepsis is insidious and difficult to diagnose with certainty. There is often strong clinical feeling, but little in the way of hard proof, that sepsis underlies the slide towards worsening kidney and multiorgan failure in patients who have been apparently successfully resuscitated from major trauma or surgery. Septicaemia is the commonest cause of death in those with acute kidney failure. The index of clinical suspicion must therefore be very high: if a patient with acute kidney failure appears to be deteriorating in any way, the question must be asked 'is this sepsis?'. Unused intravenous lines and urinary catheters should be removed, and those that are necessary but in any way 'suspicious' should be replaced. The patient should be examined regularly for signs of a septic focus. There should be a low threshold for repeated, thorough microbiological investigation. Proven infection should be treated promptly with appropriate antimicrobial agents (dose modified as required). In many cases, however, it will be necessary to start treatment 'blind', having taken specimens for culture and having made an educated guess as to the likely pathogen, with the possibility of Gram-negative septicaemia high on the list.

In the patient who appears 'obviously septic' or to be 'going off', but in whom no cause can be found, attention should be directed towards the abdomen, this being the most likely place for hidden mischief, either infective or ischaemic. Radiological investigations, in particular CT scanning, can be very useful in searching for abdominal sepsis or dead bowel, but should not be relied upon too faithfully. However, surgical exploration may be required, both to diagnose and to treat, especially in patients whose kidney failure follows previous abdominal surgical procedures.

Prescription of drugs

Many drugs are excreted by glomerular filtration or tubular secretion and must be given in reduced dosage or at longer intervals than normal in patients with kidney failure. For patients with acute kidney failure the following should not be given without very good reason: non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin-II receptor antagonists (all of which have adverse effects on renal perfusion and glomerular filtration), and aminoglycoside antibiotics (these are discussed later in this chapter). A note about two other drugs that may be given to patients with acute kidney failure is also appropriate here: both aciclovir and penicillins can cause encephalopathy if given in the doses used to treat severe infection in patients with normal kidney function. The dose of aciclovir needs to be reduced from between 5 and 10 mg/kg every 8 h to between 2.5 and 5 mg/kg every 24 h in those receiving kidney replacement therapy, and physicians should restrain themselves from prescribing the maximum recommended doses of penicillins. If in doubt, consult the manufacturer's data sheet before prescribing any drug to a patient with acute kidney failure.