Renal disease: pre-renal Flashcards
What are the three major causes of Acute Kidney Injury (AKI)?
AKI can be caused by pre-renal, renal, or post-renal factors.
What are the main causes of pre-renal AKI?
Pre-renal AKI is mainly caused by reduced perfusion to the kidneys and can be the result of an acute systemic illness. The urine dipstick usually shows a bland result. This form of AKI is usually acute and potentially reversible, accounting for 55-60% of AKI incidence.
What are the main causes of renal AKI?
Renal AKI can be caused by autoimmune diseases, acquired or inherited renal diseases, nephrotoxic drugs, or disease of the renal blood vessels. Most glomerular diseases occur without warning or a prodromal illness. The urine dipstick usually shows blood and protein present. This form of AKI often presents acutely but can result in chronic kidney disease, accounting for 35-40% of AKI incidence.
What are the main causes of post-renal AKI?
Post-renal AKI is caused by an obstruction to the flow of urine, such as ureteric stones, benign prostate obstruction, ureteric strictures, or pelvic malignancy. It is usually diagnosed radiologically or in patients with a known urological history. The urine dipstick is often blood positive. This form of AKI can present either acutely or chronically and accounts for less than 5% of AKI incidence.
What is Acute Kidney Injury (AKI) and what factors contribute to it?
AKI occurs when there is a sudden decrease in glomerular filtration rate (GFR), which is maintained by sufficient blood flow to the kidneys and nephron. If this is compromised, AKI can occur. The condition is usually reversible. GFR depends on a pressure gradient between the incoming blood at the afferent capillaries and the pressure in Bowman’s space, known as net filtration pressure.
What is pre-renal AKI and when does it occur?
Pre-renal AKI occurs when there is reduced perfusion to the kidneys through the afferent arteriole. This can happen regardless of whether the patient has hypovolaemia, euvolaemia, or hypervolaemia. The causes of pre-renal AKI can be divided into different sections.
What are the main causes of pre-renal AKI due to absolute hypovolaemia?
Causes of pre-renal AKI due to absolute hypovolaemia include:
Haemorrhage (shock) from trauma, surgery, postpartum, or gastrointestinal issues
Gastrointestinal losses, such as diarrhoea and vomiting
Renal losses, caused by drug-induced or osmotic diuresis, diabetes insipidus, and adrenal insufficiency
Losses through skin and mucous membranes, as in burns, hyperthermia, or other insensible losses
“Third-space” losses, such as pancreatitis and hypoalbuminaemia.
What are the main causes of pre-renal AKI due to decreased cardiac output?
Causes of pre-renal AKI due to decreased cardiac output include:
Diseases of the myocardium, valves, pericardium, or conducting system
Pulmonary hypertension, pulmonary embolism, positive pressure mechanical ventilation
Systemic vasodilation: Sepsis, liver failure, anaphylaxis
Drugs: antihypertensives, anaesthetics, drug overdoses.
What are the main causes of pre-renal AKI due to renal vasoconstriction?
Causes of pre-renal AKI due to renal vasoconstriction include noradrenaline, liver disease, sepsis, and hypercalcaemia.
What are the main causes of pre-renal AKI due to renovascular diseases?
Renovascular diseases causing pre-renal AKI include atherosclerosis, thromboembolic disease, and renal artery dissection.
What drugs can cause pre-renal AKI by impairing autoregulation and glomerular filtration rate?
Drugs that impair autoregulation and glomerular filtration rate, thus causing pre-renal AKI, include angiotensin-converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs that inhibit prostaglandin synthesis during renal hypoperfusion, diuretics, angiotensin II receptor blockers like candesartan, cyclosporin, and tacrolimus.
What are the primary causes of pre-renal AKI?
The primary causes of pre-renal AKI include:
Intravascular volume depletion or absolute hypovolaemia
Decreased cardiac output
Renal vasoconstriction
Renovascular diseases, and
Drugs that impair autoregulation and glomerular filtration rate by affecting the vascular tone of afferent and efferent arterioles.
What drugs are known to cause Acute Tubular Necrosis (ATN)?
Drugs that can cause Acute Tubular Necrosis (ATN) include:
Antibiotics like Vancomycin, Acyclovir, Foscarnet, Pentamidine, Aminoglycoside-Gentamicin, and Amphotericin B.
Organic solvents such as Ethylene Glycol and Toluene.
Anti-inflammatory painkillers like NSAIDs including COX 2 inhibitors.
Antihypertensives like ACE inhibitors (in patients with Bilateral Renal Artery Stenosis).
Chemotherapeutic agents such as Cisplatin and Ifosfamide.
Immunosuppressants like Cyclosporin, Tacrolimus, and IV immunoglobulin.
Radiocontrast agents.
Which drugs are known to cause tubular cell toxicity, interstitial nephritis, and crystal toxicity in AKI?
Tubular cell toxicity can be caused by Aminoglycosides, Amphotericin B, and Cisplatin.
Interstitial Nephritis can be caused by NSAIDs and Rifampicin.
Crystal Toxicity can be caused by Acyclovir and Ampicillin.
How can ACE inhibitor therapy result in worsening renal function?
ACE inhibitor therapy can worsen renal function in certain settings due to their action in decreasing glomerular filtration pressure. This can occur in conditions with already compromised renal perfusion such as bilateral renal artery stenosis or heart failure.