Renal Flashcards
State some prerenal causes of AKI due to volume depletion
diarrhoea, vomiting
burns
diuresis
haemorrhage
State some prerenal causes of AKI due to hypoperfusion
embolus renal artery stenosis NSAIDs ACEi AAA
State some prerenal causes of AKI due to hyotension
sepsis
anaphylaxis
cardiogenic shock
State some prerenal causes of AKI due to oedema
cardiac failure
cirrhosis
nephrotic syndrome
What are some renal causes of AKI
glomerular disease
tubular injury
acue interstitial nephritis
vascular disease
What drugs are nephrotoxins causing acute tubular necrosis
aminoglycosides, amphotericin and ciclosporin
What drugs are nephrotoxins causing glomerulonephritis
penicillamine, gold, captopril, phenytoin some antibiotics, including penicillins, sulfonamides and rifampicin
What drugs are nephrotoxins causing interstitial nephritis
penicillins, cephalosporins, sulfonamides, thiazide diuretics, furosemide, NSAIDs and rifampicin.
What are some causes of post-renal AKI
pelvic mass bladder cancer BPH stricture of ureters calculi
What are the key findings to diagose AKI
raise in creatinine
fall in eGFR
decreased urine output
Who is at increased risk of AKI
post surgical >65y past AKI dehydrated diabetes CKD heart failure nephrotoxic drugs liver disease use of iodinated contrast in 7/7
What is the definition of oliguria?
<0.5ml/kg/hr
Define stage 1 AKI
Creatinine rise of 26 micromol or more within 48 hours
Creatinine rise of 50–99% from baseline within 7 days* (1.50–1.99 x baseline)
Urine output < 0.5 mL/kg/h for more than 6 hours
Define stage 2 AKI
100–199% creatinine rise from baseline within 7 days* (2.00–2.99 x baseline)
Urine output** < 0.5 mL/kg/hour for more than 12 hours
Define stage 3 AKI
200% or more creatinine rise from baseline within 7 days* (3.00 or more x baseline)
Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days
Urine output < 0.3 mL/kg/hour for 24 hours or anuria for 12 hours
Any requirement for renal replacement therapy
How should i check the volume status of a patient with AKI
Core temperature.
Peripheral perfusion.
Heart rate/blood pressure (and any postural changes).
Jugular venous pressure.
Moistness of mucous membranes, skin turgor.
What signs should i look for on examination of patient with AKI
Signs of infection or sepsis.
Signs of acute or chronic heart failure.
Fluid status (dehydration or fluid overload).
Palpable bladder or abdominal/pelvic mass.
Features of underlying systemic disease (rashes, arthralgia).
What investigations should i do for a patient with AKI?
Bedside: urinalysis, ECG
Bloods: FBC, U+E, Cr, CRP, LFT, CK, ESR, coag, ANA, serum Ig. ABG if
Micro: blood culture, culture infection sources
Imaging: USS bladder, CXR (pulmoary oedema), AXR (renal calculi), CTKUB if obstruction persists after catheter
What are the indications for RRT in AKI?
uraemic pericarditis uraemic encephalopathy refractory hyperkaleamia refractory pulmonary oedema severe metabolic acidosis <7.2pH
When should a patient with AKI be referred to a nephrologist?
hyperkalaemia uraemia glomerulonephritis systemic disease no obvious reversible cause
What information does a nephrologist want to know about a patient with AKI?
history and timecourse U+E urine dipstick drugs fluid balance current volume status
What is glomerulonephritis?
inflammation of the glomeruli and nephrons!
What can cause glomerulonephritis?
minimal change disease FSGS membranous glomerulonephritis SLE amyloidosis diabetes
What drugs should be stopped in AKI due to the fact they will worsen it?
