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Renal and Hepatic Diseases and Transplant > Renal Disease > Flashcards

Renal Disease Flashcards

1
Q

What are the functions of the kidneys?

A
  1. Excretory - Excrete waste products and drugs
    - Need to assess impairment, adjust doses, hold/stop nephrotoxins
  2. Regulatory - fluid volume and composition, bp, pH
  3. Endocrine - Erythropoetin production, renin production, prostaglandin production
  4. Metabolism - Vitamin D metabolism
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2
Q

What routine tests are done to assess renal function?

A
  1. Plasma:
    - Creatinine levels (by product of protein metabolism)
    - Urea
    - eGFR
  2. Urine:
    - Albumin : Creatinine ratio (ACR)
    - Osmolarity - High particle concentration = High osmolarity
    - Specific gravity - solute concentration, higher gravity = more solutes
    Proteinuria/Microalbuminuria
    - Haematuria - Blood in the urine
    - Mid-stream urine - UTI
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3
Q

How is Creatinine Clearance calculated?

A

GFR (Glomerular filtration rate) = CrCl (creatinine clearance)

24-hour urine collection:

CrCl (ml/min) =
Urine Cr (umol/l) x Volume (ml) / Plasma Cr (umol) x Time

  • Time delays and suspect accuracy of urine collection
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4
Q

What is the Cockcroft and Gault equation and what are the limitations of using it?

A

CrCl (ml/min) =
(140-age) x wt x F* / Plasma Cr (umol/l)

(F* = 1.23 males and 1.04 females)

Limitations:
- Assumes average population data
- Unsuitable for children and pregnancy
- Renal function must be stable

Traditionally “normal” Cr= 55-125umol/l and “normal” CrCl = 120ml/min

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5
Q

How is eGFR calculated?

A

eGFR is calculated either using:

  1. MDRD - 4-variable Modification of Diet in Renal Disease equation:
    - Serum Cr, age, sex, ethnic origin
    - Less accurate when >60ml/min/1.73m2 and overestimates for elderly patients
  2. CKI-EPI - Chronic Kidney Disease Epidemiology Collaboration Formula
  • Same limitations as CrCl
  • eGFR can be calculated using and on-line calculator
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6
Q

What is Stage 1 (Normal) eGFR value?

A

> 90 ml/min/1.73m^2

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7
Q

What is Stage 2 (Mild impairment) eGFR value?

A

60-89 ml/min/1.73m^2

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8
Q

What is Stage 3A (Mild to Moderate) eGFR value?

A

45-59 ml/min/1.73m^2

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9
Q

What is Stage 3B (Moderate to Severe) eGFR value?

A

30-44 ml/min/1.73m^2

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10
Q

What is Stage 4 (Severe impairment) eGFR value?

A

15-29 ml/min/1.73m^2

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11
Q

What is Stage 5 (Established/End Stage) eGFR value?

A

<15

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12
Q

What is urea?

A

Urea is the breakdown product of protein metabolism

> 15mmol/l = Uraemia (range: 1-7 - 6.7 mmol/l)

Urea can also be raised by:
- Dehydration
- Muscle injury
- Infection
- Haemorrhage
- Excess protein intake

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13
Q

What is proteinuria / ACR?

A

The predictor of renal disease development and adverse outcomes.

Albumin - protein found in the blood, should NOT be in the urine

Albumin : Creatinine Ratio (ACR)
- Divide albumin (mg) by creatinine (g)
- >70mg/mmol in non-diabetics
- >2.5mg/mmol (Males) and >3.5 (Females) diabetics due to increased risk of developing renal disease.

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14
Q

What does ADME stand for and what does each factor indicate?

A

ABSORPTION
- Uraemia reduces drug absorption via: D&V, GI oedema
- Reduced calcium absorption (less vitamin D activation)
- Hyperphosphatemia - phosphate binder treatment reduces some drugs absorption

DISTRIBUTION
- Less protein binding (e.g. Phenytoin due to hypoalbuminemia & urea competition)
- Less tissue binding (e.g. Digoxin, increased concentrations)

METABOLISM
- Less vitamin D metabolism (less calcitriol production) = Less calcium absorption from gut and kidneys
- Less insulin metabolism
- Less elimination of pharmacologically active metabolites e.g. nor-pethidine

EXCRETION
- Less excretion
- Dose adjustments: Lower dose and/or increased dose interval
- NO adjustment to LOADING DOSES

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15
Q

What characteristics would the ideal drugs have in renal impairment?

