Week 2 Renal Chronic Kidney Disease Flashcards

1
Q

Definition of chronic kidey disease

A

GFR of less than 60 ml/min for >90 days /3 months

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

What are the 5 stages of chronic kidney disease as defined by eGFR.

Think clock into four quarters with one quarter split into 2

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

Stragtagies to prevent CKD

A
  • Control blood pressure (RAS inhibition)
  • Reduce proteinuria (RAS inhibition)
  • If diabetes, optimise glycaemic control
  • SGLT2 inhibitors (not just for diabetics, they have a protective effect on the kidneys and heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is proteinuria a marker or cause of progressive renal disease?

A

Both

Indicator of kidney damage: Protein in the urine reflects damage to the glomerular filtration barrier.

Cause: Filtered proteins can be reabsorbed by proximal tubular cells, triggering inflammation, oxidative stress, and fibrosis. The presence of protein can stimulate cytokine production and attract immune cells, worsening interstitial damage.

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

Potential toxins to avoid in CKD

A

NSAIDs / Contrast / Gentamicin /
Phosphate enemas

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

What are blood pressure treatment goals for CKD?

A

BP treatment goals
“normal” - 130/80
DM / Proteinuria 125/75

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

In CKD if the glomerulus becomes more leaky why does GFR decrease?

A

This is because although in parts there are larger holes, the overall glomerulus is damaged, in some parts the basement membrane is fibrosed resulting in no flow at all, in other parts the efferent arterioles are weakened and unable to apply pressure.

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

What happens to potassium in CKD?

What advice should you give?

A

Hyperkalaemia common as GFR declines < 25

May occur at GFR>25 if Diabetes and type 4 RTA, ACE inhibitors, High K Diet present

Advice would be a low K diet, K monitering and potential use of potassium binders

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

In CKD why are you more likely to develop acidosis?

A

Because the kidneys can’t excrete H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What advice should you be aware of with CKD and acidosis?

A

Aim to keep Serum HCO3 >22

Replace with bicarbonate

Note that animal proteins tend to contribute to higher H+ levels

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

What is the treatment for anaemia in CKD?

A

Erythropoietin

All pts with Hb < 105 and adequate iron stores should be on Epo

If poor response to EPO
Check iron stores / CRP / B12 +folate / PTH/Aluminium/ malnutrition / malignancy

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

Why does CKD lead to anaemia?

A

Erythropoietin (EPO) is a glycoprotein hormone produced by the peritubular cells of the renal cortex. This hormone stimulates red blood cell production in response to low partial pressure of oxygen (pO2). If the kindney is damaged the body makes less EPO

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

What causes renal osteodystrophy?

A

During renal failure you are unable to excrete phosphate and unable to make calcitriol resulting in hypocalcaemia.

The combination of high phosphate and low calcium trigger excessive PTH activity resulting in worsening of bones.

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

Difference between high turnover bone disease and low turnover bone disease

A

High turnover bone disease:

Secondary hyperparathyroidism - PTH rapidly breaking down bone

Low turnover bone disease:

Osteomalacia - lack of calcitriol causes bone to be unable to harden properly

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

In CKD do you see high turnover bone disease and low turnover bone disease

A

Both

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

Treatment for renal osteodystrophy

A
  1. Phosphate restrict (0.8-1.0g/kg/day)
    * diet (0.8-1.0g/kg/day)
    * binders- calcium or non-Ca binders
  2. Vitamin D therapy (alfacalcidol)
    * increases Ca / decreases PO4
  3. Monitor PTH 6/12ly
    * keep 2-3 x normal
  4. Parathyroidectomy may be required
17
Q

Consequences of hyperphosphataemia

A

Vessel calcification:

High phosphate in the blood actually begins to trick vessel cells into thinking they are osteoblasts, this phosphate then combines with calcium and begins to lay down bone in the blood vessels, this results in non-compliant vessels leading to

Systolic hypertension – L Vent Hypertrophy
Diastolic hypotension - Myocardial ischaemia

Another problem is Calciphylaxis

18
Q

With regards to vessel calcification fill in these two types

19
Q

Why is cardiovascular disease such an issue in CKD?

A

CKD leads to so many issues which could cause CKD

  • Raised BP
  • Hyperphosphataemia
  • Anaemia
20
Q

Why is malnutrician an issue in CKD?

A

Malnutrition common in CKD
* Decreased protein intake – dietary restrictions
* Decreased appetite
* Low albumin - ?related to inflammation/infxn

21
Q

What are the seven big issues that occure in CKD?

A

a) Excretory
* Salt and Hypertension
* Potassium
* Acidosis
b) Endocrine
* Anaemia
* Renal Osteodystropy
* Cardiovascular risk
* Malnutrition

22
Q

Who should you refer to a renal clinic?

A

Any patient with rapid increase in creatinine/ hypertension

Stage 3 CKD with hypertension/ proteinuria /haematuria/ rising creatinine

Any stage 4/5 CKD who is suitable for treatment

23
Q

How does peritoneal dialysis work?

A

A catheter is surgically placed into your abdomen (peritoneal cavity).

A special dialysis fluid (called dialysate) is infused into your abdomen through the catheter.

The dialysate sits in your belly for a few hours (called the dwell time).

During this time, wastes, toxins, and extra fluid pass from your blood (via the peritoneal membrane) into the dialysate.

After the dwell time, the used fluid is drained out, and fresh dialysate is put in — this process is called an exchange.

24
Q

What is the cycle of care after a kidney transplant?

25
A 70 year old woman is admitted with worsening confusion, vomiting and abdominal pain. She had a preceding four day history of diarrhoea. She has hypertension, oesophageal reflux and atrial fibrillation. She takes nifedipine, simvastatin, warfarin, digoxin and omeprazole. Her pulse is 102 bpm and blood pressure 122/80 mmHg. Investigations: Urea 12.7 mmol/L (3.0-7.0); Creatinine 210 μmol/L (60-110). Which of her drugs is most likely to have accumulated to cause her symptoms? Digoxin Nifedipine Omeprazole Simvastatin Warfarin
**Digoxin** Nifedipine Omeprazole Simvastatin Warfarin Digoxin is the only one that is metabolised by the liver so CKD causes a build up of the active drug