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Acute/Chronic Kidney Disease Flashcards

1
Q

What is acute uraemia?

A

An acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output.
Abrupt (1-7 days) and sustained rise in serum creatinine x1.5 from baseline

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2
Q

What are the causes for acute renal failure?

A
  1. Pre-renal (mostly): Dehydration, circulatory collapse, bleeding, NSAID abuse, burns, vasculitis, myeloma
  2. Parenchymal (5%): Acute tubular necrosis, acute glomerulonephritis , acute cortical necrosis, renal vascular damage, necrotising papillitis, sepsis, rhabdomyolysis (myoglobin released is very irritant), ATN, Goodpasture’s syndrome, malignant hypertension
  3. Obstructive (10%): Intratubular, ureteral, urethral (clots, stones, enlarged prostate/bladder)
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3
Q

What is the surgical triad?

A

Infection, nephrotoxic drugs and post-operative volume depletion
It is the commonest cause of hospital-acquired AKI

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4
Q

Which drugs can increase risk of AKI?

A

• ACE inhibitors and angiotensin II blockers - efferent vasodilation
• NSAIDS - afferent vasodilation
- Do not give to dehydrated patients!!!
• PPIs - Interstitial nephritis
• Lithium
• Aminoglycosides: gentamycin
Contrast medium

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5
Q

What are some of the risk factors for AKI?

A

• Advanced age >75
• Renal disease
• Malignant hypertension (180/120)
• Diabetes mellitus (glycolisation of renal vessels leading to change in tunica media causing nephropathy)
• Liver disease
• Heart disease
• Use of nephrotoxins
• Radiology contrast media - iodide component
Increased risk if has sepsis, hypotension, high EWS, hypovolaemia

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6
Q

Which drugs cause vasodilation and vasoconstriction at the afferent arteriole?

A

Constriction - NSAIDS

Vasodilation - ANP, Prostaglandins

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7
Q

Which drugs cause vasodilation and vasoconstriction at the efferent arteriole?

A

Constriction - ANP, Angiotensin II, norepinephrine

Vasodilation - ACEI/ARBs

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8
Q

Why might a patient be acidotic?

A

→ Failure to remove acid from renal system
→ Overload of buffering system
→Production of other acids e.g. lactic acid from tissue hypoxia in severely ill

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9
Q

What would a urine dipstick show in a patient with AKI

A
  • Negative usually suggest pre-renal cause
      • protein and blood: glomerular disease
      • white cells is non-specific but may suggest infection or interstitial nephritis
    • People with catheters could get false + results
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10
Q

What kind of ECG changes could occur with AKI?

A
  • Tenting of T waves
    • Widening QRS,
  • Disappearance of P waves
    Sine wave pattern
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11
Q

What is chronic kidney disease?

A

Progressive loss of nephrons resulting in permanent compromise of renal function. It is classified according to eGFR and ACR. Majority are asymptomatic.

Proteinuria or haematuria and/or reduced GFR for more than 3 months duration.

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12
Q

When is kidney damage at stage 1?

A

Stage 1 has to be GFR of >90 with evidence of kidney damage like microalbuminuria, proteinuria and haematuria. EVIDENCE OF KDINEY DAMAGE IS IMPORTANT

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13
Q

What is the ACR levels for the 3 CR categories?

A

A1 - <3
A2 - 3-30
A3 - >30

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14
Q

What is the ACR levels for the 3 CR categories?

A

A1 - <3 (only treat if have diabetes)
A2 - 3-30 (only treat if diabetes or hypertension)
A3 - >30

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15
Q

How does diabetes cause renal failure?

A

Estimated 30% of people will have CKD.

Hyperglycaemia -> oxidative stress -> matrix expansion -> increased vascular permeability -> inflammatory mediators

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16
Q

How can GFR be measured?

A

→ Using urinary clearance of an ideal filtration marker.
→ The gold standard of exogenous filtration markers is inulin.
- Inulin is a physiologically inert substance that is freely filtered at the glomerulus, and is neither secreted, reabsorbed, synthesized, nor metabolized by the kidney.
- in short supply, expensive, and difficult to assay.
→ The most common methods utilized to estimate the GFR are: measurement of the creatinine clearance; and the Cockcroft-Gault equation

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17
Q

What is the presentation of CKD?

A

→ Lethargy - anaemia is associated due to lack of erythropoietin produced in kidney
→ Concentration trouble
→ Nausea and pruritus - due to accumulation of toxic waste products
→ Poor appetite
→ Trouble sleeping
→ Muscle aches
→ Oedema - salt and water retention as the GFR declines
→ Dry, itchy skins
→ Polyuria
→ Foamy urine - proteinuria
→ Seizures - increase is neurotoxins that are not excreted in kidney
Orthopnoea & dyspnoea - due to pulmonary oedema due to reduced urine output

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18
Q

What is the pathophysiology of CKD?

