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RAHAD AHAMED
M. Pharm , Jagannath University, Dhaka
ACUTE KIDNEY INJURY
Acute kidney injury
(AKI), previously
called acute renal
failure (ARF), is an
abrupt loss of kidney
fu...
Classification and Causes of AKI
The most useful practical classification
comprises three main groups:
1. Pre-renal ( func...
Classification and Causes
1. Pre-renal acute kidney injury
a) Volume depletion resulting from:
i. Hemorrhage
ii. Renal los...
Classification and Causes
2. Renal ( Structural/ intrinsic)
a) Prolonged renal ischemia resulting from:
i. Pigment nephrop...
Classification and Causes
3. Post-renal (obstructive)
Urinary tract obstruction including:
i. Calculi( stones)
ii. Bladder...
Comparing categories of AKI
Categories Pre-renal Renal Post-renal
Etiology hypoperfusion parenchymal Obstruction
BUN value...
Diagrammatic Presentation
Pre-renal AKI Post-renal AKI
Clinical Manifestations
The patient may exhibit signs and symptoms of volume
depletion or overload, depending upon the pre...
Clinical Manifestations
Acute kidney injury with volume overload:
o Weight increased
o Orthopnoea/nocturnal dyspnoea
o An...
Diagnosis
 History collection
 Physical examination
o Asterixis and myoclonus
o Peripheral edema( if volume overload is ...
Investigation of AKI
Investigation of AKI
Investigation of AKI
Management
Effective management of AKI depends upon a rapid diagnosis. If
condition is advanced management consists mainly...
Treatment of established AKI
Uraemia and intravascular volume overload
o Intake NaCl about 1-2g/day if patient is not hyp...
Treatment of established AKI
Hypocalcaemia
o Oral calcium supplementation with calcium carbonate is usually
adequate.
o V...
Treatment of established AKI
Uraemic gastro-intestinal erosions
o Proton pump inhibitors can be efficient.
o H2 antagonis...
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Acute renal failure (ARF) is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction (usually within a 48-h period) in kidney function.
This results in an accumulation of nitrogenous waste products and other toxins. Many patients become oliguric (low urine output) with subsequent salt and water retention. In
patients with pre-existing renal impairment, a rapid decline
in renal function is termed ‘acute on chronic renal failure’.
The nomenclature of ARF is evolving and the term acute
kidney injury (AKI) is being increasingly used in clinical
practice.

Published in: Health & Medicine
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Aki updated

