Renal Flashcards
2 interventions for immediate management of hyperkalaemia?
- IV calcium gluconate/chloride
- IV insulin and dextrose
Which of the following might be indications for urgent dialysis?
Potassium 7.8 on intial bloods
Serum bicarbonate 8 on initial bloods
Creatine Kinase 20000
Creatinine 967 umol/l
Urine output 5mls/hour after 4 hours of immediate treatment
Urine output 5mls/hour for first 4 hours of admission
Pulmonary oedema after 4 hours of immediate treatments
Potassium 7.8 4 hours after insulin/dextrose
UO 5mls/hour after 4h of immediate treatment
Pulm oedema after 4h of immed treatments
Potassium 7.8 4h after insulin/dextrose
What is the most important intervention in slowing the decline in kidney function in patients with CKD?
Tight control of BP
How does hypotension cause AKI?
Acute tubular injury/necrosis
What forms the first line of filtration in the glomerulus?
What forms the second line of filtration?
Podocytes
Basement membrane
What absorption/secretion occurs in the proximal convoluted tubules?
Majority of electrolytes (Na, K, Mg, Ca, glucose) reabsorbed here
Active secretion of urea, drugs, toxins, creatinine
How does the counter-current multiplier system of the loop of Henle work?
Na/K ATPase actively pumps Na ions from ascending loop, creates hyperosmolar area so causes reabsorption of water down the osmotic gradient from the descending loop
Which cells detect changes in Na concentration in the glomerulus? What do these cells regulate?
Macula densa cells
Release of renin by the juxtaglomerular cells
ADH released from ?? stimulates what change to occur in the collecting ducts of the kidneys?
Posterior pituitary gland
Aquaporin channgels insert into collecting ducts, allows water to move into interstitial spaces, causing more concentrated urine.
Name 4 actions of angiotensin II
Direct arteriole vasoconstriction
Sympathetic activation
Aldosterone secretion by adrenal cortex– sodium reabsorption and potassium secretion
ADH release, increases water reabsorption
Give the 3 possible criteria for diagnosing an AKI
1) Rise in serum creatinine of 26micromol/L or more in the last 48h
2) Rise in >=50% rise in serum creatinine known/presumed to have occurred in past 7d/ 1.5x rise from baseline
3) Urine output <0.5ml/kg/hr for >6 hours (>8 in kids)
Give 3 pre-renal, renal and post-renal causes of AKI
Pre- sepsis, haemorrhage, renal artery stenosis, hypovolaemia, heart failure, nephrotoxics
Renal- ATN (ischaemia, nephrotoxic meds), glomerulonephritis, vasculitis, acute interstitial nephritis
Post- obstructive causes e.g. tumours, BPE, clots, calculi, strictures.
Give 5 investigations to do in a patient with AKI
- Medication review
- Urinalysis
- Bloods: FBC, U&Es, LFTs, glucose, coag screen, vasculitis screen
- ECG
- Renal US
- Relevant radiology e.g. ECHO, CXR, CTKUB
What investigation can tell you whether AKI is likely pre-renal vs ATN cause?
Fractional excretion of sodium (FEna)
<1% likely pre-renal cause. Because kidneys act to concentrate urine and retain sodium, so urinary sodium low.
>2% likely ATN. Kidneys can’t concentrate urine and retain sodium so urinary sodium is high
Outline the management plan for pts with AKI
Fluid balance, daily weight, may need catheterisation
Encourage oral fluids, may need IV
Review meds and stop nephrotoxics
Identify and treat cause
Supportive therapy e.g. O2, blood transfusion if anaemic
Urgent urology referral if severe obstruction
Monitor renal function
What is the mnemonic for when to refer for renal replacement therapy in AKI?
POPAC Pulm oedema Oedema (gen) Potassium (hyperkalaemia) Acidosis Comps of uraemia (pericarditis, encephalopathy)
A patient presents to A&E due to vomiting, muscle pain, and brown coloured urine. The Dr suspects rhabdomyolsis.
Give 3 causes.
What electrolyte abnormalities would you find?
What serum abnormality helps diagnosis?
What is treatment?
Long lies, crush injuries, compartment syndrome, seizures, ecstasy, statins (esp with clarithromycin).
HyperK+, hypocalcaemia, hyperphosphataemia
CK signif elevated
Aggressive fluids, correct electrolyte abnormalities.
What is the definition of CKD?
Kidney damage for 3+ months, secondary to structural or functional disorders/disease, with eGFR <60 on 2 separate occasions.
The KDIGO guidelines also include the degree of ? in their stratification of CKD?
Albuminuria
Which 2 pops at greater risk of CKD?
Afro-Caribbean and Asian
What are 2 common causes of CKD?
What are 2 other causes?
HTN, diabetes
renovascular disease, GN, SLE, PKD, ITN
Give 3 symptoms that might be seen in severe CKD?
Oedema, pruritus, polyuria, fatigue, muscle weakness
What is considered a normal ACR?
<30 mg/g
Give 2 indications for getting a renal US in a pt with CKD?
Symptoms of obstruction
FH of PKD
Accelerated progression of disease
Visible or persistent microscopic haematuria
What lifestyle advice would you give for CKD?
Stop smoking, healthy balanced diet, lower potassium phosphate and salt intake. Regular exercise.
What is the management of CKD?
BP control - ACE inhibitors 1st line
Manage CVD RFs - statins, antiplatelets
Manage anaemia - EPO stimulating agents, correct iron deficiency
Manage oedema - furosemide
Check for renal bone disease - adcal, bisphosphonates
How and when should you screen for renal bone disease?
Measure calcium, phosphate, vit D, PTH if eGFR <30
What is target BP in CKD?
What if ACR >70mg/mmol?
<140/90
or <130/90 if ACR >70mg/mmol
Nephrotic syndrome is characterised by what 4 features?
1) Proteinuria >3g/24hrs
2) Hypoalbuminaemia <25g/L
3) Oedema
4) Hyperlipidaemia
Give 3 causes of nephrotic syndrome?
Which is the commonest cause in children?
Which is commonest cause in adults?
Minimal change nephropathy - commonest cause in kids
FSGS
Membranous nephropathy - commonest cause in adults
How is minimal change nephropathy treated?
When is renal biopsy indicated?
What is seen on microscopy?
Prednisolone
Biopsy indicated if no response to steroids
Normal light microscopy, but podocyte fusion on electron microscopy
3 RFs for FSGS?
Biopsy may indicate what?
Treatment?
Afro-Caribbean populations, HIV, drug abuse (heroin)
IgM deposition
Steroids (or immunosuppressants if unresponsive to steroids)