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    TREATMENT FOR ACUTE KIDNEY FAILURE

     

    • Fluid and electrolyte requirements in established acute kidney failure

    A key part of the immediate assessment and management of any patient who is very ill, which will include many of those with acute kidney failure, is to make a correct assessment of the intravascular volume status and to resuscitate rapidly and effectively.


    Fluid

    Many patients with acute kidney failure are volume-depleted at the time of presentation. An urgent priority is to correct such depletion rapidly. Once this has been achieved—as judged by an improvement in peripheral perfusion, a fall in pulse rate, loss of postural drop in blood pressure, and a rise in jugular venous pressure—the perspective changes.

    In the absence of normal kidney function the greatest care must be taken to regulate the intake of fluids and electrolytes to match losses in the urine, from the gastrointestinal tract, and from other 'insensible' sources.

    As a working rule, fluid intake is limited to the volume of the previous day's urine output and gastrointestinal losses, plus 500 ml, but this allocation may need to be substantially increased in the presence of fever or in hot environments, when insensible losses may be much increased.

    However, as discussed above, fluid-balance charts are frequently inaccurate and unthinking adherence to the 'output plus 500 ml' rule can lead to grief. There is no substitute for careful, twice-daily clinical examination for signs of intravascular volume depletion or excess, supplemented by accurate daily weighing to gauge the overall net fluid balance, and an intelligent flexible response to the findings.

     

    Sodium

    In the patient who is not being dialysed, the intake of sodium must also be matched to output. Requirements are usually very small in those who are oliguric, perhaps only 15 to 30 mmol/day, but if the patient is polyuric the requirements can be considerable, with a danger of volume depletion if these are not met. The urine of a patient with polyuric kidney failure will usually contain sodium at a concentration of 50 to 70 mmol/l, hence if urine output is 3 litres/day then over 200 mmol of sodium may be required.

    On occasion, the urine output in polyuric acute kidney failure can be massive (even up to 1 litre/hour)—if the response is to administer an even greater quantity of fluid (output plus insensible losses), then it is possible to contrive a vicious cycle whereby an ever-increasing urinary output is rewarded by ever-increasing fluid infusion.

    To avoid this situation in the patient with polyuria it is best to limit input to urinary output alone, thus allowing other fluid losses to establish a mild overall negative balance, only increasing fluid input if the patient develops significant postural hypotension, which should be checked for twice daily. For unknown reasons, an excess of sodium and water in patients with tubular necrosis leads to peripheral or pulmonary oedema, whereas in those with glomerulonephritis it tends to produce hypertension.

     

    Potassium

    Because hyperkalaemia is one of the most important problems in the management of acute kidney failure, it is essential to check plasma potassium levels at least daily, and in those with hypercatabolism or gastrointestinal bleeding, or who require surgery, more frequent estimations are advisable. In oliguric cases, dietary consumption should be limited to the minimum compatible with an adequate intake of protein and amino acids (20–30 mmol/day).

    Diuretics that work on the distal tubule (for example, spironolactone, amiloride, and triamterene) promote potassium retention: they should never be used in renal failure, and it is important when reviewing the drug chart to remember that these agents are frequent constituents of tablets containing a combination of diuretic/antihypertensive compounds. Intravenous preparations of antimicrobial agents that contain large amounts of potassium should also be avoided whenever possible.

    Excretion of potassium can sometimes be enhanced in those who are oliguric by the use of high doses of furosemide (0.5–1 g daily). Oral potassium-exchange resins (e.g. Calcium Resonium), prescribed concurrently with a laxative, can be useful in controlling serum potassium for a few days or weeks, but they are not effective treatments for acute severe hyperkalaemia and are usually found to be unpalatable for long-term use. By contrast, in polyuric acute kidney failure substantial losses of potassium can occur and need to be replaced. Measurement of the urinary potassium concentration can be helpful in estimating how much potassium is required.

     

     

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