+ - 0:00:00
Notes for current slide
Notes for next slide


How to assess kidney disease

FY1 Teaching May 2025 | Robert Hunter

1 / 42

How to assess kidney disease

  • assessing kidney disease

  • common pathologies

  • investigations

  • management of AKI

  • prescribing

  • when & how to refer

2 / 42

How to assess kidney disease

  • assessing kidney disease

  • common pathologies

  • investigations

  • management of AKI

  • prescribing

  • when & how to refer

2 / 42

Often person on the team who will know the most

AKI in 10 - 20% of hospital admissions.
CKD in 10% (and therefore presumably much higher in hospital population).

750 nephrologists in UK and 250,000 doctors = 0.3%.

79F with pneumonia

Smoker, EtOH XS, hip replacement, HTN on two agents.
Getting worse after 7 days in hospital. Not for ITU.

  • SCr 60 > 80 > 198 mcM | eGFR 22 ml/min/1.73m2
  • Na 132 mM; K 5.9 mM
  • Hb 102 g/L; MCV 98; WCC 13.5; plt 566

3 / 42

79F with pneumonia

Smoker, EtOH XS, hip replacement, HTN on two agents.
Getting worse after 7 days in hospital. Not for ITU.

  • SCr 60 > 80 > 198 mcM | eGFR 22 ml/min/1.73m2
  • Na 132 mM; K 5.9 mM
  • Hb 102 g/L; MCV 98; WCC 13.5; plt 566

  • ABP 110/60 (after period of systolic in 90s)
  • JVP not visible unless lie flat
  • urine output 15 ml in past 6 hrs
  • poor oral intake since hospital admission; no IV fluids

3 / 42

79F with pneumonia

Smoker, EtOH XS, hip replacement, HTN on two agents.
Getting worse after 7 days in hospital. Not for ITU.

  • SCr 60 > 80 > 198 mcM | eGFR 22 ml/min/1.73m2
  • Na 132 mM; K 5.9 mM
  • Hb 102 g/L; MCV 98; WCC 13.5; plt 566

  • ABP 110/60 (after period of systolic in 90s)
  • JVP not visible unless lie flat
  • urine output 15 ml in past 6 hrs
  • poor oral intake since hospital admission; no IV fluids

  • increasing O2 requirement (4L/min nasal)
  • JVP elevated
  • IVI at 250 ml/hr (3L +ve in 24 hrs)
3 / 42

What is her GFR? What is the best measure of current kidney function? What would you like to know in Hx and Ex? What fluids would you prescribe? How would you manage her AKI?
Now what fluids would you prescribe? Why have the IV fluids not provoked a urine output?
Why does she have an AKI? Does she have CKD? What investigations would you request?
Would you refer to renal?


Fluids

Meta-analysis (NEJM Evidence 2022); n = 35,000 balanced vs. saline in critical care. Likely mortality benefit but v. v. small effect size (90% likely in Bayesian analysis). Evidence of harm in traumatic brain injury.

Err towards balanced crystalloids. Be aggressive in first 6 hrs (golden hours); conservative after this. Fluids are ‘thrombolysis’ for the kidney.

Special circumstances:

  • vomiting / alkalosis

  • brain injury

  • cirrhosis

  • hyponatraemia

  • hyperkalaemia


Differential diagnosis if fluid-unresponsive:

  • not enough fluid (unlikely)
  • already too congested
  • fluid going into the wrong places (leaky microcirculation)
  • established ATN (as in this case)
  • blocked catheter

Medications

  • aspirin 75 mg od

  • amlodipine 10 mg od

  • atenolol 25 mg od

  • simvastatin 40 mg od

  • paracetamol 1g qds

  • morphine sulphate 10 mg prn 1 hrly

  • dalteparin 5000 units s.c.

  • piperacillin/tazobactam 4.5g IV tds

4 / 42

What would you do with her drugs now? What would you do with her drugs next week?

Referral: when & how

  • when:

    • approaching RRT (6 Ps)
    • suspected intrinsic cause


  • know:

    • PMHx
    • drugs
    • examination findings
    • urine output
    • urine dip
    • why are you phoning?
5 / 42

Take-home messages

  • urine output = GFR now

  • always plot Cr (or eGFR)

  • blood and protein on dip = intrinsic renal disease

  • uACR or uPCR to quantify proteinuria (see the dog on fire)

  • concept of impaired autoregulation of RBF

  • correct hypovolaemia then stop

6 / 42

Reference slides

7 / 42

8 / 42

9 / 42

10 / 42

11 / 42

12 / 42

Images on left show capillaries in buccal mucosa in a patient with sepsis (Vincent & De Backer, NEJM 2013).

