Renal Flashcards
AKI DEFINITIONS
i) how is AKI defined?
ii) over what period does decline occur?
iii) is eGFR an accurate way to diagnose AKI?
iv) name the four most common causes
i) defined as an abrupt decline in kidney function from baseline
ii) decline in kidney function over days/weeks
iii) eGFR is not sensitive for AKI as it doesnt detect quick changes
AKI staging & classification?
i) what staging system is used?
ii) which two things is the staging criteria based on?
iii) is electrolyte disturbance specific for AKI?
i) KDIGO
ii) criteria based on creatinine and urine output
iii) electrolyte disturbance can be a consequence of but is not specific for AKI
PRE RENAL AKI
i) what is the broad cause of this? is there damage to the kidney itself?
ii) name four conditions that this may happen in
iii) give three modifiable and two non modafiable RF? what is the most important RF?
iv) name a drug class that causes vasoconstriction of the afferent arteriole and therefore decreased GFR?
v) name two other drugs that can cause AKI
vi) what condition can decreased blood flow to the kidneys cause?
i) reduced renal perfusion (no damage to kidney itself)
ii) can happen in shock, heart failure, haemorrhage, sepsis, dehydration
iii) mod - hypovolaemia, sepsis, infection, drugs
non mod - diabetes, HTN, CKD, liver disease
iv) NSAIDs cause vconstric of afferent arteriole > decrease in glom pressure and GFR
v) ACEi and ARBs can cause decreased activation of AG system therefore lower GFR
vi) decreased blood flow to the kidneys can cause acute tubular necrosis
MANAGEMENT OF PRE PRENAL AKI
i) name three drugs that should be stopped
ii) which antibiotic is associated with poor renal function?
iii) what potassium levels may be seen?
i) stop ACEi, diuretics, NSAIDs
ii) trimethoprim
iii) see hyperkalemia (injury of cells secreting K+ in DT)
INTRINSIC AKI
i) name three causes of renal AKI? which is the most common?
ii) name two drugs that can cause it
iii) which cancer increased risk of renal AKI?
i) glomerlonephritis, vasculitis, acute tubular necrosis (ATN is most common)
ii) nephrotoxic medication such as aminoglycosides or cisplatin
iii) myeloma
POST RENAL AKI
i) what is the most common cause of this? give three examples
ii) which type of drugs may be implicated?
iv) what happens in post renal AKI?
i) most common cause is obstruction eg, tumours, clots, stones and BPH
ii) anti cholinergic drugs can cause urine retention
iii) obstruction can cause build up of renal oressure and atrophy of cells
- also get leucocyte infiltration and cytokine release
CLINICAL FEATURES OF AKI
i) what are the presentations often related to?
ii) what general symptom is often seen?
iii) what potassium levels are seen?
iv) is there acidosis or alkalosis? what symptom may accompany this
i) related to complications of renal failure
ii) general = uraemia (build up of toxins in the blood) > malaise, pruritis, parasthesia, altered mental state
iii) hyperkalemia due to decreased potassium secretion
iv) acidosis > kussmaul breathing
MANAGEMENT OF AKI
i) what ultimately needs to be done?
ii) give two things that can be done to manage pre renal AKI
iii) give two things that can be done in intrinsic AKI
iv) three things that can be done in post renal AKI? which team should be reffered to?
v) name five situations where patient should be referred for renal replacement therapy (POPAC)
i) need to correct the underlying cause
ii) pre renal - stop nephrotoxic drugs and volume replace
ii) intrinsic - stop nephrotoxic drugs and consider immunosuppresion in some forms of glomerulonephritis
iv) post renal - catheter, nephrostomy, stent (contact urology)
v) pulmonary oedema, oedema, potassium (hyperkalemia), acidosis, complications of uraemia eg pericarditis
CKD
i) how is it defined?
ii) which three ways can it be classified?
iii) is it reversible or irreversible?
iv) what are the three most common causes in the UK?
i) defined by abnormal kidney structure or function for > 3 months
ii) can be classified on how reduced is eGFR, level of albuminuria or underlying disease
iii) irreversible
iv) most common causes are diabetes, hypertension and glomerular disease
CKD HISTORY
i) name three associated symptoms that might be important
ii) what should be looked for in the eyes and hands?
iii) what fluid levels may be seen?
iv) name three investigations to be done?
i) anaemia, nausea, headache, pruritis
ii) look for anaemia - pale conjunctiva and palmar creases
iii) may be in fluid overload
iv) eGFR, bloods, urine dipstick, CXR
MANAGEMENT OF CKD
i) what should first be managed?
ii) what are two first line drugs if there is proteinuria?
iii) what type of disease are patients with CKD at high risk of?
