Renal Flashcards
What are causes of AKI
Pre-Renal (most likely approx 70%): hypoperfusion
- hypovolaemia (bleeding, shock, dehydration)
- Oedema (cardiac /liver failure, nephrotic syndrome
- Renal hypoperfusion (renal artery stenosis, vasculitis, drugs)
Renal: intrinsic kidney damage, classified on location (vasculitis, glomerulonephritis, tubular, interstitial)
Post-Renal: obstruction to urinary flow (calculi, tumours, strictures, BPH)
what are A>E findings for AKI
A. Vomiting
B. Tachypnoea, cough (pulmonary oedema), bibasal crackles
C. Tachycardia, fluid overload
D. Confusion (uraemia), oliguria
E. Abdominal pain (retention)
what is workup for AKI
• Bedside: ECG (hyperkalaemia), urine dipstick, urine sample (MC&S, ACR), ABG (acidosis, hyperk)
• Bloods: U&E, calcium, phosphate, FBC, CRP/ESR, LFTs, CK (for rhabdo), renal screen
• Imaging: bladder scan, renal uss
Renal biopsy (if unsure of cause - rarely done)
What is management for AKI
• Treat HYPERKALAEMIA
o 10-30mL Calcium Gluconate IV over 2-10 mins (can repeat every 15 mins up to 5 doses until K+ corrected) (N.B. IV calcium gluconate must be administered by a dr due to risk of arrhythmia)
o 10 U Actrapid with 100mL 20% glucose IV over 10 mins
o Consider 5 mg Salbutamol nebuliser
o Monitor ECG and ensure quick access to defibrillator
o Repeat U&E
o ABG to check for acidosis
Review drugs - stop drugs that reduce renal perfusion (NSAIDS) are nephrotoxic (aminoglycosides) are renally escreted (metforming) can cause hyperk (ACEi/ARB)
- Fluid resus
- Catheterise, monitor UO
- Treat the CAUSE
o Hypovolaemia > IV fluids
o Retention > catheterise
o Pulmonary oedema > cautious use of furosemide
What are indications for dialysis
Acidosis (refractory to treatment / severe <7.2)
Electrolyte imbalance (refractory hyperkalaemia)
Intoxication (CKD stage 5; GFR <15)
Oedema pulmonary /overload of fluid
Uraemia complications (encepalopathy, nausea, pruritus, pericarditis)
How can you define AKI
KDIGO guidelines:
- increase serum creat >26 within 48hours
- increase serum creat >1.5x baseline within past 7 days
- urine vol <0.5ml/kg/h for 6 hours
How can you classify AKI
Based on creatinine compared to baseline or based on URINE OUTPUT
What is presentation of AKI
oliguria / anuria
dehyrdation, thirst, dry mouth
confusion
uraemia: malaise, nausea, vomiting, pruritus, drowsiness
hypotension, hypovolaemia (if prerenal)
palpable bladder (if postrenal)
renal bruits (if renovasc disease)
dehydration
What are two blood markers of renal function
Urea
Creatitinine
What is creatinine
breakdown of protein metabolism within muscles
How does creatinine travel through kidneys
creatinine enters the blood
is freely filtered through kidneys
what pathology can alter creatinine amount in the blood
and why
Creatinine is produced and excreted through kidneys at constant rate
So if RENAL FUNCTION DECREASES
You reduce creatinine excretion > increased in creatinine in blood
what is eGFR
Serum creatinine + age + sex + ethnicity
What is creatinine clearance
eGFR + height + weight
why is creatinine clearance importannt
because the amount of creatinine produceed is dependent on our muscle mass
What is urea
a nitrogenous waste product
what conditions can cause urea to be elevated in the blood
DEHYDRATION - as urea is reabsorbed by kidneys when dehydrated
UGI BLEED - as RBC breakdown cause increased urea
What is classification of AKI
KDIGO stages 1-3
Stage1: serum creatinine 1.5 to 1.9x reference; bodyweight in urine mLs every 2 hours for <12 hours
Stage 2: serum creatinine 2.0 to 2.9x reference; bodyweight in urine mLs every 2 hours for over 12 hours
Stage 3: serum creat >3; anuric >12h
Drugs that need to be stopped in AKI
DAMN
Diuretics
ACEi, ARB
Metformin
NSAID
What are three forms of renal replacement therapy
Haemodialysis
Peritoneal dialysis
Renal transplant
How does peritoneal dialysis work
Peritoneum is used as semipermeable membrane. Dialisate is instilled in peritneum
What is advantage and disadvantage of peritoneal dialysis
Advantage: can be done at home
Disadvantage: risk of infection
Explain how haemodialysis works
Access via AV fistula / tesio
Takes blood out, passes it through dialysate. It is separated from dialysate via a semipermeable membrane
Electrolyte imbalances are corrected via diffusion; fluid overload is corrected via negative pressure in the dialysate (draws out water from blood=)
What are problems that occur with renal failure (link back to the specific renal function)?
