renal general revision Flashcards
(71 cards)
1
Q
when should you refer people with CKD to a nephrologist?
A
CKD 4 GFR<30 people losing kidney function quickly ACR>70 ACR>30 and non-visible haematuria HTN on 4 agents suspecting a rare cause RA stenosis
2
Q
why does CKD produce anaemia (2 reasons..)
A
- Fe-def anaemia
- kidney can;t clear waste products from the liver
- hepcidin in particular builds up
- high levels of hepcidin block Fe absorption in the gut - stopping the body absorbing Fe
(inhibits the Fe transporter in the gut epithelium)
- produces an Fe def anaemia - decreased EPO production
3
Q
who is at risk of AKI?
think main related systems
A
CKD DM myeloma atherosclerotic disease CCF cirrhosis elderly
4
Q
list some causes of AKI (Prerenal / intrinsic / post renal)
A
Pre: (Major causes - ischaemia / lack of blood flowing to the kidneys) - hypovolaemia (D&V) - renal artery stenosis Instrinsic: glomerulonephritis ATN AIN rhabdomyolysis / tumour lysis syndrome Postrenal: obstruction - renal calculi in ureter / bladder -BPH - external compression of ureter - oliguric
5
Q
what are the 3 criteria for an AKI?
A
- increase in serum creat of 26 or more over 48hrs
- increase in serum creat of 50% or more over the past 7 days
- Oliguric - UO<0.5ml/kg/hr for >6hrs
6
Q
how can liver cirrhosis cause an AKI?
A
- liver doesn’t remove vasodilators from bloodstream
- splanchnic vessels dilate
- bloodflow diverted away from kidneys
- renal bloodflow decreases
AKI
7
Q
how would you investigate an AKI?
A
Urine dip
Estimate renal function (Creatinine / UO / GFR)
Fluid status
Biochemistry - HCO3 (will drop in AKI as not reabsorbed) Bone biochem if more chronic
Renal USS (Avg size 9-12 - 1.5cm variation allowed) (especially if suspected obstruction / no identifiable cause)
Immunology - ANCA / Anti-GBM / myeloma screen /
8
Q
GFR is calculated using what variables?
A
serum creat
age
gender
ethnicity
9
Q
which drugs must be stopped in AKI as they may worsen renal Fn
A
NSAIDs / aminoglycosides / ACEis / ARBs / diuretics / metformin
NB - may need to alter Li / digoxin
don’t need to alter aspirin / paracetamol
10
Q
how would you manage an AKI:
A
ABCDE approach - potassium - haemodynamics - UO charting - frequent observations Urine dip Medications (hold metformin / nsaids / ACEis / ARBs / diuretics - alter doses of renally excreted drugs eg. Li / dig Dialysis..
11
Q
what are the indications for dialysis in AKI?
A
F.U.H.A. hyperkalaemia acidosis uraemic Sx (pericarditis - ALWAYS LISTEN TO THE HEART IN AKI - PERICARDIAL RUB) / encephalopath / AMS Fluid overload
12
Q
why would you use haemofiltration over haemodialysis?
A
haemofiltration is more suitable if the patient is haemodynamically unstable
13
Q
why do you get polyuria in hypercalcaemia?
A
Ca2+ blocks ADH receptor in kidneys (collecting tubules)
14
Q
what drug used to treat pyelonephritis can cause an AKI?
A
Gentamicin - intrinsic AKI
15
Q
what feature on blood results might suggest dehydration rather than an AKI?
A
urea raised proportionally MORE than creatinine
16
Q
how would you differentiate primary and secondary hyperaldosteronism?
A
look at the renin levels?
if renin normal - 1y hyperaldosteronism - eg. Conn’s syndrome (aldosterone producing adenoma)
if high renin - 2y hyperaldosteronism - eg. RAS
17
Q
what might a very raised blood urea nitrogen concentration suggest in the context of a serious ill patient (raised far more that Cr)
A
Upper GI bleed
‘blood meal’
18
Q
what is fanconi’s syndrome
how does it present
A
insult to the PCT (the workhorse of the kidneys)
(NB - is rare…)
Px with:
glycosuria / met acidosis / phosphatura - osteomalacia / rickets as are pissing out all your phosphate
19
Q
what are some causes of Fanconi Sx?
