Renal : AKI + CKD Flashcards

1
Q

🫘 What is the function of the kidneys?

A
  • 🚮 filter waste substances (urea, creatinine,ammonia, uric acids) and xs water from the blood
  • 🏭 produce hormones - ie calcitonin 🦴 (activated vitamin D), erythropoietin 🩸 and angiotensin 2 🫀
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2
Q

How do we diagnose AKI and CKD?

A
  • 🛌 assessment of patient signs, sympotms and risk factors
  • 💧 urine output
  • 🩸 serum creatinine levels (waste products of muscle break down)
  • 📉 we can also look at renal function - eGFR
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3
Q

What is the name of the tool used and endorsed by NHSE to identify potential cases of AKI based on creatinine levels in the lab?

A

The Acute Kidney Injury algorithm.

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4
Q

What is the eGFR a measure of?

A

⏰ a blood test which measures how good your kidneys are at filtering out waste from the blood.

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5
Q

What does a HIGH eGFR rate indicate?

A

😊 good kidney clearance → the kidneys can filter out a lot of blood per minute

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6
Q

What does a LOW eGFR rate indicate?

A
  • 😢 poor renal clearance - the kidney can only filter a small (n) of blood per minute
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7
Q

Which populations of patients might the eGFR appear HIGHER and thus BETTER than it actually is?

A
  • 👴🏼the elderly
  • 🥗those on low protein diet
  • 🦾 amputees
  • 💪those with muscle wasting disorder (ie myesthenia gravis, late stage muscular dystrophy)
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8
Q

Which population of patients might the eGFR appear LOWER and thus WORSE than it actually is?

A
  • 🏋️‍♀️ high muscle mass (e.g high - level sport or body builder)
  • 🥩 High protein diet (e.g taking protein supplements)
  • 🛏️ Muscle breakdown (e.g after heavy exercise, myosotis, muscular dystrophy)
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9
Q

How do we measure the creatine clearance in px with a stable renal function?

A

Cockcroft - Gault equation
CrCl

⚠️ it is not used clinically as it doesn’t use standardised creatine values and thus can give inaccurate values

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10
Q

🫘 What is chronic kidney disease?

A

Abnormalities in the structure and or function of the kidney present for >3 months where px have an eGFR of 60ml/min/1.73m2 or less.

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11
Q

What are some examples of kidney disease markers? (Ie indicators of kidney disease in the px)?

A
  • 🥩 albuminuria (ACR > 3 mg/mmol),
  • 🩸 haematuria (or presumed or confirmed renal origin)
  • 💧 electrolyte abnormalities due to tubular disorders
  • 🫘 renal histological abnormalities
    -🩻 structural abnormalities detected by imaging (e.g. polycystic kidneys, reflux nephropathy)
  • a history of kidney transplantation
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12
Q

What are some common causes of CKD?

A
  • 💊 Drugs that are potentially Nephrotoxic (NSAIDS, ACEi, ARBS), bisphosphonates, calcineurin inhibitors, diuretics, Li, MTX, PPIs
  • 🫀conditions associated with intrinsic kidney disease → HTN, T1/T2DM (essp not managed or controlled well), and glomerular disease.
  • 🫘current or previous hx of AKI
  • 🥵kidney infections
  • ⭕️ Polycystic kidney disease → an inherited condition where cysts develop in the condition
  • 🪢 glomerulonephritis (inflammation of the glomeruli of the kidneys)
  • 🙅‍♀️conditions associated with Obstructive Kidney Disease
  • 🤝 multi-system diseases that may involve the kidney.
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13
Q

Name some potentially Nephrotoxic drugs that may contribute to CKD?

A
  • 💊 NSAIDS
  • 🫀 ACEi, ARBS
  • 🦴 bisphosphonates
  • calcineurin inhibitors
  • 💧 diuretics
  • 🪙 Li
  • MTX
  • 🥛 PPIs
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14
Q

How NSAIDS cause renal dysfunction (ie AKI/CKD)?

A

NSAIDs work by inhibition of COX enzymes and thus inhibiting the production of prostaglandins

PG are invovled in efferent arteriolar constriction which is used to maintain a pressure gradient in the glomerulus.