A
  • A wide therapeutic index
  • Cleared by the liver
  • Drugs not affected by fluid balance, protein binding or tissue binding
  • Not nephrotoxic

Can be essential to use a nephrotoxic drug:
- Monitor renal function and toxicity
- In end-stage renal failure - no further renal function damage or decline. Monitor for toxic accumulation side effects.

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16
Q

What are the 3 classifications (cause types) of renal disease?

A
  1. Pre-renal
  2. Intrinsic
  3. Post-renal
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17
Q

What is pre-renal failure?

A

Reduced renal perfusion

For example:
- Hypovolaemia (burns, dehydration, haemorrhage)

  • Reduced cardiac output - heart failure, MI
  • Infection
  • Liver disease - chronic, blood flow through the liver reduces, lack of blood supply ongoing to the kidney
  • Medications causing impaired renal regulation - ACEIs, NSAIDs, Ciclosporin, Tacrolimus - Diuretics, Laxative abuse or D&V side effects
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18
Q

Explain the pharmacology of pre-renal failure.

A
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19
Q

What is intrinsic renal failure?

A

Damage to renal tissue.

Can be secondary from pre-renal failure and prolonged reduced perfusion.

For example:
- Glomerular
- Tubular
- Renovascular
- Infection
- Nephrotoxicity - NSAIDs, Contrast media
- Metabolic (e.g. Hypercalcaemia, hyperuricaemia)
- Congenital

Nephrotoxicity:
1. Hypersensitivity reactions (unpredictable)
- Glomerulonephritis - Phenytoin, Pencillins
- Interstitial damage - Penicillins, Cephalosporins, Allopurinol, Azathioprine

  1. Directly toxic (more predictable)
    - Aminoglycosides, amphotericin, cyclosporin
    - Can occur from a single dose
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20
Q

What is post-renal failure?

A

Obstruction to urinary flow

For Example:
- Stones blocking ureter (e.g. calcium oxalate)
- Structural (e.g. tumour, stricture)
- Nephrotoxicity (e.g. cytotoxic medication, high dose sulphonamides)
- Outside urinary tract (e.g. Ovarian tumour, prostatitis, BPH)

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21
Q

What does AKI stand for?

A

Acute kidney injury

22
Q

What does CKD stand for?

A

Chronic kidney disease

23
Q

What is acute kidney injury (AKI)?

A

Rapid decline (hours/days) in someone’s usual level of kidney function, which has an up to 90% mortality rate if not identified and treated.

24
Q

How is acute kidney injury diagnosed?

A
  • Serum creatinine rises by over 26.5umol/L within 48hrs
    OR
  • Serum creatinine rises by >1.5 fold from their baseline value, which is known or presumed to have occurred within the last 7 days
    OR
  • Urine output is < 0.5ml/kg/hr for 6 hours
25
Q

What are the risk factors of acute kidney injury?

A
  • Diabetes
  • CKD
  • Previous AKI
  • Hepatic disease
  • Congestive cardiac failure (CCF) or Peripheral vascular disease (PVD)
  • > 65 years old
26
Q

What are the main causes of acute kidney injury?

A
  • Most common cause of AKI is pre-renal disease
  • Reduced perfusion due to low blood volume and reduced circulation
  • Hypotension/Sepsis/Infection/Dehydration
27
Q

What medications are prescribed for acute kidney injury?

A

Triple Whammy:
1. ACEI/ARB
2. NSAIDs
3. Diuretics

28
Q

How can acute kidney injury be prevented?

A
  • Avoid nephrotoxics in those at risk e.g. NSAIDs in elderly
  • Monitor renal function for those taking high risk drugs/with hight risk comorbidities
  • Review medication known to exacerbate
  • Educate patients e.g. sick day rules to manage long term higher risk medication
29
Q

What are the management options for acute kidney injury?