Fluid balance»_space; FLuid overload
Electrolyte homeostasis»_space; hyperkalaemia, acidosis
Waste excretion»_space; uraemia
Hormone production»_space; anaemia, hypercalcaemia (hyperphosphataemia)
Ix for CKD
UE
blood glucose
K+
FBC
Antibodies, USS, biopsy
stages of CKD
1: eGFR >90
2: eGFR >60
3: eGFR >30
4. eGFR >15
5. eGFR <15
How do you manage CKD
- modify RF => antihypertensives, good dlycaemic control)
- fluid balance => restrict fluid + salt
- Anaemia => EPOstimulating agents
- hypocalcaemia => phosphate binders, vit D supplements
- consider renal replacement therapy
Nephritic syndrome triad
BPH
Blood (Haematuria)
proteinuria
Hypertension
What are causes of nephritic syndrome
Immune-mediated
- IgA nephropathy
- Post strep glomerulonephriitis
- Henoch Schonein , HUS, SLE, Goodpastures
CAUSE INFLAMMATION OF GLOMEROLUS AND NEPHRON > CAPILLARY BECOMES LEAKY
Describe what occurs in IgA nephropathy
Following resp/GI infection
Abnormal IgA is produced
Immune system makes antibodies against it
Sticky immune complexes are produced
Explain how IgA nephropathy presents
5-7 days post infection
Abdo pain, rash, arthritis
Explain how Post-Strep Glomerulonephritis presents
4-6 weeks post infection
What must you manage in Post-Strep Glomerulonephritis
HTN
what is triad of nephrotic syndrome
PHO
Proteinuria
Hypoalbuminaemia
Oedema
+ Thrombosis (due to loss of antithrombin III thhrough kidneys)
Causes of nephrotic syndrome
Minimal change diisease
FOcal segmenral glomerulonephritis (MOST COMON)
Membranous glomerulonephritis
what are causes of CKD
long term renal injury
usually linked to:
- DM
-HTN
- chronic inflammation (glomeerulonephritis, vasculitis, myeloma, amyloidosis)
what is mode of inheritance for PKD
Autoomal dominant
what occurs in PKD
multiple renal cysts develop and cause damage to adjacent nephrons
how and when does PKD present
in > 30 years old
liver cysts: flank pain, haematuria, HTN
berry aneurysm: SAH
Mitral valve prolapse
HOw can you manage PKD
give TOLVAPTAN to slow down progression
what is the usual cause of RAS
atherosclerosis
what occurs to renal enzymes in RAS
Renal hypoperfusion> increased angiotensin 2, increased aldosterone > increased BP
whhat drug is AWFUL if you have RAS and wy
ACEi
because in RAS renal perfusion is actually maintained by constriction of the efferent arteriole
ACEi remove that constriction > glomerular filtration pressure drops > little blood flows to kidey > severe AKI
Gold standard Ix for RAS
Digital subtraction angiography
WHAT IS fibromuscular dysplasia
Proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow.