NSAIDs • Aminoglycosides • ACE inhibitors • Angiotensin II receptor antagonists • Diuretics
What are the features of hypokalaemia on ECG/
u waves
flattened t waves
prolonged QT interval
Name some reasons for extrarenal loss of K+
vomiting
diarrhoea
villous adenoma
Name some reasons for renal loss of K+
diuretics - loop and thiazide mineralocorticoid excess - Conn's - Cushing's - corticosteroids - ectopic ACTH renal tubular acidosis
What is the mechanism for loop and thiazide diuretics causing hypokalaemia
loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule,
activation of the renin-angiotensin-aldosterone system
Increased aldosterone stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion,
What is the mechanism of loop diuretics?
inhibit the sodium-potassium-chloride cotransporter in the thick ascending limb
leads to a significant increase in the distal tubular concentration of sodium, reduced hypertonicity of the surrounding interstitium, and less water reabsorption in the collecting duct.
diuresis (increased water loss) and natriuresis (increased sodium loss)
What is the mechanism of thiazide diuretics
inhibit the sodium-chloride transporter in the distal tubule
Name some reasons for the shift of K+ into cells causing hypokalaemia
insulin
salbutamol
catecholamines
Name some reasons decreased intake of K+ causing hypokalaemia
prolonged fasting
anorexia
What are the clinical features of hypokalaemia?
lethargy muscle weakness u waves on ECG ileus arrhythmias cardiac arrest
What is the treatment for hypokalaemia
oral KCL
IV KCL if <2.5 or at risk of arrhythmias
correct underlying cause
What broad categories can be the cause of hypokalaemia
reduced intake
uptake into cells
renal loss
GI loss
What causes of hypokalaemia are associated with alkalosis?
vomiting
diuretics
Cushing’s syndrome
Conn’s syndrome
Why can diuretics cause alkalosis
the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
The increased hydrogen ion loss can lead to metabolic alkalosis.
What causes of hypokalaemia are associated with acidosis?
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
What drug can hypokalaemia increase the toxicity of?
digoxin
What is the most worrying consequence of hyperkalaemia
VF
cardiac arrest
Broadly speaking, what are the reasons that hyperkalaemia occurs
excess release from cells
potassium retention
What are the causes of potassium retention leading to hyperkalaemia
renal failure
decreased mineralocorticoids - Addison’s, ACEi, ARB
diuretics - K+ sparing, spironolactone
Describe the mechanism of action of potassium sparing diuretics
directly inhibit ENaC
inhibiting sodium reabsorption, so less potassium and hydrogen ions are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.
can cause hyperkalaemia
Describe the mechanism of aldosterone receptor antagonists
antagonize the actions of aldosterone (increased Na+ excretion by ENaC, at the distal segment of the distal tubule.
causes more sodium to pass into the collecting duct and be excreted in the urine.
less potassium and hydrogen ion are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.
What are the causes of excess potassium release leading to hyperkalaemia
rhabdomyolysis
haemolysis
GI bleed
acidosis
What are the signs of hyperkalaemia on ECG
tall-tented T waves, small P waves, prolonged PR interval widened QRS - sine wave appearance asystole
What are the steps in treatment of hyperkalaemia in an emergency
stabilise cardiac membrane - 10ml 10% calcium gluconate over 2 mins
move K+ into intracellular space - insulin + glucose (10 units actrapid in 50ml 20% glucose), nebulised salbutamol
remove K+ from body - calcium resonium
dialysis if refractory
When is hyperkalaemia considered an emergency?
K+ >6.5
ECG changes seen
What is the treatment for mild hyperkalaemia
restrict oral and IV potassium
What are common causes of CKD
hypertension diabetes nephrotoxic drugs SLE vasculitis glomerulonephropathy polycystic kidney disease recurrent pylonephritis obstruction
Which drugs can cause CKD
lithium ciclosporin aminoglycosides tacrolimus mesalazine
What are the key investigations in suspected CKD
Bedside: urine dipstick, urine sample A:Cr, urinalysis
Bloods: FBC, U+E, Cr, glucose, autoantibodies, Ca2+, phpsphate, vit D, PTH
Micro: urine MC+S
Imaging: AXR, USS KUB, CTKUB
special tests: biopsy if kidneys normal size
What complications does uraemia cause in CKD?
pericarditis encephalopathy nausea vomiting bleeding neuropathy
What causes renal bone disease?
loss of renal function that activates vitamin D (1-alpha hydroxylation)
less absorption of dietary Ca2+
increased PTH
hyperphosphateaemia
destruction of bones by osteoclasts to raise Ca2+
osteodystrophy
Why does anaemia develop in CKD
reduced EPO
bone marrow not stimulated
less red blood cells made
How is renal bone disease treated?
