ACUTE RENAL FAILURE (ACUTE KIDNEY INJURY-AKI)

Definition

• Acute renal failure is the sudden interruption of kidney function due to obstruction, reduced circulation or renal parenchyma disease.

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• It is usually reversible with medical treatment otherwise may progress to end-stage renal disease(ESRD), uremic syndrome and death.

CAUSES

• The causes of renal failure can be classified under
• PRE-RENAL CAUSES (60%-70%)

Prerenal causes of AKI are factors external to the kidneys, and affect flow of blood to the kidneys

• Haemorrhage
• Renal loses (diuresis)
• Gastrointestinal loses (vomiting, diarrhoea, NG suction)
• Myocardial infarction
• Congestive heart failure
• Cardiogenic shock
• Sepsis
• Anaphylaxis

�B. INTRA-RENAL CAUSES (25%)

• Nephrotoxic Agents (Aminoglycosides, Heavy metals (lead, mercury) Arsenic, NSAIDs (Diclofenac), ACE inhibitors and contrast media
• Infections (Acute Glomerulonephritis, Acute pylonephritis)
• Prolonged renal ischemia resulting from transfusion reaction, haemolytic anaemia, sickle cell anaemia.
• Acute tubular necrosis is the most common cause of Acute Kidney Injury (AKI) for hospitalized patients.

C. POST-RENAL CAUSES(<10%)

• Renal calculi (stone)
• Tumors/cancers of the urinary tract
• BPH
• Strictures
• Blood clots
• Pregnancy
• Trauma (back, pelvis, perineum
• Spinal cord disease
• Neuromuscular disorders

�PATHOPHYSIOLOGY�

• The prerenal factors reduce systemic circulation, causing a reduction in renal blood flow.
• This leads to decreased glomerular perfusion and filtration of the kidneys.
• Although kidney tubular and glomerular function is preserved, glomerular filtration is reduced as a result of decreased perfusion.

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PATHOPHYSIOLOGY

• The oliguria is caused by a decrease in circulating blood volume (e.g., severe dehydration, heart failure, decreased cardiac output) and is readily reversible with appropriate treatment.
• Prerenal azotemia results in a reduction in the excretion of sodium (less than 20 mEq/L), increased sodium and water retention, and decreased urine output.

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Pathophysiology cont’d

• The damage from intrarenal causes usually results from prolonged ischemia, nephrotoxins
• Nephrotoxins can cause obstruction of intrarenal structures by crystallizing or by causing damage to the epithelial cells of the tubules.
• Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction.
• Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI

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�Pathophysiology Cont’d�

• Postrenal causes of AKI involve mechanical obstruction in the outflow of urine.
• Urine refluxes into the renal pelvis, impairing kidney function.
• Bilateral ureteral obstruction leads to hydronephrosis (acummulation of urine in the kidneys), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive decline in kidney function.

Pathophysiology Cont’d

• If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely.
• After 12 weeks, recovery is unlikely. Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis.

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PHASES OF ACUTE RENAL FAILURE

There are four (4) clinical phases;

1. initiation phase/period
2. period of oliguria (10-20 days)
3. period of diuresis
4. period of recovery

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�PHASES OF ACUTE RENAL FAILURE CONT’D�

A. Initiation phase/period

• This is when initial insult occurs and ends when oliguria develops

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�PHASES OF ACUTE RENAL FAILURE CONT’D�

b. Period of oliguria (10-20 days)

• Rise in concentration of substances that are usually excreted by the kidneys
• Urinary output is less than 400mls/day
• Uraemic symptoms first appear
• Oliguria usually occurs within 1 to 7 days of the injury to the kidneys.
• If the cause is ischemia, oliguria often occurs within 24 hours. In contrast, when nephrotoxic drugs are involved, the onset may be delayed for as long as 1 week.
• The oliguric phase lasts on average about 10 to 14 days but can last months in some cases.

Phases of Acute Renal Failure Cont’d

C. PERIOD OF DIURESIS

• Gradual increase in urinary output which signals that glomerular filtration has started
• Laboratory values for serum urea an d creatinine remain high because the tubules are unable to concentrate the urine
• Uremic symptoms may still be present

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D. PERIOD OF RECOVERY

• Signals the improvement of renal function (3-12months)
• Laboratory values return to normal
• There is permanent 1% to 3% reduction in GFR

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�SIGNS AND SYMPTOMS�

• Lethargy
• Persistent nausea and vomiting
• Diarrhoea
• Dry skin and mucous membrane from dehydration
• Breath may have the odor of urine (uremic fetor)

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�SIGNS AND SYMPTOMS CONT’D�

• CNS symptoms may include drowsiness, twitching and seizures, irritability
• Hematemesis
• Pruritus
• Anaemia

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SIGNS AND SYMPTOMS CONT’D

• Urinary output may be scanty
• Peripheral oedema
• Uraemic frost
• Pulmonary oedema

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SIGNS AND SYMPTOMS

• Hypertension
• Petechiae, ecchymoses
• Anuria –rare
• Metabolic acidosis (Kussmaul’s respiration)

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DIAGNOSIS

• Blood analysis; increase creatinine, BUN, K⁺, phosphorus , H⁺ levels, decrease calcium

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• Urinary analysis – (output scanty or normal), haematuria, casts, proteinuria

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• X-ray
• Renal scan
• Retrograde pyelography
• Hb – low

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�MEDICAL MANAGEMENT�

• Treat the underlying causes
• Maintain fluid and electrolyte balance (dialysis)
• Diuretics are prescribed and administered
• Regular Insulin IV to correct hyperkalaemia.
• Sodium Bicarbonate to correct acidosis shift of potassium into cells.
• Phosphate binding agents. eg. calcium, lanthanum carbonate.

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�NURSING MANAGEMENT�

• Offer patient psychological support
• Promote bed rest to conserve energy

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OBSERVATIONS

• Monitor the patient vital signs
• Monitor intake and output (check fluid excess or deficit)
• Assess the patient urine – casts, consistency, amount, odour and colour
• Asses for signs of dehydrations
• Monitor for presence of oedema

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OBSERVATIONS CONT’D

• Weigh patient daily
• Monitor for side effects of drugs
• Watch for symptoms of hyperkalaemia (malaise, anorexia, paresthesia [abnormal tingling or feeling of needle and pins], muscle weakness, and irritability)

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�DIET �

• - Provide high carbohydrate diet(providing 30 to 35 kcal/kg )
• - Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat.
• Offer the patient low protein diet (1g/kg during oliguria phase)
• Encourage the patient to take in low sodium diet
• Low potassium and phosphorus intake (avoid banana, citrus fruits and juices)

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�DIET CONT’D �

• After diuretic phase, the patient is placed on high protein diet and high calorie diet
• Dietary vitamin supplement
• Restrict fluids intake

COMPLICATIONS

• Hyperkalaemia
• Metabolic acidosis
• Chronic renal failure
• Anaemia
• Shock