Nephrology Flashcards
How can we divide up the causes of AKI?
Prerenal
Lack of blood flow to the kidneys
Intrarenal
Intrinsic damage to the glomeruli, renal tubules or interstitium
Postrenal
Obstruction to the urine coming from the kidneys
What findings can be expected in AKI?
Reduced urine output (<0.5ml/kg/hour is termed oliguria)
Fluid overload
Rise in molecules that the kidney normally excretes/maintains balance of, e.g. potassium, urea and creatinine
Symptoms of AKI
Reduced urine output
Pulmonary/peripheral oedema
Arrhythmias (due to potassium levels)
Uraemia features (pericarditis/encephalopathy)
What should we test in all AKI patients?
U+Es
Urinalysis
When should we do a renal ultrasound in AKI?
If there’s no identifiable cause for the deterioration OR are at risk of a urinary tract obstruction
What commonly used drugs should be stopped in AKI?
Metformin Lithium Digoxin NSAIDs Aminoglycosides ACEi Diuretics Angiotensin II receptor antagonists
How should we treat hyperkalaemia should it arise in AKI?
IV calcium gluconate Combined insulin/dextrose infusion Nebulised salbutamol Loop diuretics Calcium resonium Dialysis (last line)
Blood supply of the kidneys?
Renal arteries + veins
What is the normal blood urea nitrogen (BUN):creatinine ratio?
Causes of pre-renal AKI
Decreased bloodflow due to:
Absolute loss of fluid - Major haemorrhage Vomiting Diarrhoea Severe burns
Relative loss of fluid -
Distributive shock
Congestive heart failure (blood pools in the venous system)
Local to the kidney -
Renal artery stenosis
Embolus
What is azotemia?
High levels of nitrogen containing blood
What happens to the RAAS system during AKI?
Kidneys activate the RAAS, causing adrenal glands to secrete aldosterone which tells the kidneys to reabsorb sodium
Sodium reabsorption results in increased water reabsorption AND urea reabsorption
Is urine more concentrated in pre-renal AKI?
Yes. There is more urea relative to water than usual
What is the BUN:creatinine ratio in pre-renal AKI?
> 20:1
What is the most common cause of intrarenal AKI?
Acute tubular necrosis:
What are causes of acute tubular necrosis?
Ischaemia to the tubular cells Nephrotoxins: Aminoglycosides Heavy metals (e.g. lead) Myoglobin (from damaged muscle) Ethylene glycol (anti-freeze) Radiocontrast dye Uric acid (tumour lysis syndrome during cancer treatment)
How can you prevent uric acid causing tubular necrosis during cancer treatment?
Make sure they stay well hydrated
Give medications: allopurinol, urate oxidase
Trying to reduce the effects of tumour lysis syndrome
What happens to the tubule during acute tubular necrosis?
For whatever reason there is cell death. These cells then go into the tubule lumen and plug the tubule. This increases the pressure and makes it harder for fluid to flow down the tubules, reduced eGFR
What do you get a build up of in the blood during acute tubular necrosis resulting in AKI?
Acid (metabolic acidosis)
Hyperkalaemia
What might you find in the urine of someone with an acute tubular necrosis?
Brown grannular casts (these are the clumps of dead cells from the necrosis)
What is glomerulonephritis?
Inflammation of the glomerulus causing a reduction in eGFR. It is often caused by the deposition of antigen-antibody complexes in glomerular tissue
What do the antigen-antibody complexes activate in glomerulonephritis?
The complement system. This then attracts macrophages and neutrophils to the site. These release lysosomal enzymes which then damage podocytes in the glomerulus
Function of podocytes
They are negatively charged and have small gaps in between them. As a result larger molecules cannot get through.
What happens when podocytes are damaged (e.g. by lysosomal enzymes from neutrophils etc.)
They allow larger molecules to pass through (e.g. proteins and red cells)
Fluid leakage also reduces pressure difference which means lower GFR
This causes fluid build up and therefore oedema and HTN