1alpha hydroxycholecalciferol = alfacalcidol = vitamin D analogue
calcium supplements
phosphate binders - decrease phosphate absorption
how is anaemia treated in CKD
EPO
how is acidosis treated in CKD
sodium bicarbonate supplements
how is oedema treated in CKD
loop diuretics
fluid restriction
how is hypertension treated in CKD
ACEi or ARB
How is the risk of CVD managed in CKD
statin
aspirin
What can cause increase the rate of progression of CKD
AKI Heart failure - chronic, Peripheral arterial disease Hypertension and/or proteinuria . Diabetes Smoking. NSAIDs Nephrotoxic drugs such as lithium, ciclosporin, and diuretics. Untreated urinary outflow tract obstruction Structural renal tract disease renal calculi. Multi-system diseases with potential kidney involvement, such as systemic lupus erythematosus (SLE).
What is the MDRD
Modification of Diet in Renal Disease (MDRD) equation
used to estimate the GFR using serum creatinine
What variables are used when calculating the MDRD
serum creatinine
age
gender
ethnicity
What are the limitations of eGFR
may be affected after protein rich meal 12 hours before test - rasied creatinine
not validated in mild renal disease
affected by muscle mass
pregnancy
If a patient with CKD is discovered to have proteinuria, what is the best management?
blood pressure control - ACEi
Depending on ACR result, what is the best course of action in CKD
An ACR of less than 3 mg/mmol does not require further action.
An ACR of 3-30 does not usually require action, though would be checked annually.
An ACR of greater than 30 suggests significant leakage of protein through the kidneys, and the higher the level the more concern, especially if it is over 100.
What should be done before prescribing any drug in CKD?
check how its administration should be altered!
renal drug handbook!
Which drugs are particularly significant in terms of dose modification in CKD
aminoglycosides cephalosporins heparin lithium opiates digoxin
What are the indications for dialysis in CKD
uraemic pericarditis uraemic encephalopathy hyperkalaemia acidosis pulmonary oedema
What defines end stage renal failure
need for RRT
GFR <15
What defines stage 1 CKD
GFR >90
with presence of kidney damage
What counts as ‘presence of kidney damage’ in the CKD stages
proteinuria
haematuria
evidence or abnormal anatomy
evidence of systemic disease
What defines stage 2 CKD
GFR 60-89
with presence of kidney damage
What defines stage 3a CKD
GFR 45-59
What defines stage 3b CKD
GFR 30-44
What defines stage 4 CKD
GFR 15-29
What defines stage 5 CKD
GFR <15
State the basic mechanism of action of haemodialysis
AV fistula formed
blood and dialysis fluid separated by semipermeable membrane
flow in opposite directions
solutes move from blood to fluid
How long does it take for an AV fistula to be usable after it has been formed
8 weeks
why do the dialysis fluid and blood need to flow in opposite directions in haemodialysis
so the blood always meets a less concentrated solution
allows diffusion down concentration gradient from blood to fluid
State the basic mechanism of action of peritoneal dialysis
uses peritoneum as semipermeable membrane
permanant catheter inserted into peritoneal cavity
isotonic/hypertonic glucose solution infused into peritoneal cavity
solutes move from blood into peritoneum
drained after several hours
Why is hypertonic fluid used in peritoneal dialysis
removes excess fluid from body
What are the key indications for renal transplant?
ESRF polycystic kidney disease diabetes pyelonephritis glomerulonephritis
What are the contraindications for renal transplant
Cancer. Active infection. Uncontrolled ischaemic heart disease. AIDS with opportunistic infections. Active viral hepatitis. Extensive peripheral vascular disease.
