Overview
Prerenal failure is azotemia caused by poor perfusion of the nephrons. Low perfusion reduces glomerular pressure, which reduces the pressure difference between afferent arterioles and Bowman’s spaces. This ultimately leads to reduced glomerular filtration rate (GFR). Reduced perfusion is sensed by juxtaglomerular cells, which secrete renin to activate the RAAS in an attempt to raise blood pressure. Aldosterone increases overall reabsorption, including sodium, water and blood urea nitrogen (BUN).
| Pathology | Cause |
|---|---|
| Reduced vascular volume | Haemorrhage, hypovolemia, diarrhoea and vomiting, burns, pancreatitis, hypoaldosteronism (Addison’s disease), third-spacing (hypoalbuminemia) |
| Reduced cardiac output | Cardiogenic shock, myocardial shock |
| Systemic vasodilation | Sepsis, drugs |
| Renal vasoconstriction | NSAIDs, ACE-i, ARBs, hepatorenal syndrome, renal artery stenosis |
Renal Artery Stenosis
Renal artery stenosis is narrowing of the renal artery, commonly due to atherosclerotic disease (80%) or bilateral fibromuscular dysplasia in young women.
- Pathophysiology
- Low kidney perfusion activates RAAS
- Increased angiotensin II constricts efferent arteriole and raises blood pressure (hypertension)
- Increased aldosterone increases intravascular volume and causes hypokalemia
- Signs and symptoms
- Often asymptomatic
- Secondary hypertension in a young patient (< 30)
- New-onset hypertension in an older patient ( > 55)
- Unexplained, sudden pulmonary oedema
- Physical exam
- Bruit inferior to the posterior costal margin
- Investigations
- U/E/Cs
- Elevated BUN
- Elevated creatinine
- Elevated BUN/Cr ratio (> 20:1)
- Hypokalemia
- Urinalysis: to exclude intrarenal failure
- Unremarkable
- Serum aldosterone:renin ratio: to exclude primary hyperaldosteronism
- < 20
- Duplex ultrasound: best initial imaging modality to diagnose renal aretry stenosis
- CT angiogram or MRA: to confirm renal artery stenosis
- U/E/Cs
- Treatment
- ACEi + statin + aspirin in unilateral atherosclerotic etiology
- ACEi in unilateral fibromuscular dysplasia
- Stenting in bilateral or refractory stenosis
NSAID induced prerenal falure
NSAIDs can cause prerenal failure in patients with pre-existing renal disease by inhibiting prostaglandin synthesis which leads to constriction of the afferent areterioles and reduced glomerular filtration ratio. NSAIDs are also associated with acute tubular necrosis and acute interstitial nephritis
- Treatment
- Discontinue NSAIDs
Dehydration and Systemic Hypotension
Dehydration and Systemic hypotension are the most common causes of acute renal failure. It is easily reveresed by replacing fluid and has a good prognosis. Diagnosis is clinical.
- Treatment
- Fluid replacement
Hypoaldosteronism
Hypoaldosteronism causes poor sodium and water reabsorption leading to hypovolemic hyponatremia. It is commonly caused by Addison disease (autoimmune) and Waterhouse-Friderichsen Syndrome (infectious)
- Patient history
- Hyperpigmentation (Addison disease)
- History of meningococcal infection (Waterhouse-Friderichsen syndrome)
- Signs and symptoms
- Weakness
- Hypotension and syncope
- Salt craving
- Hypoglycemia (due to low cortisol)
- Uremia
- Investigations
- U/E/Cs
- Hyponatremia
- Hyperkalemia
- Elevated BUN
- Elevated Cr
- Elevated BUN/Cr
- Urinalysis
- No abnormalities
- Complete blood count
- Anaemia
- Neutropenia
- Lymphocytosis
- Plasma renin
- High
- Serum aldosterone
- Low
- U/E/Cs
- Treatment
- Prednisone and fludrocortisone
Hepatorenal syndrome
Hepatorenal syndrome is an idiopathic prerenal failure caused by severe liver disease. It presents with a prerenal picture with features of liver failure (hypoalbuminemia, hyperbiliubinemia, prolonged PT). It is a diagnosis of exclusion and is usually diagnosed when there is prerenal azotemia in the setting of liver faillure.
- Pathophysiology
- Increased Nitric Oxide production → systemic vasodilation → activation of renal sympathetic nervous system → vasoconstriction of afferent arterials → reduced renal perfusion and glomerular filtration rate → activation of RAAS → vasoconstriction → further decrease in GFR → azotemia
- Signs and symptoms
- Jaundice
- Pruritus
- Asterixis
- Ascites
- Spider angioma
- Peripheral edema
- Investigations
- U/E/Cs
- Elevated BUN
- Elevated Cr
- Elevated BUN/Cr
- Complete blood count
- Anaemia
- Thrombocytopenia
- LFTs
- Hypoalbuminaemia
- Hyperbilirubinaemia
- Coagulation panel
- Prolonged PT
- Paracentestis and culture of ascitic fluid: to rule out spontaneous bacterial peritonitis
- Elevated PMNs
- Positive culture
- U/E/Cs
- Treatment
- Vasoconstrictors e.g. terlipressin
- Human albumin
- 1500 mL normal saline (improvement excludes hepatorenal syndrome)
- Ceftriaxons (for SBP, until ascitic culture returns negative)
- Paracentesis for symptomatic ascites
- Monitor electrolytes and correct as needed
- Dialysis if needed