A
Cystinosis (build up of cysteine - commonest cuase in paeds)
multiple myeloma
sjogrens
Wilson’s disease
nephrotic Sx
20
Q
what does the DCT do?
A
mostly sodium reabsorption (hence water reabsorption)
under control of aldosterone
21
Q
what electrolyte abnormalities do you see in Conn’s?
A
conns is primary hyperaldosteronism
aldosterone - loads of it - causes the reabsorption of Na+ - so K+ is excreted in DCT and H+ is also excreted with K+
hence pts are hypokalaemia, hypernatraemic and alkalotic (losing all their H+)
and obvs have HTN because water stays with Na+
22
Q
Addisons - what metabolic picture (K+ and acid-base)
A
hyperkalaemic acidosis
not enough aldosterone produced - because of adrenal insufficiency
so Na+ is lost along with water, and H+ and K+ are retained because they always travel in the opposite direction to Na+ when aldosterone is involved..
AT RISK OF MASSIVE HYPOTENSIVE CRISIS
23
Q
what medications cause hypokalaemia?
A
loop diuretics
(work on the Na+/K+/Cl- transporter NKCC2 in the loop of henle)
furosemide / bumetanide
thiazide diuretics
acts on the DCT to block the Na+/Cl-
bendroflumethiazide
24
Q
what medications can cause hyperkalaemia
A
spironolactone (aldosterone antagonist) - hence why..
amiloride - potassium sparing diuretic -block ENaC in the DCT
ARBs - block AT2
ACEis - both work on the RAAS system that ends up with aldosterone….
trimethoprim
calcineurin inhibitors
25
if planning to manage someone with a kidney stone conservatively, what medication can you give:
1. strong pain relief - IM diclofenac
2. meds to help them pass the stone
a-adrenergic blockers
Ca2+ blockers
26
when should you do an IMMEDIATE CT KUB
and what is your timeline if not urgent but suspecting kidney stones...
1. urgent if fever / one kidney / ?diagnosis - may be ruptured AAA
14 hours within otherwise..
27
what is the first line treatment of an acute urinary tract obstruction due to stones+infection...
Nephrostomy
28
```
PREVENTION OF KIDNEY STONES
HOW DO YOU PREVENT:
1. calcium
2. oxalate
3. uric acid?
```
4. cysteine?
1. low animal protein diet
well hydrated
low salt
thiazide diuretics
2. cholestyramine and pyridoxine reduce urinary oxalte secretion...
3. allopurinol
urinary alkalinisation - makes the uric acid more soluble and less likley to crystallise..
4. chelation therapy - penicillamine
29
what is your main ddx to be excluded for AKI?
AAA rupture!!
30
categorise the intrinsic renal causes of AKI?
vascular - vasculitis / TTP
glomerular - glomerulonephritis / nephrotic syndrome
ATN - ischaemic cause or nephrotoxic...?
31
ecg changes in
1. hyperkalamia
2. hypokalaemia
1. tall tented t waves
small p waves
WIDE QRS - becomes sinusoidal (sine waves) periarrest
V fib
2. small/inverted t waves (opposite of hyper.)
prominent U waves (after t wave...)
long PR
depressed ST segments
32
giving potassium - what should you remember?
NEVER give K+ as a fast stat bolus dose- lethal injection
give K+ cautiously at no more than 20mmol/hr
never more concentrated than 40mmol/L
ie. dilute well in bags of saline...
if severe:
40mmol KCl in 1L* 0.9% NaCl BD or TDS
infusion rate - 10ml of K+ / 250ml of 0.9% NaCl per hour
33
if someone is very ill - ABG + ECG is rarely going to hurt!
ie in AKI etc..
