Lecture 19: Clinical Problem Solving: Kidney Failure

Question 1

What is kidney failure?

Answer 1

Reduction in GFR (Glomerular Filtration Rate)

• High potassium (poor filtration, therefore not peeing out K+)
• Uraemia
• High creatinine (?)
• Oliguria (not passing much urine, may or may not happen)

Question 2

What do you want to know about a patient?

Answer 2

1. History (symptoms)

2. Examination (signs)

Question 3

Examples of History taking

Answer 3

1. Pass urine –> at night?
2. Breathless
3. Vomitted blood?
4. Abdominal pain
5. Diabetes –> kidneys involved/damaged –> any medication
6. Familial inheritable diseases

Question 4

JVP measurement as part of Examination

Answer 4

Look at patient ar 45 degrees. Internal Jugular in neck
- Check how many cm pulsation of JVP is above the sternal notch
Normal :1-2cm
If had to lie patient flat in order to get JVP –> -ve
If could see JV pulsating at ear level –> +ve –> fluid overload/congestive HF
- Linked to low BP (e.g. 90/60)

Question 5

Patient Signs from Examination:
- Afebrile, Looks unwell. BP 90/60, Dry skin, Chest clear, JVP: 0cm, increased creatinine levels, Normal/slightly dropped Hb levels, Normal Calcium, Increased Potassium

Answer 5

Acute:
- history of diarrhea and vomiting + dehydrated
= Pre-renal

Question 6

Role of Blood Tests

Answer 6

Dont tell you whether it is Acute or Chronic Kidney Failure

- Just that it is Kidney Failure (LOW eGFR)

Question 7

What other blood tests may help distinguish whether it is acute or chronic kidney failure?

Answer 7

HAEMOGLOBIN test (anaemia)

• elevated ESR (in KF)
• Liver function tests are irrelevant, and Calcium and phosphate levels dont help distinguish

Question 8

What are Hb levels relevant to distinguishing b/w acute or chronic kidney failure?

Answer 8

RBC life = 120 days –> if EPO levels decrease due to KF will take a long time (chronic) to show and hence become anaemic
Therefore slightly low Hb levels = Acute KF
Very low Hb levels = Chronic KF –> as KF (hence decreased EPO production) must have lasted 120 days to show anaemia

Question 9

Cycle to produce low Hb levels

Answer 9

Kidney functions:

1. Kidney’s get rid of lfuid and electrolytes
2. Produce EPO erythropoietin
3. Alpha-hydroxylate Vit D (storage form –> active form –> so can absorb Vit D from bone)

Question 10

Acute Renal Failure

Answer 10

Acute deterioration of kidney function over a short period of time
Usually reversible
Often associated with other illnesses
- diarrohea and vom. –> dehydration –> affects kidney

Question 11

Pre-renal KF

Answer 11

Due to decreased perfusion of kidneys
Generally low BP (due to low vol.)
- Bleeding
- Sepsis (cytokines –> vasiodilation –> decreased BP)
- Dehydration
- HF ( no heart pumping –> cardiogenic shock –> decreased BP)
Some progress to become intrinsic renal damage (Acute Tubular necrosis)

Question 12

Renal KF

Answer 12

Mainly ATN (Acute Tubular Necrosis) --> due to pre-renal that wastnt treated early enough
- Acute= Toxins. Tubular= Renal

Question 13

Causes of Renal KF

Answer 13

Aminoglycosides: antibiotics for gram -ve infections
Contrast: CT, angiograms
NSAIDS: neurophen w/o hydration
Rhabdomyolysis:
- acute muscle breakdown –> toxin release –> acute kidney failure
- trauma
-venom/toxin (crack/cocaine/heroine/ bee stings)

Question 14

Other causes of intrinsic renal failure (not ATN)

Answer 14

RPGN (Rapid Progressive GlomeruloNephritis)

• Rapid acute renal failure (from glomerulus inflammation)
• Cresents in glomeruli on biopsy
• Red cells and cast cells in urine (SLE/Lupis, vasculitis, post-Streptococcal GN)

Question 15

What is the best test for Post-Renal AKI?

