Renal Flashcards
(58 cards)
Best way to differentiate between CKD and AKI
renal USS - CKD should have bilateral small kidneys
Why do CKD patients have low vitamin D
the kidneys activate vitamin D absorbed from sun and diet allowing it to be involved in parathyroid function, cell growth, bone health and calcium and phosphorus metabolism
Most common inheritable kidney disease
ADPKD
Screening test for ADPKD
as well as knowing about family hx
USS to see how many cysts they have
Ofc they should already have bloods done showing renal failure
MX for ADPKD
tolvaptan (vasopressin receptor 2 antagonist) may be an option. NICE recommended it as an option for treating ADPKD in adults to slow the progression of cyst development and renal insufficiency only if:
they have chronic kidney disease stage 2 or 3 at the start of treatment
there is evidence of rapidly progressing disease and
the company provides it with the discount agreed in the patient access scheme.
Features of ADPKD
hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones
Other than the kidneys, what else can ADPKD affect
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
Features of alports syndrome
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy
What is alports syndrome
Alport’s syndrome is usually inherited in an X-linked dominant pattern*. It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure.
Alports syndrome and failing transplant - what to think
the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.
Diagnosis of alports syndrome
molecular genetic testing
renal biopsy
electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
What is the role of calculating an anion gap
To determine if someone is in a metabolic acidosis
What is a raised anion gap
In excess of 14 mmol
This shows metabolic acidosis
Causes of raised anion gap and metabolic acidosis
lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
How to calculate an anion gap
(sodium + potassium) - (bicarbonate + chloride)
Causes of chronic kidney disease
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease
Diet recommendations in CKD
Low protein
Low phosphate
Low sodium
Low potassium
The reason: these products are typically renally excreted in a well kidney; therefore reduction in intake puts less strain on kidneys
Why is creatinine not a reliable measure of kidney function
This is due to the variation which occurs in creatinine numbers based on muscle mass
This is why in CKD we measure eGFR
What are the stages of CKD
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
CKD and hypertension mx
ACE inhibitors are useful as they decrease filtration pressures at the level of the glomerulus
Furosemide is useful as a anti-hypertensive in patients with CKD, particularly when the GFR falls to below 45 ml/min*. It has the added benefit of lowering serum potassium. However, be aware of dehydration if pt has gastroenteritis
When to worry about an eGFR drop if you recently started an ACE inhibitor with known CKD
NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs). A rise greater than this may indicate underlying renovascular disease.
Two causes of diabetes insipidus
decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)
Causes of cranial DI
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis
Causes of nephrogenic DI
genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
