ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY

The term ‘renal failure' means failure of renal excretory function as a result of reduction of the GFR. This is accompanied to a variable extent by failure of erythropoietin production, vitamin D hydroxylation, regulation of acid-base balance, regulation of salt and water balance and blood pressure control.

Definition

The term ‘acute kidney injury' has replaced the term acute renal failure. AKI is an abrupt sustained rise in serum urea and creatinine due to a rapid decline in GFR leading to loss of normal water and solute homeostasis. It is usually but not invariably reversible or self-limiting. In contrast CKD implies long-standing, and usually progressive, impairment in renal function. There are universal criteria for diagnosis of AKI with three levels of increasing kidney dysfunction and two outcomes (Table 9.10).

Classification

Renal failure results in reduced excretion of nitrogenous waste products of which urea is the most commonly measured. A raised serum concentration (uraemia) is classified as (i) prerenal, (ii) renal (intrinsic) or (iii) postrenal. This classification allows the clinician to consider the cause of the injury systematically for the purposes of diagnosis and management. AKI may also result from a combination of these factors, e.g. in post-surgical AKI, fluid depletion (prerenal), systemic infection and nephrotoxic drugs (renal) may all play a role. Acute injury may also complicate CKD (‘acute-on-chronic').

Table 9.10 RIFLE classification for acute kidney injury

Grade

Serum creatinine

Urine output criteria

Risk

↑ SCr to ≥ 1.5 X from baseline

<0.5 mưkg/h ≥6 h

Injury

↑ SCr ≥ 2 X from baseline

<0.5 mL/kg/h ≥12 h

Failure

↑ SCr ≥ 3 X from baseline or SCr ≥350 μmol/L with an acute increase ≥40 μmol/L

<0.3 mL/kg/h ≥24 h

Loss

Persistent AKI > 4 weeks

ESKD

Persistent renal failure >3 months

SCr, serum creatinine; ESKD, end-stage kidney disease.
• Baseline SCr is considered to be within 1 week.
• When baseline SCr is not known and in the absence of a history of chronic kidney disease, calculate a baseline SCr using the Modification of Diet in Renal Disease equation for assessment of kidney function, assuming a glomerular filtration rate of 75 mL/min/1.73 m2.
• Only one criterion (SCr or urine output) has to be fulfilled to qualify for a stage.
• AKI should be both abrupt (within 1–7 days) and sustained (more than 24 hours).

Prerenal failure

There is impaired perfusion of the kidneys with blood due to one or more of hypovolaemia, hypotension, impaired cardiac pump efficiency, or vascular disease limiting renal blood flow. The kidney is normally able to maintain glomerular filtration in spite of wide variations in the renal perfusion pressure and volume status - so-called ‘autoregulation'. Maintenance of a normal GFR in the face of decreased systemic pressure depends on the intrarenal produc-tion of prostaglandins and angiotensin II. With severe or prolonged hypo-volaemia there is eventually a drop in glomerular filtration, termed ‘prerenal failure'. Drugs that impair renal autoregulation, such as ACE inhibitors and NSAIDs, increase the tendency to develop prerenal uraemia.

Prerenal uraemia is characterized in the early stages by lack of structural damage and rapid reversibility once normal renal perfusion has been restored. However, all causes of prerenal uraemia may, if sustained, lead to ischaemic tubule cell injury (ischaemic intrinsic AKI) from which recovery will be delayed.

A number of criteria have been proposed to differentiate between prerenal and intrinsic renal causes of uraemia (Table 9.11).

■ Urine specific gravity and urine osmolality are easily obtained measures of concentrating ability but are unreliable in the presence of glycosuria or other osmotically active substances in the urine.

■ Urine sodium is low if there is avid tubular reabsorption, but may be increased by diuretics or dopamine.

Table 9.11 Criteria for distinction between prerenal and intrinsic causes of renal failure

Prerenal

Intrinsic

Urine speciíic gravity

>1.020

<1.010

Urine osmolality (mOsm/kg)

>500

<350

Urine sodium (mmol/L)

<20

>40

Fractional excretion of sodium (Na+)

<1%

>1%

Fractional excretion of Na+ = urine [sodium] + urine [creatinine] X 100 plasma [sodium] plasma [creatinine]

where [ ] is the concentration.

■ Fractional excretion of sodium (FENa) the ratio of sodium clearance to creatinine clearance, increases the reliability of this index but may remain low in some ‘intrinsic' renal diseases, including contrast nephropathy and myoglobinuria.

The urinary indices do not, however, completely segregate the two conditions and they are no substitute for a proper clinical assessment.

Management

Prerenal uraemia due to hypovolaemia or hypotension should be treated with prompt replacement of the appropriate fluid (e.g. blood in the case of post-haemorrhagic shock or crystalloid in the case of vomiting, diarrhoea or polyuria) to correct the problem and prevent development of ischaemic renal injury and established AKI. In some cases, e.g. with a very sick patient, volume replacement is guided by measurement of the central venous pres-sure (CVP) (p. 581). With pure prerenal uraemia, urine output should increase with volume replacement. If the problem relates to cardiac pump insufficiency or occlusion of the renal vasculature the management is to try to correct the underlying cause.

Postrenal uraemia

Postrenal uraemia occurs when both urinary outflow tracts are obstructed or when the tract is obstructed in a patient with a single functional kidney (p. 381). It is usually quickly reversed if the obstruction is relieved. All patients with AKI must be examined for evidence of obstruction (enlarged palpable kidneys or bladder, large prostate on rectal examination, pelvic masses on vaginal examination in women) and undergo renal ultrasonography to look for hydronephrosis and dilated ureters. Bladder outflow obstruction is ruled out by flushing of an existing catheter or insertion of a urethral catheter (which should then be removed unless a large volume of urine is obtained).