Inhibition of the PG means that the constriction of the efferent arteriole is loser and thus the intraglomerular pressure is also lost - AKI/CKD

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15
Q

💊 Explain how ACEi and ARBs can lead to AKI/CKD? (Kidney damage)

A
  • ACEi and ARBs both result in the inaction or lack of angiotensin 2 a hormone needed to maintain the dilated afferent arteriole of the glomerulus

As a result the afferent arteriole of the glomerulus is constricted resulting in reduced blood flow int the kidney - reduced perfusion of the kidney - AKI (hypoperfusion)

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16
Q

💊 How do we generally treat CKD?

A
  • ✅ usually based on the management of the conditions that occur as complications associated with CKD (ie malnutrition, CVD, HTN, PAD, HF)
  • 🛑 withhold or reduce any potentially Nephrotoxic drugs that may cause AKI → explain why to the patient
  • blood pressure control, management of renal bone disease, renal anaemia, preservation of kidney function and metabolic acidosis.
    • Statins and oral platelet and anti coagulation therapy may also be offered for secondary prevention of CVD

💊An SGLT2 inhibitor may also help (ie Dapagliflozin)

🏃‍♀️Lifestyle modifications and addressing risk factors

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17
Q

What are some lifestyle modifications we can advise to a patient with CKD to reduce their risk of the condition worsening?

A
  • 🚬if the smoke → advise that they stop!
  • 🍷drinking alcohol in moderation
  • 🧈maintain a healthy body weight
  • 🏃‍♀️regular exercise
  • 🥗eating a healthy diet
  • 💊OTC analgesia → avoid NSAIDS and where possible avoid herbals 🌱, paracetamol may be a better option.
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18
Q

What is the name of the drug that used as an option to treat stage 3 and 4 CKD (with albimunuria) associated with T2DM in adults?

A

Finerenone -

19
Q

What are the two key parameters we need to measure before we can Rx and initiate this drug?

A
  • eGFR
  • serum [K]
20
Q

Why is Finerenone used to prevent the worsening of/ treat stage 3 CKD in px with diabetes?

A

Finerenone is a non-steroidal mineralocorticoid receptor antagonist that inhibits receptor-mediated sodium reabsorption (thus more is peed out!) and decreases receptor overactivation, thereby reducing the inflammation and fibrosis that lead to kidney damage.

21
Q

Why do we need to measure the serum [K] before initiating finerenone?

A

In the kidneys, sodium is re absorbed in enhanced for potassium secretion.

Finerenone works to increase secretion of Na, thus we need the K+ to be not too high. If they are TOO high we cannot initiate Finerenone bc it will cause the K+ to be higher restyling in problems with the heart

22
Q

What is Acute Kidney Injury?

A

The rapid decline in renal function over hrs - days that results in the failure of the kidneys to maintain serum fluids, produce hormones, and maintain electrolyte + acid base homeostasis.

23
Q

What are the stages of AKI?

A
  • 🤫 In the early stages, AKI may be symptomless
  • a common indicator at first is the rapid decline in urinary output - indicative of dehydration!
  • new or worsening confusion 😵‍💫, fatigue 🥱, or drowsiness 😴
24
Q

What are some of the risk factors for developing an AKI?

