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Renal Dysfunction Flashcards

1
Q

What are the main causes of AKI?

A

Pre-renal (~80%) causes:
Dehydration – low blood volume reduces blood flow to kidneys
Sepsis – low ejection fraction reduces blood flow to kidneys.
Heart failure - low ejection fraction reduces blood flow to kidneys.
GI bleed – low blood volume reduces blood flow to kidneys
Hypotension– reduced blood flow to kidneys

Post renal causes (~10%)
Obstructions e.g., kidney stones, enlarged prostate – affect drainage of kidney

Intrinsic causes (~10%)
Injury
Major surgery

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2
Q

What are symptoms of AKI?

A

Nausea and vomiting - When the kidney cannot remove waste, it builds up and causes nausea and vomiting
Hypertension - The kidney is involved in blood pressure homeostasis due to the angiotensin aldosterone system
Dehydration
Confusion
Reduced urine output or changes to urine colour
Back ache
Abdominal pain
Oedema

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3
Q

What suggests AKI diagnosis?

A

A rise in serum creatinine of 26 micromol/L or greater in 48 hours
A 50% or greater rise in serum creatinine within the past 7 days.
A fall in urine output to less than 0.5ml/kg/hour for more than 6 hours

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4
Q

Following diagnosis of AKI, what should be done?

A

Identify the cause by performing a urine dipstick test testing for blood, protein, leucocytes, nitrites, and glucose.

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5
Q

What is used to treat hyperkalaemia in AKI?

A

Calcium resonium (calcium polystyrene sulfonate)

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6
Q

How does calcium resonium treat hyperkalaemia in AKI?

A

It is a polystyrene cation exchange resin which removes excess potassium from the body by exchanging it for the cation ion (Ca++) in the resin.

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7
Q

What are some common drug interactions of resonium?

A

Digoxin - cardiac side effects of digoxin exaggerated if hypokalaemia and/hypercalcaemia develop.

Lithium - decrease in lithium absorption

Thyroxine - decrease in thyroxine absorption

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8
Q

What adverse effects does calcium resonium cause?

A

Hypokalemia - Monitor serum potassium and for signs of hypokalaemia such as irritability, confusion, muscle weakness, and ECG abnormalities.

Faecal impaction and constipation - in rectal use.

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9
Q

When should calcium resonium treatment be stopped?

A

When serum potassium reaches 5.5mmol/L, as effects are long lasting and levels will continue to decrease after treatment cessation.

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10
Q

What is hyperkalaemia?

A

Serum potassium >5.5mmol/L

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11
Q

What is hypoklaemia?

A

Serum potassium <3.4mmol/L.

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12
Q

When is renal replacement therapy required?

A

If any of the following does not respond to treatment following AKI/CKD:
Hyperkalaemia
Metabolic acidosis
Fluid overload
Pulmonary oedema
Symptoms/complications or uraemia e.g., pericarditis or encephalopathy.

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13
Q

Name 8 types of medications which can contribute to impaired renal function.

A

Contrast media
ACEis/ARBs - alter haemodynamics and impair kidneys ability to maintain GFR. Also can lead to hyperkalaemia.
NSAIDs - altered haemodynamics within kidney lead to under-perfusion and reduced glomerular filtration.
Thiazide and loop diuretics -hypoperfusion can cause or exacerbate AKI. Can cause tinnitus and deafness if renal function reduced.
Potassium-sparing diuretics – hypoperfusion can lead to hyperkalaemia.
Anti-hypertensives – hypotension can exacerbate renal hypoperfusion
Methotrexate - crystal nephropathy
Metformin – avoid if GFR <30ml/min due to lactic acidosis and accumulation leading to hypoglycaemia.

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14
Q

Which key medicines should have a reduced dose in renal impairment due to renal excretion?

A

Opioids
Benzodiazepines
Antibiotics such as acyclovir, aminoglycosides, fluconazole, and penicillin.
Pregabalin and Gabapentin
Phenytoin
Antihistamines

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15
Q

What is CKD?

A

Abnormalities in kidney function or structure present for more than 3 months, with implications for health.

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16
Q

What is the MDRD formula for eGFR?

A

GFR (ml/min/1.73m2 = 175 x serum creatinine^-1.154 x age^-0.0203x1.212 if black x 0.742 if female

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17
Q

What is the Cockcroft-Gault formula for Creatinine clearance?

A

CCr (ml/min) = (((140-age) x weight)/(72x serum creatinine)) x 0.85 if female)

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18
Q

Which calculation (MDRD or CG) is preferred for estimating renal function?

