Clinical Vignette

A 54 year old man with a history of type 2 Diabetes Mellitus and Coronary Artery Disease is
admitted to the coronary care unit with worsening angina and hypertension. His pain is
controlled with intravenous nitroglycerin, and he is treated with aspirin, beta-blockers to lower
his heart rate, and angiotensin-converting enzyme (ACE) inhibitors to lower his blood pressure.
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 at that time reveals that he is afebrile, his heart rate is regular at 62 bpm, and his
blood pressure is 109/65 mmHg. His ophthalmoscopy reveals dot haemorrhages and hard
exudates, his neck veins are flat, his chest is clear, and 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, with normal pusles 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
23/06/2015

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.

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

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

Diagnosis

Differential Diagnosis

Chronic renal failure

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

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

Indication for renal replacement

therapy
-

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