Acute Kidney Injury
Definition
• A sudden, sustained, and usually reversible decrease
in the glomerular filtration rate (GFR) occurring over
a period of hours to days.
KDIGO Definition of AKI ( 2012 )
• Increase in SCr by ≥0.3 mg/dL within 48 hours
• Increase in Scr by ≥1.5 times baseline, which is
known or presumed to have occurred within the
prior seven days
• Urine volume >0.5 ml/kg/h for 6 hours.
Predisposing factors
 etiologic factors:
• Volume restriction (eg, low fluid intake, gastroenteritis)
• Nephrotoxic drug ingestion (eg, nonsteroidal anti-
inflammatory drugs [NSAIDs], aminoglycosides)
• Exposure to iodinated contrast agents within the past week
• Trauma or unaccustomed exertion
• Blood loss or transfusions
• Exposure to toxic substances, such as ethyl alcohol or ethylene glyc
ol
• Exposure to mercury vapors, lead, cadmium, or other heavy metals,
which can be encountered in welders and miners
A higher risk for developing AKI:
• Diabetes
• Hypertension
• Chronic heart failure
• Liver disease
• Autoimmune diseases
• Connective tissue disorders
symptoms
 Urine output:
- AKI is usually accompanied by oliguria or anuria. However, polyuria may occur due
to either reduced fluid reabsorption by damaged renal tubules, or the osmotic
effect of accumulated metabolites.
- Abrupt anuria suggests an acute obstruction, acute and severe glomerulonephritis,
or acute renal artery occlusion.
- Gradual diminution of urine output may indicate a urethral stricture or bladder
outlet obstruction - eg, benign prostatic hyperplasia.
 Nausea, vomiting.
 Dehydration.
 Confusion.
 Abdominal pain & fever
 Lower limb edema
 Hypertension
 Osteoporosis
 Muscle Weakness & fatigue
• diabetic patient (hypoglycemic)
• Electrolyte disturbance
• orthostatic hypotension
• hemorrhage
• orthopnea and paroxysmal nocturnal dyspnea(heart failure)
• hematuria
• recent radiologic examinations
Diagnosis
• History
- Drugs
- Occupational
- Urinary symptoms.
- Past medical history.
• Examination
- Signs of infection or sepsis.
- Signs of acute or chronic heart failure.
- Fluid status (dehydration or fluid overload).
- Palpable bladder or abdominal/pelvic mass.
- Features of underlying systemic disease (rashes, arthralgia).
Investigation
• Urinalysis
- blood, nitrates, leukocytes, glucose and protein
- Urine osmolality
• Blood tests
- Infection
- Creatinine
- Antinuclear antibody (ANA)
- Virology: hepatitis B and C; HIV
• Ultrasound
-obstruction
Management
1. Stop nephrotoxic drugs where possible
2. Monitor creatinine, sodium, potassium, calcium,
phosphate, glucose
3. Identify and treat infection
4. Optimise fluid balance
5. Urgent relief of urinary tract obstruction
6. Identify and treat acute complications
-Hyperkalaemia.
-Acidosis.
-Pulmonary oedema.
-Bleeding.
• Drug options
-There are no drugs which have been shown to limit
progression of, or speed up recovery from, AKI.
-Treatment as appropriate for complications.
-Loop diuretics are not routinely used. They may be
considered for treatment of fluid overload or
oedema while awaiting renal replacement therapy
(RRT) or when renal function is recovering.
Prevention
• Close monitoring of urinary output and creatinine levels for
risk patients allows early detection.
• Avoidance of nephrotoxic drugs as NSAIDs and ACE inhibitors
• Control diabetes & hypertention
• Early treatment of infections/sepsis
• Early treatment/prevention of dehydration
• Correcting hypovolaemia
• Good nutrition & fluid

Acute kidney injury

  • 1.
  • 2.
    Definition • A sudden,sustained, and usually reversible decrease in the glomerular filtration rate (GFR) occurring over a period of hours to days. KDIGO Definition of AKI ( 2012 ) • Increase in SCr by ≥0.3 mg/dL within 48 hours • Increase in Scr by ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days • Urine volume >0.5 ml/kg/h for 6 hours.
  • 4.
    Predisposing factors  etiologicfactors: • Volume restriction (eg, low fluid intake, gastroenteritis) • Nephrotoxic drug ingestion (eg, nonsteroidal anti- inflammatory drugs [NSAIDs], aminoglycosides) • Exposure to iodinated contrast agents within the past week • Trauma or unaccustomed exertion • Blood loss or transfusions • Exposure to toxic substances, such as ethyl alcohol or ethylene glyc ol • Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners
  • 5.
    A higher riskfor developing AKI: • Diabetes • Hypertension • Chronic heart failure • Liver disease • Autoimmune diseases • Connective tissue disorders
  • 7.
    symptoms  Urine output: -AKI is usually accompanied by oliguria or anuria. However, polyuria may occur due to either reduced fluid reabsorption by damaged renal tubules, or the osmotic effect of accumulated metabolites. - Abrupt anuria suggests an acute obstruction, acute and severe glomerulonephritis, or acute renal artery occlusion. - Gradual diminution of urine output may indicate a urethral stricture or bladder outlet obstruction - eg, benign prostatic hyperplasia.  Nausea, vomiting.  Dehydration.  Confusion.  Abdominal pain & fever  Lower limb edema  Hypertension  Osteoporosis  Muscle Weakness & fatigue
  • 8.
    • diabetic patient(hypoglycemic) • Electrolyte disturbance • orthostatic hypotension • hemorrhage • orthopnea and paroxysmal nocturnal dyspnea(heart failure) • hematuria • recent radiologic examinations
  • 9.
    Diagnosis • History - Drugs -Occupational - Urinary symptoms. - Past medical history. • Examination - Signs of infection or sepsis. - Signs of acute or chronic heart failure. - Fluid status (dehydration or fluid overload). - Palpable bladder or abdominal/pelvic mass. - Features of underlying systemic disease (rashes, arthralgia).
  • 10.
    Investigation • Urinalysis - blood,nitrates, leukocytes, glucose and protein - Urine osmolality • Blood tests - Infection - Creatinine - Antinuclear antibody (ANA) - Virology: hepatitis B and C; HIV • Ultrasound -obstruction
  • 11.
    Management 1. Stop nephrotoxicdrugs where possible 2. Monitor creatinine, sodium, potassium, calcium, phosphate, glucose 3. Identify and treat infection 4. Optimise fluid balance 5. Urgent relief of urinary tract obstruction 6. Identify and treat acute complications -Hyperkalaemia. -Acidosis. -Pulmonary oedema. -Bleeding.
  • 12.
    • Drug options -Thereare no drugs which have been shown to limit progression of, or speed up recovery from, AKI. -Treatment as appropriate for complications. -Loop diuretics are not routinely used. They may be considered for treatment of fluid overload or oedema while awaiting renal replacement therapy (RRT) or when renal function is recovering.
  • 13.
    Prevention • Close monitoringof urinary output and creatinine levels for risk patients allows early detection. • Avoidance of nephrotoxic drugs as NSAIDs and ACE inhibitors • Control diabetes & hypertention • Early treatment of infections/sepsis • Early treatment/prevention of dehydration • Correcting hypovolaemia • Good nutrition & fluid