A
  • 🩸 A major risk of actor for AKI is renal hypoperfusion → ie a reduced blood flow to the kidneys.
  • 💊 Drugs (NSAIDS, ACEi, ARBS)
  • 🫀conditions associated with intrinsic kidney disease → HTN, T1/T2DM (essp not managed or controlled well), and glomerular disease.
  • 🥵Sepsis
    • 💧🧂Intense sodium and water retention
  • 🍸DEHYDRATION
  • ⚠️ Elderly patients and those that are taking medication that is deemed as “nephrotoxic” or those that cause dehydration are at greater risk of incurring an AKI.
  • There are many additional risk factors such as poor blood pressure control, diabetes and sepsis in the elderly
25
Give 3 examples of analgesia that may increase the risk of developing an AKI? - what should we do if the px takes these drugs and has an AKI?
- ⚠️ NSAIDS - withdraw in px at high risk - ⚠️ opioids - avoid long acting preparations - 📉 pregabalin and gabapentinoids - reduce their dose
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27
🫀 Give 7 examples of drug classes that are **CARDIOVASCULAR MEDICATIONS** that may increase the risk of AKI? - what would we do if the px takes these and has an AKI?
- 🫀 antihypertensives (CCBs, alpha and beta blockers) - **withhold** - 🩸 ACEi, ARBs, Aliskiren - **consider withholding** - 💧 diuretics (loop + thiazide) - **consider withholding** - K+ sparing diuretics - STOP 🛑 in AKI - 🧈 statins 🛑 STOP in AKI - 🌳 digoxin - 📉 reduce dose - 🩸 DOACS - - **consider withholding**
28
🦠 Give 3 examples of drug classes that are USED TO TREAT INFECTION that may increase the risk of AKI?
- Aciclovir → reduce the dose, encourage the patient to drink plenty - Trimethoprim and co - trimoxazole → avoid or reduce dose (essp if the px already taking ACEi,ARB or spiro) - Phenytoin → monitor levels, correct phenytoin levels for uraemia and low serum albumin
29
🍫 Give two examples of drug classes that are used to TREAT DIABETES that may increase the risk of AKI?
- **Hypoglycaemic drugs**→ the accumulation of AKI may increae the risk of AKI - **Metformin** → risk of lactic acidosis is increased → accumulation can also lead to hypoglycaemia in poor renal function
30
How does **colchicine** increase risk of AKI?
- colchicine - Used to treat pain and inflammation (in gout) → may cause diarrhoea, vomiting causing hypovolaemia if AKI
31
What are the complications of using Li in AKI?
can cause nephrogenic diabetes insipidus (xs thirst and urination bc the urine isnt concentrated) , care rarely also associated with NMS
32
If a px is taking colchicine , or Li, and has an AKI, what should we do?
- colchicine → use lower doses or consider steroids, **do not use NSAIDS for gout** in AKI - NSAIDS worsen AKI!!!! - Lithium → avoid where possible, monitor lithium and electrolyte levels
33
What are the 3 classes of the causes for AKI?
- 🔴 pre - renal - 🟡 intra - renal - 🟢 post - renal
34
What is **pre - renal AKI **?
Any sort of renal damage that occurs before the kidneys. Reduced blood flow to the kidneys - anything that results in **hypoperfusion** of the kidneys
35
What arte some causes of hypo - perfusion to the kidneys and therefore pre - renal AKI?
- 💧 hypovolaemia -> reduced blood volume in the circulatory system - 🫀 reduced cardiac output - 🩸 reduced systemic vasodilation - 🪢 afferent arterial constriction - 🪢 efferent arterial dilation
36
How does hypovolaemia lead to *pre - renal AKI* and what are some causes of hypovolaemia?
causes of hypovolaemia → burns 🔥 , trauma 😣 + haemorrhage 🩸, px taking diuretics 💧 , GIT issues (ie excessive vomiting 🤮 and diarrhoea 💩 ).
37
Which conditions may cause a decreased cardiac output and thus pre - renal AKI?
- CO → the (n) of blood ejected from the heart every minute - usually caused by heart diseases, ie HF, PE
38
What is **intra - renal AKI**?
The structural damage to the kidney tissue. It my be categorised as vascular 🩸 glomerular 🧶 , tubular 🦯, or interstitial (ie allergic response in the tissues - acute interstitial nephritis → usually caused by antibiotic drugs) depending on which area of the kidneys is affected
39
What is **post renal AKI**?
This is damage to structures after the kidneys → ie the ureters, bladder and urethra → usually some sort of **obstruction.** - *ie some sort of tumour 🤒* - *Some sort of renal stone 🪨* - *Benign prostatic hyperplasia 🧍‍♂️* - Due to obstruction of the flow of urine out of the kidneys
40
Which patient groups are at increased risk of developing AKI in primary care?
- px with DM 🍫 - px with CKD - px with dementia 👴🏼 - px with HF (taking ACEi and diuretics) - older px 👵 - self neglected px - ie dehydrated, malnutrition - 💩 px abusing laxatives or diuretics - px taking recreational drugs
41
Typically how do we treat AKI?
- 📋 first we review their medicines thoroughly to eliminate any potential causes (ie drug induced, also looking at what type of px they are (ie elderly, female, cancer, overweight, NSAIDS,HF etc) - 🛑 in many cases we’ll need to **withold** medications (ie essp cardiac drugs and diuretics) - until the px resolves - explain this temporary witholding of medications to the px - that its likely its the reason for the decline in renal function
42
We can also look at the patients bloods to identify AKI or CKD. Looking at the [K+] and [Na+] which results may indicate AKI?
- 📈 Hyperkalemia - kidneys are not filtering and secretion K well - 📉 hyponatremia - H2O retention - not being filtered well - dilution of Na+ - 📈 hypernatremia - more Na+ being retained less being filtered out of the kidneys
43