  1. 1. RAHAD AHAMED M. Pharm , Jagannath University, Dhaka
  2. 2. ACUTE KIDNEY INJURY Acute kidney injury (AKI), previously called acute renal failure (ARF), is an abrupt loss of kidney function that develops within 7 days. This results in an accumulation of nitrogenous waste products and other toxins.
  3. 3. Classification and Causes of AKI The most useful practical classification comprises three main groups: 1. Pre-renal ( functional/ hypoperfusion) 2. Renal ( Structural/ intrinsic) 3. Post-renal (obstructive)
  4. 4. Classification and Causes 1. Pre-renal acute kidney injury a) Volume depletion resulting from: i. Hemorrhage ii. Renal losses(diuretics) iii. GI losses (vomiting, diarrhea) b) Impaired cardiac efficiency resulting from: i. MI ii. Heart failure iii. Dysrhythmias iv. Cardiogenic shock c) Vasodilation resulting from: i. Sepsis ii. Anaphylaxis iii. Antihypertensive medications or other medication that cause vasodilation
  5. 5. Classification and Causes 2. Renal ( Structural/ intrinsic) a) Prolonged renal ischemia resulting from: i. Pigment nephropathy ii. Myoglobinuria( trauma, crush injury, burns) iii. Hemoglobinuria( transfusion reaction, hemolytic anemia) b) Nephrotoxic agents such as: i. Aminoglycosides antibiotics ii. Radiopaque contrast media iii. Heavy metals iv. NSAIDS, ACE inhibitors c) Infectious processes such as: i. Acute pylonephritis ii. Acute GN
  6. 6. Classification and Causes 3. Post-renal (obstructive) Urinary tract obstruction including: i. Calculi( stones) ii. Bladder tumor iii. BPH iv. Stricture v. Blood clots vi. Medications
  7. 7. Comparing categories of AKI Categories Pre-renal Renal Post-renal Etiology hypoperfusion parenchymal Obstruction BUN value Increased Increased Increased Creatinine increased increased increased Urine output Decreased Varies, often decreased Varies, may be decreased or sudden anura Urine sodium Decreased to <20 mEq/L Increased to > 40mEq/L Varies, decreased to <20 mEq/L Urinary sedimentation Normal, few hyaline cast Abnormal casts and debris Usually normal Urine osmolarity Increased to 500 mOsm About 350 mOsm Similar to serum Varies, increased or equal to serum Urine specific gravity Increased Low normal Varies
  8. 8. Diagrammatic Presentation Pre-renal AKI Post-renal AKI
  9. 9. Clinical Manifestations The patient may exhibit signs and symptoms of volume depletion or overload, depending upon the precipitating conditions, course of the disease and prior treatment.  Acute kidney injury with volume depletion: o Fatigue o Loss of appetite o Headache o Nausea and vomiting o Gastrointestinal hemorrhage o Muscle cramp o Tachycardia o Blood pressure o Postural hypotension o Cold extremities o Reduced skin turgor
  10. 10. Clinical Manifestations Acute kidney injury with volume overload: o Weight increased o Orthopnoea/nocturnal dyspnoea o Ankle swelling o Oedema o Jugular venous pressure distension o Pulmonary crackles
  11. 11. Diagnosis  History collection  Physical examination o Asterixis and myoclonus o Peripheral edema( if volume overload is present) o Pulmonary rales( if volume overload is present) o Elevated right atrial pressure ( if volume overlaod is present) o Identification of precipitating cause o Serum creatinine and BUN level o Urine analysis o Renal bladder ultra sound o Renal scan o CT scan and Mri o The urine will be examined under a microscope o Biopsy
  12. 12. Investigation of AKI
  13. 13. Investigation of AKI
  14. 14. Investigation of AKI
  15. 15. Management Effective management of AKI depends upon a rapid diagnosis. If condition is advanced management consists mainly of supportive strategies, with close monitoring and appropriate correction of metabolic, fluid and electrolyte disturbances. Patients with acute AKI require renal replacement therapy with regular dialysis. Patients with immune mediated causes of AKI should be treated with appropriate immune suppressive agents. Early preventive and supportive strategies o Identification of patients at risk o Withdrawal and avoidance of nephrotoxic agents o Optimization of renal perfusion o Establishing and maintaining an adequate diuresis Drug therapy and renal auto-regulation
  16. 16. Treatment of established AKI Uraemia and intravascular volume overload o Intake NaCl about 1-2g/day if patient is not hyponatraemic. o Intake total fluid to less than 1L/day Acidosis o Treated orally with sodium bicarbonate 1-6g/day in divided doses o 50-100mmol of bicarbonate ions intravenously. Hyperkalaemia o Dietary potassium should be restricted to less than 40mmol/day o 10-30mL of calcium gluconate 10% intravenously over 5-10 min o 50 mL of 50% glucose with 8-12 units of soluble insuline over 10min o Nebulised salbutamol has been used to lower potassium.
  17. 17. Treatment of established AKI Hypocalcaemia o Oral calcium supplementation with calcium carbonate is usually adequate. o Vit. D may be used to treat the hypocalcaemia. Hypophosphatemia o Phosphate binding agents may be used to retain phosphate ions in the gut. o Most commonly used agents are calcium carbonate or acetate and are given with food. Infection o Broad spectrum antibiotics are used.
  18. 18. Treatment of established AKI Uraemic gastro-intestinal erosions o Proton pump inhibitors can be efficient. o H2 antagonists are an appropriate alternative. Nutrition o Electrolyte free amino acid solutions is usually supplied as 12-30 g/day. o Mg and Zn supplementation may be required. o Parenteral glucose may be required in AKI patients.

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