HMO education - kidney function Flashcards

1
Q

Creatinine as a measure of renal function - in what way is it subpar?

A

Freely filtered by glomerulus, not reabsorbed, but 15% actively secreted by the tubules

In advanced renal failure the % tubular secretion increases…

It also varies with muscle mass and diet (small amount)

  • Strict vegans, less cr intake, underestimates Cr therefore overestimates eGFR
  • More muscle mass, more Cr released, overestimates Cr, underestimates eGFR

Serum Cr also only starts to increase substantially when approx 50% renal function is lost

If you really need to know the exact GFR - nuclear medicine studies (DTPA/MAG3). This is better than eGFR from Cr clearance and than 24 hour collections

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

Indications for 24 hour urine collection

A

Higher quality egFR for chemo dosing

24 hour bence jones protein, light chains in MM

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

BPT EXAM QUESTIONS: which drug increases serum Cr without impacting on eGFR

A

cotrimoxazole!!!

Everything goes back to normal once the drug is stopped

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

Factors that increase plasma Cr

A

Decreased GFR
Increased muscle mass
Cotrimoxazole effect

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

Factors that increase plasma urea

A

Decrease GFR
Dehydration (ADH response to dehydration)
Increased oral protein intake (diet/GI bleeding)

Increased catabolic rate and protein breakdown (sepsis, steroids, some tetracyclines)

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

Haematuria on dipsticks - false positives and negatives

…. compared to when you actually look under the microscope and see RBCs

A

False positives:

  • haemoglobinuria
  • myoglobinuria
  • iodine contamination
  • oxidising agents in container

false negatives:

  • high urinary nitrate
  • high urinary vit c
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Proteinuria on dipstick… false positives and negatives

A

Normal <150mg / 24 hours or double in pregnancy

False positives: very alkaline urine, very concentrated urine, reading delay

false negatives
dilute urine
bence jones protein (need to specifically test)

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

Which organisms will not show up with nitrites on urine dipstick?

A

strep faecalis!!!!

others may be: staph, acinetobacter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Urine casts types

A

ACELLULAR

Hyaline - normal

Granular - cellular injury (e.g. ATN), immunoglobulin light chains, plasma proteins (e.g. albumin)

Fatty casts - hyaline casts with fat deposits (e.g. nephrotic syndrome)

waxy casts - ESRF

CELLULAR

  • red, white
  • tubular cells (ATN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a bland vs abnormal vs active urinary sediment?

A

Bland: Nothing in urine to imply glomerular pathology

Abnormal: either casts of abnormal degree of protein - ddx may include GN

Active sediment: - includes red cell/glomerular casts –> implies glomerulonephritis!

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

Urgent indications for renal biopsy

A

Rapid deterioration of renal function with abnormal urinary sediment

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

Strong indications for renal biopsy

A

Proteinuria+ haematuria

Proteinuria >1g/day (not diabetic)

Renal impairment with either proteinuria or haematuria

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

What is microalbuminaemia an independent risk factor for?

A

Cardiac disease!!!!

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

Prerenal causes of AKI

A

Hypovolaemia

  • bleeding
  • low cardiac output
  • hepatorenal
  • renovascular stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Renal causes of AKI

A
  • ATN (ischaemic or toxic)
  • GN
  • Small/medium vessel - disease (vasculitis)
  • Tubular obstruction (urate crystals, MM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is ATN?

A

Tubules are quite sensitive to ischaemia (blood supply is last in the line in the medulla)

Most risk of necrosis and cell death

Generally reversible. but once hypovol corrected you need to restrict fluid intake and correct electrolyte imbalances. May need dialysis to support.

Lasts 10-14 days classically

Polyuria with dilute urine may occur in recovery period

17
Q

Hypovol vs progression to ATN - labs to differentiate

A

Urinary Na+
Pre-renal <20, ATN >40 (lost function of tubules, can’t retain Na)

Plasma urea/creatinine ratio
Pre-renal > 80
ATN < 80

Urine osmolality
Pre-renal > 500
ATN > 350

18
Q

Ix for every AKI + initial clinical steps

A
  • Bloods: VBG, UEC, LFT, FBE, CK, CMP, coags, CRP
  • Urine: dipstick, MCS, protein:cr
  • Imaging: USS or CT

Initial clinical steps:

  • fluid balance / IDC insertion if required
  • bladder scan
19
Q

Criteria for post-obstructive diuresis

A

UO 200mls/hour for 2 hours
OR
>3L in 24 hours

Can cause severe dehydration and electrolyte imbalances

20
Q

Management of post-obstructive diuresis

A
  • N saline at 50-80% urine output / hour (depending on PO intake) –> slightly less than match to avoid continuing to drive polyuria
  • 12 hourly UECs/CMP
  • Replace electrolytes
  • Accurate fluid balance
  • Investigate the underlying cause of obstruction: constipation, tumour, stone, clot, etc.
21
Q

Mechanism of triple whammy

A

NSAIDs: inhibit PGs at the afferent arteriole (constricts aff. art)
ACEi: reduce angiotensin II production at efferent arteriole (dilates eff art.)

22
Q

Mechanisms of renal protection of ACEI in CKD

A

In a well patient…. ACEi protect the nephrons:

  • Anti-proteinuric
  • Reduced intraglomerular stress
  • Delays progression of CKD
  • Good antihypertensive
23
Q

PPIs and AKI?

A

Can be associated with interstitial nephritis

24
Q

Indications for dialysis

A
A - acidosis 
E - electrolytes (hyperK)
I - intoxication 
O - overload (refractory to diuretics - can't make them pee despite large amounts of diuretics)
U - uraemic pericarditis (right now!)
25
Q

Glomerular injury

A
  • Ischaemic: thromb microangiopathy, micro emboli, vasculitis
  • Inflam: GN
  • Toxins: drugs causing TMA, drugs causing GN
26
Q

Tubular injury

A

Ischaemic: prolonged pre-renal insult
Inflam: AIN, drugs, infection, autoimmune
Toxins: tubulotoxic drugs, hypercalcaemia, rhabdo, contrast nephropathy, myeloma/light chains, crystalluria

27
Q

How to tell if its a glomerular or tubular injury

A

Microscopic red cells and protein in the urine –> is this GN

28
Q

GN screen

A
HIV/HCV/HBV
ANA/ENA/dsDNA?ANCA/anti-GBM
Complement - c3/c4
SEP-UPEP/BJ protein 
ASOT
29
Q

GN tutorial by Kristeen

A

https://kristeenbarker.thinkific.com