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YR5 Chemical Pathology > Assessment of Renal Function 2 > Flashcards

Assessment of Renal Function 2 Flashcards

1
Q

What is the difference between AKI and CKD?

A

AKI:

Abrupt decline in GFR

Potentially reversible

Tx targeted to precise dx + reversal of disease

CKD:

Longstanding decline in GFR

Irreversible

Tx targeted to prevention of complications of CKD + limitation of progression

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2
Q

Define AKI.

A

Rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base + fluid homeostasis.

Medical emergency necessitating referral to a nephrologist for dx + tx

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3
Q

What are the stages of AKI?

A

1. Increase in sCr ≥ 26 µmol/L

or 1.5-1.9x reference sCr.

2: sCr 2.0-2.9x reference sCr.

3: sCr ≥3x reference sCr

or increase ≥ 354 µmol/L.

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4
Q

What are the three different types of AKI?

A

Pre-renal

Renal

Post-renal

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5
Q

What are features of pre-renal AKI?

A

Reduced renal perfusion:

as part of generalised reduction in tissue perfusion

or selective renal ischaemia.

No structural abnormality.

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6
Q

What is the normal response to reduced circulating volume ?

A

Activation of central baroreceptors

Activation of RAAS

Release of vasopressin

Activation of sympathetic system

Vasoconstriction, increased cardiac output, renal Na retention

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7
Q

When does pre-renal AKI occur?

A

When normal adaptive mechanisms fail to maintain renal perfusion when there is reduced circulating volume

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8
Q

What are 5 causes of pre-renal AKI?

A

True volume depletion (unable to drink)

Hypotension

Oedematous states (3 failures)

Selective renal ischaemia (e.g. RAS in atherosclerotic disease)

Drugs affecting glomerular blood flow

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9
Q

What is this?

A

Renal artery stenosis

(on RHS of image)

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10
Q

Which drugs can predispose patients to develop pre-renal AKI?

A

NSAIDs

Calcineurin inhibitors

ACEi or ARBs

Diuretics

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11
Q

How do NSAIDs predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease afferent arteriolar dilatation

Ibuprofen

Diclofenac

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12
Q

How do Calcineurin inhibitors predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease afferent arteriolar dilatation

Cyclosporine

Tacrolimus

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13
Q

How do ACEi or ARBs predispose patients to developing pre-renal AKI? Give 2 examples

A

Decrease efferent arteriolar constriction

Enalopril

Losartan

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14
Q

How do diuretics predispose patients to developing pre-renal AKI? Give an example

A

Affect tubular function, decrease preload

Loop: Furosemide

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15
Q

What is the difference between pre-renal AKI and acute tubular necrosis?

A

Pre-Renal AKI is not associated with structural renal damage + responds immediately to restoration of circulating volume.

Prolonged insult leads to ischaemic injury.

ATN does NOT respond to restoration of circulating volume.

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16
Q

A 68M with previously normal renal function is found to have a creatinine of 624μmol/l.

Renal USS shows the following appearance in both kidneys. What is the likely cause of his AKI? What makes you think this?

A

Benign prostatic hypertrophy

Hydronephrosis in both kidneys, calyces very dilated, shows obstruction distal to kidneys

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17
Q

What causes post-renal AKI?

A

Physical obstruction to urine flow

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18
Q

What are common sites of obstruction in post-renal AKI?

A

Intra-renal obstruction

Ureteric obstruction (bilateral)

Prostatic/urethral obstruction

Blocked urinary catheter

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19
Q

What are different things which may cause obstruction in post-renal AKI?

A

Luminal: Stones, clots.

Mural: Malignancy (ureteric, bladder, prostate), BPH, urethral strictures.

Extrinsic compression: Malignancy (pelvic e.g. ovarian mass), prostatic hypertrophy.

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20
Q

What is the pathophysiology of obstructive uropathy?

A

GFR is dependent on the hydraulic pressure gradient.

