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Nephrology

Question 118 of 180

A 54 year old man presents to the Emergency Department with a 5 day history of productive cough. He has no significant past medical history. His wife is concerned as he has become confused and has not passed urine for more than 24 hours. On examination you hear coarse crepitations at the right lung base. A chest x-ray confirms a right lower zone pneumonia. His observations are recorded as:

  • Heart rate: 114 beats per minute
  • Blood pressure: 95/65 mmHg
  • Respiratory rate: 24 breaths per minute
  • Oxygen saturations: 94% on 15/L min

You suspect sepsis secondary to pneumonia that may be complicated by an acute kidney injury (AKI). Which of the following does NOT meet the criteria for detecting AKI?

Answer:

Acute kidney injury (AKI) is characterised by a decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte, and acid-base homeostasis. AKI can be detected by using any of the following criteria:
  • A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
  • A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days.
  • A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours.
If there is doubt whether a person with chronic kidney disease has worsening of their condition or has acute-on-chronic kidney disease, consider it to be acute and manage accordingly.

Acute Kidney Injury

Acute kidney injury (AKI) is characterised by a decline in renal excretory function over hours or days that can result in failure to maintain fluid, electrolyte, and acid-base homeostasis.

AKI can be detected by using any of the following criteria:

  • A rise in serum creatinine of 26 micromol/L or greater within 48 hours.
  • A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days.
  • A fall in urine output to less than 0.5 mL/kg/hour for more than 6 hours.

If there is doubt whether a person with chronic kidney disease has worsening of their condition or has acute-on-chronic kidney disease, consider it to be acute and manage accordingly.

Causes

  • Pre-renal - due to reduced perfusion of the kidneys and leading to a decreased glomerular filtration rate (GFR)
    • Hypovolaemia e.g. haemorrhage, gastrointestinal losses, renal losses, burns
    • Reduced cardiac output e.g. cardiac failure, liver failure, sepsis, drugs
    • Drugs that reduce blood pressure, circulating volume, or renal blood flow e.g. ACE inhibitors, ARBs, NSAIDs, loop diuretics
  • Renal - due to structural damage to the kidney (may be caused by persistent pre- or post- renal causes)
    • Toxins and drugs e.g. antibiotics, contrast, chemotherapy
    • Vascular e.g. vasculitis, thrombosis, thromboembolism, dissection
    • Glomerular e.g. glomerulonephritis
    • Tubular e.g. acute tubular necrosis, rhabdomyolysis, myeloma
    • Interstitial e.g. interstitial nephritis, lymphoma infiltration
  • Post-renal - due to acute obstruction of urinary flow resulting in increased intratubular pressure and decreased GFR
    • Obstruction e.g. renal stones, blocked catheter, enlarged prostate, genitourinary tract tumours/masses, neurogenic bladder

Risk factors

Groups at increased risk of acute kidney injury include the following:

  • People aged 65 years or over
  • A history of acute kidney injury
  • Chronic kidney disease (estimated glomerular filtration rate [eGFR] less than 60mL/min/1.73m2)
  • Symptoms or history of urological obstruction or conditions which may lead to obstruction
  • Chronic conditions such as heart failure, liver disease, and diabetes mellitus
  • Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer)
  • Sepsis
  • Hypovolaemia
  • Oliguria (urine output less than 0.5mL/kg/hour)
  • Nephrotoxic drug use within the last week (especially if hypovolaemic)
  • Exposure to iodinated contrast agents within the past week
  • Cancer and cancer therapy (risk will depend on the type of cancer, proposed treatment and premorbid risk factors)
  • Immunocompromise (for example HIV infection)
  • Toxins (for example some herbal remedies, poisonous plants and animals)

Clinical features

Suspect acute kidney injury (AKI) in anyone with:

  • Symptoms and signs such as:
    • Nausea and vomiting, or diarrhoea, evidence of dehydration
    • Reduced urine output or changes to urine colour
    • Confusion, fatigue, and drowsiness
  • An acute illness and any of the risk factors listed above
  • An illness with no clear acute component and any of the following:
    • Chronic kidney disease (especially stage 3B, 4, or 5), or urological disease
    • New onset or significant worsening of urological symptoms
    • Symptoms or signs of a multi-system disease affecting the kidneys and other organ systems (for example signs or symptoms of acute kidney injury, plus a purpuric rash in thrombotic thrombocytopenic purpura)
    • Symptoms suggesting the presence of complications of acute kidney injury
  • An acute kidney injury warning stage test result generated from electronic detection systems in a biochemistry laboratory

