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Y3 Lecture weeks > Lab5: Biochemistry in renal disase (2) > Flashcards

Lab5: Biochemistry in renal disase (2) Flashcards

1
Q

What do we look at urine dipstick - signs of renal disease?

A
  • Protein
  • Blood (haematuria)
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2
Q

What’s normal amount of protein in the urine in 24 hr period?

A

<0.15 g/24hr

*more than 50% of the above is Tamm-Horsfall ( aka uromodulin) - momucoprotein (secreted by renal cells)

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3
Q

What is overflow proteinuria?

A

Large amount of urinary protein is being filtered - excess of protein goes through the kidney and through the urine

e.g. in Myeloma

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4
Q

What’s glomerular proteinuria?

A

Damage to glomerular membrane -> large molecular weight protein (not normally filtered through the membrane), but in that case they will be and they will come out in the urine

Main protein seen: albuminuria (as more abundant protein in the blood - so seen with damage)

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5
Q

What’s tubular proteinuria?

A

It’s when kidney tubules cannot reabsorb low molecular weight protein (e.g. beta 2) *

*low molecular weight protein are normally filtered through the glomerular membrane

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6
Q

What’s secreted proteinuria?

A

Excess of proteins that are normally secreted by renal cells

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7
Q

What do we test for when we want to test for glomerular proteinuria

A
  • 24 hr total protein
  • urine dipstic (0.3/L) protein -> 0.3/L upwards only detected by urine dipstic
  • protein:creatinine ratio (PCR)
  • Microalbumin
  • Albumin:creatinine ratio (ACR)
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8
Q

What proteins would indicate glomerular proteinuria?

A
  • Increase in high molecular weight proteins in the urine
  • albumin is the main protein lost (most abundant in plasma)
  • more severe glomerular damage - loss of larger proteins
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9
Q

What is detected via micro-albumin test?

A

Very low levels of albumin in the urine - early renal dysfunction

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10
Q

What to do if ACR (albumin: creatinine ratio) is between 3mg/mmol and 70 mg/mmol?

A

Confirm bu subsequent early morning sample

Condirmed ACR or >/= 3 mg/mmol = significant proteinuria

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11
Q

What is classified as significant proteinuria?

A

condirmed ACR or >/= 3 mg/mmol

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12
Q

Do we need to repeat ACR test for proteinuria if ACR is 70 mg/mmol or more?

A

No, this indicated significant proteinuria straight away

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13
Q

What tests to do for tubular proteinuria?

A

Tubular = low molecular weight protein in the urine

  • 24 hr total protein
  • Protein: creatinine ratio (PCR)
  • specific proteins e.g. NAG, RBP, alpha 1 -microglobulin

* albumin: creatinine ratio normal (glomerular function intact)

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14
Q

High PCR (protein: creatinine ratio) and low ACR (albumin : creatinine ratio)

What does it indicate?

A

Increased low molecular weight protein -> possible tubular damage

*as Albumin gets through filtration membrane in glomerular damage; PCR will show microglobulins which are normally reabsorbed in the tubules

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15
Q

What proteins may be seen in overflow proteinuria?

A

Low molecular weight protein - examples:

  • Myoglobin - serum creatinine kinase
  • Bence-Jones protein
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16
Q

What are the urine casts?

A

Aggregation of molecular in distal/collecting duct -> damage to the nephrons / necrosis of renal tubules

e.g. Red cell casts, cellular debris, Tamm-Horsfall protein - hyaline, white cells

Look for it by MICROSCOPY

17
Q

The most common types of stones

A
18
Q

What are physiological inhibitors of stone growth?

A

mucopolysaccharides, citrate and pyrophosphate

19
Q

What urine pH favours formation of renal stones

A

alkaline

20
Q

What do we look at in the urine analysis when we suspect renal stones?

A
  • calcium
  • phosphate
  • urate
  • oxalate
  • cysteine
  • pH
  • sodium
  • magnesium
  • citrate
  • microbiology
21
Q

What is diagnostic of CKD?

A
  • abnormalities in kidney function or structure present for >/= 3 months

and/or

  • GFR <60 ml/min/1.73 m2 on at least 2 occasions separated by a period of at least 90 days
22
Q

CKD signs and symptoms

A
  • early stages are asymptomatic
  • uremic syndrome (weakness, fatigue, loss od appetite, nausea, vomiting, tremors, altered mental function)
  • nocturia

- polyuria

  • pain

- oedema

23
Q

Reduced GFR -> what biochemical abnormality can be seen?

A

Increased serum urea/creatinine

24
Q

What biochemical abnormality can be seen in reduced tubular function?

A

Hyponatremia

Reduced tubular function = sodium loss, inability to concentrate or dilute urine

25
Q

What biochemical abnormality can reduced GFR lead to?

A

Hyperkalaemia

26
Q

How can CKD lead to metabolic acidosis?

A
  • Reduced GFR -> reduced H+ ion excretion and reduced PO4 excretion
  • Reduced tubular function – bicarb reabsorption
27
Q

Why hypocalcaemia is associated with CKD?

A

Reduced 1,25 –vitamin D (1alpha hydroxylase)

28
Q

What test should be used for eGFR?

A

CKD-EPI creatinine equation

*advise people not to eat meat in 12 hours before having a blood test for creatinine/eGFR

29
Q

What Ix should be used for proteinuria?

A

Urine ACR

30
Q

What other /2nd line test to use to confirm/rule out CKD if eGFR with creatinine is borderline?

A

Cystatin C

*it is in the guidelines but not many places use it because of the cost and therefore not many labs offer it

31
Q

What’s the aim of treatment of CKD?

A
  • No cure
  • Treatment to manage complications
  • slow down the progression
  • to reduce CVD risks
32
Q

What findings would suggest the increased risk of progression of CKD?

A
33
Q

What findings (in GFR) would indicate an increased risk of progression to end-stage kidney disease? (2)

A
  • a sustained decrease in GFR of 25% or more over 12 months

OR

  • a sustained decrease in GFR of 15 ml/min/1.73 m2 or more over 12 months
34
Q

What’s ASSIST?

A

CKD from Renal Registry

  • scheme aiming to increase early identification of CKD

Aim: to reduce the unplanned need for dialysis

*to look at eGFR over time and to alert the clinicians of significant changes

35
Q

Pre-renal. What would increase more: creatinine or urea?

A

Urea > creatinine

pre renal -> less blood flow to the nephron -> slower filtrate flow through the nephrone -> filtrate spends longer in the nephron -> more time for the urea to be reabsorbed -> more urea reabsorbed -> more serum urea

36
Q

A response of sodium and water to hypovolaemia in AKI in:

  • pre-renal cause
  • intrinsic
A
  • pre- renal: sodium and water retention (tubule function initially is intact)
  • intrinsic: sodium and water loss (tubular dysfunction so not able to reabsorb)
37
Q

Management of AKI

A
  • determine the cause and treat
  • give fluids - if dehydrated
  • stop nephrotoxic drugs
  • treat metabolic complications - hyperkalaemia
  • monitor (U&E, fluid balance chart)
  • nephrology referral
  • renal replacement therapy - if needed

Y3 Lecture weeks (65 decks)

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