Obstruction results in increased tubular pressure.

Results in an immediate decline in GFR.

Huge rise in Creatinine

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21
Q

Describe the recovery from obstructive uropathy

A

Immediate relief: Restores GFR with no structural damage e.g. via urethral catheter insertion (or subrapubic catheter)

Prolonged obstruction: structural damage

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22
Q

What does prolonged obstructive uropathy result in?

A

Glomerular ischaemia

Tubular damage

Long-term interstitial scarring

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23
Q

What is the cause of intrinsic renal AKI?

A

CELLULAR/ INTRINSIC DAMAGE.

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24
Q

Where is the abnormality in intrinsic renal AKI?

A

Vascular disease: vasculitis

Glomerular disease: glomerulonephritis

Tubular disease: ATN

Interstitial disease: analgesic nephropathy

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25
What are the most common causes of direct tubular injury in intrinsic renal AKI?
**Most commonly ischaemic.** **Endogenous toxins:** Myoglobin + Immunoglobulins **Exogenous toxins- contrast, drugs:** Aminoglycosides, Amphotericin, Acyclovir
26
What are common conditions of immune dysfunction causing intrinsic renal injury?
Glomerulonephritis Vasculitis Cause renal inflammation
27
What conditions lead to infiltration/ abnormal protein deposition causing intrinsic renal AKI?
Amyloidosis Lymphoma Myeloma-related renal disease
28
Which 2 measures can be used to predict severity of AKI?
**SERUM CREATININE** **URINE OUTPUT**
29
Why do some cases of AKI not resolve?
Acute wounds heal via 4 phases: Haemostasis, Inflammation, Proliferation, Re-modelling Imbalance between scarring + remodelling: Replacement of renal tissue by scar tissue Results in chronic disease.
30
What are the stages of CKD? What is the prevalence in the population of each?
1. Kidney damage with normal GFR: \>90ml/min Prev: 3.3% 2. Mild decreased GFR: **60-89** ml/min Prev: 3% 3. Moderate decreased GFR: **30-59** ml/min Prev: 4.3% 4. Severe decreased GFR: **15-29** ml/min Prev: 0.2% 5. End-stage kidney failure, GFR: \<15 or dialysis Prev: 0.2%
31
What are the 6 most common causes of CKD?
Diabetes Atherosclerotic renal disease HTN Chronic Glomerulonephritis Infective or obstructive uropathy PKD
32
What are the four broad categories of consequences of CKD?
**Progressive failure of homeostatic function:** Acidosis + Hyperkalaemia **Progressive failure of hormonal function:** Anaemia + Renal Bone Disease **Cardiovascular disease:** Vascular calcification + Uraemic cardiomyopathy **Uraemia + Death**
33
What is renal acidosis? pathophysiology? consequence? treatment?
Metabolic acidosis. Failure of renal excretion of protons. Results in: Muscle + protein degradation Osteopenia due to mobilization of bone calcium Cardiac dysfunction Tx: Sodium bicarbonate PO
34
What are common ECG findings in hyperkalaemia? What may this progress to?
Tall tented T-wave Flattening of P-wave Widened QRS VT + VF
35
What is anaemia of chronic renal disease?
Progressive decline in EPO-producing cells with loss of renal parenchyma. Usually when GFR \< 30mL/min. Normochromic, normocytic anaemia.
36
What are 3 erythropoiesis-stimulating agents (ESAs) and what do they treat?
Erythropoietin alfa (Eprex) Erythropoietin beta (NeoRecormon) Darbopoietin (Aranesp) Anaemia of CKD
37
What are 5 reasons for CKD not responding to ESA treatment?
Iron deficiency TB Malignancy B12 + folate deficiency Hyperparathyroidism
38
What is renal bone disease?
Complex entity resulting in reduced bone density, bone pain + fractures: Osteitis fibrosa Osteomalacia Adynamic bone disease Mixed osteodystrophy
39
What is the pathophysiology of renal bone disease?