Complications

Complications from acute kidney injury (AKI) arise as a result of impairment of the kidneys excretory, endocrine, and metabolic actions. Complications include:

  • Hyperkalaemia
    • This is usually asymptomatic until severe, but can then cause muscle weakness, paralysis, cardiac arrhythmias, or (in extreme cases) cardiac arrest
  • Other electrolyte imbalances e.g. hyperphosphataemia, hyponatraemia, hypermagnesaemia, hypocalcaemia
  • Metabolic acidosis
    • Can present with altered level of consciousness, circulatory collapse, and hyperventilation
  • Volume overload (peripheral and pulmonary oedema)
    • Signs include tachypnoea, tachycardia, cyanosis, and lung crepitations
  • Uraemia
    • Symptoms include confusion, lethargy, and altered level of consciousness
  • Chronic kidney disease
    • People who have experienced AKI have an increased risk of hypertension and chronic kidney disease (CKD), which can be end-stage

Assessment

For a person with acute kidney injury, assess:

  • Volume status by checking:
    • Fluid intake and losses
    • Peripheral perfusion (capillary refill time)
    • Heart rate/blood pressure (and any postural changes)
    • Jugular venous pressure
    • Moistness of mucous membranes, skin turgor
    • Changes in urination pattern
    • For peripheral oedema and pulmonary crackles
  • Renal function and potassium level
  • For possible underlying causes by asking about:
    • Current symptoms, if the person is unwell (for example diarrhoea, vomiting).
    • Any recent symptoms that may suggest an underlying obstructive cause (for example lower urinary tract symptoms, bloating from a pelvic mass, renal colic).
    • History of cardiovascular disease increasing the risk of impaired renal perfusion.
    • Symptoms of an underlying inflammatory process (for example vasculitic rash, arthralgia, epistaxis, or haemoptysis).
    • Drug history including any medicines that could cause or exacerbate AKI or accumulate and cause harm.
    • Possibility of rhabdomyolysis, for example, skeletal muscle injury, muscle overexertion, crush injury, prolonged immobility.
  • For renal disease by performing urine dipstick testing for blood, protein, leucocytes, nitrites, and glucose
    • AKI with negative urinalysis usually indicates a pre-renal cause, but drugs should also be considered.
    • Positive protein and blood indicators on urinalysis may suggest glomerular disease (particularly with more strongly positive results, for example, 2+ blood, 2+ protein).
    • Increased white cells are non-specific but may suggest infection (most common) or interstitial nephritis.
  • The stage of acute kidney injury:
    • Stage 1
      • Creatinine rise of 26 micromol or more within 48 hours OR
      • Creatinine rise of 50–99% from baseline within 7 days OR
      • Urine output < 0.5 mL/kg/h for more than 6 hours
    • Stage 2
      • 100–199% creatinine rise from baseline within 7 days OR
      • Urine output < 0.5 mL/kg/hour for more than 12 hours
    • Stage 3
      • 200% or more creatinine rise from baseline within 7 days OR
      • Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days OR
      • Urine output < 0.3 mL/kg/hour for 24 hours or anuria for 12 hours

Investigations

  • Bloods
    • Urea and electrolytes (including creatinine and bicarbonate) are the key investigations.
    • Also request liver function tests, C-reactive protein, full blood count, and blood cultures if infection suspected.
  • Urinalysis
    • As above
  • Renal ultrasound
    • Do not routinely offer ultrasound of the urinary tract when the cause of the acute kidney injury has been identified.
    • When pyonephrosis (infected and obstructed kidney[s]) is suspected with acute kidney injury, offer immediate ultrasound of the urinary tract (to be performed within 6 hours of assessment).
    • When adults have no identified cause of their acute kidney injury or are at risk of urinary tract obstruction, offer urgent ultrasound of the urinary tract (to be performed within 24 hours of assessment).
  • Further diagnostic tests (e.g. immunology, kidney biopsy) may be indicated according to the suspected cause of AKI.

