Medicine - Renal Flashcards
What are the 2 main types of dialysis?
Haemodialysis
Peritoneal dialysis
What is required for haemodialysis?
- Dialysis machine (patient’s blood is pumped OUTSIDE the body and through this machine)
- Vascular access is required via an AV fistula (longterm), or a temporary CVC
What happens inside a haemodialysis machine (broadly)?
Blood flows through tiny semi-permeable tubes surrounded by a dialysis solution (dialysate)
Filtration occurs via osmosis and diffusion - dialysis fluid contains solutes at a similar level to the level they would be in a healthy patient’s blood
Can add bicarbonate (to combat acidosis), EPO and drugs if needed
Heparin always added
How often should haemodialysis be performed?
4 hour treatment 3 times per week
What are the 3 main possible complications of dialysis
- Blood infection (more common in peritoneal dialysis)
- Thrombosis
- Internal bleeding (due to added heparin)
What is peritoneal dialysis?
Dialysis fluid is introduced into the patient’s abdominal cavity for several hours, and the peritoneum serves as the natural filter
Can be done automatically at night during sleep
Recall some pros of peritoneal dilaysis
- Offers more flexibility (can be done overnight)
- Is better tolerated by patients
- Less expensive
What is a tesio line?
- Tunneled dual lumen central line
- Used as a ‘bridge’ before an AV fistula can be put in
- One lumen enters the right atrium, the other
sits outside the RA in the vena cava - Both lumens exit the body (with a central line, only 1 lumen enters the skin)
Why is a normal vein unsuitable for haemodialysis, and why is an AV fistula used?
Normal vein would easily collapse/ thrombose with recurrent venepuncture
Vein in an AV fistula hypertrophies in response to turbulent flow of blood from artery and so can withstand repeated venepuncture
Recall some contra-indications to renal biopsy in acute renal failure
- Obvious pre or post renal cause (these are contra-indications)
- Significant coagulopathy
- Infection at the site
What group of diseases is the most common cause of nephritic syndrome?
Proliferative glomerulonephritis
Recall 5 causes of the nephrotic syndrome
Amyloidosis Diabetes Focal segmental glomerulosclerosis Membranous glomerulonephritis Minimal change disease
What are the most common causes of AKI?
Remember STOP:
- Sepsis/dehydration / heart failure (decrease blood supply)
- Toxins (NSAIDs, nephrotoxic drugs),
- Obstruction in the urinary tract (back pressure
- Parenchymal kidney disease (gnpehritis, inephritis, ATN) - decrease filtration of blood
pre renal, renal & post renal
What are the most common causes of CKD?
Diabetic nephropathy
Other causes: HTN, age, gnpehritis, PKD, Nsaids, PPis, lithium
Hypertensive nephropathy
What are the primary functions of the kidney?
Balance:
- Water
- Electrolyte
- Acid-base
Endocrine:
- erythropoietin
- vit D activation
- renin-angiotensin system
- BP control
Excretion:
- Waste
- Metabolites
What symptoms might you expect from someone with CKD?
Fluid overload (pedal oedema, pleural effusion, ascites, tiredness)
Anaemia (SOB, tiredness, LoC, headcaches)
Hyperkalaemia (palpitations, cardiac arrest, asymptomatic)
Uremia (pruritis, confusion, pericarditis, encephalopathy)
Acidosis (nausea, vomiting,
tiredness)
Increased drug action (e.g. opioid side effects)
Reduced urine output
What diet should be followed in patients with very low creatinine clearance?
Low phosphate (eg. avoid chocolate, shellfish, nuts)
Low potassium (avoiding chocolate, bananas etc)
Fluid restricted (avoiding alcohol, avoid too much tea/coffee)
Low salt (avoiding processed foods)
Can take phosphate binders if diet restriction alone doesn’t succeed
Recall a mnemonic that can be used to remember the most common indications for emergency dialysis
A – acidosis
E – electrolyte imbalance (K+ of 6.5+ and refractory to
medical management)
I – intoxication (certain drugs require dialysis to
clear the blood)
O – overload of fluid (refractory to diuretic treatment)
U – uraemic encephalopathy & pericarditis
BLAST mnemonic for drugs that can be dialysed out - Barbiturates Lithium Alcohol Salicylates Theophylline
What can be used as an alternative to calcium gluconate in hyperkalaemia as a cardioprotective infusion?