Unable to excrete phosphate from kidneys (despite high PTH). Phosphate retention stimulates production of FGF23 + Klotho (lowers levels of activated vit D). Unable to make activated vit D (no 1a-hydroxylase). Phosphate retention + low levels of activated vit D leads to **hypocalcaemia**. Phosphate retention also causes end-organ resistance to PTH, which further leads to hypocalcaemia. Hypocalcaemia leads to increased PTH (2 HPT) + eventually leads to autonomous secretion + 3 HPT. Increased phosphate in blood complexes with calcium, which lowers free calcium in blood. In response to high circulating PTH, bone will become resistant to PTH.
40
What is osteitis fibrosa?
Osteoclastic resorption of calcified bone + replacement by fibrous tissue Due to 2 HPT Lesions (Brown tumours) of fibrous tissue
41
What is osteomalacia?
Insufficient mineralization of bone osteoid Due to low active Vit D
42
What is adynamic bone disease?
Excessive suppression of PTH results in low turnover + reduced osteoid
43
What are management strategies for renal bone disease?
**Phosphate control:** Dietary + Phosphate binders **Vit D receptor activators:** 1-alpha calcidol + Paricalcitol (As can't hydroxylate) **Direct PTH suppression:** Cinacalcet
44
What is the most important consequence of CKD?
Cardiovascular disease
45
What is the association between GFR and cardiac events?
Risk of cardiac event is directly predicted by GFR. As eGFR reduces, risk of mortality massively increases
46
How does atherosclerosis arise in CKD?
Role of traditional RFs less well defined in patients with renal disease Though control of Cholesterol + HTN shown to slow progression/ risks
47
What is vascular calcification?
Renal vascular lesions characterised by heavily calcified plaques (rather than traditional lipid-rich atheroma)
48
What is this?
Vascular calcification LAD = WHITE due to being full of calcium
49
What are the 3 phases of uraemic cardiomyopathy?
Left ventricle (LV) hypertrophy LV dilatation LV dysfunction
50
What are contraindications for renal transplant? What are not contraindications for renal transplant?
**CI: Active sepsis** **Not CI:** HIV, BMI \>30, \>65, any malignant disease are not CI (depends on disease).
51
What is haemodialysis?
Blood is passed through a dialyser which removed most waste products. ~3x/ week for ~6h. Home dialysis possible
52
What is peritoneal dialysis?
Peritoneal cavity is filled with fluid + peritoneal membrane is used as dialysing membrane. Can be done at home.
53
Patient has new onset AKI. What is the likely diagnosis?
Rhabdomyolysis Fall, long lie, muscle breakdown Myoglobin in urine
54
A 40F presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure?
Systemic vasculitis Non blanching rash, young, no other insult
55
What measures can be used to predict risk of outcomes in CKD?
eGFR Albumin : Creatinine ratio (ACR)
56
List 5 functions of the kidney
Excretion of water-soluble waste Water balance Electrolyte balance Acid-base homeostasis Endocrine functions: produces EPO + renin, hydroxylates Vit D
57
What is a major cause of hyperkalaemia in patients with CKD?
Dietary intake High K+ found in milk, chocolate, dried fruits, tomatoes
58
Why does hyperkalaemia cause pathology? In which CKD patients is this particularly common? What medications can precipitate it?
K+ is the major intracellular cation Hyperkalaemia causes membrane depolarisation: cardiac + muscle disruption Diabetic CKD patients ACEi, Spironolactone, Potassium sparing diuretics
59
How do you distinguish Anaemia of chronic renal disease from other common causes of anaemia?
Iron deficiency: microcytic B12 +/- folate deficiency: macrocytic
60
Why is uraemic cardiomyopathy uncommon in the UK?
Uraemia is a consequence of end stage CKD Patients receive dialysis In LIC there is less access to dialysis so is more common

YR5 Chemical Pathology (16 decks)

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