What are the common problems caused by haemodialysis
inconvenience - 4h 3xweek high cost increased risk cardiovascular disease fluid restriction fistula problems - thrombosis, infection disequilibration syndrome hypotension
What are the common problems caused by peritoneal dialysis
peritonitis
exit site infection
Which organisms commonly cause peritonitis in peritoneal dialysis patietns
Staphylococcus epidermidis
Staphylococcus aureus
What are the common problems caused by renal transplant
immunosupression leads to infection and malignancy
graft failure
cardiovascular disease
What cancers are more likely after immunosupression following renal transplant
lymphoma
skin
Name some common drugs used for immunosupression following renal transplant
tacrolimus ciclosporin azathioprine prednisolone sirolimus monoclonal antibodies
Name some of the infections that are likely after immunosupression following renal transplant
HSV
Candida
Pneumocystis jirovecii
CMV
What are the side effects associated with tacrolimus and cicllosporin
hypertension, tremor, increased incidence of diabetes mellitus and renal impairment
What are the side effects associated with azathioprine and mycophenolate
neutropenia
Define nephrotic syndrome
proteinuria >4.5g in 24h
hypoalbuminaemia <30g/L
peripheral oedema
What is the pathophysiology behind nephrotic syndrome
damage to podocytes leads to widening of filtration barrier
high molecular weight proteins can leak through the basement membrane and into the glomerulus
not reabsorbed, so lost in urine
What are the causes of nephrotic syndrome
glomerulonephritis - minimal change, membranous, FSGS diabetes amyloidosis SLE multiple myeloma
Describe the key features of minimal change disease
affects children
mainly idiopathic
can be due to NSAIDs or Hodgkin’s lymphoma
responds well to steroids
Describe the key features of membranous glomerulonephritis
can be caused by infection, rheumatoid drugs and cancer
thickened BM
IgG and C3 present
Describe the key features of FSGS glomerulonephritis
mainly idiopathic
IgM and C3
What investigations should be done in suspected nephrotic syndrome
urinalysis, BP, 24hr urine collection, urine P:Cr
FBC, U+E, glucose, lipid profile, ANA, Ig screen
USS KUB
renal biopsy
What is the differential diagnosis in nephrotic syndrome
CCF
liver disease
What are the compliciations of nephrotic syndrome
hypercoaguability - leads to DVT, renal vein thrombosis
hypercholesterolaemia
increased susceptibility to infection - esp pneumococcal
Why does hypercoaguability occur in nephrotic syndrome
loss of ATIII in urine
Why does increased susceptibility to infection occur in nephrotic syndrome
loss of Ig
What is the treatment for nephrotic syndorme
reduce oedema - loop diuretics eg IV furosemide
prevent loss protein - ACEi
reduce complications - anticoagnulation. statins, pneumococcal vaccine
treat underlying cause
What are the key investigations to rule out multiple myeloma?
plasma electrophoresis
urine electrophoresis - Bence-Jones proteins
Define nephritic syndrome
haematuria
mild proteinuria
inability to excrete fluids - leading to oedema and HTN
reduced eGFR - leading to uricaemia
What are the causes of nephritic syndrome
rapidly progressive glomerulonephritis
- due to Goodpasture’s, Wegener’s SLE
IgA nephropathy
Describe the key features of Goodpasture’s syndrome
affects lungs and kidney
anti-GBM antibody
leads to acute renal failure and pulmoanry haemorrhage
Describe the key features of Wegener’s granulomatosis
affects upper airway, lungs and kidneys
cANCA
crescents seen in glomeruli on microscopy
Describe the key features of SLE
affects joints, kidneys and skin
ANA, anti dsDNA
Describe the key features of IgA nephropathy
history of upper respiratory infections
mesangial IgA deposits
What are the features of chronic GN on USS kidneys
small shrunken kidmeys
What investigations should be done in suspected glomerulonephritis
urine dipstick, urine microscopy, urine protein
FBC, U+E, eGFR, Cr, ANA, dsDNA, antiGBM, cANCA
blood cultures
USS kidneys
renal biopsy
What are the features of atherosclerotic renal artery stenosis
HTN - due to reduced blood flow to kidneys, so increased RAAS
fluid overload of bilateral
small kidney on USS