iv) which two electrolytes should only be consumed in small amounts in the diet?
i) manage hypertension first
ii) if proteinuria give an ACEi or ARB
iii) high risk of CV disease
iv) low pbosphate/potassium diet
WHAT IS SEEN IN CKD?
i) what eGFR levels and creatinine levels are seen?
ii) what phosphate levels are seen?
iii) what blood related disorder is seen?
iv) what calcium levels are seen?
v) name a nephrotoxic drug that should be avoided
i) low GFR and high creatinine
ii) high phosphate levels
iii) anaemia (lack of EPO production)
iv) hypocalcaemia
v) avoid NSAIDs
CKD MECHANISM
i) what does the kidney initially do in response to renal injury? what does it try to maintain?
ii) how does this affect glom permeability? what effect does this have on mesangial cells?
iii) which molecule is also upregulated in renal injury? how does this lead to more scarring of the glom?
iv) which scoring category is used? what two things is this based on?
i) In response to renal injury, there is thought to be an increase in intra-glomerular pressure with glomerular hypertrophy, as the kidney attempts to adapt to nephron loss to maintain constant glomerular filtration.
ii) An increase in glomerular permeability to macro-molecules such as transforming growth factor-beta (TGF-beta), fatty acids, pro-inflammatory markers of oxidant stress, and protein may result in toxicity to the mesangial matrix, causing mesangial cell expansion, inflammation, fibrosis, and glomerular scarring.
iii) Additionally, renal injury results in an increase in angiotensin II production, causing an upregulation of TGF-beta, contributing to collagen synthesis and renal scarring within the glomerulus.
iv) KDIGO > based on albuminuria and GFR
Both the structural alterations and accompanying biochemical, cellular, and molecular changes seem to account for progressive renal scarring and loss of kidney function.
All forms of CKD are also associated with tubulo-interstitial diseases; the exact mechanism of injury is not known, but is thought to be secondary to a reduction in blood supply in addition to an infiltration of lymphocytes and inflammatory mediators that result in interstitial fibrosis and tubular atrophy.
HYPERPARATHYROIDISM IN CKD
i) what does parathyroid hormone do - by what three mechanisms does it do this? when is it released? what type of hyperparathyroidism is seen in CKD? what does this mean?
ii) why do you get hyper PT in CKD?
iii) how is phosphate implicated?
i) released from PT gland when calcium levels are low > increases calcium reabs in kidney (via vitamin D) resorption of bone and increases calcium abs from small intestine (by decreasing phosphorus abs)
secondary hyperPTH - secondary to hypocalcaemia
ii) secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D
- elevation of parathyroid hormone (PTH) in response to hypocalcemia induced by phosphate retention and reduced calcitriol synthesis as a consequence of reduced renal function
iii) in CKD - decreased phosphate clearance > hyperphosphataemia > hypocalcaemia > stim of PT glands
UTI
i) what is it? what is the most common type? why does it affect women more? what is the most common causative organism?
ii) name four risk factors? what is uncomplicated/complicated/recurrent/relapsing?
iii) name three symptoms? how is an upper UTI more likely to present? (3)
iv) what investigation should be done? what two things are likely to be seen if a UTI is presennt?
v) what is offered to men? what abx is given? what is offered to women? what is given if complicated/uncomplicated? what should be done if symptoms persist?
vi) which group of people should always be sent for culture with asymptomatic bacteruria
i) infection of urethra, bladder or kidneys
* cystitis is the most common
* mostly affects women due to shorter urethra length - in men should always warrant clinical suspic
* Ecoli most common organism
ii) RF > immunosupression, diabetes, underlying renal tract abnorms
Uncomplicated > normal underlying GU anatomy and physiology
Complicated > underlying anatomy or physiol predisposes to UTI (outflow obstruc)
Recurrent > repeat infection with new organism
Relapsing > repeat infection with the same organism
iii) Dysuria, increased freq or urgency
* smelly urine
* upper UTI - more likely to px systemically unwell with fever, loin pain, back pain
iv) Urine Dip
Working dx of UTI given typical symptoms and leucocyte esterase/nitrites on urine
v) drink fluids and wipe from front to back
- Men - offer symp relief with paracetamol and treat lower UTI without assoc indewelling catheters with trimethiprim 200mg BD for 7 days
- Women - symp relief with paracetamol or NSAIDS
* if uncomplicated - trimethoprim 200mg BD for 3 days /nitrofurantoin 50mg QDS for 3 days
* complicated - consider prolonging abx therapy for 3 days
* if symptoms persist > send for MC&S
vi) all pregnant women with asymp bacteruria should be sent for culture and treated with 7 days of nitro
