Clinical Vignette

A 54 year old man with a history of DM Type II and CAD

Admitted with worsening angina and hypertension
His pain is controlled with IV GTN and treated with ASA, betablocker and ACE inhibitors
Cardiac enzymes are normal
He undergoes coronary angiography, which reveals significant
stenosis
By the next day his urine output has diminished to 200 mL over 24
hours.
Examination reveals: afebrile, HR at 62 bpm, BP of 109/65 mmHg
Ophthalmoscopy reveals dot haemorrhages and hard exudates

Clinical Vignette contd

Neck veins are flat, chest is clear, his heart rhythm is
normal with an S4 gallop and no murmur or friction
rub.
His abdomen is soft without masses or bruits
He has no peripheral oedema or rashes, normal pulses
in all extremities
Current laboratory studies include: Na 140 mEq/L, K
5.3 mEq/L, Cl 104 mEq/L, CO2 19 mEq/L and blood
urea nitrogen (BUN) 69 mg/dL. His creatinine (Cr) level
has risen to 2.9 mg/dL from 1.6mg/dL on admission.

Acute Kidney Injury

Paul Scavella II
4th Year Medical Student
Medicine Junior Clerkship
30/06/2015

Definition
Acute kidney injury (AKI) is the abrupt (1 to 7 days) and
sustained (more than 24 hours) decrease of kidney function,
resulting in the retention of urea and other nitrogenous waste
products and in the dysregulation of extracellular volume and
electrolytes. It can be mild to severe. The term AKI has largely
replaced acute renal failure (ARF), reflecting the recognition
that smaller decrements in kidney function that do not result
in overt organ failure are of substantial clinical relevance and
are associated with increased morbidity and mortality.
-

Palevsky et. al.

Definition Contd

Epidemiology
- ~ o.1% of UK population (2000 ppm/year)
- 20x incidence of new ESKD
- 10% require dialysis (200 ppm/year)
- 2x incidence of new ESKD
- 3-7% of admitted patients
- 25 - 30 % of ICU patients
- Aggregated cost of nearly $4.7 billion for ~ 498,000 US
hospital stays in US
- Up to 90% recovery rate, but up to 50% do not return to

Epidemiology contd
The spectrum of acute renal failure in a developing country.

Total 1,014 cases, 98 were analyzed

Nearly 50% had non-oliguric ARF
Mortality 36.1% and 67.3% in non-oliguric and oliguric groups, respectively
21% had complete recovery
24% had renal insufficiency
Overall mortality rate was 55%, comparable to first world countries

A W Sawyer, R L Knowles, R Roberts, H Munnings

Risk Factors

Advanced age
Diabetes
High blood pressure
Kidney disease
Liver disease

Aetiology
The Aetiology falls into 3 broad categories:
1. Prerenal
2. Renal/Intrinsic
3. Postrenal

Aetiology Contd
Prerenal AKI - is the result of decreased blood
flow
1) Hypovolemia:
o Dehydration, inadequate oral fluid intake
o Hemorrhage, burns
o Vomiting, diarrhea, excessive use of diuretics
2) Hypotension:
o Cardiogenic shock (e.g. myocardial infarction)
o Massive peripheral vasodilation: septic shock (e.g. gram-negative sepsis
due to UTI), neurogenic shock (e.g. spinal cord injury), anaphylactic shock
(e.g. bee sting)

Aetiology Contd
3) Low cardiac output:
o CHF (congestive heart failure)
o Constrictive pericarditis
o Coarctation of aorta (decreased cardiac output to lower extremities, including
the kidneys)
4) Hypoalbuminemia:
o Cirrhosis
o Nephrotic syndrome
o Burns
o Malabsorption
5) Renal artery stenosis
6) Hepatorenal syndrome
7) Hepatopulmonary syndrome

Aetiology Contd
Renal AKI - acute tubular necrosis or
ischaemia/toxins
1) Glomerular diseaseacute glomerulonephritis, usually due to rapidly proliferative
glomerulonephritis (RPGN):
o Type I RPGN: Goodpasture syndrome
o Type II RPGN: Poststreptococcal glomerulonephritis, Lupus nephritis, IgA
nephropathy
o Type III RPGN: Granulomatosis with Polyangiitis (formerly Wegener
granulomatosis)

Aetiology contd
2) Tubulointerstitial disease:
o Acute tubular necrosis (ATN): Can be caused by ischemic or nephrotoxic
insult. Ischaemic ATN is the most common cause of AKI. Microscopic
examination of urine reveals epithelial casts which have degenerated to form
pigmented, muddy-brown renal tubular casts in urine.
o Drug-induced interstitial nephritis
3) Vascular disease:
o Intrarenal vascular occlusione.g., renal artery/vein thrombosis, thrombotic
microangiopathies: hemolytic uremic syndrome (HUS), thrombotic
thrombocytopenic purpura (TTP)
o Intrarenal vasculitise.g. Granulomatosis with Polyangiitis

Aetiology contd
Postrenal AKI - obstruction of urine flow
1) Prostate Disease (MCC of postrenal AKI)
2) Renal Stones
3) Pelvic Malignancies

Pathophysiology
1. Disruption of the actin cytoskeleton
2. Loss of cell polarity
3. Cell death
4. Shedding of viable and nonviable cells
5. Tubular obstruction
6. Backleak of glomerular filtrate

Clinical Presentation
Prerenal
Vomiting, diarrhoea
Intestinal obstruction
NPO
Look for
Thirst
Reduced JVP
Decreased skin turgor
Dry mucous membrane

Clinical Presentation Contd

Renal
Oliguria, HTN, Hypertension ---> AGN
Intake of nephrotoxic drugs
h/o atrial fibrillation

Clinical Presentation Contd

Postrenal
Anuria
Flank pain
h/o prostatic disease

Differential Diagnosis

Chronic renal failure

Dehydration
Diabetic ketoacidosis
Gastrointestinal (GI) bleeding
Heart failure
Metabolic acidosis
Obstructive uropathy
Protein overloading
Renal calculi

Work Up
History
Physical
Ancillary Investigations
o

o
o

Lab Investigations
General
Specific
Imaging
Biopsy

Work Up contd
History
Physical

Work Up contd
Lab Investigations
o
o
o
o

Urinalysis
CBC
Serum Creatinine
Fractional excretions of sodium

Workup Contd
CBC

Work Up Contd
Serum Creatinine
o

Assuming no renal function, the rise in creatinine

can be predicted using the following formulas:
Males: Wt. (kg) x [28 - 0.2(age)]/total body water
in mg/dL added to the creatinine value
Females: Wt. (kg) x [23.8 - 0.17(age)]/total body
water in mg/dL added to the creatinine value

Work Up Contd

Fractional excretions of sodium

o Distinguishing prerenal from intrinsic renal causes
o Defined by the formula:

asdfasd

Work Up Contd
Imaging
Renal ultrasound
Computed tomography
Magnetic resonance imaging

Work Up Contd
Biopsy
Patients whom prerenal and postrenal
causes r/o with no clear intrinsic cause

Treatment
- Optimization of haemodynamic status
- Avoidance of further renal insults
- If, necessary institution of renal replacement
therapy

Indication for renal replacement

therapy
-

Symptoms of uraemia
Uraemic pericarditis
Refractory volume overload
Refractory hyperkalaemia
Refractory metabolic acidosis

THANK YOU!

MCQs
All of the following are correct except:
a. Biopsy is reserved for finding the pathology in AKI where
prerenal and postrenal causes are excluded
b. A value less than 1 percent indicates a prerenal cause of acute
kidney injury
c. Renal replacement therapy is indicated for symptoms of
uraemia