A
  1. IDENTIFY THE CAUSE:
    - Investigations
  • Medication history: Review and hold medication known to exacerbate AKI (ACEI, Diuretics), Adjust doses of other medication to prevent harm (Metformin, DOACs)
  1. RESTORE AND MAINTAIN RENAL FUNCTION (VOLUME STATUS and BP):
    - Aggressive, early fluid resuscitation to mimic the nature of fluid lost i.e. blood, sodium chloride
  • Monitor input and output
  • Hypovolaemic - positive fluid balance to hydrate the patient and increase renal perfusion
  • Dialysis can be used in 1/3 patients to maintain renal function while treating the underlying cause (rapidly rising Cr/Urea, severe hyperkalaemia, metabolic acidosis)

In fluid overloaded patients:

  1. Loop diuretics
    - Only is no issue with renal perfusion - caution to avoid dehydration
    - Diuresis, reduced tubular cell metabolic demands, increase renal blood flow
    - High doses: 1-2g IV over 24hrs
    - 4mg/min max rate (higher risk of ototoxicity)
  2. Dopamine - ITU
    - Low dose 2mcg/kg/min = renal vasodilatation through DA1 receptors increasing perfusion and urine output
    - Higher dosing (>5mcg/kg/min) can cause vasoconstriction
  3. OTHER TREATMENTS
    Antibiotics if infective cause

Electrolyte correction - hyperkalaemia
- Over 6.5mmol/L potassium = muscle weakness, ECG changes, v-fib, cardiac arrest
- Over 6mmol/L and AKI should ve urgently treated in AKI patients

30
Q

What does CDK stand for?

A

Chronic Kidney Disease

31
Q

What is Chronic Kidney Disease?

A

It the worsening, progressive and irreversible loss of kidney function.

It can lead to end stage kidney failure - Permanent damage/loss of function.

The UKKA (The UK Kidney Association) defines CKA as a patient with abnormalities of kidney function or structure present for more than 3 months.
- The definition includes all individuals with markers of kidney damage or those with an eGFR of less than 60ml/min/1.73m2 on at least 2 occasions 90 days apart.

32
Q

What are the causes of CKD?

A
  1. Acute kidney injury (AKI) - Irreversible intrinsic damage
  2. Hypertension (HTN) - Vessel thickening and narrowing leading to less blood flow (RAS system worsens and can cause glomerulosclerosis)
  3. Diabetes - nephropathy leading to fibrosis, membrane thickening and sclerosis
  4. Glomerulopathies/vasculitis/polycystic kidney disease
    |
    V
    Kidney Sclerosis
33
Q

Name some complications of Chronic Kidney Disease.

A
  • Water and electrolyte balance
  • Hypertension
  • Acid/base balance
  • Muscle dysfunction
  • Renal bone disease
  • Uraemia
  • Anaemia
34
Q

What happens in the kidneys when it’s unable to regulate water and/or electrolytes?

A

Early stages:
- Polyuria / nocturia (regular need to urinate)
- Osmotic effect of urea (>40mmol/l)
- Loss of ability to concentrate urine

CDK progression:
- Kidneys are unable to excrete Na+ and Water
- Peripheral and pulmonary oedema
- Ascites
- 80% have volume dependent hypertension

Hyperkalaemia:
Due to kidneys inability to excrete, risk of cardiac arrest

Acidosis:
Due to inability to remove H+ ions = Reduced bicarbonate levels

35
Q

How do we treat the inability to regulate water?

A
  1. Fluid restriction - turn off the tap:

~ Not yet on dialysis and still able to pass urine - Restriction at a minimum of 1L /day (Hemodialysis not passing urine may be a lot less)
~ Sodium restriction - dietary measure

  1. Diuretics - take the plug out

~ If fluid restriction alone does not achieve optimal dry weight
~ Diuretics - Loop diuretics 1st line (Furosemide up 2g daily), Bumetanide absorbed better if theres a lot of fluid accumulation in the abdomen
~ Metolazone - cautious addition as a very strong diuretic, closely monitor

Monitor - Daily weights at home and blood pressure

36
Q

How do we treat the inability to regulate electrolytes?