34
briefly outline the KDIGO system for staging an AKI
3 stages
1. creat 1.5-2x higher than normal
<0.5ml/kg/hr urine in >6hrs (ie just over the threshold for AKI)
2. Creat 2-3x higher than normal - <0.5ml'kg/hr urine in >12hrs
3. creat >3x higher than normal - <0.3ml/kg/hr urine in >24hrs / ANURIA FOR >12 HOURS
35
what is 'flash' pulmonary oedema and why does it occur in AKI
reduced GFR means decreased fluid clearance
reduced renal perfusion also activates the RAAS - further reducing the fluid clearance by the kidneys
XS fluid overload
oedema
in peripheries and in the lungs
DANGEROUS - MAY NEED DIALYSIS
36
management of flash pulmonary oedema in AKI and CKD?
```
O2
diuretics
nitrates
opiates
haemodialysis
ventilation support if required
```
37
further management (ie post resus) of AKI
1. nutrition -
2. observe kidney function
3. prevent further complications / insults...
38
what side effects do loop diretics have and why?
hyponat
hypokal
hypochlor
hypotension
(NB -+ indirect loss of calcium and magnesium and hydrogen ions)
inhibit uric acid excretion - may lead to gout
39
what is bartter's syndrome?
what is the main pathophysiology
how do children present?
AR disease of early childhood
essentially like being overdosed on a loop diuretic
defective NaCl channel in the loop of Henle
```
unable to concentrate urine
Na+ loss
volume depletion
RAAS SYSTEM ACTIVATED
hypokalaemia
met alkalosis
increased urinary K+ and Cl-
```
Px:
failure to thrive
polyuria
polydipsia
Tx:
NSAIDs (inhibit prostaglandins)
ACEi's
K+ replacement
40
causes of AKI?
```
sepsis
major surgery
cardiuogenic shock
other hypovolaemia
drugs
hepatorenal syndrome
obstruction
```
41
when can a patient NOT go on dialysis
absoilute CIs
temporary CIs
Relative CIs
aboislute - cancer with mets
temporary - active infection / HIV with high viural load / uunstable CVD
relative.. - CCF / CVD
42
what does glomerulonephritis cover?
covers a number of conditions that are:
1. caused by pathology in the glomerulus
2. associated with proteinuria / haematuria / both..
3. dxed on a renal biopsy
4. cause CKD
5. can progress to kidney failure (apart from M-C-disease)
all the conditions exist on a spectrum from proteinuria to haematuria
43
how can a classically nephritic (mostly haematuria) GN cause proteinuria?
if a GN causes scarring
leading to podocyte damage
proteinuria can occur
44
what bedside test should you ALWAYS do in oedema (*bear in mind these are renal flashcards..)
URINE DIPSTICK
45
how do you investigate glomerular disease?
essentially want to work out the potential damage, and find the cause...
```
1. Bedside
urine dipstick
urine sample for:
-mc&s
- Bence-Jones protein
-
```
2. bloods
fbc / u&e / LFT / CRP / immunoglobulins / electrophoresis of plasma / complement C3/C4 / ana / anca / anti-GBC / anti-dsDNA (lupus..)
3. imaging
CXR - check for pulmonary haemorrhage eg. in goodpastures
Renal USS - size and anatomy for biopsy
4. special tests:
RENAL BIOPSY REQUIRED FOR DIAGNOSIS
46
what treatments can you give in CKD to slow disease progression?
1. BP - target systolic BP <140 and diastolic <90
IF DM OR A:CR>70 THEN 10 LOWER...
2. RAAS - offer an ACEi or ARB (RAAS antagonist) to Dm / HTN / CKD if they also have a raised A:CR (doesn;t need to be raised much in HTN, and even less in DM)
Glycaemic control - target HBa1C of 53
Lifestyle - low salt / exercise / healthy weight / smoking cessation
47
what complications of CKD may you need to treat?