A

MDRD for eGFR is preferred as the CG for creatinine clearance can sometimes overestimate kidney function which can lead to a risk of overdosing drugs with a narrow therapeutic index.

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19
Q

What indicates CKD?

A

GFR of <60ml/min/1.73m2 on at least 2 occasions separated by at least 90 days, with or without markers of kidney damage.

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20
Q

What is ACR testing?

A

Albumin to creatinine ratio aka urine microalbumin.
Detects amount of albumin in urine, and compares to amount of creatinine. A higher amount of albumin/ higher ACR indicates impaired kidney function.

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21
Q

What indicates more severe CKD?

A

Higher ACR and lower GFR.

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22
Q

What is accelerated progression of CKD?

A

A sustained decrease in GFR of 25% or more and a change in GFR category within 12 months
OR
A sustained decrease in GFR of 15ml/min/1.73m2 per year.

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23
Q

What increases risk of CKD? (9)

A

Untreated urinary outflow obstruction
NSAID use (chronic)
CVD, hypertension, diabetes
AKI, African, Asian
Proteinuria
Smoking

UNCAPS

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24
Q

How does CKD cause renal anaemia?

A

The kidneys can’t produce enough erythropoietin (EPO), the hormone which stimulates red blood cell production. Low EPO levels causes RBC counts to drop and anaemia to develop.

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25
Q

What are some symptoms of anaemia?

A

Hb <110g/L
Tiredness
SOB
Lethargy
Palpitations

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26
Q

How is iron deficiency determined in renal anaemia?

A

% Hypochromic red blood cells (%HRC) - % of RBC with haemoglobin deficiency. Anaemia = >6%.
OR
Reticulocyte Hb content (CHr) - amount of Hb in reticulocytes (early erythrocytes). Indicates amount of iron available for Hb production in bone marrow. Anaemia = <29pg.

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27
Q

How is renal anaemia treated?

A

Erythropoetic stimulating agents (ESA) therapy - epoetin alfa.
Iron - ferric carboxymelose.

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28
Q

When receiving treatment for renal anaemia, what monitoring is required?

A

Iron every 1-3 months
Hb every 2-4 weeks in ESA induction phase, then every 1-3 months.
Blood pressure - ESA hypertension, Ferinject hypotension

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29
Q

What are some adverse effects of ESA/epoietin alfa?

A

Hypertension
Skin reactions
Headache
Seizures, more common in first 90 days - avoid driving.
Irritation at injection site
Takes 6 weeks to work so symptoms of anaemia will resume in this period.

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30
Q

What are some adverse effects of Ferric carboxymaltose?

A

Dizziness
Rash
GI discomfort
Hypotension
Hypersensitivity
Irritation at injection site

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31
Q

What is renal bone disease caused by?

A

In CKD, the kidneys fail to excrete the phosphorous, resulting in hyperphosphatemia. High phosphate can cause body changes which pull calcium from the bones and elsewhere in the body, leading to hypocalcaemia.
Also, damaged kidneys stop converting vitamin D to calcitriol, which further creates an imbalance of calcium.
In addition, kidney damage affects the parathyroid gland, causing it to release excess parathyroid hormone which moves calcium from the bones to the blood.

The lack of calcium in the bones causes them to become brittle and weak, putting them at higher risk of fractures.

32
Q

How is hypocalcaemia in renal bone disease/CKD treated?

A

Alfacalcidol (vitamin D analogue). Quickly converted into calcitrol (active vitamin D) by the liver to replace the deficiency in the kidney. It increases serum calcium levels by stimulating intestinal calcium absorption, reabsorption from bone, and renal reabsorption.

33
Q

Why is alfacalidol first line for hypocalcaemia in CKD?

A

It is more effective than other vitamin D analogues such as colecalciferol as they require the kidneys to convert them into active calcitriol, while alfacalcidol is converted efficiently in the liver.

34
Q

What are some potential adverse effects of alfacalcidol?

A

Dizziness
Rash
Hypercalcaemia : GI discomfort, weakness, fatigue, headache, thirst, metallic taste in mouth, confusion (severe).

35
Q

What monitoring does alfacalcidol require?

A

Baseline and every 2-4 weeks (or 3 months if less deemed necessary):
Alkaline phosphate
Parathyroid hormone
Serum calcium
Serum creatinine
Serum phosphate
U&Es
Vitamin D (25-hydroxy vitamin D)

36
Q

How does CKD affect phosphate levels?

A

Poor excretion results in hyperphosphataemia.

37
Q

How is hyperphosphatemia treated?

