Acute kidney injury Flashcards
(73 cards)
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.