A

→ Renal injury -> increase intra-glomerular pressure -> glomerular hypertrophy (adapting to nephron loss to maintain GFR)
→ Increase in glomerular permeability -> toxicity to mesangial matrix -> mesangial cell expansion, inflammation, fibrosis and scarring
Injury results in increased angiotensin II production -> increase TGF beta -> collagen synthesis -> renal scarring

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19
Q

What could be the differential diagnosis for CKD?

A

a. Diabetic kidney disease - a. history of poorly controlled diabetes
b. Hypertensive nephrosclerosis
c. Ischaemic nephropathy
d. Obstructive uropathy - more common in men [prostate enlargement]
e. Nephrotic syndrome
f. Glomerulonephritis

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20
Q

What are the symptoms of hypercalcaemia?

A

Painful bones, renal stones, abdominal groans and psychic moans (low mood, confusion, insomnia)

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21
Q

Can tertiary hyperparathyroidism occur due to CKD?

A

Yes, longstanding CKD is a common cause of tertiary hyperparathyroidism

This would differ from secondary hyperparathyroidism which would show high phosphate instead of low

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22
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

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23
Q

Causes of persistent non-visible haematuria

A 
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
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24
Q

False haematuria causes - red/orange urine, where blood is not present on dipstick

A

foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin

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25
How does hypernatraemia present?
Symptoms of this include diarrhoea or vomiting, impaired thirst, weight loss, oliguria and other signs of hypovolemia.
26
How does hyponatraemia present?
Mental status changes, including altered personality, lethargy and confusion. If the concentration falls lower, other signs can include hyperreflexia and seizures. Na+ - <135
27
How does hypomagnesemia present?
Symptoms of this include nausea, vomiting, lethargy, weakness, tremor and muscle fasciculations, including Trousseau and Chvostek's sign.
28
How does hypocalcaemia present?
Symptoms of this include muscle cramps, and if over a long period of time it can cause symptoms of confusion, memory loss, delirium, and depression.
29
What is Trousseau's sign?
Trousseau's sign is a carpopedal spasm caused by inflating the blood-pressure cuff to a level above the systolic blood pressure in patients with hypocalcaemia
30
What is Chvostek's sign?
Chvostek's sign is also seen in hypocalcemia; tapping over the facial nerve causes twitching of the facial muscles.
31
How can CKD lead to osteomalacia?
High phosphate levels in CKD 'drags' calcium from the bones, resulting in osteomalacia Alendronic acid is a bisphosphonate that reduces the rate of bone turnover and strengthens the bone.
32
Difference between haemodialysis and peritoneal dialysis:
Haemodialysis: Performed 3X a week, for four hours each time Usually done in a hospital Major food and fluid restrictions Fatigue, hypotension and risk of septicaemia Fistula is well concealed and easy to maintain ``` Peritoneal dialysis: Performed daily, for shorter periods Can be performed at home or when travelling No food or fluid restrictions Increased risk of peritonitis Permanent catheter may be embarrassing ```
33
What tests are performed to match donor and recipient compatability?
They are blood type, crossmatch and HLA testing. 1)Blood typing is the first step in identifying the level of compatibility o Blood group O is the universal donor o Blood group AB is the universal recipient o Blood group A can receive from A and O o Blood group B can receive from B and O 2) HLA typing is also called tissue typing – these are present on the plasma surface of the cells  There are 6 main antigens that have been identified in playing a major role in rejection: A, B and DR (two antigens for each letter)  You inherit HLAs from your parents (3 from each) 3)Crossmatch is a test done just prior to transplantation, to determine if the body already has antibodies against the donor’s antigens – it is done by mixing the blood from the donor and recipient.
34
What is the treatment for hypocalcaemia?
Usually treated with Vit D compounds Remember role of Kidney in 1α-Hydroxylation as an essential step for activation of vitamin D alfacalcidol (1α-hydroxycholecalciferol)calcitriol (1,25-dihydroxyvitamin D3 or 1,25-dihydroxycholecalciferol) – can be used in renal failure colecalciferol (vitamin D3), ergocalciferol (vitamin D2) – need a functioning kidney
35
How to treat hyponatraemia?
Risk of osmotic demyelination syndrome (cerebral oedema etc). Need to check bloods every 24h and don't want Na+ to rise/fall more than 10mmol/L
36
What is tolvaptan?
Tolvaptan is a competitive antagonist at vasopressin V2 receptors. Its major action is in the renal collecting ducts to reduce water reabsorption and produce aquaresis without sodium loss, thus increasing free water clearance and correcting dilutional hyponatraemia
37
How to treat hypercalcaemia