Calcium chloride
How might a chest x ray appear in Goodpasture’s syndrome?
Bilateral widespread airspace opacities
Which diagnosis classically has the symptoms of haematuria and haemoptysis in a young person?
Goodpasture’s
What is the likelihood of complete recovery of kidney function following an AKI if there is no pre-existing CKD?
80%
Recall 3 ECG changes in hyperkalaemia
Tented T waves
Widening QRS complex
Small p waves
What is the most common cause of nephrotic syndrome in adults?
Membranous glomerulonephritis
What are the components of the annual review for patients with type 2 diabetes?
Retinopathy screening Foot assessment for both sensation and doppler testing of vascular supply Albumin:creatinie ratio U+E Serum cholesterol HBa1c Review of any glucose monitoring Weight assessment Smoking status assessment
What are the indications for dialysis?
Refractory hyperkalaemia Refractory fluid overload Metabolic acidosis Uraemia symptoms CKD stage 5
What will the urinary sodium be in pre-renal vs intrinsic renal ARF?
Pre-renal: urinary sodium low
Intrinsic renal: urinary sodium high
Recall the symptoms of HUS vs TTP
HUS: MAHA, thrombocytopaenia, AKI
TTP: MAHA, thrombocytopaenia, AKI, neurological impairment and fever
Recall some key nephrotoxic drugs that should be stopped in AKI
stop the DAMN drugs Diuretics ACEi and ARBs Metformin NSAIDs
At what GFR would you do a routine nephrology referral?
Either at GFR <30 or a reduction in GFR over 12 months of >25% >15mL/min/1.73m^2
How can CKD be managed by diet?
- Reduce dietary phosphate, sodium, potassium, fluids
- Sevelamar (phosphate binder) - reduces uric acid and lipid levels
- Vitamin D
Recall 4 features of adult polycystic kidney disease
Liver cysts
Berry aneurysms
Mitral valve prolapse
Renal failure signs
What is the medical management of adult polycystic kidney disease?
Tolvaptan
Does IgA nephropathy cause nephrotic or nephritic syndrome?
Nephritic (rarely nephrotic)
Recall some signs and symptoms of IgA nephropathy
Purpuric rash (100%)
Arthralgia (60-80%)
Abdominal pain (60%)
Glomerulonephritis (20-60%)
How should IgA nephropathy be managed?
Most cases will resolve spontaneously in 4w
Joint pain –> NSAIDs
Scrotal involvement/severe oedema/ severe abdominal pain –> oral prednisolone
Renal involvement –> IV corticosteroids
What type of cancer is left varicocele most associated with?
Renal cell carcinoma
What is the most common form of renal tumour?
Clear cell carcinoma
Which urological cancer is most associated with painless haematuria?
Transistional cell carcinoma
In patients with CKD, what should be done before any scan that uses contrast?
Give IV saline –> volume expansion –> reduced chance of cast nephropathy
What are the variables in the Modification of Diet in Renal Disease equation, that affect eGFR?
CAGE: Creatinine Age Gender Ethnicity
What medication should be started in patients with CKD who have an ACR of >30?
ACE inhibitor
How long does it take for an AV fistula to develop
6-8 weeks
How does the size of kidneys differ in chronic diabetic nephropathy vs ckd of another cause?
Chronic diabetic nephropathy = large/normal kidneys
CKD = small kidneys
Nice criteria for a AKI
cr rise > 25 in 48 hrs
50% in 7 days
urine output < 0.5 for more than 6 hrs
Main Rf for AKI
Age
Cardiac
Liver
CKD
Age
Drugs e.g. NSAIDS / ACEi
contrast medium
Glucose in urine
Diabetes
Mx of AKI
fluid - pre renal
stop nephrotoxic meds
relieve obstruction
Complications of AKI
Hyperkalaemia
Fluid overload
metabolic acidosis
uraemia - encephalopathy
Main Ix for CKD
eGFR - two test 3 months apart
proteinuria
haematuria
renal USS
eGFR staging
90
60-89
45-59
30-44 (3b)
15-29
15 - end stage renal failure
Main complications of CKD
anaemia
renal bone disease
cvd
peripheral neruopathy
dialysis
Specialist referral ckd
30 egfr
70 ACR
decrease of egfr of 15 / 25 % in 1 yr
uncontrolled htn on 4 hypertensives
Treat complications of CKD
sodium bicarbonate for metabolic acidosis
iron and erythropoietin anaemia
vit d for bone disease
dialysis for end stage renal failure
renal transplant
Why should blood transfusions be limited with treating ckd over erythopoietin?
