Acute Kidney Injury Flashcards
What 3 principles are desirable in theory for a good assessment of renal function?
- Measurable
- Reproducible
- Consistent
Which of the following is not a desirable, theoretical good assessment of renal function?
A. Reproducible
B. Consistent
C. Measurable
D. Traceable
D. Traceable
What is used as a measurement of renal function?
GFR/eGFR
What is the equation for GFR?
[X]urine x urine flow rate / [X] plasma
What is the ideal criteria for a marker of GFR?
Principles of GFR marker: GFRR
• Gain: Appear in plasma at constant rate
• Filtered: Freely filtered at glomerulus
• Reabsorbed: Not reabsorbed or secreted by renal tubule
• Renal: Does not undergo extra-renal elimination
Which of the following is not a criteria for a marker used to estimate GFR?
A. Appear in the plasma at a constant rate
B. Freely filtered at the glomerulus
C. Reabsorbed/secreted by renal tubule
D. Does not undergo extra-renal elimination
C. Reabsorbed/secreted by renal tubule
What is the most commonly used marker for estimation of GFR?
A. Inulin
B. Cystatin
C. Creatinine
D. Urea
C. Creatinine
What is inulin and why is it good as an exogenous marker of GFR?
Why may it not be useful?
Plant polysaccharide of fructose.
Constant injection of inulin for 3 hour at 18mg/min with timed urine and blood collection to measure inulin at midpoints of collection period
+ Gold standard
+ Fulfils marker criteria (constant, not produced elsewhere, not secreted/absorbed, only renally excreted)
+ Comprehensive assessment via blood and urine output/sampling
- Time-consuming
- Resources
- Difficult to perform
What is cystatin and why is it good as an marker of GFR?
Why may it not be useful?
Cysteine protease inhibitor present on surface of nucleated cells shed into plasma and excreted by glomerular filtration
+ More stable than creatinine
+ Less interpersonal and intrapersonal variation
+ Better for elderly populations
+ Freely filtered, reabsorbed and metabolised by PT cells, not produced elsewhere, only renally excreted)
+ 13kDa
- Expensive
- Difficult (laboratory specific)
- Not validated
What is Creatinine and why is it good as an marker of GFR?
Why may it not be useful?
Metabolic product of creatine and phosphocreatine released at a constant rate by the body
Note: Plasma creatinine inversely related to GFR by 2 thus halving GFR ≈ x2 plasma creatinine concentration
+ Does not bind plasma proteins
+ Freely filtered
+ Little reabsorption
+ Low M/w 113Da
- Secreted by tubules (breakdown from muscle) - Increased error at lower GFR
- Relations to muscle mass - Inaccuracy in GFR determination by creatinine clearance due to collection and measurement
- Insensitive in acute kidney injury (AKI)
- Deranged in diet (meat), muscle mass (elevated), age (decrease), vegetarians (decrease),
- Drugs interfere: Trimethoprim, cimetidine compete for secretion and other substances (bilirubin, cephalosporin, high glucose)
What is Urea and why is it good as an marker of GFR?
Why may it not be useful?
Metabolic product of amino acids and exogenously acquired from protein intake
+ Freely filtered
+ Low M/w of 60Da
- 50% reabsorbed by PCT depending on water/Na reabsorption
- Deranged by liver disease (reduced urea plasma levels)
- Proteinolysis in the intestines raises urea
Which of the following markers is useful in elderly populations and has less interpersonal variation?
A. Inulin
B. Cystatin
C. Creatinine
D. Urea
B. Cystatin
Which of the following markers is endogenous and does not bind plasma proteins?
A. Inulin
B. Cystatin
C. Creatinine
D. Urea
C. Creatinine
Which of the following markers is endogenous and can be interfered with in AKI or Drugs?
A. Inulin
B. Cystatin
C. Creatinine
D. Urea
C. Creatinine
Which of the following markers is endogenous and is freely filtered but up to 50% is reabsorbed by PCT?
A. Inulin
B. Cystatin
C. Creatinine
D. Urea
D. Urea
What are the indications when clearance measurements based on serum creatinine may be inaccurate?
- Old age
- BMI
- MSK diseases
- Paraplegia/Quadriplegia
- Diet (carnivorous or vegetarian)
- Rapidly changing kidney function
- Pregnancy
What is the relationship between age and GFR?
Increasing age from 20 onwards leads to a gradual, physiological reduction in GFR
How can eGFRs be calculated? List the main formulas used.
1. MDRD: Formula to estimate GFR • Computerised • Useful is stable creatinine • Clinically used • Modifier for F (0.742) and Black (1.21)
• Less accurate if near normal GFR
- CKD-EPI: Formula estimating GFR
• Best estimation of GFR
• Clinically used (for donors)
• Modifier for Age (0.993), F (1.018), Black (1.159)
• Not validated yet (used for donors)
- Cockcroft-Gault Equation: Based on serum creatinine alone
• Advised for narrow therapeutic index drugs
- Inaccurate for rapidly changing creatinine levels
- Uses IBW at extremes of BW
- Adults only
- Not adjusted for SA
Which of the following equations is used for donors and gives the best estimation of GFR?
A. CKD-EPI
B. Cockcroft-Gault Equation
C. MDRD
A. CKD-EPI
Which of the following equations is used for clinically and useful is stable creatinine?