A

Phosphate binders such as calcium acetate.

38
Q

How does calcium acetate work?

A

This binds to phosphate from the diet to produce calcium phosphate, which is poorly absorbed by the body and is excreted by the faeces

39
Q

What are potential adverse effects of calcium acetate?

A

Mild-severe hypercalcaemia:
GI discomfort, weakness, fatigue, headache, thirst, metallic taste in mouth, confusion (severe).

40
Q

What monitoring does calcium acetate require?

A

Serum calcium and phosphate levels regularly.

41
Q

How does metabolic acidosis occur?

A

Usually, the body removed acid through the urine and retains the right amount of bicarbonate (base). However, in CKD, the kidneys can’t remove enough acid leading to metabolic acidosis, where bicarbonate levels <22mmol/l and/or arterial blood pH <7.35.

42
Q

What are some symptoms of metabolic acidosis?

A

Rapid/long deep breathing
Fatigue
Confusion
Dizziness

43
Q

How is metabolic acidosis treated?

A

If serum bicarbonate levels are <20mmol/L and GFR <30ml/minm/1.73m2, consider oral sodium bicarbonate to raise the blood pH.

44
Q

What are some side effects of sodium bicarbonate?

A

Can lead to metabolic alkosis (pH >7.45) which causes headache, muscle pain and twitching, nervousness/restlessness, nausea and vomiting, and headache.

Sodium can induce sodium and water retention leading to hypernatremia, hypokalaemia, and oedema.

45
Q

Do any drugs interact with sodium bicarbonate?

A

Sodium bicarbonate also reduces the acidity levels in the stomach, so can interfere with absorption of some medications, generally recommend waiting 2 hours between taking sodium bicarbonate and other medications.

46
Q

What monitoring does sodium bicarbonate require?

A

Blood pH
Serum bicarbonate
Blood gases - increases CO2
Serum electrolytes - hypokalaemia, hypernatraemia

47
Q

How does CKD cause cause hyperkalaemia?

A

Decrease in renal potassium excretion.
Use of ACEis and ARBs can exacerbate hyperkalaemia.

48
Q

What are some symptoms of hyperkalaemia?

A

Can be asymptomatic
Muscle weakness and stiffness
Fatigue
Severe: arrythmias leading to cardiac arrest and death.

49
Q

Other calcium resonium, how else can hyperkalaemia be reduced by CKD treatment?

A

Sodium bicarbonate for treatment of metabolic acidosis has an alkalinising effect on the blood which causes an intracellular shift of potassium via hydrogen and potassium exchange, thus reducing serum potassium levels.

50
Q

What is haemodialysis?

A

A process by which the blood passes through a tube into an artificial kidney/filter called a dialyzer which is divided into 2 parts separated by a thin wall/membrane. This filters waste products from the blood into dialysate fluid which is pumped out of the dialyser while the filtered blood is passed back into the body.

51
Q

How often do patients require dialysis?

A

Usually 3 4-hour sessions a week.

52
Q

What are some side effects of dialysis?

A

During treatment:
Nausea and dizziness due to rapid changes in blood volume throughout treatment.

Generally:
Breathlessness
Fatigue
Insomnia
Poor appetite
Thirst
Weakness
Muscle cramps
Body image concerns
Itchy skin
Sexual dysfunction

53
Q

What symptoms indicate a need to start dialysis?

A

Uremia symptoms impacting daily life
Uncontrollable fluid overload
*eGFR of 5-7ml/min/1.73m2

54
Q

What is uremia?

A

A buildup of waste products in your blood that occurs as a result of untreated kidney failure.

55
Q

What are common symptoms of uremia?

A

Nausea
Vomiting
Weight loss
Difficulty concentrating
Fatigue.

56
Q

What does a dialysis diet have to be?

A

High protein
Low salt, potassium, and phosphorous (found in many fruits and veg)
Limited fluids

57
Q

Why do dialysis patients have to take supplement vitamins such as Renavit?

A

Water soluble vitamins are lost during dialysis.
Also, their diet is often restricted.

58
Q

What does Renavit contain?

A

B1
B2
B3
B5
B6
B8
B9
B12
C

59
Q

What is the aim of immunosuppression in transplant patients?

A

Prevent acute rejection and optimise function of the transplanted kidney, while minimising the adverse effects of immunosuppression such as increased risk of infection, cancer, diabetes, and CVD.

60
Q

What is first line immunosuppression for kidney transplant?

A

Induction: Basiliximab
Maintenance: immediate release Tacrolimus + Mychophenolate Mofetil (+ Prednisolone)

61
Q

What is Basiliximab?

