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Download Acute and Chronic Renal Failure by Michael Boulton-Jones MB, B.CHIR, MRCP (auth.) PDF

By Michael Boulton-Jones MB, B.CHIR, MRCP (auth.)

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2. 5 mEq/I). 3. Marked acidosis with a bicarbonate of below 12 mmol/l (12 mEq/I). 4. Fluid overload, particularly in the presence of pulmonary oedema. 5. A confused uncooperative patient in whom conservative management is impracticable. Although renal failure itself does not cause confusion, convulsions or abnormal neurological signs except terminally, it probably contributes to their appearance in patients who have widespread infection or inappropriate drug 32 Acute and Chronic Renal Failure therapy.

The remaining nephrons hypertrophy to cope with the increased load, and are capable of adapting their function to do so. The patient remains well until so many nephrons are lost that hypertrophy of the remainder no longer maintains the GFR, which then progressively declines. As further nephrons are lost the remainder are unable to acidify, concentrate or dilute the urine normally and the patient develops acidosis and a urine of fixed concentration. However, even at this stage, the function of the surviving tubules remains evident in some important aspects.

Clinically folate deficiency appears first (often as thrombocytopenia), but this may be because it is most easily recognized. It is best to start patients on folic acid and other water soluble vitamins as soon as dialysis is undertaken. Infections Infections are the main or contributing cause of A TN in about one-third of patients and develop in a further 50 per cent. The management and prevention of these infections is of major importance and the failure of therapy is a common cause of death. The common sites are the lung, urine and wounds; septicaemia is found in about 15 per cent of patients.

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