A
  1. Potassium (Target 4.0 - 6.0 mmol/L pre-dialysis in hemodialysis patients):
    - Acute management
    - Medication review - medications/fluids contributing

Long term management:
- Calcium resonium ~ binds to potassium in the GI tract - Releases calcium ions in exchange and constipation s/e ~ prescribed lactulose alongside

  • Sodium Zirconium cyclosilicate and patiromer calcium approved by NICE for acute and chronic hyperkalaemia meeting certain criteria ~ Allow CKD patients to stay of ACEI/ARB for longer or at a higher dose ~ better adherence
  1. Acidosis - Sodium bicarbonate PO 500mg TDS
37
Q

What are the symptoms of uraemia related CKD and how cane it be treated?

A

Uraemia (>15mmol/L) - Effective treatment requires dialysis

Symptoms:
- Anorexia
- Nausea and vomiting
- Constipation
- Foul taste
- Pruritis
- Skin discolouration

NICE approved the use of Difelikefalin for pruritis in hemodialysis patients.

38
Q

What is muscle dysfunction in relation to CKD and how can it be treated?

A

Muscle dysfunction includes cramps and restless legs especially at night.

Nutritional deficiencies and electrolytes disturbances.

Treatment:
- Lifestyle measures + check iron levels
- Quinine 300mg ON (cramps)
- Ropinirole 250mcg ON (restless legs)

39
Q

What is hypertension in relation to CKD?

A

Circulatory volume expansion due to sodium & water retention

Leads to artery stenosis = renin release = hypertension increases and increased rate of renal function decline

Proteinuria:
- Sustained hypertension can lead to protein in the urine
- Over 2g in 24hr = Glomerular disease
- Over 5g in 24hrs = Severe disease (nephrotic syndrome)

40
Q

How do we manage hypertension in CKD patients?

A
  1. Targets as per NICE guidelines in all stages of CKD:
  • Proteinuria low (ACR <70 or PCR <100) - Target blood pressure <140/90 mmHg
  • Proteinuria high (ACR >70 or PCR >100) - Target blood pressure < 130/80mmHg
  1. Encourage ACR testing to identify CKD earlier and ensure appropriate intervention
  2. CKD, Hypertension and ACR >30mg/mmol OR Diabetes and ACR is 3mg/mmol or more:
  • ACEI/ARB started and optimised
  • ACEI/ARB may be also offered to CKD patients who do not have existing hypertension or diabetes if ACR is 70mg/mmol or more
  1. ACEI/ARBs
    - Monitor potassium prior to treatment & 1-2 weeks after initiation/dose change (Potassium binder may be required if hyperkalaemia on repeat sample)
  • Creatinine monitoring - 1-2 weeks after initiation/dose incrementation

CONTRAINDICATION in renal artery stenosis:
- Atherosclerosis in renal arteries supplying blood to the kidney = reduced GFR

  • RAS system constricts the efferent arteriole to maintain pressure and perfusion
  • RAS blockers (ACEI/ARB) block this compensatory mechanism
  1. CCBs - For ankle oedema
  2. Diuretics - Not usually for hypertension, mainly oedema
    - Thiazide diuretics (except metolazone) ineffective CrCl <25ml/min
  • Potassium soaring diuretics increase hyperkalaemia risk
  1. Beta blockers - cardio selective e.g. Metoprolol (cleared by the liver), low dose and titrate
  2. Alpha blockers - e.g. Doxazosin, cleared via the liver
  3. Vasodilators - Only used if struggling to control with other agents
    - S/E: Reflex tachycardia (use with B-blockers), fluid retention (use with diuretics) and minoxidil causes excess hair growth
41
Q

How is SGLT2 (Dapagliflozin) used in chronic kidney disease?

