Acute renal failure

Published on 01/03/2015 by admin

Last modified 22/04/2025

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Acute renal failure

Renal failure is the cessation of kidney function. In acute renal failure (ARF), the kidneys fail over a period of hours or days. Chronic renal failure (CRF) develops over months or years and leads eventually to end-stage renal failure (ESRF). ARF may be reversed and normal renal function regained, whereas CRF is irreversible.

Aetiology

ARF arises from a variety of problems affecting the kidneys and/or their circulation. It usually presents as a sudden deterioration of renal function indicated by rapidly rising serum urea and creatinine concentrations. As acute renal failure is common in the severely ill, sequential monitoring of kidney function is important for early detection in this group of patients.

Usually, urine output falls to less than 400 mL/24 hours, and the patient is said to be oliguric. The patient may pass no urine at all, and be anuric. Occasionally urine flow remains high when tubular dysfunction predominates.

Kidney failure or uraemia can be classified as (Fig 18.1):

Fig 18.1 The classification of acute renal failure.

Pre-renal: the kidney fails to receive a proper blood supply.

Post-renal: the urinary drainage of the kidneys is impaired because of an obstruction.

Renal: intrinsic damage to the kidney tissue. This may be due to a variety of diseases, or the renal damage may be a consequence of prolonged pre-renal or post-renal problems.

Diagnosis

In nearly all cases the clinical history and presentation will indicate that a patient has, or may develop, ARF. The first step in assessing the patient with ARF is to identify any pre- or post-renal factors that could be readily corrected and allow recovery of renal function. The history and examination of the patient, including the presence of other severe illness, drug history and time course of the onset of the ARF, may well provide important clues. Factors that precipitate pre-renal uraemia are usually associated with a reduced effective ECF volume and include:

decreased plasma volume because of blood loss, burns, prolonged vomiting, or diarrhoea

diminished cardiac output

local factors, such as an occlusion of the renal artery.

Pre-renal factors lead to decreased renal perfusion and reduction in GFR. Both AVP and aldosterone are secreted maximally and a small volume of concentrated urine is produced.

Biochemical findings in pre-renal uraemia include the following:

Serum urea and creatinine are increased. Urea is increased disproportionately more than creatinine because of its reabsorption by the tubular cells, particularly at low urine flow rates. This leads to a relatively higher serum urea concentration than creatinine, which is not so readily reabsorbed.

Metabolic acidosis: because of the inability of the kidney to excrete hydrogen ions.

Hyperkalaemia: because of the decreased glomerular filtration rate and acidosis.

A high urine osmolality.

Post-renal factors cause decreased renal function, because the effective filtration pressure at the glomeruli is reduced due to the back pressure caused by the blockage. Causes include:

renal stones

carcinoma of cervix, prostate, or occasionally bladder.

If these pre- or post-renal factors are not corrected, patients will develop intrinsic renal damage (acute tubular necrosis).

Acute tubular necrosis

Acute tubular necrosis may develop in the absence of pre-existing pre-renal or post-renal failure. The causes include:

acute blood loss in severe trauma

septic shock

specific renal disease, such as glomerulonephritis

nephrotoxins, such as the aminoglycosides, analgesics or herbal toxins.

Patients in the early stages of acute tubular necrosis may have only modestly increased serum urea and creatinine that then rise rapidly over a period of days, in contrast to the slow increase over months and years seen in chronic renal failure.

It may be difficult to decide the reason for a patient’s oliguria. The biochemical features that distinguish pre-renal uraemia from intrinsic renal damage are shown in Table 18.1.

Table 18.1

Biochemical features in the differential diagnosis of the oliguric patient

Biochemical feature	Pre-renal failure	Intrinsic renal damage
Urine sodium	<20 mmol/L	>40 mmol/L
Urine/serum urea	>10 : 1	<3 : 1
Urine/plasma osmolality	>1.5 : 1	<1.1 : 1

Management

Important issues in the management of the patient with ARF include:

Correction of pre-renal factors, if present, by replacement of any ECF volume deficit. Care should be taken that the patient does not become fluid overloaded. In cardiac failure, inotropic agents may be indicated.

Treatment of the underlying disease (e.g. to control infection).

Biochemical monitoring. Daily fluid balance charts provide an assessment of body fluid volume. Serum creatinine indicates the degree of impairment of the GFR and the rate of deterioration or improvement. Serum potassium should be monitored closely.

Dialysis. Indications for dialysis include a rapidly rising serum potassium concentration, severe acidosis, and fluid overload.

There may be three distinct phases in the resolving clinical course of a patient with acute renal failure (Fig 18.2). An initial oliguric phase, where glomerular impairment predominates, is followed by a diuretic phase when urine output is high, as glomerular function slowly improves but tubular function remains impaired. During a recovery phase, complete renal function may return. Careful clinical and biochemical monitoring is necessary throughout the course of the patient’s illness.