Renal Flashcards
Why is someone with nephrotic syndrome at increased risk of thromboembolism?
They are losing antiithrombin 3 and plasminogen in the urine
What are some complications of nephrotic syndrome?
Infection, thromboembolism, hyperlipidaemia, hypocalcaemia, acute renal failure
If a patient is prescribed clarithromycin what would you do about their regular statin medication?
Get them to stop taking the statin temporarily while taking clarithromycin because of rhabdmyolysis risk
What are some complications of rhabdomyolysis?
Metabolic acidosis, hyperkalaemia, hypocalcaemia
Which glomerular nephritises cause nephrotic syndrome?
Minimal change, focal-segmental glomerular sclerosis, membranous glomerular nephritis
Which glomerular nephritises cause nephritic syndrome?
IgA nephropathy, post streptococcal, alport’s syndrome
What are the main side effects of oxybutynin?
Dry mouth, dizziness, confusion, blurred vision
at roughly what level do the kidneys sit in the retroperitoneum?
T12 to L3
which kidney sits a little lower than the other?
the right as it is displaced down slightly by the liver
which specialised cells are responsible for detecting any changes in Na concentration and filtrate osmolality?
macula densa cells
which cells release renin and sit adjacent to the bowmans capsule and afferent arteriole of the nephron?
juxtagglomerular cells
how does ADH affect the collecting duct and resulting urine?
ADH stimulates aqauporin channels to insert themself into collecting duct allowing water to move via osmosis into the intersitial spaces
resulting in more concentrated urine
what does renin do?
converts angiotensinogen into angiotensin 1
what does ACE (angiotensin converting enzyme) do?
converts angiotensin1 to angiotensin 2
what are the effects of angiotensin 2?
increases blood pressure by vasoconstriction:
- direct arteriole constriction
- aldosterone secretion leading to sodium reabsorption
-ADH release
what are some causes of pre-renal AKI?
hypovolaemia, haemorrhage, sepsis, renal artery stenosis
what are some causes of renal AKI?
glomerulonephritis, vasculitis, acute tubular necrosis
what are the two types of acute tubular necrosis?
ischaemic and nephrotoxic (from medications)
what triad of symptoms is classically associated with acute interstitial nephritis?
rash, fever and eosinophilia
how would approach assessing a patient in AKI?
fluid assessment (hypovolaemic? pulmonary oedema?)
feel for bladder- distended?
venous gas for potassium (ECG?), lactate if signs of sepsis
catheterise- helps with obstruction and monitoring output
how would you investigate AKI?
urine dipstick (haem/proteinuria may suggest renal cause)
USS kidneys within 24 hrs
LFTs (hepatorenal)
platelets (HUS?/TTP?)
what are the criteria for diagnosing AKI? (NICE 2019)
- rise in creatinine >25micromol/L in 48 hrs
- rise in creatinine >50% in 7 days
- urine output less than 0.5ml/kg/hr for >6 hrs
what is acute tubular necrosis?
damage and death of the epithelial cell of the renal tubules. most common intrinsic cause of AKI
what finding on urinalysis confirms ATN?
brown muddy casts
what is prognosis following acute tubular necrosis?
the epithelial cells can regenerate so once underlying cause treated recovery should take 1-3 weeks
what is acute interstitial nephritis?
acute inflammation of the interstitium (space between tubules and vessels), caused by an immune response associated with drugs/infections/autoimmune conditions
how is acute interstitial nephritis treated?
steroids
what are complications of uraemia?
uraemic encephalopathy, pericarditis
what are some causes of metabolic acidosis with a raised anion gap?
lactic acidosis, salicylate poisoning, methanol poisoning, diabetic ketoacidosis, alcoholic ketoacidosis, renal failure
what are some causes of metabolic acidosis with a normal anion gap?
diarrhoea, renal tubular acidosis, interstitial renal disease, dehydration
what bloods can be sent to investigate for a renal cause of AKI?
immunoglobulins, paraproteins, complement, autoantibodies (ANA, ANCA, anti-GBM)
what kind of questions will renal team likely ask you when referring a patient with AKI to them?
are they passing urine?
fluid status?
renal USS and urinalysis results
any nephrotoxic drugs?
baseline renal function?
what are the different stages of CKD?