Bisphosphonates (IV alendronic acid) | IV fluids
38
How can Rhabdomyolysis cause AKI?
Myoglobin released from muscle tissue is toxic to the kidneys and will produce acute kidney injury. Raised creatinine kinase, and raised potassium levels are typical features of rhabdomyolysis.
39
How would a Rhabdomyolysis typically present in the exam?
Patient who has fallen or had a prolonged epileptic seizure with AKI on admission
40
How does haemodialysis work?
Involves regular filtration of the blood through a dialysis machine in hospital. Most patients need dialysis 3 times per week, with each session lasting 3-5 hours. At least 8 weeks before treatment, the patient must undergo surgery to create an arteriovenous fistula, which provides the site for haemodialysis. Most commonly in the lower arm.
41
How does peritoneal dialysis work?
Filtration occurs within the patient's abdomen. Dialysis solution is injected into the abdominal cavity through a permanent catheter. The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum. After several hours of dwell time, the dialysis solution is then drained, removing the waste products from the body, and exchanged for new dialysis solution.
42
List some of the complications of haemodialysis
``` Infection Endocarditis Stenosis at side Hypotension Cardiac arrhythmia Air embolus Anaphylactic reaction Disequilibrium syndrome ```
43
List some of the complications of peritoneal dialysis
``` Peritonitis - Staphylococcus Epidermidis (coagulase -) or Staph aureus Catheter infection/ blockage Constipation Fluid retention Hyperglycemia Hernias Back pain Malnutrition ```
44
List some of the complications of renal transplantation
``` DVT/PE Graft rejection Infection Bone marrow suppression Recurrance of disease Urinary tract obstruction CVD ```
45
Causes of hypercalcaemia:
1. Hyperparathyroidism 2. Malignancy, melanoma, PTHpP from squamous cell lung cancer 3. Sarcoidosis 4. Vit D intoxication 5. Thyrotoxicosis 6. Milk-Alkali syndrome 7. Drugs: Thiazides 8. Addison's disease 9. Paget's disease of the bone
46
Example of corticosteroid with very high mineralocorticoid activity but low glucocorticoid activity
Fludrocortisone
47
Example of corticosteroid with very high glucocorticoid activity but low mineralocorticoid activity
Dexamethasone | Betmethasone
48
Example of corticosteroid with high mineralocorticoid activity and glucocorticoid activity
Hydrocortisone
49
Example of corticosteroid with low mineralocorticoid activity and predominant glucocorticoid activity
Prednisolone
50
Treatment for Rhabdomyolysis
Rehydration IV normal saline Hartmann's solution has potassium content which isn't favorable in AKI
51
What is the most common and important viral infection in solid organ transplant recipients?
Cytomegalovirus
52
Which drugs can cause gynaecomastasia?
``` Spironolactone (most common drug cause) Cimetidine digoxin Cannabis Finasteride Gonadorelin analogues e.g. Goserelin, buserelin Oestrogens, anabolic steroids ```
53
eGFR can be inaccurate due to what reasons?
Increased muscle mass Pregnancy Eating red meat 12h prior to sample being taken
54
Would calcium be low in chronic or acute kidney failure
Chronic rather than acute
55
Patients who have received an organ transplant are at risk of developing what cancer?
Skin Cancer - particularly squamous cell carcinoma | Due to long term immuno
56
How is hyperkalaemia managed?
IV Calcium gluconate (stabilises cardiac membranes)
57
What is meant by acute-on chronic kidney injury
Decline in renal function with potential reversibility
58
What is normal eGFR
80-120 (around 100)
59
How can you have CKD but normal eGFR
If presence of proteinuria e.g. diabetic nephropathy Polycystic kidney disease patients - genetic disease (might have CKD but normal eGFR for now)
60
Common-est cause of post-renal kidney failure in patients not in hospital is:
BPH
61
What would be the commenest pathology leading to a neurogenic bladder?
Diabetic neuropathy This can lead to post-renal kidney failure
62
Why is it not so common to see posterior urethral valves as a cause of post-renal failure
Picked up on neonatal screening so should have been surgically fixed
63
What can cause pure acute tubular injury in a patient?
Gentamycin
64
What is the commonestcause pure acute interstitial injury in a patient?
Drugs like amoxicillin, NSAIDS or PPIs
65
Symptoms of uraemia
``` Pruritus Anorexia Changes in cognitive function Confusion, coma Myoclonic jerk Chest pain - due to pericarditis ```
66
What is Nephrotic syndrome?
hypoalbuminaemia •>3.5 g proteinuria/day •dyslipidaemia •salt and water retention, leading to oedema.
67
Most common cause of nephrotic syndrome in children?
Minimal change GN But cannot be diagnosed without biopsy - normally just given treatment and hoped for the best Second most common: Focal segmental glomerular sclerosis
68
Most common cause of nephrotic syndrome in adults?
Membranous nephropathy Focal segmental GS
69
What is Nephritic syndrome?
Haematuria Oliguria Hypertension Oedema
70
What is the complication of correcting hyponatraemia too rapidly?
Osmotic demyelination syndrome
71
What is the complication of correcting hypernatraemia too rapidly?
Cerebral oedema

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