Clinical pathology of renal disease Flashcards

1
Q

What are the functions of the kidney? And which one are affected first by AKI and CKD?

A

Excretion and homeostasis –> Waste products, acid-base balance, etc

Endocrine functions –> RAAS, erythopoietin production, hydroxylation of vitamin D

E&H are damaged early in AKI and late in CKD, while Endocrine functions are damaged in CKD.

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2
Q

What are the causes of renal AKI?

A

1) Renal underpefusion
2) Intrinsic renal damage
3) Obstruction

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3
Q

What can causes renal underperfusion?

A

1) Hypovolaemia –> Haemorrhage, Dehydration (elderly, postsurgery)
2) Sepsis (vasodilatation)
3) Renal artery stenosis /atherosclerosis
4) Pump failure (heart)

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4
Q

What can cause intrinsic renal damage?

A

1) Ischaemia
2) Nephrotoxins–> Drugs, poisons, myoglobin (rhabdomyolysis), paraproteins (myeloma)
3) Infection (pyelonephritis)
4) Trauma

5) Early stage of inflammatory causes of chronic kidney
disease (glomerulonephritis, interstitial nephritis)

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5
Q

What are the causes of renal obstruction?

A

1) Stones
2) Tumour
3) Prostatic hypertrophy (most common)

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6
Q

How would sodium be effected in a pre-renal uraemia and in intrinsic renal damage?

A

1) Pre-renal uraemia
- -> Urine sodium is <15
- -> Serum sodium is HIGH (helps to preserve water)

2) Intrinsic renal damage
- -> Urine sodium is >40
- -> Serum sodium is LOW (kidney stopped working)

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7
Q

When should fluids be given in AKI?

A

Fluid cures in the pre-renal uraemia state.
–> Fluid resolves low GFR from low renal perfusion.

Fluid kills in the intrinsic renal damage stage.

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8
Q

What biochemical changes occur in AKI?

A

Hyperkalaemia –> Retain potassium to help neutralise acid pH (metabolic acidosis).

Life threatening when….

1) Plasma pH <7.0
2) Potassium > 8mmol/l

Retain nitrogenous waste products.

Hyponatraemia –> First sign of fluid retention –> Will eventually lead to fluid overload.

REMEMBER you do not see endocrine changes in AKI.

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9
Q

What drugs should you avoid in AKI?

A

ACE inhibitors
ARBs
NSAIDs
And other nephrotoxic drugs

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10
Q

What are some causes of CKD?

A
Diabetes Mellitus, Hypertension
Polycystic Kidney Disease
Recurrent pyelonephritis / reflux nephropathy
Glomerulonephritis
Interstitial nephritis
Multisystem disease
Drugs
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11
Q

What tests do you use to monitor early and late CKD?

A

EARLY –> eGFR

LATE –> Serum creatinine

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12
Q

What are the ranges for albumin to creatinine ratio (ACR) in CKD?

A

A1 <3

A2 3-30

A3 >30

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13
Q

What biochemical changes occur in CKD stage 3-4?

A

1) Elevated creatinine, reduced eGFr, Elevated ACR

2) Endocrine changes
- -> Reduced 1alpha hydroxylation of Vitamin D
- -> Hypocalcaemia and secondary hyperparathyroidism
- -> Reduced Erythropoietin, causing anaemia

3) Lipids –> Elevated Cholesterol & Triglyceride partly accounts for increased risk of CHD
4) Impaired immune function

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14
Q

What biochemical changes occur in CKD stage 4-5?

A

1) Elevated creatinine AND urea
2) High phosphate
3) Acidosis
4) Hyperkalaemia –> offset by increased gut losses until late stage

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15
Q

Most patients with CKD do NOT get oliguria until very late stage, except when the cause of the CKD is….

A

Glomerular damage (EG: glomerulonephritis)

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16
Q

How does lack of vitamin D cause bone damage?

Osteomalacia and osteitis fibrosa

A

Vit D is unable to absorb calcium in the gut so plasma calcium decreases.
Therefore parathyroid hormone increases to absorb calcium from bone.

Also metabolic acidosis causes bone buffers to be dissolved –> osteoporosis (from reduced GFR)

Also get increased plasma phosphate which binds to calcium –> Metastatic calcifications

17
Q

What are the two main causes of hypokalaemic acidosis?

A

1) GI loss –> diarrhoea, laxatives

2) Renal tubular acidosis –> renal loss of potassium