Renal Flashcards

1
Q

How do you calculate the plasma creatinine clearance value at the
bedside, by body weight?

A

The Cockcroft–Gault method is widely used:
Creatinine clearance = (140- age) x bodyweight (kg) x 1.23 (males) or
1.04 (females)/serum creatinine (μmol/L)
The Modification of Diet in Renal Disease (MDRD) is another measure
that uses serum creatinine level, sex and ethnicity to calculate estimated
glomerular filtration rate (eGFR). It is calculated automatically on
read-outs from many chemical pathology laboratories. A further formula
is the National Kidney Foundation clinical practice guidelines formula.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Can you tell me whether administering low doses of dopamine to
increase renal blood flow is today considered obsolete?

A

The effect of low-dose dopamine on renal blood flow has been
questioned. The effect of increasing urine output is now thought to be
largely due to the rise in cardiac output. Low-dose dopamine is still used
and is not obsolete, as it often helps in shock whatever the mechanism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why does haemoglobinuria cause anuria?

A

Haem pigment casts obstruct the tubules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is albumin infusion contraindicated in nephrotic syndrome? If not, then
what are the indications?

A

No, albumin infusion is not contraindicated but its effect is transient. It
is sometimes used in diuretic-resistant nephrotic syndrome patients with
an albumin of less than 20 g/L. It is combined with diuretic therapy,
e.g. furosemide. There is no good evidence, however, of its clinical
usefulness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Listed under the drug causes of nephrotic syndrome, it has been
stated that high doses of captopril can induce an immune-complexmediated
membranous glomerulonephritis. If a patient with nephrotic
syndrome has hypertension, is it detrimental to give captopril as a
treatment for his hypertension? Could this exacerbate the patient’s
nephrotic syndrome?

A

Proteinuria sufficient to cause the nephrotic syndrome has been
described with captopril. Angiotensin II receptor antagonists would be
better in the circumstances you describe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Please explain the pathophysiology of ascites in the nephrotic
syndrome?

A

Expansion of the interstitial compartments (i.e. the peritoneal cavity in
ascites) is secondary to the accumulation of sodium in the extracellular
compartment. Sodium retention occurs because of increased Na/K-
ATPase expression and activity in the cortical collecting duct. Additional
factors include elevated tumour necrosis factor alpha (TNF-α) levels and
an increase in circulating atrial natriuretic protein (ANP) levels, which
change capillary permeability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does the nephritic syndrome cause hyperkalaemia? I don’t seem
to be able to find a definitive answer in the textbooks that I have
consulted.

A

Acute nephritic syndrome with acute kidney injury causes hyperkalaemia.
Nephrotic syndrome does not, unless acute kidney injury supersedes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

You say that the investigation of first choice for urinary tract infections
(UTIs) in males or children, or recurrent UTIs in females, is intravenous
urography (IVU); in Oxford Handbook of Clinical Medicine it is ultrasound
(US). Which is best?

A

IVU shows the anatomical detail better than US and was regarded by
many as first choice. US does not show pelvicalyceal anatomy as well
but it does rule out major abnormalities, e.g. obstruction, and many
urologists do not now use IVU. US followed by contrast-enhanced
computed tomography has become more common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Other than amoxicillin, what other orally administered drug is
    recommended for the treatment of a urinary tract infection (UTI)
    caused by enterococcus?
  2. What is the recommended dosage for antibiotics in the prophylactic
    treatment of recurrent UTI in pregnancy? Is amoxicillin clavulanic
    acid safe to use during pregnancy?
A
  1. Trimethoprim, an oral cephalosporin, or ciprofloxacin is used. A
    pretreatment urine culture should be obtained if possible and the
    treatment can then be changed according to bacterial sensitivities and
    clinical response.
  2. Dose: amoxicillin 250 mg every 8 hours for 5 days. Co-amoxiclav is
    safe in pregnancy. Bacteruria should always be treated in pregnancy
    and shown to be eradicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the advantage of intermittent self-catheterization over an
indwelling catheter? How is bladder training done while on an
indwelling catheter?