1. renal
anaemia - investigate / treat deficiencies / DONT MISS CHRONIC BLOOD LOSS - May need to tx with EPO if Hb<110g/L and likely to benefit in terms of function and QOL
acidosis - may need sodium bicarb supplements if eGFR<30 and low serum bicarb
oedema - fluid restrict to 1.5l/day and Na+ restrict
high doses of loop diuretics (+ thiazide if needed to inhibit diustal tubule Na+ excretion)
CKD-bone mineral disorders.. - ckd causes an increase in serum phosphate and a decrease in the hyproxylation of vitamin D by the kidneys
if egfr less than 30 - measure Ca2+ / HCO3- / ALP / PTH / 25-OH vitD
may need phosphate binders if high
may also need Vit D supplements if deficient
if PTH persistently increasing - tx with an activated Vit D analogue eg. calcitriol
2. other
CV risk
- antipllatelets if at risk for atherosclerotic events
atorvastatin 20mg
preparation for RRT
48
give 4 examples of nephritic glomerulonephritides:
```
IgA nephropathy
HSP
Post-strep gn
anti-GBM (goodpastures)
rpgn
```
49
describe the presentation. Dx and Tx of IgA nephropathy
COMMONEST PRIMARY GN IN HIGH INCOME COUNTRIES
Px: ASx non-vis haematuria / episodic haematuria
may occur within 12-72hrs of pharyngitis
hypertension seen
proteinuria usually <1g
slow indolent diseaes
half progress to renal failure over 30yrs
men have worse prognosis/ as do increased creat / higher BP / proteinuria
Dx:
ACEi or ARB reduce proteinuria and protect RFn
Corticosteroids and fish oil if perssistent proteinuria >1g despite RAAS antagonist for at least 6 months
50
descriobe the presentation, Dx and Tx of HSP
complications?
small vessel vasculitis
the sort of systemic variant of IgA nephropathy - IgA gets deposited in joints / skin / gut as well as the kidney.
Px:
a triad + nephritis
1. Flitting polyarthritis
2. purpuric rash on extensor surfaces esp on legs
3. abdo pain
Nephritis - micro or macroscopic haematuria
MONITOR BP - renal compllications
Cx - renal involvement - common - manage as with IgA nephropathy
steroids for gut involvement
51
post strep-GN
breif pathoiphys?
px
dx
tx
occurs after a throat (2/52) or skin (~4/52) infection
the streptococcal antigen deposits in the glomerulus - leads to immune complex formation -> inflammation (nephritis)
not usually very much proteinuria
px:
somewhere between haematuria and acute nephritis (haematuria / htn / oedema (from salt retention) - but not as much as in nephrotic syndrome / oliguric
dx:
evidence of strep infection (anti-streptolysin o titre / increased anti-DNAse B / decreased c3 (*ie. decreased c3 so can't clear the infection...?)
tx:
supportive
abx to clear the nephritogenic bacteria
52
anti -gbm disease
px
dx
tx
```
px - lung (pulm haemorrhage in most...) and renal disease
dx - anti-gbm in kidney
tx - plasma exchange
cs
cyclophosphamide
```
53
rpgn
px
dx
rx
px:
aggresive gn, often presents as AKI
causes include anti-GBM / SLE / ANCA+ve vasculitis
dx:
bad and fast - breaks in the gbm allow influx of inflamm cells - crescents seen on renal biopsy
tx:
corticosteroids / cyclophosphamide
other txs depend on the aetiology..
plasma xchange if ANCA+ve vasculitis / anti-GBM
?MAb in lupus nephritis.
