Acute kidney injury Flashcards
What percentage of drug-induced acute kidney injury is accounted for by acute interstitial nephritis?
Acute interstitial nephritis accounts for 25% of drug-induced acute kidney injury.
What are the most common drug causes of acute interstitial nephritis?
The most common drug causes include antibiotics such as penicillin, rifampicin, NSAIDs, allopurinol, and furosemide.
What systemic diseases can cause acute interstitial nephritis?
Systemic diseases include SLE, sarcoidosis, and Sjogren’s syndrome.
What infections are associated with acute interstitial nephritis?
Infections include Hanta virus and staphylococci.
What histological features are seen in acute interstitial nephritis?
Histology shows marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules.
What are the clinical features of acute interstitial nephritis?
Clinical features include fever, rash, arthralgia, eosinophilia, mild renal impairment, and hypertension.
What investigations are used to diagnose acute interstitial nephritis?
Investigations show sterile pyuria and white cell casts.
Who is most commonly affected by tubulointerstitial nephritis with uveitis (TINU)?
TINU usually occurs in young females.
What symptoms are associated with tubulointerstitial nephritis with uveitis?
Symptoms include fever, weight loss, and painful, red eyes.
What findings are seen in urinalysis for tubulointerstitial nephritis with uveitis?
Urinalysis is positive for leukocytes and protein.
What is acute kidney injury (AKI)?
AKI describes a reduction in renal function following an insult to the kidneys. Around 15% of patients admitted to hospital develop AKI.
What are the potential outcomes of AKI?
Most patients with AKI recover renal function, but some may have long-term impaired kidney function. AKI can also result in acute complications, including death.
What are the causes of AKI?
Causes of AKI are divided into prerenal, intrinsic, and postrenal causes.
What are prerenal causes of AKI?
Prerenal causes relate to ischaemia or lack of blood flow to the kidneys. Examples include hypovolaemia secondary to diarrhoea/vomiting and renal artery stenosis.
What are intrinsic causes of AKI?
Intrinsic causes involve damage to the kidneys themselves, often due to toxins or immune-mediated conditions. Examples include glomerulonephritis, acute tubular necrosis (ATN), and rhabdomyolysis.
What are postrenal causes of AKI?
Postrenal causes relate to obstruction of urine flow from the kidneys. Examples include kidney stones and benign prostatic hyperplasia.
Who is at increased risk of AKI?
Risk factors include chronic kidney disease, other organ failure, history of AKI, use of nephrotoxic drugs, age 65 or over, and oliguria.
How can AKI be prevented?
Identifying patients at risk of AKI can help reduce incidence. For example, providing IV fluids during investigations requiring contrast.
What happens when kidneys stop working?
Key indicators of AKI include reduced urine output (oliguria) and fluid overload, along with a rise in potassium, urea, and creatinine.
What are the symptoms and signs of AKI?
Symptoms may include reduced urine output, pulmonary and peripheral oedema, arrhythmias, and features of uraemia.
How is AKI detected?
Detection involves blood tests for urea and electrolytes (U&Es) and urinalysis. NICE criteria include a rise in serum creatinine or a fall in urine output.
What is the management of AKI?
Management is largely supportive, focusing on fluid balance and reviewing medications. Certain drugs may need to be stopped or adjusted.
What treatments are not recommended for AKI?
Routine use of loop diuretics and low-dose dopamine is not recommended. However, loop diuretics may be used for significant fluid overload.
What is the treatment for hyperkalaemia in AKI?
Treatment includes stabilisation of the cardiac membrane, short-term potassium shift, and removal of potassium from the body.
When is specialist input required in AKI management?
Specialist input is needed for severe AKI or unknown causes, and all patients with suspected AKI secondary to urinary obstruction require urologist review.
What is renal replacement therapy?
Renal replacement therapy, such as haemodialysis, is used when a patient does not respond to medical treatment of complications.
Management
Hyperkalaemia treatments
What is the urine sodium level in pre-renal uraemia?
< 20 mmol/L
What is the urine sodium level in acute tubular necrosis?
> 40 mmol/L
What is the urine osmolality in pre-renal uraemia?
> 500 mOsm/kg
What is the urine osmolality in acute tubular necrosis?
< 350 mOsm/kg
What is the fractional sodium excretion in pre-renal uraemia?
< 1%
fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100
What is the fractional sodium excretion in acute tubular necrosis?
> 1%
What is the response to fluid challenge in pre-renal uraemia?
Good
What is the response to fluid challenge in acute tubular necrosis?
Poor
What is the serum urea:creatinine ratio in pre-renal uraemia?