A

This depends on the clinical need. Intermittent catheterization is
associated with fewer urinary infections. Bladder training involves
closing off the catheter intermittently for increasing lengths of time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Kindly tell me about the role of pulse wave velocity (PWV) in early
diagnosis of arteriosclerosis. How is it useful in cardiac, diabetic and
renal medicine?

A

Pulse-wave velocity is an indicator of arterial stiffness measured by
Doppler ultrasound. Its use is not widespread but some studies suggest
that it indicates atherosclerosis independent of blood pressure and might
therefore be of prognostic value. The properties of the arterial wall, its
thickness and the arterial lumen diameter are factors that influence PWV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

You say that no convincing evidence was found that chronic
hyperuricaemia causes nephropathy and nor can it be corrected by
allopurinol. However, some patients we see have high serum uric
acid and creatinine, which both come down with allopurinol. Please
comment.

A

There is evidence to suggest that chronic hyperuricaemia causes
nephropathy, but this does not happen as often as was originally
thought.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Can aspirin cause analgesic nephropathy? If yes, then how could we
justify its use in primary prevention of coronary artery disease (CAD),
even in high-risk patients? I have read that regular use of analgesics for
3 years could cause analgesic nephropathy.

A

Aspirin in large doses used over a long time can produce analgesic
nephropathy; this was well described in Australia some years ago. In
small doses, e.g. 75–150 mg a day, aspirin appears very safe and should
be used for secondary prevention of further coronary events.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the probability that a patient on a moderate daily dose of nonsteroidal
anti-inflammatory drugs (NSAIDs; ibuprofen 800 mg once daily
for tension headache) will develop analgesic nephropathy?

A

Renal lesions are rare and at this dose and frequency the patient is very
unlikely to develop analgesic nephropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Do daily doses of paracetamol with the dosage range of 1 g/day cause
analgesic nephropathy. If so, after what length of time?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Allopurinol is used for the treatment of uric acid stones; it is also one
of the aetiologies of renal calculi. Could you please explain its actual
effect.

A

Allopurinol blocks the enzyme xanthine oxidase which converts xanthine
into urate. The level of urate in the blood falls, as does the amount in the
urine. It does not cause uric acid stones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why should we avoid angiotensin-converting enzyme (ACE) inhibitors
as hypertensive therapy in the presence of renal artery stenoses? How
can they lead to acute renal failure? What else can we prescribe for this
patient to regulate the hypertension?

A

In renal artery stenosis there is reduced renal perfusion, reduced
transglomerular pressure and reduced glomerular filtration rate (GFR),
which leads to acute renal failure. The response is intrarenal activation
of the renin–angiotensin system, which leads to efferent arterial
vasoconstriction. This restores transglomerular pressure and glomerular
filtration rate. Angiotensin-converting enzyme (ACE) inhibition or
blockade prevents angiotensin release and stops the resultant response.
Use other drugs, such as nifedipine or a beta-blocker.

18
Q

Is the use of angiotensin-converting enzyme (ACE) inhibitors

contraindicated in cases of unilateral renal artery stenosis?

A

yes

19
Q
  1. How effective is renal duplex in detecting renal artery
    stenosis?
  2. Is magnetic resonance angiography superior to renal duplex in
    detecting renal artery stenosis?
A
  1. Duplex scanning compared to arteriography is over 90% sensitive and
    specific.
  2. Yes, and this is now best practice for the diagnosis.
20
Q

How accurate is ultrasonography in detecting renal calculi?

A

Small calculi might be missed

21
Q

Please explain the most effective way to manage a case of intrauterine
fetal unilateral hydronephrosis in the 32nd week of pregnancy.

A

This is a very specialized area and consultation with a paediatric
urologist is essential. In general, hydronephrosis is being detected
more frequently as routine ultrasonography becomes more common.
In most cases, fetal surgery has not been beneficial. The most common
cause of hydronephrosis is pelviureteric obstruction, which does not generally impair renal function. Expectant management with follow-up
at 2-monthly intervals is the best approach.