54
nephritic syndrome and aki
rpgn
55
nephritic syndrome, young adult, haematuria immediately (12-72hrs) post URTI
IgA nephropathy
56
child with nephrotic syndrome
minimal change disease
57
Mixed nephritic/nephrotic presentation
Diffuse proliferative glomerulonephritis
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE
```
Membranoproliferative glomerulonephritis (mesangiocapillary)
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy
```
58
Typically presents with nephrotic syndrome (proteinuria, oedema)
Minimal change disease
typically a child with nephrotic syndrome (accounts for 80%)
causes: Hodgkin's, NSAIDs
good response to steroids
Membranous glomerulonephritis
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease
Focal segmental glomerulosclerosis
may be idiopathic or secondary to HIV, heroin
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
59
Typically presents with nephrotic syndrome (proteinuria, oedema)
Minimal change disease
typically a child with nephrotic syndrome (accounts for 80%)
causes: Hodgkin's, NSAIDs
good response to steroids
Membranous glomerulonephritis
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease
Focal segmental glomerulosclerosis
may be idiopathic or secondary to HIV, heroin
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
60
nephrotic syndrome with underlyinh infection / malignancy
Membranous glomerulonephritis
61
nephrotic glomerulonephritides - three main ones:
minimal change
fsgs
membrabnous neohropathy
membranoproliferative glomerulonephropathy
minimal change - dx with electron microscopy - tx with pred 1mg/kg
treat all the others with ACE-i/ARB and BP control
can give corticosteroids and other immunosuppresion..
62
which out of ADPKD and ARPKD is more common?
AD is more common (makes sense....)
63
definition of nephrotic syndrome
management of nephrotic syndrome (general...)
triad of:
1. hypoalbuminaemia
2. hyperlipidaemia
3. oedema (pitting..)
principles of management:
1. reduce the oedema:
64
definition of nephrotic syndrome
management of nephrotic syndrome (general...)
triad of:
1. hypoalbuminaemia
2. hyperlipidaemia
3. oedema (pitting..)
principles of management:
1. reduce the oedema:
fluid restriction (1L./day) and salt restriction
loop diuretics
NB - if gut oedema afffects the absorption of oral diuretics - give them IV
aim 0.5-1kg weight loss per day to avoid iv volume depletion - 2y aki
CAN ADD THIAZIDE DIURETICS IF RESISTANT TO LOOPS
2. treat the underlying cause
Adults need a renal biopsy
in children - give steroids as minimal change is the commonest cause - then if they don't work / another cause looks more likely (arthritis / rash / anaemia) then may need biopsy
3. reduce proteinuria
ACEi/ARB
4. Complications - manage..
Thromboembolism - lmwh - may need to dose adjust if low gfr
5. infection - give pneumoccoccal injection?
6. hyperlipidaemia - may need a statin?
65
prescribing maintenance fluyids
1. adults
2. children
1. 30ml/kg/24hrs
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis
2. 100ml/kg/24hrs for first 10kg
then 50 for next 10
then 20 for all after that..
66
evaluating the cause of an AKI - what would point you more towards a prerenal cause of an AKI rather than an ATN..?
ATN or prerenal uraemia? In prerenal uraemia think of the kidneys holding on to sodium to preserve volume - so there wont be much Na in the urine - whereas in ATN the tubules are a bit fucked so can't hold on to the Na+...
67
whatb is the most common and most important viral infection in solid organ transplant recipients...
and the Tx??
Cytomegalovirus is the most common and important viral infection in solid organ transplant recipients
tx with Ganciclovir
68
triad of rash, fever and eosinophilia (rarely all at the same time) - arthralgia, sterile pyuria and white cell casts
after a drug tx eg ABx
what is it
what does it commonly arise after?
Acute interstitial nephritis
Acute interstitial nephritis (AIN) typically arises following drug therapy in the majority of cases (~75%), with infections and systemic vasculitides forming the rest. The most common drug causes include: non steroidal anti-inflammatories (NSAIDs), penicillins, sulphur-based medications, proton pump inhibitors (PPIs), ciprofloxacin and allopurinol.
69
name a good vit d supplement for end stage renal disease
alfacalcidol - ideal as it does not require activation by the kidneys
70
what do you need to diagnose CKD 1 and 2 as well as the eGFR measurements...?
and what are the gfr cutoffs for the different stages..
Chronic kidney disease is only diagnosed in this situation if supporting tests such as urinalysis or renal ultrasound are abnormal / normal U&Es and no proteinuria
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
71
what areb the variables in gfr?
eGFR variables - CAGE - Creatinine, Age, Gender, Ethnicity