Management

  • Supportive treatment
    • Perform an urgent septic screen and implement your local care bundle (e.g. Sepsis Six) within 1 hour if infection is suspected.
    • Stop/avoid exposure to any nephrotoxins (e.g. non-steroidal anti-inflammatory drugs [NSAIDs], aminoglycoside antibiotics) and to any other agents that may reduce kidney function (e.g. ACE inhibitors, angiotensin-II receptor antagonists). Review and adjust dosing of all other medications in line with the degree of kidney injury. Consider withholding diuretics and other antihypertensive medications.
    • If hypovolaemic, start immediate intravenous fluid resuscitation to improve kidney perfusion but take care to use close monitoring to avoid volume overload. Give a 500 mL intravenous bolus of crystalloid over 15 minutes and then continue with goal-directed fluid therapy. Escalate to critical care for consideration of vasopressors if the patient remains severely hypotensive despite adequate volume resuscitation.
    • Closely monitor and manage volume status and electrolytes.
    • Identify and treat reversible causes (e.g. relief of any urinary tract obstruction).
    • Treat life-threatening complications (e.g. hyperkalaemia and acidosis).
    • Refer to nephrology if there is:
      • Uncertainty about the cause or a poor response to treatment or complications that fail to respond to medical management
      • A specific diagnosis that might need specialist treatment (e.g. vasculitis, glomerulonephritis, myeloma)
      • Stage 3 AKI or AKI in a patient with pre-existing CKD stage 4 or 5
      • A history of kidney transplant
  • Relieving urological obstruction
    • Insert a bladder catheter if obstruction is suspected clinically and cannot be quickly ruled out by ultrasound.
    • Refer all people with upper tract urological obstruction to a urologist. Refer immediately when one or more of the following is present:
      • Pyonephrosis
      • An obstructed solitary kidney
      • Bilateral upper urinary tract obstruction
      • Complications of acute kidney injury caused by urological obstruction
    • When nephrostomy or stenting is used to treat upper tract urological obstruction in people with acute kidney injury, carry it out as soon as possible and within 12 hours of diagnosis.
  • Pharmacological management
    • Do not routinely offer loop diuretics to treat acute kidney injury.
    • Consider loop diuretics for treating fluid overload or oedema while:
      • a person is awaiting renal replacement therapy or
      • renal function is recovering in a person not receiving renal replacement therapy.
  • Renal replacement therapy
    • Discuss any potential indications for renal replacement therapy with a nephrologist and/or critical care specialist immediately to ensure that the therapy is started as soon as needed.
    • Base the decision to start renal replacement therapy on the condition of the patient as a whole and not on an isolated urea, creatinine or potassium value.
    • Refer adults immediately for emergency renal replacement therapy if any of the following are not responding to medical management:
      • Hyperkalaemia (potassium >6.5 mmol/L)
      • Metabolic acidosis (pH <7.15)
      • Symptoms or complications of uraemia (for example, pericarditis or encephalopathy)
      • Fluid overload
      • Pulmonary oedema

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  • Biochemistry
  • Blood Gases
  • Haematology
Biochemistry Normal Value
Sodium 135 – 145 mmol/l
Potassium 3.0 – 4.5 mmol/l
Urea 2.5 – 7.5 mmol/l
Glucose 3.5 – 5.0 mmol/l
Creatinine 35 – 135 μmol/l
Alanine Aminotransferase (ALT) 5 – 35 U/l
Gamma-glutamyl Transferase (GGT) < 65 U/l
Alkaline Phosphatase (ALP) 30 – 135 U/l
Aspartate Aminotransferase (AST) < 40 U/l
Total Protein 60 – 80 g/l
Albumin 35 – 50 g/l
Globulin 2.4 – 3.5 g/dl
Amylase < 70 U/l
Total Bilirubin 3 – 17 μmol/l
Calcium 2.1 – 2.5 mmol/l
Chloride 95 – 105 mmol/l
Phosphate 0.8 – 1.4 mmol/l
Haematology Normal Value
Haemoglobin 11.5 – 16.6 g/dl
White Blood Cells 4.0 – 11.0 x 109/l
Platelets 150 – 450 x 109/l
MCV 80 – 96 fl
MCHC 32 – 36 g/dl
Neutrophils 2.0 – 7.5 x 109/l
Lymphocytes 1.5 – 4.0 x 109/l
Monocytes 0.3 – 1.0 x 109/l
Eosinophils 0.1 – 0.5 x 109/l
Basophils < 0.2 x 109/l
Reticulocytes < 2%
Haematocrit 0.35 – 0.49
Red Cell Distribution Width 11 – 15%
Blood Gases Normal Value
pH 7.35 – 7.45
pO2 11 – 14 kPa
pCO2 4.5 – 6.0 kPa
Base Excess -2 – +2 mmol/l
Bicarbonate 24 – 30 mmol/l
Lactate < 2 mmol/l
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