Renal Flashcards
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
Features of DI
polyuria and polydipsia
due to ADH not working (whether cranial or nephrogenic), water will not be reabsorbed. This will result in low urine osmolality due to vol of H20 lost. Will have high plasma osmolality.
Mx of DI
nephrogenic diabetes insipidus
thiazides
low salt/protein diet
central diabetes insipidus can be treated with desmopressin
Mechanism of spironolactone
spironolactone aldosterone antagonist which acts in the cortical collecting duct.
Why do patients with liver cirrhosis benefit from spironolactone
liver cirrhosis results in portal hypertension…this results in vasodilation causing subsequent activation of RAAS from a drop in systemic BP. Spironolactone is an aldosterone antagonist therefore stops RAAS.
As well as liver cirrhosis, what other indications are there for spironolactone?
nephrotic syndrome
Conn’s syndrome
Hypertension
HF
Adverse affects of spironolactone
hyperkalaemia
gynaecomastia
What type of AKI does rhabdomyolysis cause
intrarenal AKI
Causes of rhabdomyolysis
seizure
collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)
Features of rhabdo
acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
the CK is significantly elevated, at least 5 times the upper limit of normal
elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology
myoglobinuria: dark or reddish-brown colour
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis
Mx of rhabdo
IV fluids to maintain good urine output
urinary alkalinization is sometimes used
Which malignancy are patients at risk of following renal transplant
SCC or BCC
Renal transplant medication example regime
initial: ciclosporin/tacrolimus with a monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus
add steroids if more than one steroid responsive acute rejection episode
Ciclosporin mechanism
inhibits calcineurin, a phosphotase involved in T cell activation
Mycophenolate mofetil (MMF) mechanism
blocks purine synthesis by inhibition of IMPDH
therefore inhibits proliferation of B and T cells
side-effects: GI and marrow suppression
Common side effects of renal transplant medication
Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia.
Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney
Malignancy (SCC and BCC)
Features of a hyeracute graft rejection in renal transplant
Minutes to hours
due to pre-existing antibodies against ABO or HLA antigens
an example of a type II hypersensitivity reaction
leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
no treatment is possible and the graft must be removedW
Which system is used to determine which kidney is compatible with which patient
HLA typing which is found on chromosome 6
Features of acute graft failure
(< 6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants
Features of chronic graft rejection
> 6 months
both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)
Starry sky on immunoflueresence
URTI 1-2 weeks ago
Blood and protein in urine
HTN
Post strep glomerulonephritis
URTI 1-2 days ago, macro haematuria
Young male
IgA nephropathy
When might contrast related nephrotoxicity show on bloods and what are the risk factors
2 -5 days after administration; will be a 25% increase in creatinine
RFs: known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
Prevention of nephrotoxicity due to contrast
f intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure
Raised anion gap causes
lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol
AKA metabolic acidosis
Lactate driven metabolic acidosis consider which drivers
sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin
Renal cell carcinoma triad
haematuria, loin pain, abdominal mass
Features of renal cell carcinoma
haematuria, loin pain, abdominal mass
pyrexia of unknown origin
left varicocele (due to occlusion of left testicular vein)
endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
When to urgently refer hematuria
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 hematuria
Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection
Wilms nephroblastoma is likely in who
children under 5 years of age, with a median age of 3 years old.
It is the commonest childhood malignancy
Features of wilms nephroblastoma
abdominal mass (most common presenting feature)
flank pain
painless haematuria
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients
Think 3 year old, painless haematuria ongoing with no organisms
TCC
ATN causes raised urine sodium - why
tubular damage resulting in sodium ion loss
ATN causes low urine osmolality - why
damage to the renal tubule means that damage is happening at the loop of henle impairing its ability to concentrate urine
