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Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Best way to differentiate between CKD and AKI

A

renal USS - CKD should have bilateral small kidneys

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2
Q

Why do CKD patients have low vitamin D

A

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

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3
Q

Most common inheritable kidney disease

A

ADPKD

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4
Q

Screening test for ADPKD

A

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

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5
Q

MX for ADPKD

A

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.

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6
Q

Features of ADPKD

A

hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones

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7
Q

Other than the kidneys, what else can ADPKD affect

A

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

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8
Q

Features of alports syndrome

A

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

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9
Q

What is alports syndrome

A

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.

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10
Q

Alports syndrome and failing transplant - what to think

A

the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.

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11
Q

Diagnosis of alports syndrome

A

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

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12
Q

What is the role of calculating an anion gap

A

To determine if someone is in a metabolic acidosis

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13
Q

What is a raised anion gap

A

In excess of 14 mmol
This shows metabolic acidosis

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14
Q

Causes of raised anion gap and metabolic acidosis

A

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

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15
Q

How to calculate an anion gap

A

(sodium + potassium) - (bicarbonate + chloride)

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16
Q

Causes of chronic kidney disease

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

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17
Q

Diet recommendations in CKD

A

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

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18
Q

Why is creatinine not a reliable measure of kidney function

A

This is due to the variation which occurs in creatinine numbers based on muscle mass

This is why in CKD we measure eGFR

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19
Q

What are the stages of CKD

A

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

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20
Q

CKD and hypertension mx

A

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

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21
Q

When to worry about an eGFR drop if you recently started an ACE inhibitor with known CKD

A

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.

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22
Q

Two causes of diabetes insipidus

A

decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

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23
Q

Causes of cranial DI

A

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

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24
Q

Causes of nephrogenic DI

A

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

25
Q

Features of DI

A

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.

26
Q

Mx of DI

A

nephrogenic diabetes insipidus
thiazides
low salt/protein diet
central diabetes insipidus can be treated with desmopressin

27
Q

Mechanism of spironolactone

A

spironolactone aldosterone antagonist which acts in the cortical collecting duct.

28
Q

Why do patients with liver cirrhosis benefit from spironolactone

A

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.

29
Q

As well as liver cirrhosis, what other indications are there for spironolactone?

A

nephrotic syndrome
Conn’s syndrome
Hypertension
HF

30
Q

Adverse affects of spironolactone

A

hyperkalaemia
gynaecomastia

31
Q

What type of AKI does rhabdomyolysis cause

A

intrarenal AKI

32
Q

Causes of rhabdomyolysis

A

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)

33
Q

Features of rhabdo

A

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

34
Q

Mx of rhabdo

A

IV fluids to maintain good urine output
urinary alkalinization is sometimes used

35
Q

Which malignancy are patients at risk of following renal transplant

A

SCC or BCC

36
Q

Renal transplant medication example regime

A

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

37
Q

Ciclosporin mechanism

A

inhibits calcineurin, a phosphotase involved in T cell activation

38
Q

Mycophenolate mofetil (MMF) mechanism

A

blocks purine synthesis by inhibition of IMPDH
therefore inhibits proliferation of B and T cells
side-effects: GI and marrow suppression

39
Q

Common side effects of renal transplant medication

A

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)

40
Q

Features of a hyeracute graft rejection in renal transplant

A

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

41
Q

Which system is used to determine which kidney is compatible with which patient

A

HLA typing which is found on chromosome 6

42
Q

Features of acute graft failure

A

(< 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

43
Q

Features of chronic graft rejection

A

> 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)

44
Q

Starry sky on immunoflueresence
URTI 1-2 weeks ago
Blood and protein in urine
HTN

A

Post strep glomerulonephritis

45
Q

URTI 1-2 days ago, macro haematuria
Young male

A

IgA nephropathy

46
Q

When might contrast related nephrotoxicity show on bloods and what are the risk factors

A

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

47
Q

Prevention of nephrotoxicity due to contrast

A

f intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

48
Q

Raised anion gap causes

A

lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol

AKA metabolic acidosis

49
Q

Lactate driven metabolic acidosis consider which drivers

A

sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin

50
Q

Renal cell carcinoma triad

A

haematuria, loin pain, abdominal mass

51
Q

Features of renal cell carcinoma

A

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

52
Q

When to urgently refer hematuria

A

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

53
Q

non urgent referral for hematuria

A

Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

54
Q

Wilms nephroblastoma is likely in who

A

children under 5 years of age, with a median age of 3 years old.

It is the commonest childhood malignancy

55
Q

Features of wilms nephroblastoma

A

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

56
Q

TCC

A
57
Q

ATN causes raised urine sodium - why

A

tubular damage resulting in sodium ion loss

58
Q

ATN causes low urine osmolality - why

A

damage to the renal tubule means that damage is happening at the loop of henle impairing its ability to concentrate urine

Medicine (8 decks)

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