1= >90
2= 60-90
3a= 45-60
3b= 30-45
4= 15-30
5= <15
how do we quantify protienuria in CKD?
urine albumin:creatinine ratio
how is a diagnosis of CKD made?
consistent results over 3 months of either:
eGFR below 60 or urine ACR above 3
when should patients with CKD be referred to a renal specialist?
eGFR less than 30
urine ACR more than 70
accelerated progression (eGFR drop of 15 or 25% in a year)
5 year risk of requiring dialysis >5%
uncontrolled hypertension despite four or more antihypertensives
how do we treat CKD?
optimise glycaemic control, blood pressure, avoid nephrotoxic drugs where appropriate. if glomerulonephritis is the cause then treat this
what are some medications that help slow disease progression in CKD?
ACEi and SGLT-2 inhibitors
why does renal bone disease occur?
diseased kidneys excrete less phosphate and don’t metabolise vitamin into its active form. this reduces serum calcium leading to a secondary hyperparathyroidism
why does osteosclerosis occur in CKD?
osteoblasts respond to increased osteoclast activity by increasing their rate of activity creating new tissue in the bone. because of low calcium levels this new bone isnt properly mineralised
what is a characteristic finding on spinal X-ray seen with renal bone disease?
rugger jersey spine
(involves sclerosis of both ends of each vertebral body with osteomalacia in the centre so looks like strips on a rugby shirt)
what is the treatment of renal bone disease?
phosphate binders, calcium and vitamin D supplementation and bisphosphonates
what symptoms can be seen in later stages of CKD?
fluid overload (SOB, peripheral oedema), pruritus, anorexia, nausea, vomiting, restless legs, fatigue, bone pain, weakness, impotence
how might kidneys appear on USS of a patient with CKD?
usually small <9cm
can be big in infiltrative causes (amyloidosis, myeloma) and polycystic kidney disease
what is the target BP for a patient with CKD?
140/90
or 130/80 if diabetic or has A:CR >70
what is a good resource to use when queries arise regarding prescribing for patient with renal failure or are on renal replacement therapy?
renal drug database
what are some immunosupressing drugs used following renal transplant?
monoclonal antibodies e.g basilixamab
calcineurin inhibitors e.g tacrolimus, ciclosporin
anti metabolites e.g azathioprine
steroids
where can a transplanted kidney be palpated?
in the iliac fossa area
what kind of scar is typically seen following renal transplant?
hockey stick scar
what signs can be looked for on examination that may be the results of imunnosupressive treatment?
seborrhoeic warts and skin cancer
tacrolimus causes a tremor
cyclosporin causes gum hypertrophy
steroids cause cushings features
what is anti GBM disease also known as?
good pastures syndrome
how does anti-GBM (glomerular base membrane) disease typically present?
renal disease (oliguria, AKI) and lung disease (pulmonary haemorrhage causing haemoptysis+SOB)
what murmur and relating heart defect is associated with autosomal dominant polycystic kidney disease?
late systolic murmur with systolic click
caused my mitral valve prolapse
what is the pathophysiology of alports syndrome?
an X-linked genetic condition where a defect in the gene coding for type 4 collagen results in an abnormal glomerular basement membrane
why might a patient with alports syndrome have a transplant fail?
the body may see the normal type 4 collagen of the new kidneys basement membrane as foreign as it has never had that- leading to a goodpastures type presentation
if a patient presents with haematuria following a recent URTI, how would the diagnosis differ if they presented within a couple days of the URTI compared to a couple weeks later?
concurrent or after a couple days = IgA nephropathy
after a couple weeks = post-strep glomerulonephritis
