Chronic Kidney Disease Flashcards

1
Q

What are the functions of the kidney?

A

1 - Water and salt homeostasis (H+, Na+, K+, PO4-, others)
2 - Filters the blood - removal of toxins and waste
3 - Endocrine Function
4- Urea Production

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2
Q

What are the endocrine functions of the kidney?

A

Renin - regulates blood pressure and water levels
Kallikrein - coagulation
EPO - RBC Production
Calcitriol - Final activation of vit d3

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3
Q

What are the RF for CKD

A

Male
Hypertensive
Smoking
Diabetes
Age >50 years old
Black and Hispanic
FHX
Autoimmune diseases

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4
Q

What is CKD defined as?

A

Chronic kidney disease (CKD) can be defined by the presence of kidney damage or reduced kidney function for >3MONTSHS

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5
Q

What investigations can be used to assess renal function or structure

A

Renal Chemistry:
Serum: Electrolytes (K+H+Na+), Glucose, Urea, Creatinine, EPO
Bloods - Anaemia - Normocytic?
Serum creatinine
Urine analysis: Haematuria +/- Proteinuria, Glucosuria

**GOLD STANDARD - KDIGO Classification
Urinary albumin: creatinine ratio
Estimated of eGFR (glomerular filtrations rate) **

Imaging -
Renal US: eGFR G4/G5
- Kidney swelling, atrophy, hydronpheresis, stones
Biopsy - Nephrotic or nephritic

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6
Q

What can cause CKD? Name 7 causes

A

MC - Diabetes - Diabetic nephropathy glycation of glomerular endothelium and arterioles leading to fibrosis
2. Hypertension and CVD - Thickening of arterioles - less perfusion
3. Glomerulopathies - Nephritic / Nephrotic
4. Congenital causes -Polycystic kidney disease
5. Obstruction - renal colic, BPH, Tumour
6. Nephrotoxic drugs - NSAIDs, Anti-depressants, Loop diuretics
7. Pyelonephritis - Persistent infection/inflammation of the kidneys

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7
Q

Pathophysiology of CKD

A

Regardless of the aetiology, the end result is structural alterations-> interstitial fibrosis and tubular atrophy

Damage/loss of nephrons -> persistent inflammation -> Scarring and loss of function

  • glomerular hypertrophy to compensate for loss
  • WCC and inflammatory mediator infiltration
  • Increase in glomerular permeability - loss of macromolecules & exposure to nephrotoxic molecules
  • Renin-angiotensin 2 - excess collagen release

The resultant kidney failure is responsible for a number of complications including:

Metabolic derangement (uraemia and hyperkalaemia),
Anaemia (reduced erythropoietin),
CKD-mineral bone disease (CKD-MBD).

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8
Q

What is the classification system used for CKD? and what a parameter is used?

A

KDIGO Kidney Disease: Improving Global Outcomes (KDIGO) classification

KDIGO classifies CKD based on cause (C), glomerular filtration rate category (G), and albuminuria category (A).

Cause : Identified via patient history (HTN, DM, Drugs)

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9
Q

What are the classification ranges for GFR rate according to KDIGO?

A

Glomerular filtration rate (GFR) category is based on GFR (mL/minute/1.73 m²):

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10
Q

What are the classification ranges for Albuminuria according to KDIGO?

A

Albuminuria category is based on albumin excretion rate (AER) or albumin to creatinine ratio (ACR):
The recommended method to evaluate albuminuria is to measure urinary ACR in a spot urine sample

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11
Q

If both creatinine and albumin are measures of kidney excretion, why would we measure the ratio of both?

A

Concentration of creatinine and albumin in urine can vary. Thus there is a need for standardization.

The ACR corrects for these differences by dividing the amount of albumin in the urine by the amount of creatinine in the urine
Creatinine is excreted at a relatively constant rate and so creatinine levels in urine can act as a standardizing factor.

This allows us to compare ACR values across different samples and get a better sense of the amount of albumin being excreted relative to creatinine.

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12
Q

RISK STRATIFICATION OF KDIGO CLASSIFICATION SYSTEM

A
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13
Q

How would CKD Present?

A

Asx until ESRF ~ fatigue, nausea, pruritus

Symptoms and signs are associated with function

1.Anemia (EPO)
Anemia Sx- headache, pallor, fatigue, intermittent claudication, tachycardic, exertional dyspnoea

  1. Uraemia (Less urea excretion)
    Sx- Uraemic frost, pruritus, Nausea, Reduced appetite, restless legs
  2. Oliguria (reduced urination) ~ 0.5ml/kg/hr or less than 500ml/day

= Fluid retention - peripheral adn pulmonary Oedema, increase JVP

  1. Hyperkalaemia - Arrhythmias, msucle cramps, weakness, reduced tone
  2. Metabolic acidosis - excess H+ retention
  3. MBD Mineral bone disease due to: Hypocalcaemia, hyperphosphatemia, and reduced active vitamin D into calcitriol. Hypocalcaemia leads to secondary Hypoparathyroidism.
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14
Q

What other investigation should be considered to rule out differentials/identify cause

A

Fundoscopic eye examination - Identifies diabetic/htn retinopathy -markers of microvascular complications

DRE - BPH associated with obstructive uropathy

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15
Q

How to treat CKD

A

Treatment

To slow progression:
Maintain BP, treat hypertension (<130/80)
E.g.
ACEi/ARB - Ramipril

2nd line other Anti-HTN drugs: CCBs (verampril) , BB(Atenolol),
Diuretic (thiazide)

Adjunct:
+ SGLT2i - Dapagliflozin
+ Statin - Atorvastatin
+ Vitamin D - MBD
+ Epoetin alfa - if Anaemic

Stage 4-5 Refer to nephrology

For end-stage kidney disease: stage 5
Dialysis:
- Peritoneal dialysis (daily, abdominal
catheter)
- Haemodialysis (3x/week, need fistula)

3rd line: Transplant + lifelong immunosuppression

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16
Q

what can affect serum creatinine levels?

A

Serum creatinine levels have a high individual variation changing with disease states, muscle mass, pregnancy and dietary intake.

17
Q

What are the complications of CKD

A

CVD ~ fluid overload/anemia = HF
MSK - MBD mineral bone disease
Endocrine - Secondary hyperparathyroidism
Heamatological- Anemia
Metabolic acidosis

18
Q

What are the indications for dialysis?

A

eGFR stage 5 AFUK
Anemia
Persistent oedema
Electrolyte imbalance
Severe uraemia ~ seizures
Acidosis non responsive to bicarbonate