Images on right show stripping of capillary glycocalyx in rat model of sepsis.

13 / 42

14 / 42

15 / 42

Causes of low renal perfusion

  • hypovolaemia (including third-space losses)
  • low effective arterial blood volume (CCF, cirrhosis)
  • distributive causes (sepsis, hepatorenal)
  • drugs (ACEi, NSAIDs, CNIs)
  • macro-vascular obstruction (RAS, dissection, cross-clamp)
  • micro-vascular (accelerated HTN, atheroembolism, SRC, TMA)

Think twice about drugs & sepsis (STOP)

Thadhani et al (NEJM, 1996); Abeulo et al (NEJM 2007); Vincent & De Backer (NEJM, 2013)

16 / 42

17 / 42

18 / 42

Drugs in AKI


19 / 42

Red = directly nephrotoxic
Purple = accumulate in renal failure
Blue = harmful when stopped and not re-started

Should we stop ACEi?

Should we have sick day rules?

Supplemental slides

Cr plot gallery
volume assessment
renal haemodynamics
proteinuria

20 / 42

Cr plot gallery

21 / 42

22 / 42

Myeloma + contrast

23 / 42

DKD

24 / 42

AIN (Sjogrens)

25 / 42

ATI (sepsis / ortho)

26 / 42

RAS + ACEi

Volume assessment

27 / 42

Volume assessment

  • peripheral perfusion
  • peripheral oedema
  • JVP
  • blood pressure (relative & absolute)

  • postural changes

  • always helpful…

    - urine output (+/- catheter)
    - fluid balance chart
    - weight chart
28 / 42

Potential confounders in peripheral perfusion / postural changes… Oedema – where / semi-quantitative / absence of oedema Lie flat for JVP Relative hypotension: Liu et al (NDT 2009)

Tricky volume assessment

  • sepsis

  • heart failure

  • cirrhosis

  • nephrotic syndrome

  • young people

  • old people
  • Black African family origin

Vincent & De Backer (NEJM, 2013)

29 / 42

Tricky volume assessment

  • individual signs unreliable (unless at extremes – e.g. JVP < 1 or > 10 cm)

  • quantify oedema (can even be negative!)

  • almost never “intravascularly deplete but extravascular overload”

  • Bayesian approach


EABV = “a poorly measurable quality of arterial filling determined primarily by blood volume, cardiac output, and vascular tone”

30 / 42

Blood distributed 85 % in venous; 15 % arterial. The description “ECF overload but intravascularly deplete” is usually wrong. Rather there is reduced EABV. Studies in CCF and cirrhosis – showing overall vascular expansion but re-distribution into venous (e.g. splanchnic) circulations.

Renal haemodynamics

31 / 42

32 / 42

33 / 42

34 / 42
  • low Cl at MD (or NKCC2i) stimulates COX2
  • PGE2 stimulates aa vasodilatation (counteracts vasopressors in volume depletion)...
  • ...and also renin release
  • hence role in maintaining glomerular perfusion in hypovolaemia
  • hence hyperPGE2 in Bartter

35 / 42

36 / 42

Proteinuria

37 / 42

38 / 42

39 / 42

Proteinuria

- usually ignore trace results  
- dip ‘+’ = 30 mg/dL = PER 0.5 g/d = overt proteinuria  
- dip ‘+++’ = 300 mg/dL = PER 1–2 = heavy proteinuria  
- to convert PCR to PER, divide by 100  
- ACR >220, PCR >350, PER > 3.5 g/d = nephrotic
40 / 42

41 / 42

https://edren.org/ren/handbook/unithdbk/ckd/proteinuria/

42 / 42

How to assess kidney disease

  • assessing kidney disease

  • common pathologies

  • investigations

  • management of AKI

  • prescribing

  • when & how to refer

2 / 42
Paused

Help

Keyboard shortcuts

↑, ←, Pg Up, k Go to previous slide
↓, →, Pg Dn, Space, j Go to next slide
Home Go to first slide
End Go to last slide
Number + Return Go to specific slide
b / m / f Toggle blackout / mirrored / fullscreen mode
c Clone slideshow
p Toggle presenter mode
t Restart the presentation timer
?, h Toggle this help
oTile View: Overview of Slides
Esc Back to slideshow