22
Q

In renal failure, why does oedema first occur in the periorbital area and
nowhere else?

A

In renal failure, oedema is due (as in other conditions) to fluid retention.
The oedema is generalized but is often first noticed in the lax tissues
around the eyes (periorbital area).

23
Q

How does sodium valproate decrease serum urea concentration and GI
bleed increases it?

A

Blood is protein and therefore contains nitrogen, which is converted
to urea; hence the rise in urea concentration with a gastrointestinal
bleed. It is unclear whether sodium valproate does decrease the urea
concentration but it does have a number of metabolic effects. Valproate
produces anorexia, which reduces protein intake, and this could lower
the serum urea. Of course, you also get a low urea in severe liver disease,
which very rarely occurs with sodium valproate. Sodium valproate also
raises the ammonia level, again rarely, which could affect the urea level

24
Q
  1. What clinical information can be obtained by checking the blood urea
    nitrogen (BUN) level that cannot be obtained by checking the blood
    urea and serum creatinine alone?
  2. What is the signifying difference between blood urea and BUN?
A

BUN is shorthand for blood urea nitrogen; that is the blood urea. We now
do not measure blood urea, we measure serum or plasma urea. There is,
therefore, no difference between the BUN and the serum urea

25
Q
  1. Does uraemia cause dysentery with blood and mucus mixed with the
    stools?
  2. Is it correct to use the term ‘uraemic dysentery’?
  3. Does uraemia cause finger clubbing?
A

no
no
no

26
Q

What are the causes of a low serum creatinine?

A

Small body mass.

27
Q

Why does oliguria occur in the early stages of acute tubular

necrosis (ATN)?

A

There are many mechanisms but vasopressin levels are elevated so that
free water and urea excretion are reduced. Angiotensin II and aldosterone
are also increased, reducing sodium and hence water excretion

28
Q

Is renal impairment induced by lithium therapy in bipolar affective
disorders irreversible? How often does it occur?

A

Renal impairment is usually reversible but cases have been reported
in which progression occurs when lithium has not been stopped
immediately. It is uncommon if lithium therapy is monitored with serum
levels.

29
Q

Can you please explain why a patient with chronic renal failure (CRF)
might present with either oliguria or polyuria?

A

CRF can present with polyuria, which is due to failure of tubular
reabsorption. When depression of glomerular filtration occurs, oliguria tends to replace polyuria. Because tubular dysfunction always
accompanies glomerular disease to some extent, the urine output is not a
useful guide to renal function. The oedema occurs because of increased
sodium tubular reabsorption

30
Q

What are uraemic frost conditions?

A

This is a term used for the appearance of the skin, literally ‘a frost’, which
occurs only in terminal renal failure. In the age of dialysis and renal
transplantation it is now not seen in developed countries.Terlipressin has been most used and a response occurs in about 60% of
patients, usually over a few days. It improves circulatory function by
vasoconstriction of the dilated splanchnic arteries, which subsequently
suppresses the activity of the endogenous vasoconstrictor systems,
resulting in increased renal perfusion. The response, however, is
frequently transient: most patients with the hepatorenal syndrome
require liver transplantation.

31
Q

What is the role of terlipressin or novapressin in the management of
hepatorenal syndrome?

A

Terlipressin has been most used and a response occurs in about 60% of
patients, usually over a few days. It improves circulatory function by
vasoconstriction of the dilated splanchnic arteries, which subsequently
suppresses the activity of the endogenous vasoconstrictor systems,
resulting in increased renal perfusion. The response, however, is
frequently transient: most patients with the hepatorenal syndrome
require liver transplantation.

32
Q

What is the rationale of angiotensin-converting enzyme (ACE) inhibitors
in chronic renal disease?

A

ACE inhibitors reduce intraglomerular pressure and proteinuria as well
as blood pressure in chronic renal failure. They slow progression of the
renal disease

33
Q

What procedure is recommended for post renal transplant if this is the
second graft?