Treatment of obstruction is usually by a temporary measure, e.g. urethral/ suprapubic catheterization or percutaneous nephrostomy, until definitive treatment of the obstructing lesion can be undertaken (p. 383).

Acute uraemia due to renal parenchymal disease

This is most commonly due to acute tubular necrosis as a result of renal ischaemia or direct renal toxins (Table 9.12). Other causes include diseases affecting the interstitium (drug hypersensitivity, infections), the renal vascu-lature (vasculitis, accelerated hypertension, cholesterol embolism, haemo-lytic uraemic syndrome, thrombotic thrombocytopenic purpura) and acute glomerulonephritis.

Clinical and biochemical features

The early stages of AKI are often completely asymptomatic. It is not the accumulation of urea itself that causes symptoms, but a combination of many different metabolic abnormalities.

■ Alteration of urine volume. Oliguria usually occurs in the early stages. Recovery of renal function typically occurs after 7-21 days and in the

Table 9.12 Some causes of acute tubular necrosis
Haemorrhage
Burns
Diarrhoea and vomiting, fluid loss from fistulae
Acute pancreatitis
Diuretics
Myocardial infarction
Congestive cardiac failure
Endotoxic shock
Snake bite
Myoglobinaemia
Haemoglobinaemia (due to haemolysis, e.g. in falciparum malaria, ‘blackwater fever’)
Hepatorenal syndrome
Radiological contract agents
Drugs, e.g. aminoglycosides, non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, platinum derivatives
Abruptio placentae
Pre-eclampsia and eclampsia

recovery phase, which may last some weeks, there is often passage of large amounts of dilute urine.

■ Biochemical abnormalities include hyperkalaemia, metabolic acidosis (unless there is loss of hydrogen ions by vomiting or aspiration of gastric contents), hyponatraemia (due to water overload from continued drinking after the onset of oliguria or administration of 5% glucose), hypocal-caemia due to reduced renal production of 1,25 dihydroxycholecalciferol and hyperphosphataemia due to phosphate retention.

■ Symptoms of uraemia are weakness, fatigue, anorexia, nausea and vom-iting, followed by mental confusion, seizures and coma. There may be pruritus and bruising. Breathlessness occurs from a combination of anaemia and pulmonary oedema secondary to volume overload. Pericar-ditis occurs with severe untreated uraemia and may be complicated by a pericardial effusion and tamponade. Impaired platelet function causes bruising and exacerbates gastrointestinal bleeding. Infection occurs due to immune suppression.

Investigation of the uraemic emergency

The purpose of investigation, together with clinical examination, is threefold:

1. To differentiate acute from chronic uraemia (p. 392).

2. To document the degree of renal impairment and obtain baseline values so that the response to treatment can be monitored. This is accomplished by measurement of serum urea and creatinine.

3. To establish whether AKI is prerenal, renal or postrenal, and to determine the underlying cause so that specific treatment (e.g. intensive immunosuppression in Wegener's granulomatosis) may be instituted as early as possible and thus prevent progression to irreversible renal failure.

Investigations

■ Blood count: anaemia and a very high erythrocyte sedimentation rate (ESR) may suggest myeloma or a vasculitis as the underlying cause.

■ Urine and blood cultures to exclude infection.

■ Urine dipstick testing and microscopy: glomerulonephritis is suggested by haematuria and proteinuria on dipstick testing and by the presence of red cell casts on urine microscopy (p. 361).

■ Urinary electrolytes (Table 9.11) may help to exclude a significant pre-renal element to AKI.

■ Serum calcium, phosphate and uric acid.

■ Renal ultrasound excludes obstruction and gives an assessment of renal size; CT is useful for the diagnosis of retroperitoneal fibrosis and some other causes of urinary obstruction, and may also indicate cortical scarring.

■ Histological investigations: renal biopsy should be performed in every patient with unexplained AKI and normal-sized kidneys.

■ Optional investigations (depending on the case):

■ Serum protein electrophoresis for myeloma

■ Serum autoantibodies, ANCAs (p. 299) and complement

■ Antibodies to hepatitis B and C and HIV may suggest polyarteritis (HBV), cryoglobulinaemia (HCV) or HIV as the cause of AKI.

Management

The best form of management of AKI is prevention, e.g. by optimizing fluid balance in hospitalized patients (p. 326) and volume expansion (0.9% sodium chloride at 1 mL/kg/h for 12 hours before the procedure and several hours afterwards) in patients with impaired kidney function (eGFR below 60 mL/min/1.73m2) undergoing radiological contrast studies. The principles of management of established AKI are summarized in Emergency Box 9.1. Hypovolaemia (prerenal) and obstruction (postrenal) must be excluded as contributing factors in all patients. Dialysis and haemofiltration are some-times necessary; they do not hasten recovery from AKI but are performed as a bridge while patients are receiving treatment for the underlying cause or there is a natural improvement in kidney function. Indications for dialysis are listed in Table 9.13. Whether haemodialysis, haemofiltration or peritoneal dialysis (p. 396) is used depends on the facilities available and the clinical circumstances.

Prognosis

This depends on the underlying cause. The most common cause of death is sepsis as a result of impaired immune defence (from uraemia and malnutri-tion) and instrumentation (dialysis and urinary catheters and vascular lines). In those who survive, renal function usually begins to recover within 1-3 weeks. AKI is irreversible in a few patients, probably because of cortical necrosis which, unlike tubules which regenerate, heals with the formation of scar tissue.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

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Infectious diseases

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Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
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HEPATITIS
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TESTICULAR TUMOUR
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