This most commonly affects YOUNG WOMEN
Susceptible to AKI after the initiation of an ACE inhibitor.
On MR angio: ‘string of beads’ appearance.
What are stimuli for renin secretion
low Na
low perfusion
sympathetic stimulation (beta adrenergic receptors)
how does renin act on the RAS
Renin releasedd from JGA
Renin converts angiotensinogen to Angiotensin 1
What occurs to angiotenssin 1
Angiotensin 1 is cleaved in lung by ACE to At2
What is function of At2
Stimulates adrenal production of aldosterone
also constricts arterioles
how do you distinguish glomerulonephritis from AIN on urine dip
glomerulonephritis = NEPHRITIC syndrome = blood and protein in urine
AIN = NePHROTIC syndrome = protein and WCC
what do you do if a patient has CKD but needs a scan with contrast?
give IV saline before and after - this reduces the risk of precipitating an AKi
what CK levels are you expecting for rhabdomyolysis
CK >10 000
otherwise (if lower than that) it could just be a soft tissue injury
what histopathological findings do you expect with a carcinoma
nuclear enlargement
hyperchromasia
pleomorphism
difference between IgA and post infection nephropathy in terms of timing
IgAA is FEW DAYS
post-infectious is FEW WEEKS
How does urinary sodium differ between prerenal and renal AKI, and why?
prerenal: LOW urinary sodium
because the kidney works fine and is desperately trying to hold on to sodium to raise BP
renal: HIGH urinary sodium
because the kidney is damaged so loses lots of sodium
classify and name causes or intrinsic renal AKI
VASCULITIS - affects the blood vessels
- small vessels (microangiopathic): HUS, TTP, DIC, GPA
- large vessel (obstructive): renal artery / vein thrombosis or embolus
GLOMERULONEPHRITIS - affects the glomerolus
- minimal change disease (in children)
- membranous glomerulonephritis (in adults)
ATN - affects tubules
- rhabdomyolisis, post-hypovolaemia
AIN - affects intersttium
- NSAIDS, PENICILLIN, SULFA-DRUGS, PPI, CIPROFLOX, ALLOPURINOL, FUROSEMIEDE
most common extarenal presentation of PKD
cystic liver > hepatomegaly
what is a dangerous unique complication of haemodysalisis
Dialysis disequilibrium syndrome
causes cerebral oedema (headache, drowsiness)
why do you need to STOP LITHIUM in AKI?
because may cause toxic accumulation of lithium (although lithium itself does not actually cause AKI)
what dose of aspirin can you continue for AKI
low dose (75 mg)
how do you treat cranial DI
DESMOPRESSIN
how do you treat nephrogenic DI
thiazide
when does a GP need to refer to nephrology someone with CKD
if;
- eGFR below 30
- eGFR falls progressively by > 15 in a year
what else other than GFR do you need to diagnose CKD stages 1 and 2
you need supportive evidence (e.g. from urine dip, USS, symptoms)
otherwise likely not CKD, as GFR is simply variable in peoopke
what dose of potassium is safe to give IV per hour WITHOUT CARDIAC MONITORING
10mmol / h
what must a patient be on if receiving 20mmol KCl /h
requires cardiac monitoring
via central line preferred
what is the pathophysiology of goodpasture
anti-GBM antibodies against T4 collagen
what are symptoms of goodpasture
pulmonary haemorrhage > haemoptisis
glomerulonephritis > NEPHRITIC syndrome (proteinuria + haemoaturia)
how much does creatininee need to increase by to recognise an AKI
> 26 micromol / L
what are the three ways of removing potassium from the body (rather than merely shifting it into cells) in hyperkalaemia
calcium resonium (enema > oral)
loop diuretics
dialysis
what electrolyte imbalance can large volumes of NaCL cause
hyperchloraemic metabolic acidosis
which vit D supplement is good for end stage kidney disease a
alpha calcidiol
