CKD Flashcards

1
Q

What is the role of the kidney? (5).

A

(1. ) Excretion of by-products of metabolism
- Drug metabolites- Creatinine
- K+, Urea, Phosphate excretion
- Keep in plasma proteins, cells

(2. ) Vitamin D activation: Ca and PTH regulation, important for bone, vasculature, nerve health
(3. ) Fluid balance and BP: RAAS
(4. ) Epo production: RBC production

(5. ) Acid-base pH homeostasis
- drop in pH sensed by kidney -> cells excrete acid and absorb bicarbonate to correct pH

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

What is CKD and RF?

A
  • Irreversible deterioration in renal function over years
  • Initially it manifests as biochemical abnormalities then loss of excretory, metabolic, endocrine function of the kidney leads to clinical Sx and signs of renal failure
  • Ultimately without RRT it leads to chronic stage 5, ESRD
RF 
- HTN, DM, vascular disease
- >65y
- using nephrotoxics e.g. ibroprofen
These are high risk groups and should be targeted for screening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pathophysiology of CKD (note: this is a simplified answer) (6)

A

(1. ) Nephron damage:
- GFR drops causing RAAS activation
- inc BP and systemic resistance thus HTN
- pedal & pulmonary oedema

(2. ) Reduced excretion:
- Uremic, hyperkaliaemic (late stage)
- Drug toxicity
- Albuminuria

(3. ) Reduced PO excretion and vitamin D activation
- Low serum Ca
- PTH excreted (in response to hi serum PO, low Ca)
- secondary hyperparathyroidism, which inc bone resorption & can lead to renal osteodystrophy (CKD-MBD)

(4. ) High serum PO and HTN causes endothelial damage and calcification. This inc BP and CVD risk
(5. ) Reduced intercalated cells available means there’s reduced bicarbonate in relation to H+, so become acidotic.
(6. ) Reduced EPO production means less RBC are formed -> anaemic

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

Aetiology of CKD

A
  • DM
  • HTN/atheroma/renovascular (renal-CVD)
  • Glomerulonephritis
  • Unknown
  • Infective
  • Obstructive
  • Cystic or congenital e.g. POK
  • Others: Medication, Myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dx of CKD

A

KDIGO criteria:

  • Abnormalities of the kidney structure or function
  • Present for >3m with implication for health

Therefore, Dx requires:

  • Abnormal function = either GFR <60ml or albuminuria (urine ACR >3mg/mmol)
  • Abnormal structure = histological or radiological evidence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is staging of CKD based on?

A
  • GFR and albuminuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical features of CKD

A

(1. ) Asymptomatic usually
- Raised creatinine & urea found accidentally
- Low GFR but <30ml at this point

(2. ) Nocturia
(3. ) Tiredness, Breathlessness: due to renal anaemia or fluid overload

(4.) Sx of further deterioration: Pruritus, anorexia, wt loss, N+V

(5. ) Sx of advanced deterioration
- Kussmaul breathing: due to metabolic acidosis
- Muscle twitching
- Drowsiness
- Coma

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

CKD Ix

A

Approach

  • Hi Creatinine & urea requires rapid investigation, repeat in 2w
  • identify cause, exacerbating factors e.g. HTN, obstruction
  • screen for complications (CVD, bone etc)

(1. ) U&E, electrolytes: hyperkalaemia? acidosis?
(2. ) Urinalysis: quantify proteinuria, haematuria may indicate GN
(3. ) Ca, phosphate, PTH, 25(OH)D: renal osteodystrophy?

(4. ) FBC, Albumin, glucose, lipids:
- anaemia?
- nephrotic syndrome?
- CV risk

(5. ) Renal US
(6. ) Hepatitis, HIV Serology

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

Aims of CKD Management (4.)

A

Aims of Mx in CKD is to:

(1. ) Monitor renal function
(2. ) Slow down further renal damage and limit complications
(3. ) Treat CVD RF
(4. ) Prepare for RRT if appropriate

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

CKD Management (5.)

A

(1.) Monitor renal function every 6m in stage 3,4,5 CKD. Predict when ESRF would be reached

(2. ) Reduce rate of progression:
- ACEi, ARBs: reduce proteinuria

(3. ) Tx of complications
(a. ) Electrolyte & fluid imbalances = reduce dietary protein, K, Na, fluid. Consider diuretics.

(b.) Acidosis: Na bicarbonate supps

(c. ) CKD-MBD:
- Reduce dietary PO
- Active vitamin D supps

(d. ) Anaemia: iron supps, ESA
(e. ) Glycaemic Control

(4. ) Tx of CVD risk
- healthy lifestyle, wt loss, exercise, smoking cessation, statin

(5. ) Renal Replacement Therapy RRT:
- Haemodialysis
- Peritoneal dialysis
- Kidney Transplant

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

What are non-modifiable and modifiable factors that affect CKD progression?

A

Non-modifiable

  • underlying cause of renal disease
  • race (CKD progresses faster in black than white)

Modifiable

  • BP
  • Proteinuria
  • Nephrotic use
  • Underlying disease activity
  • Further renal insults
  • Dyslipidaemia
  • Inc phosphate
  • Acidosis
  • Anaemia
  • Smoking
  • Glycaemic control if diabetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does RRT not do? (2)

A
  • Activate vitamin D
  • Produce EPO
  • So pts still required - active Vit D, EPO injections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is Dialysis indicated? (4)

A
  • Fluid overload
  • Hyperkalemia
  • Uraemia
  • Metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When is kidney transplant contraindicated? (4)

A

active malignancy
vasculitis
CVD
high risk of renal failure

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