A

Monocloncal antibody which acts as an interleukin-2 receptor antagonist to prevent T-cell activation.

62
Q

How is Basiliximab given for induction immunosuppression?

A

20mg IV 2 hours before surgery and 4 days after surgery.

63
Q

How does tacrolimus work?

A

Inhibits calcineurin phosphate to prevent calcium-dependent events such as IL-2 gene transcription (preventing T-cell activation), cell degranulation, and apoptosis.

64
Q

Why is Tacrolimus brand specific?

A

Switching brands is associated with toxicity and organ rejection.

65
Q

What are some counselling points for tacrolimus?

A

Take on an empty stomach
Avoid fatty foods and grapefruit juice
Ensure serum levels are monitored
Check interactions with other medications as it is metabolised by CYP450 system

66
Q

What monitoring is required for tacrolimus?

A

Baseline, then from 3 months, weekly until stable, then every 2-4 weeks, then from 4 months, every 4-6 weeks, then from 12 months, every 3-6 months:
* BP
* Clotting screening – can be altered.
* Fasting blood glucose – for post-tranaplsnt diabetes.
* Visual acuity – for optic neuropathy leading to blindness.
* FBC .
* LFTs
* Plasma proteins
* serum creatinine or eGFR
* U&Es, especially potassium

ECG – for hypertropic changes. Baseline and then at 3, 9, and 12 months.
Tacrolimus serum level - TDM due to narrow therapeutic window. Twice a week. 12 hours postdose.
Lipids - annually.
HepB surface antibodies - annually. Revaccinaye if too low.

T DM
A ntibodies
C lotting
R enal
O ptics
L ipids and LFTs
I love sugar (FBG)
M yo (ECG)
U &Es
S erum proteins

FBC and BP

67
Q

What is mycophenolate mofetil?

A

Anti-metabolite which inhibits inosine-5-monophosphate dehydrogenase to deplete guanosine nucleotides in T and B lymphocytes to inhibit their proliferation, thereby suppressing cell-mediated immune responses.

68
Q

What are some couselling points for mycophenolate mofetil?

A

Brand specific
Take at same time each day
Take on an empty stomach 1h before or 2h after meals until dosage stabilised, then can take with food.
Higher risk of skin cancer, so limit sun exposure and use SPF.
Avoid antacids, cholestyramine, and calcium-free phophate binders as they reduce the absorption.
Ensure effective contraception used during treatment.

69
Q

What are some adverse effects of mycophenolate mofetil?

A

Anaemia
Leukopenia
GI toxicity
Increased skin cancer risk

70
Q

What monitoring does mycophenolate mofetil require?

A

Pregnancy test – baseline and use contraception. Can cause miscarriage and severe birth defects.
Albumin – low albumin increases clearance. Baseline and every 2 weeks for 6 weeks until stable, then 3 monthly
BP – baseline
FBC – baseline and every 2 weeks for 6 weeks until stable, then 3 monthly
Height - baseline
Weight - baseline
LFTs – baseline and then AST or ALT every 2 weeks for 6 weeks until stable, then 3 monthly
Serum creatinine or eGFR– baseline and every 2 weeks for 6 weeks until stable, then 3 monthly
Vaccination status – baseline for pneumococcus and influenza

71
Q

How does prednisolone work for immunosuppression?

A

Reduces transcription of inflammatory cytokines.

72
Q

What are some counselling points for prednisolone?

A

Long-term use can cause adrenal insufficency, diabetes, and osteoporosis.
Can cause gastric ulcers and bleeds due to increased acid secretion, and decreased gastric mucus and prostaglandin synthesis. May require concurrent PPI use.
Keep steroid card on you at all times.
Don’t stop taking suddenly as can cause withdrawal symptoms due to reduced cortisol.

73
Q

Other than immunosuppression, what is routinely given to transplant patients?

A

A 6-month course of prophylactic co-trimoxazole for prevention of pneumocystis pneumonia caused by the fungus pneumocystis jirovecci which is common in immunosuppressed patients.

74
Q

What are the symptoms of Pneumocystis pneumonia?

A

Severe fungal lung infection causing:
Cough
Fever
Difficulty breathing
SOB
Weakness
Fatigue

75
Q

What is co-trimoxazole?

A

Antibioticcontaining trimethoprim (dihydrofolate reductase inhibitor) and sulfamethoxazole (inhibit conversion of PABA to dihydrolate) which each inhibit a different step in bacterial protein synthesis.

76
Q
A

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