A

If by ‘procedure’ you mean immunosuppressive regime, then for a highrisk
patient (e.g. after a previous graft), CD25 monoclonal antibodies (e.g.
basiliximab or dacluzimab) are used as induction therapy, followed by
mycophenolate (replacing azathioprine) and tacrolimus

34
Q

Do the cysts in autosomal-dominant polycystic kidney disease (PCKD)
undergo malignant transformation and in what percentage?

A

Malignant transformation does not occur in PCKD

35
Q

In a 69-year-old patient with a 2-cm hard prostatic nodule on digital
rectal examination, what is the more appropriate way to make a
definitive diagnosis of prostate cancer: prostate biopsy or serum prostatespecific
antigen (PSA)?

A

Prostate biopsy. A histological diagnosis is essential; the Gleason Scoring
System, which guides treatment and includes prognosis, depends on this

36
Q

A 50-year-old patient complains from slight lower urological symptoms
(mild difficulty in urination). By digital rectal examination a mass of
(1) hypertrophy can be palpated. His family history contains cases of
prostate cancer (in some relatives). What is the next investigation to do in
this patient?
● Titration of serum prostate-specific antigen (PSA): Is it useful in such a
patient? Why?
● Transrectal ultrasound (TRUS)?
● TRUS-guided needle biopsy?

A

The risk of prostate cancer is approximately two-fold in men with firstdegree
relatives affected. There is perhaps a trend to an increase when
other relatives are affected. In the particular instance of the 50-year-old
man the correct procedure is rectal ultrasound-guided needle biopsy.
The serum prostate-specific antigen (PSA) is useful in that:
● a PSA 4 is normal
● a PSA 4.1–10 means the cancer is confined to the prostate
● a PSA 10 indicates the likelihood of extraprostatic extension by up
to 30- to 40-fold.

37
Q

What are the causes of urinary incontinence in the elderly?

A
The causes of urinary incontinence are represented by the acronym
DIAPPERS:
● Delirium
● Infection
● Atrophic urethritis
● Pharmacological (drugs)
● Psychological
● Excess urine output (e.g. diabetes, congestive cardiac failure)
● Restricted mobility
● Stool impaction
38
Q

For how long could urinary retention persist after major gastrointestinal
tract surgery? Will cholinesterase inhibitors be of benefit in enhancing
emptying of the bladder?

A

Urinary retention can persist for days, particularly in elderly men with
enlarged prostate glands. After 24 hours, catheterization is usually
performed. Cholinesterase inhibitors are now not used because of
side-effects.

39
Q
  1. What are the possible causes of a large, white kidney?

2. What is the physiological significance of a giant cell?

A
  1. Amyloid involvement of the kidneys produces enlarged, pale kidneys.
  2. Giant cells are due to the fusion of activated macrophages and are
    seen in chronic inflammation, e.g. tuberculosis
40
Q

What is the amount of 24-hour urinary albumin excretion above which a
diabetic patient is said to have microalbuminuria?

A

Normal people excrete 30 mg of albumin in 24 hours. Excretion of
30–300 mg is called microalbuminuria. Above 300 mg in 24 hours protein
can be detected by dipstix and is termed ‘albuminuria’.

41
Q

How is forced diuresis induced in cases of prerenal failure?

A

Prerenal failure is due to hypovolaemia, hypotension or fluid and
electrolyte depletion. You need, therefore, to replace fluids initially with
0.9% saline with potassium (20 mmol). Monitor the pulse, blood pressure
and venous pressure. A diuresis will occur when volume repletion has
taken place.

42
Q

Treatment
Patients with chronic kidney disease and proteinura >1 g/24 hours

additional measures

A

● Angiotensin-converting enzyme inhibitor increasing to maximum dose
● Add angiotensin receptor antagonist if goals are not achieved*
● Add diuretic to prevent hyperkalaemia and help to control blood pressure
● Add calcium-channel blocker (verapamil or diltiazem) if goals not achieved

● Statins to lower cholesterol to 4.5 mmol/L
● Stop smoking (threefold higher rate of deterioration in chronic kidney disease)
● Treat diabetes (HbA1C 7%)
● Normal protein diet (0.8–1 g/kg bodyweight)