Acute kidney injury (AKI), formerly called acute renal failure (ARF), is defined as an abrupt decline in renal function over hours to weeks. It is commonly caused by decreased renal blood flow, direct kidney damage, or urine flow obstruction. AKI is diagnosed through increased levels of blood urea nitrogen and creatinine and confirmed by kidney imaging and biopsy if needed. Treatment focuses on reversing the underlying cause, managing complications like fluid overload, and providing renal replacement therapy like hemodialysis if severe. The prognosis depends on the cause, with community-acquired AKI having a better prognosis than hospital-acquired AKI which is often part of multi-organ failure.

1. Acute Renal Failure
By Dr. Sarah D’souza
BDS
©

2. Acute kidney injury (AKI), formerly called acute renal
failure (ARF), is commonly defined as an abrupt decline in
renal function, clinically manifesting as a reversible acute
increase in nitrogen waste products (measured by blood
urea nitrogen [BUN] and serum creatinine levels) over the
course of hours to weeks.
INTRODUCTION

3. • Risk (R) - Increase in serum creatinine level X 1.5 or decrease in GFR by
25%, or UO < 0.5 mL/kg/hr for 6 hours
• Injury (I) - Increase in serum creatinine level X 2.0 or decrease in GFR by
50%, or UO < 0.5 mL/kg/hr for 12 hours
• Failure (F) - Increase in serum creatinine level X 3.0, decrease in GFR by
75%, or serum creatinine level ≥4 mg/dL with acute increase of >0.5 mg/dL;
UO < 0.3 mL/kg/h for 24 hours, or anuria for 12 hours
• Loss (L) - Persistent AKI, complete loss of kidney function >4 weeks
• End-stage kidney disease (E) - Loss of kidney function >3 months
CLASSIFICATION
(RIFLE)

4. ETIOLOGY
Broadly grouped into three
major categories:
• Decreased renal blood
flow (pre-renal causes;
40-70% of cases)
• Direct renal
parenchymal damage
(intrinsic renal causes;
10-50% of cases)
• Obstructed urine flow
(post-renal or obstructive
causes; 10% of cases).

5. ETIOLOGY
Principal pre-renal causes:
•Hypovolaemia
Haemorrhage
Volume depletion (vomiting, diarrhoea, burns)
•Renal hypoperfusion
NSAIDs/selective cyclo-oxygenase 2 inhibitors
Angiotensin converting enzyme inhibitors/angiotensin II receptor antagonists
Renal artery stenosis/occlusion
•Hypotension
Cardiogenic shock
Distributive shock (for example, sepsis, anaphylaxis)
•Oedematous states
Cardiac failure
Hepatic cirrhosis
Nephrotic syndrome

6. ETIOLOGY
Principal causes of intrinsic ARF:
•Glomerular disease
Inflammatory - post-infectious glomerulonephritis, SLE, cryoglobulinaemia
Thrombotic - disseminated intravascular coagulopathy, thrombotic microangiopathy
•Interstitial nephritis
Drug induced - NSAIDs, antibiotics
Infiltrative - Lymphoma
•Tubular Injury
Ischaemia - prolonged renal hypo perfusion
Toxins - drugs (aminoglycosides), pigments (myoglobin)
•Vascular
Vasculitis
Cryoglobulinaemia
Cholesterol emboli

7. ETIOLOGY
Principal post-renal causes of ARF:
• Intrinsic
Intra-luminal—stone, blood clot, papillary necrosis
Intra-mural—urethral stricture, prostatic hypertrophy
•Extrinsic
Pelvic malignancy
Retroperitoneal fibrosis

8. SIGNS AND SYMPTOMS
Skin: Digital ischemia, butterfly rash
Palpable purpura: systemic vasculitis
Maculopapular rash: Allergic interstitial
nephritis
Track marks (ie, intravenous drug abuse)
Eyes: Keratitis, iritis
Signs of diabetes mellitus
Signs of hypertension
Ears: Hearing loss- Alport disease and
aminoglycoside toxicity
Mucosal or cartilaginous ulcerations:
Granulomatosis with polyangiitis (
Wegener granulomatosis)

9. SIGNS AND SYMPTOMS
Cardiovascular examination:
Irregular rhythms (ie, atrial fibrillation)
Murmurs: Endocarditis
Abdomen:
Pulsatile mass or bruit: Atheroemboli
Abdominal or costovertebral angle tenderness
Pelvic, rectal masses; prostatic hypertrophy; distended
bladder
Limb ischemia, edema
Pulmonary examination:
Rales: Pulmonary edema, infectious pulmonary process
Hemoptysis: ANCA (antineutrophilic cytoplasmic
antibodies) vasculitis

11. DIAGNOSIS
• Kidney function studies: Increased levels of blood urea
nitrogen (BUN) and creatinine are the hallmarks of renal
failure; the ratio of BUN to creatinine can exceed 20:1 in
conditions that favor the enhanced reabsorption of urea,
such as volume contraction (this suggests prerenal AKI).
• Complete blood count.
• Peripheral smear (eg, schistocytes such as thrombotic
thrombocytopenic purpura).
• Serologic tests: These may show evidence of conditions
associated with AKI

12. DIAGNOSIS
• Complement testing
• Bladder pressure: Patients with a bladder pressure
above 25 mm Hg should be suspected of having AKI
caused by abdominal compartment syndrome.
• Ultrasonography
• Aortorenal angiography: Can be helpful in establishing
the diagnosis of renal vascular diseases, such as renal
artery stenosis
• Renal biopsy: Can be useful in identifying intrarenal
causes of AKI and directing targeted therapy.

13. MANAGEMENT -
Supportive treatment
• Correction of fluid overload with furosemide.
• Correction of severe acidosis with bicarbonate administration,
which can be important as a bridge to dialysis.
• Correction of hyperkalemia.
• Correction of hematologic abnormalities (eg, anemia, uremic
platelet dysfunction) with measures such as transfusions and
administration of desmopressin or estrogens.
• Treatment of AKI ideally should begin before the diagnosis is
firmly established. A high index of suspicion is often necessary
to diagnose early AKI. Significant decreases in GFR frequently
occur before indirect measures of GFR reveal a problem. All
seriously ill medical patients (eg, elderly patients, diabetic
patients, hypovolemic patients) should have AKI included early
in their differential diagnosis.

14. MANAGEMENT -
Supportive treatment
•Reversal of hypovolemia by rapid fluid infusion
often is sufficient to treat many forms of AKI.
•Placement of a urinary catheter early in the
workup of a patient with KI not only allows
diagnosis and treatment of urethral and bladder
outlet urinary obstruction but also allows for
accurate measurement of urine output.
•The principal methods of renal replacement
therapy (RRT) are intermittent hemodialysis
(IHD), continuous venovenous hemodiafiltration
(CVVHD), and peritoneal dialysis (PD).

15. PROGNOSIS
Because most cases of community-acquired acute
kidney injury are secondary to volume depletion, as
many as 90% of cases are estimated to have a
potentially reversible cause.
Hospital-acquired AKI often occurs in an ICU setting and
is commonly part of multiorgan failure.