A
  1. Renal protective effect
  2. Mechanism unknown:
  • Proposed via inhibiting sodium reabsorption this activates adenosine = vasoconstriction of the afferent arteriole (tubuloglomerular feedback)
  • Prevents prolonged high pressure and damage in the glomerulus
  1. Dapagliflozin is the only licensed currently for CKD:
  • Add-on to optimised standard care including highest tolerated ACEI or ARB - unless contraindicated
  • eGFR 25-75ml/min1.37m2 at the start of the treatment with type 2 diabetes or uACR of at least 22.66mg/mmol
  1. Warnings/education
  • Sick day rules - held when acutely unwell particularly in dehydration or acute hospital admission
  • MHRA warning - Diabetic ketoacidosis that can be euglycemic
  • MHRA warning - Fournier’s Gangrene
42
Q

What is hyperphosphataemia in relation to renal bone disease?

A
  • Less excretion of phosphate by the kidneys which results in build up in the blood
  • Symptoms include pruritis
43
Q

How does low vitamin D cause renal bone disease?

A
  • There is less activation of vitamin D
  • Cholecalciferol converted to calcitriol by hydroxylation in 25 position in the liver, and 1alpha position in the kidney (hence 2nd step impaired)
  • Which ultimately results in defective bone mineralisation and osteomalacia (bone softening)
44
Q

What is hypocalcaemia in relation to renal bone disease?

A
  • Less vitamin D = Less absorption of Ca from GI tract and kidneys
  • More phosphate = more sequestering of calcium as calcium phosphate in bones
  • Increased bone turnover to release calcium into the bloodstream
  • Weakening on the bone architecture (osteitis)
  • Osteopenia and osteoporosis are common
  • Increased fracture risk
  • Bone hardening (osteosclerosis)
45
Q

How do we treat hyperphosphatemia?

A
  1. Diet - Phosphate intake
  2. Phosphate binders e.g. calcium acetate, sevlamer, lanthanum
  3. Bind with phosphate in the gut (take with/before meal and dose accordingly)
  4. High adherence issue - large tablets/tablet burden/GI side effects
46
Q

How do we treat hypocalcaemia and low vitamin D?

A

Vitamin D3 analogue:
E.g. Calcitriol (activate), Alfacalcidol (activated in the liver)

47
Q

How do we treat hyperparathyroidism?

A
  • Parathyroidectomy (removal of the parathyroid glands)
  • Cinacalcet - lowers PTH levels by increasing sensitivity of calcium receptors (calcimimetic)
  • Paricalcitol - IV Vitamin D analogue (expensive)
48
Q

What are the target aims for renal bone disease?

A
  1. PTH: >2x and <4x upper limit of normal
  2. Phosphate: 1.1 - 1.5mmol/l
    - 1.1 - 1.7mmol if on dialysis
  3. Calcium (corrected): 2.2 - 2.6mmol/l

Targets will vary depending on the stage of chronic kidney disease, dialysis and the unit.

49
Q

What is renal anaemia?

A

DEFINITION ADD

  • Iron deficiency - reduced absorption ability
  • Need sufficient stores for erythropoietin treatment to be effective

Target Ferritin Range: 200-500mcg/L (Max 800mcg/L and minimum >100mcg/L)

  • PO iron may be sufficient for pre-dialysis patients
  • Most patients will need IV replacement e.g. Ferinject, Venofer - Serum Ferritin <200mcg/L
  • AVOID blood transfusions - renal transplantation in the future
50
Q

What are the symptoms of renal anaemia?

A
  • Fatigue
  • Breathlessness
  • Angina
51
Q

How do we treat renal anaemia?

A
  1. Recombinant human erythropoietins by injection (IV/SC):
  • Epoetin alfa (Eprex)
  • Darbepoetin (Aranesp)
  • Epoetin beta (NeoRecormon)
  • S/E - Hypertension, pre red cell aplasia (Eprex only)
  1. HIF stabilisers - Roxadustat - involved in gene expression in erythropoiesis to increase Hb production and improve iron response
  2. Hb target: 100-120g/L
52
Q

What complications are considered for CKD patients?

A
  1. Vitamins
    - Renavit - contains water soluble vitamins alongside dietary advice
  • Particularly on dialysis as removes water soluble vitamins
  1. Hepatitis B vaccination
    - 5 yearly booster for all CKD patients with blood manipulation, particularly haemodialysis (monitored yearly for antibodies)
  • Doses are doubled at 3x 40mcg doses

Renal and Hepatic Diseases and Transplant (2 decks)

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