Allosensitation - transplant organs more likely to be rejected
iv iron in dialysis
Main complications of periotoneal dialysis
bacterial periotonities - glucose infusion = growth area
peritoneal sclerosis - thickening and scarring
ultrafilrtation failure - absorb dextrose in solution - reduce gradient
weight gain as absorb carbs in dextrose
psychosocial - sleep with machine
Types of haemodialysis and complications
Tunnelled cuffed catheter - tube through vein sits at svc, dacron cuff for healing of tissue to cuff making more permanet and avoid bacteria - infection and blood clots
AV fistula - connection between artery and vein - surgical op 4 week to 4 month before use
skin integrity, aneurysms, palpable thrill, machinery murmu
- infection, thrombosis, stenosis, steal syndrome, high output heart failure
steal syndrome
inadequate flow to distal limb from av fistula - distal ischaemia
high output heart failure
quick flow artery to vein, rapid return blood to heart - increase pre load- hypertrophy of heart muscle
Features of renal transplant
HLA matching
life long immunosuppression e.g. tacrolimus
rejection, failure and electoryle imbalance
immuno comp - IHD, t2dm, infeection, pcp, cmv, pjp, non hodgkin, skin cancer SCC
Features of nephritic syndrome
haematuria
oliguria - reduced urine output
proteinuria <3g tho
fluid retention
Features of nephrotic syndrome
peripheral oedema
proteinuria >3g
serum albumin less than 25g
hypercholesterolaemia
increase clotting
MCD = child, focal segmental glomeruloscelrosis = adults
Interstitial nephritis
inflammation space between cells and tubules of intersititum of kidneys - acute and chronic
Acute - AKI and HTN, hypersensitivity - drugs / infection - rash, fever, eosinophilia - cause and steroids
Chronic CKD, autoimmune, infetion etc - cause and steroids
Causes of glomerulosclerosis
glomerulonephritis
obstructive uropathy
focal segmental glomerulosclerosis
Glomerulopehritis treatments
steroids
blood pressure control
IgA nephropathy
common primary glomerulonephritis
20s
IgA deposits and glomerular mesangial proliferation
Membranous glomerulonephritis
most common overall
20s 60s
IgG and complement deposits on basement membrance
idiopathic
secondary to malignany, rheumatoid and drugs
Diffuse proliferative glomerulonephritis (post strep)
under 30
1 to 3 weeks post strep
nephritic yndrome
receover
Good pastures syndrome
anti-gbm
Gn + pulmonary haemarry attack basement membrance
AKI + haemoptysis
Rapidly progressive glomerulonephritis
crescentic GN
very acute with sick
secondary to good pastures
Featres of diabetic nephropathy
high levels of glucose cause scarring
proteinuira feature due to damage
ACR and U&Es
blood pressure and sugar optimising
Acute tubular necrosis
death of epithelial cells of renal tubules - most common AKI - ischaemia / toxins - reversible 7-21 day recovery
Ish - shock, sepsis, dehydration
Toxin - radio contrast dye, gentamicin, nsaids, lithium, heroin
urinalysis - muddy brown casts
Mx - AKI - supportive fluids, cause, stop drugs, and treat complications
Renal tubular acidosis
metabolic acidosis in the tubules of the kidney
4 types
type 1 - distal tubule unable to excrete hydrogen ions e.g genetic, SLE< sjogren, PBC, HT, sickle, marfans
- failure to thrive, hyperventilation to compensate, ckd, bone disease
- hypokalaemia, met acid, high urinary ph
- oral bicarbonate
type 2 - proximal tubule, unable to reabsorb bicarbonate, excess in urine
- fanconis, jews, bone marrow failure, acute myeloid, cafe au lait
- hypokalaemai, met acid and high urinary ph
- same as above
type 3 - both
type 4 - reduced aldosterone - hyperkalaemic renal tubular acidosis, suppress ammonia, acid urine most common
- adrenal insufficinecy- ACE / spironolactone - SLE / diabetes / HIV
- hyperkalaemia, high chloride, meta acidosis, low urinary pH
- fludrocortisone and bicarbonate
Haemolytic uraemic syndrome
thrombosis in small blood vessels - shiga toxin
Haemo anaemia, AKI, Low platelet count
e coli 0157
gastroenteririts - then 5 days after, brusing + kidney symptoms
Emergency - supportive anti HTN, blood transfusions and dialysis
features of rhabdomyolysis
overuse / underuse muscle breakdown
myocyte death 0 myoglobin, potassium, phosphate, CK released
myoglobin toxic to kidney - AKI, acccumulate products more in the blood
red brown urine
ECG for hyperkalaemia but CK main test