Raised
What is the serum urea:creatinine ratio in acute tubular necrosis?
Normal
What is the fractional urea excretion in pre-renal uraemia?
< 35%
fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100
What is the fractional urea excretion in acute tubular necrosis?
> 35%
What is the urine:plasma osmolality ratio in pre-renal uraemia?
> 1.5
What is the urine:plasma osmolality ratio in acute tubular necrosis?
< 1.1
What is the urine:plasma urea ratio in pre-renal uraemia?
> 10:1
What is the urine:plasma urea ratio in acute tubular necrosis?
< 8:1
What is the specific gravity in pre-renal uraemia?
> 1020
What is the specific gravity in acute tubular necrosis?
< 1010
What is the urine sediment like in pre-renal uraemia?
Normal/ ‘bland’ sediment
What is the urine sediment like in acute tubular necrosis?
Brown granular casts
Acute tubular necrosis vs prerenal uraemia
What increases the risk of Acute Kidney Injury (AKI)?
Emergency surgery, intraperitoneal surgery, chronic kidney disease (CKD) with eGFR < 60, diabetes, heart failure, age > 65 years, liver disease, and use of nephrotoxic drugs such as NSAIDs, aminoglycosides, ACE inhibitors/angiotensin II receptor antagonists, and diuretics.
What are the diagnostic criteria for AKI?
- Rise in creatinine of 26µmol/L or more in 48 hours OR 2. ≥ 50% rise in creatinine over 7 days OR 3. Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR 4. ≥ 25% fall in eGFR in children/young adults in 7 days.
What are the KDIGO staging criteria for AKI?
Stage 1: Increase in creatinine to 1.5-1.9 times baseline, or increase by ≥26.5 µmol/L, or reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours.
Stage 2: Increase in creatinine to 2.0 to 2.9 times baseline, or reduction in urine output to <0.5 mL/kg/hour for ≥12 hours.
Stage 3: Increase in creatinine to ≥ 3.0 times baseline, or ≥353.6 µmol/L, or reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or initiation of kidney replacement therapy, or in patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2.
When should a nephrologist be referred for AKI?
Refer if there is renal transplant, ITU patient with unknown cause of AKI, vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma, AKI with no known cause, inadequate response to treatment, complications of AKI, stage 3 AKI, CKD stage 4 or 5, or if qualifying for renal replacement due to hyperkalaemia, metabolic acidosis, complications of uraemia, or fluid overload (pulmonary oedema).
Kidney disease staging criteria
What is acute tubular necrosis (ATN)?
ATN is the most common cause of acute kidney injury (AKI) seen in clinical practice.
What severely affects the functioning of the kidney in ATN?
Necrosis of renal tubular epithelial cells.
Is ATN reversible?
In the early stages, ATN is reversible if the cause is removed.
What are the two main causes of ATN?
Ischaemia and nephrotoxins.
What are some causes of ischaemia leading to ATN?
Shock and sepsis.
What are some nephrotoxins that can cause ATN?
Aminoglycosides, myoglobin secondary to rhabdomyolysis, radiocontrast agents, and lead.
What are features of AKI in ATN?
Raised urea, creatinine, potassium, and muddy brown casts in the urine.
What are the histopathological features of ATN?
Tubular epithelium necrosis, loss of nuclei, detachment of tubular cells from the basement membrane, dilatation of the tubules, and necrotic cells obstructing the tubule lumen.
What are the phases of ATN?
Oliguric phase, polyuric phase, and recovery phase.
Necrotic desquamated epithelial cells inside the tubular lumens
Section of the renal cortex with diffuse necrosis and tubular dilatation. The glomeruli are normal
Severe dilatation of the tubules
What is Rhabdomyolysis typically associated with in exams?
A patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission.
What are some causes of Rhabdomyolysis?
Seizure, collapse/coma (e.g. elderly patient collapses at home, found 8 hours later), ecstasy, crush injury, McArdle’s syndrome, drugs (statins, especially if co-prescribed with clarithromycin).
What are the features of Rhabdomyolysis?
Acute kidney injury with disproportionately raised creatinine, elevated creatine kinase (CK), myoglobinuria (dark or reddish-brown colour), hypocalcaemia, elevated phosphate, hyperkalaemia, metabolic acidosis.
What is the significance of elevated creatine kinase (CK) in Rhabdomyolysis?
The CK is significantly elevated, at least 5 times the upper limit of normal. Elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology.
What is the management for Rhabdomyolysis?
IV fluids to maintain good urine output. Urinary alkalinization is sometimes used.
