Renal Flashcards

(34 cards)

1
Q

Define Acute Kidney Injury (AKI)

A

An abrupt decline in kidney function i.e. glomerular filtration rate (can be hours or days)

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2
Q

What are the 3 classifications of AKI?

A
  • Pre-renal
  • Post-renal
  • Intrinsic
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3
Q

Define Pre-renal AKI

What is is caused by? (6)

A
  • Blood flow to kidneys reduced, can cause ischaemic injury if not managed
  • Reduced BP, hypovolaemia (blood loss), dehydration, GI bleed, sepsis and liver failure
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4
Q

Define Post-renal AKI

What can it be caused by?

A
  • Obstruction to the outflow from kidneys
  • Benign prostatic hypertrophy (BPH), prostate cancer, renal calculi, retroperitoneal fibrosis (scar tissue at back of abdomen)
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5
Q

Define Intrinsic AKI

A
  • Damage to the function tissues of the kidney
  • Acute interstitial nephritis (inflammation of renal interstitium), hypersensitivity reaction (often drug induced), myeloma (type of blood cancer), vasculitis (immunological renal disease
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6
Q

How can glomerular filtration rate measured?

A
  • eGFR (ml/min/1.73m2)

- Creatinine clearance (ml/min)

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7
Q

What is the formulae used to calculate creatinine clearance

A

CrCl = F(140 - age) x weight / Serum Creatinine

F = 1.04 female F = 1.23 male

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8
Q

In what patients MUST creatinine clearance be calculated?

A
  • Patients taking: Direct Oral Anticoagulants (DOACs) e.g. Dabigatran
    Nephrotoxic drugs e.g. Cisplatin, Methotrexate, ACE
    inhibs, Cyclosporine, NSAIDs, Tacrolimus
    Drugs excreted renally e.g. antibiotics, beta-blockers,
    diuretics, lithium, digoxin
  • > 75 years
  • Extremes of muscle mass
  • Narrow therapeutic index drugs e.g. Digoxin
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9
Q

What are the steps taken after a patient is found to have a low CrCl?

A
  • Establish AKI or CKD
  • Review all medications and assess adjustments e.g. always stop ACE inhibs in AKI, BUT not CKD as it is renal protective
  • Check dosing based on eGFR

-

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10
Q

Define Chronic Kidney Injury (CKD)

A

Abnormalities of kidney function or structure present, for > 3 months, with health implications

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11
Q

What is ACR?

A
  • Albumin : Creatinine ratio
  • Normally proteins are not filtered into tubules of nephron, they remain in blood due to size
  • As CKD progresses, structure breaks down causing ‘leaks’ allowing protein to be filtered and into the urine where it can be detected
  • Greater amount of albumin in urine = more severe CKD
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12
Q

What are the risk factors for CKD? (6)

A
  • Hypertension (more strain on tubules)
  • UTIs, especially recurrent ones
  • Medication e.g. Lithium, NSAIDs
  • CVD
  • Age
  • Malignancy
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13
Q

How is CKD testing prompted?

A
  • Albumin, proteins or blood in urine

- Ultrasound or biopsy results

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14
Q

What are the clinical complications of CKD? (8)

A
  • Acidosis
  • Anaemia
  • Dyslipidaemia
  • Fluid overload
  • Hyperkalaemia
  • Hypertension
  • Mineral & bone disorder
  • Uraemia
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15
Q

What is acidosis?

How is it managed?

What are the SE of treatment?

A
  • Result of blood becoming more acidic due to kidneys inability to excrete H+ and reabsorb HCO3-
  • Long term sodium bicarbonate (1g TDS)
  • Increase in Na = water retention (Na and water diffuse together)
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16
Q

What is renal anaemia?

What causes it?

How do you manage it?

A
  • When quality or quantity of RBC are below normal
  • Lack of circulating iron: by blood loss, dietary inadequacy, poor absorption of Fe due to uraemia or use of phosphate binders, impaired erythropoiesis due to lack of erythropoietin, long term use of immunosuppressants
  • Pre-dialysis management: oral iron, 3 months MAX
  • Dialysis patients: IV iron, given after dialysis
17
Q

What is erythropoietin?

A
  • A naturally occurring hormone produce by the kidneys
  • Stimulates bone marrow to produce red blood cells (erythrocytes)
  • CKD patients have little to no circulating EPO
18
Q

How can you manage a lack of erythropoietin?

A

Erythropoietin stimulating agents (ESA)

  • Eprex: recombinant human EPO, given SC once weekly
  • Aransep: Given IV to dialysis patients, once weekly
19
Q

What is dyslipidaemia?

How do you manage?

A
  • Abnormal lipid metabolism in CKD
  • Causes high rate of CVD in CKD
  • Atorvastatin 20mg OD
20
Q

How does fluid overload occur in CKD?

A

Due to kidneys inability to maintain Na and fluid balance

21
Q

How would you manage fluid overload in CKD?

A
  • Restrict Na diet (salt), and fluid intake
  • Diuretic therapy: Loop diuretic e.g. furosemide in high dose
  • If medication ineffective = dialysis
  • AVOID meds with high Na e.g. effervescent medication
22
Q

What can be the consequence of hyperkalaemia (high potassium)?

A
  • Damaging to hear muscles and cause abnormal rhythms
23
Q

How would you manage hyperkalaemia in CKD? (4)

A

Non-pharmacological: restrict dietary potassium

Pharmacological:

  • Calcium resonium orally TDS
  • IV Calcium gluconate
  • Actrapid insulin (pushed K+ into cells, avoiding heart)
  • Dialysis as last option

BEWARE drugs exacerbating hypokalaemia e.g. potassium sparing diuretics e.g. Spironolactone) Digoxin and NSAIDs

24
Q

How would you manage hypertension in CKD?

A
  • ACE inhibitor e.g. Ramipril
  • Angiotensin Receptor Blockers (ARBs) e.g. _____sartan

RENOPROTECTIVE IN CKD

25
Why are mineral and bone disorders such an issue in CKD?
- Kidneys responsible for balancing potassium and calcium in blood - These are essential for bone development and regrowth
26
How do the kidneys balance calcium in the blood? (4)
- Healthy kidneys activate Vitamin D into calcitriol - Calcitriol maintains blood calcium levels - Healthy kidneys also remove excess phosphorus
27
What happens to mineral levels in CKD?
- Production of calcitriol stops - Causes reduction in calcium in blood (hypocalcaemia) - Phosphorus levels in blood rise
28
How is calcitriol deficiency managed in CKD?
- Alfacalcidol (activated Vit D)
29
How is high phosphorus in blood (Hyperphosphatemia) managed in CKD?
- Phosphate binders e.g. Sevelemar or Lanthanum carbonate TDS - Restricted phosphate diet
30
What is Hyperparathyroidism?
- Parathyroid hormone is continually stimulated to release parathyroid hormone (PTH) - Parathyroid gland becomes enlarged as a result - Result is hypercalcaemia
31
how is Hyperparathyroidism managed?
- Cinacalcet | - Parathyroidectomy (removal of gland)
32
What is uraemia?
- Build up of urea in blood - Serious and result in emergencies e.g. encephalopathy and pericarditis (irritation or infection to heart muscle tissue)
33
How is uraemia managed?
Dialysis to remove waste products
34
What medications are given to diabetes patients with CKD?
- Metformin 1st line IF CrCl > 30 ml/min - CAUTION: Sulphonylureas in renal failure, increased risk of hypoglycaemia --> risk in elderly (falls) - Pioglitazone fine in renal failure BUT contra-indicated in heart failure