Iv fluids encourage filtration
sodium bicarbonate / mannitol increase gfr and reduce oedema
Features of hyperkalaemia
arrhythmias and ventricular fibrillation
aki/ckd/rhadb/adrenal insuff.tumour lysis
drugs - spiro/ace/AII/nsaids/potassium
always repeat sample
tall t waves, flattened p waves and broad qrs complex
insulin dextrose and calcium gluconate
drive postasium into cels , stabilise cardiac muscle
neb salbutamol - potassium into cells
resonium- out of gut and into stool potassium - good for milder
Polycystic kidney disease features
cysts in kidney
associated with hepatic cysts and cerebral aneurysms
USS and genetic testing
AD
- PKD1 most common
- mit regrug, colonic diverticula, aortic root dilatation
- loin pain, HTN, CVD, haematuria with cyst rupture, renal stones, end stage renal failure
AR
- oligohydramnios
- underdeveloped lungs - not adults
Mx
- tolvaptan - vasopressin receptor antagonist - slow cysts and progression of renal failure
- supportive
- avoid contact sport, drugs regular monitoring
When someone has a AKI what should be done?
Renal DRs26
If no identifiable cause of AKI is found what should be done
renal USS within 24 hrs of assessment
Drugs safe to continue on AKI
- Paracetamol
- Warfarin
- Statins
- Aspirin (at a cardioprotective dose of 75mg od)
- Clopidogrel
- Beta-blockers
Drugs that should be stopped with AKI
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
Drugs that may need to be stopped with AKI
- Metformin
- Lithium
- Digoxin
Levels of hyperkalaemia
mild: 5.5 - 5.9 mmol/L
moderate: 6.0 - 6.4 mmol/L
severe: ≥ 6.5 mmol/L
Why are rectal calcium resonium enemas more useful for removing potassium than oral
potassium is excreted rectally
Maintainence fluid levels
25-30 ml/kg/day of water and
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis
Risk of using large volumes of 0.9% saline
hyperchloraemic metabolic acidosis
Why should hartmanns not be used in patients with hyperkalaemia
contains potassium
Causes of hyperchloraemic metabolic acidosis
gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia
ureterosigmoidostomy
fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
Causes of raised anion gap acidosis
lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol
metformin type 2 lactic acidosis
Nephrogenic DI treatment
thiazides
low salt/protein diet
Associated conditions with diabetic nephropathy
alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura
AKI vs CKD
CKD - bilateral small kidneys on USS + hypocalcaemia
exception:
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy
Extra renal features of PCKD
liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
Factors that affect eGFR
pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken
Anaemia in CKD
correct iron levels before starting EPO agents
if target levels not reached after 3 months - start on IV iron
How does myoglobin cause renal failure
tubular cell necrosis
How quick should fluids be given with AKI
within 15 minutes avoid potassium based ones like hartmanns
What is pre-renal disease?
kidneys hold onto sodium to preserve volume, rasied urine osmoliatiy
Iron deficiency in elderly
endoscopy to rule out sinister causes
Urgent referral for haematuria criteria
Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection
Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
Non urgent referral for haematuria criteria
Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection
Patients present with acute or subacute deterioration in renal function (suggested in this patient who is passing less urine), joint pain, and hypersensitivity features (fever and rash). Urinalysis will show a raised urine white cell count.
Acute interstitial nephritis
Rf for contrast based nephrotoxicity
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
withhold metformin due to risk of lactic acidosis
Most common extra manifestation of ADPKD
liver cysts
Maximum rate of potassium infusion
The maximum recommended rate of potassium infusion via a peripheral line is 10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring
Management of bone disease with CKD
reduce dietary phosphate levels
phosphate binders
vit d
remove parathyroid gland
calcium binder of phosphate - hypercal + vascular calcification
Why is nephrotic syndrome associated with a hypercoaguble state?
loss of antithrombin III via the kidneys
and plasminogen
dvt