Answer 15

Renal Ultrasound

• can always palpate bladder, but only useful if obstruction is at bladder outlet (enlarged prostate)
• not urine volume or looking for haematuria
• can only palpate a polycystic kidney

Question 16

Treatment for having an enlarged bladder

Answer 16

Hydronephrosis –> needs draining

Question 17

Hypervolemia

Answer 17

Fluid overload

1. Edema (swelling) - particularly feet and ankles
   - 3kg of fluid per leg. press hard on shin bone
2. Difficulty breathing while lying down (orthopnea - difficulty breathing when lying flat in bed)
3. Crackles on auscultation (when breathing)
4. High BP
5. Irritated cough
6. Jugular Vein distension
7. Shortness of breath (dyspnea)
8. Strong, rapid pulse (tachycardia)

Question 18

Meaning of 6ml/min

Answer 18

6% of normal kidney function

Question 19

Presentation of Chronic KF

Answer 19

Most people wont have an acute presentation until their renal function is really bad
GFR 30/40 = no signs/symptoms
GFR Less 15 = some KF symptoms (Uraemia)

Question 20

Uraemia

Answer 20

Nausea, vomiting, cold intolerance, itchiness, breathlessness

Question 21

Patient Signs from Examination:

- 10 days of vomitting, unwell, past history, diabetes 15 years, hypertension, very anaemic, no history of bleeding

Answer 21

Chronic KD

Question 22

Signs of CKD

Answer 22

1. (protein) malnutrition : Wasted, weight loss, look unwell
   - cant eat as feel to sick and nauseated
2. Fluid overload
   - High BP, oedema (swelling), pulmonary oedema
3. Rash (uremic toxin build up in skin/ hyperphosphatemia makes itchy)
4. Pericardial Rub ( inflammation b/w pleural layers –> fluid in pericardium –> crunchy noise –> pleural rub heard when breathing)

Question 23

Blood rests to help distinguish b/w acute or chronic KF

Answer 23

Most blood tests that are abnormal in KF are abnormal just becuase the kidney doesnt work properly
- High potassium, urea, creatinine and phosphate
Same for both acute and chronic
BUT Hb is LOW in chronic Renal Failure (average RBC lifespan of 120 day)

Question 24

Diabetes rates

Answer 24

Main cause for CKD
Increased risk proportionately in Maori, pacifica and asian populations (23.5%)
Type II common in NZ
For every diagnosed diabetic there is another undiagnosed (therefore rates are actually high than expected)

Question 25

What tests might be helpful to confirm diagnosis?

Answer 25

1. Kidney size (normal 10-11cm) (see on US)

2. Presence of obstruction

Question 26

State of Kidney in CRD re tests to confirm diagnosis

Answer 26

1. Small (6cm) kidney size

- check for post-acute kidney failure

Question 27

Main causes of CKD

Answer 27

1. Diabetes (main reason)
2. Hypertension (Increased BP) 20%
3. Glomerular disease 20%

Question 28

Renal Ultrasound

Answer 28

Normal Kidney size 10-11cm

Kidneys less than 8cm highly likely to be due to CRF

Question 29

What is the best treatment to treat deterioration of CKD?

Answer 29

TREAT BP

• treating the anaemia wil help the patient feel better, and slows the progression of chronic kidney disaese
• HbA1c <7.0 - glycemic control- helps slow development into neuropathy. NO help if you ALREADY have CKD
• Can give dialysis to decreased BP, but will just Delay death, wont prevent/cure end stage Kidney failure/death

Question 30

BP control

Answer 30

BP control (BP under 130) is the best treatment to help prevent patients from getting worsened renal function
High Bp = massively increased risk of developing end stage kidney failure
Normal (<120/80) or optimal (<110/70) = being is either of these BP ranges both leads to a massively lower risk of develping end-stage renal fialure

Question 31

What best BP treatment for CKD works the best?

Answer 31

ACE inhibitors/ Receptor blockers
Note: most people require multiple BP lowering pills, as the key treatment is having BP control
- Beta blockers, Diuretics

Question 32

Why are ACE inhibitors/Receptor blockers the best treatment for High BP in CKD?

Answer 32

RAAS 1. slat and h2o control
RAAS 2. vasoconstriction and angiotensin
3. Preferentially vasodilates the Efferent arteriole –> decreased BP in glomeruli –> decreased ongoing damage to glomerulus itself due to the High BP

Question 33

Where do ACE inhibitors and ACE receptor blockers act?

Answer 33

ACE inhibitors: no AI –ACE–> AII

ACE Receptor Blockers: no AII binding to AI1 receptor

Question 34

What happens when you decrease the BP in the glomerulus?

Answer 34

Decreased damage to glomerulus itself –> decreased ongoing structural damage
- done by ACE inhibitors by both RAAS steps 1 and 2, but also by step 3 Preferentially vasodilating the efferent arteriole in the glomerulus