A. CKD-EPI
B. Cockcroft-Gault Equation
C. MDRD
C. MDRD
Which of the following equations is used when narrow therapeutic index drugs are used?
A. CKD-EPI
B. Cockcroft-Gault Equation
C. MDRD
B. Cockcroft-Gault Equation
Which of the following equations is only applicable to adults?
A. CKD-EPI
B. Cockcroft-Gault Equation
C. MDRD
B. Cockcroft-Gault Equation
What relationship does renal blood flow have on kidney function? What endogenous marker is used? Equation used to calculate RPF?
Renal blood flow (Renal plasma flow ≈ RPF) ≈ hydraulic pressure in glomerulus based on afferent and efferent arteriolar radius ≈ ∆ GFR
- Kidneys take 20% CO ≈ 20% of 5L/min ≈ 1/L min
Which of the following is a marker for Renal Plasma Flow (RPF)?
A. Butyric acid
B. Urea
C. Para-aminohippurate
D. Creatining
C. Para-aminohippurate
What impact would an increase in the diameter of the afferent arteriole have on filtration?
A. Increase as less perfusion
B. Increase as more perfusion
C. Decrease as less perfusion
D. Decrease as more perfusion
B. Increase as more perfusion
What impact would a decrease in the diameter of the afferent arteriole have on filtration?
A. Increase as less perfusion
B. Increase as more perfusion
C. Decrease as less perfusion
D. Decrease as more perfusion
C. Decrease as less perfusion
What impact would an increase in the diameter of the efferent arteriole have on filtration?
A. Increase as less perfusion
B. Increase as more pressure across the glomerulus
C. Decrease as less perfusion
D. Decrease as reduced pressure across the glomerulus
D. Decrease as reduced pressure across the glomerulus
What impact would a decrease in the diameter of the efferent arteriole have on filtration?
A. Increase as less perfusion
B. Increase as more pressure across the glomerulus
C. Decrease as less perfusion
D. Decrease as reduced pressure across the glomerulus
B. Increase as more pressure across the glomerulus
What effect does NSAID have on GFR?
A. Agonist of COX-1 and COX-2 at peroxidase site thus increase conversion of arachidonic acid to PDH2 synthetases and subsequent prostaglandin increasing GFR
B. Antagonist of COX-1 and COX-2 at peroxidase site thus reduce conversion of arachidonic acid to PDH2 synthetases and subsequent prostaglandin decreasing GFR
C. Antagonist of COX-1 and COX-2 at cycloxygenase site thus reduce conversion of arachidonic acid to PDH2 synthetases and subsequent prostaglandin decreasing GFR
D. Antagonist of COX-1 and COX-2 at cycloxygenase site thus reduce conversion of arachidonic acid to PDH2 synthetases and subsequent prostaglandin decreasing GFR
D. Antagonist of COX-1 and COX-2 at cycloxygenase site thus reduce conversion of arachidonic acid to PDH2 synthetases and subsequent prostaglandin decreasing GFR
What impact does ACEi have on GFR?
A. Inhibit AGT-II production thus constrict afferent arterioles to reduce GFR
B. Increase AGT-II production thus dilate afferent arteriole to increase GFR
C. Inhibit AGT-II production ≈ dilate efferent arterioles ≈ reduce pressure gradient across glomerulus to reduce GFR
D. Inhibit AGT-II production ≈ constrict efferent arterioles ≈ reduce pressure gradient across glomerulus to increase GFR
C. Inhibit AGT-II production ≈ dilate efferent arterioles ≈ reduce pressure gradient across glomerulus
What impact do ARBs have on GFR?
A. Inhibit AGT-II production thus constrict afferent arterioles to reduce GFR
B. Increase AGT-II production thus dilate afferent arteriole to increase GFR
C. Inhibit AGT-IIR binding ≈ dilate efferent arterioles ≈ reduce pressure gradient across glomerulus to reduce GFR
D. Inhibit AGT-IIR binding ≈ constrict efferent arterioles ≈ reduce pressure gradient across glomerulus to increase GFR
C. Inhibit AGT-IIR binding ≈ dilate efferent arterioles ≈ reduce pressure gradient across glomerulus to reduce GFR
Which radionuclide is best for envisaging renal scarring and mass?
A. MAG3
B. DMSA
C. 51Cr-EDTA
D. Creatinine
B. DMSA
Which radionuclide is an independent indicator of ERPF and renal function?
A. MAG3
B. DMSA
C. 51Cr-EDTA
D. Creatinine
A. MAG3
Which radionuclide emits a lower radiation dose thus may be safer relatively?
A. MAG3
B. DMSA
C. 51Cr-EDTA
D. Creatinine
C. 51Cr-EDTA
Which radionuclide has a high extraction fraction of 40-50%?
A. MAG3
B. DMSA
C. 51Cr-EDTA
D. Creatinine
A. MAG3
Define Proteinuria.
≥ 0.3g in 24 hours (albumin)
List 3 states/conditions which may give variations in urinary albumin.
- Posture
- Exercise
- Acute diuresis
- Menstruation
- Does not detect light chains in urine (e.g. Bence Jones protein)
What are the two sites of EPO production?
1) Kidney: 90%
2) Liver: 10%
What impact does acidosis have on Haemoglobin production?
Outline the physiological mechanism for this.
Acidosis reduces Erythropoiesis.
MOA: Acidosis ≈ reduced O2 affinity of Hb thus increasing tissue oxygenation ≈ reduce EPO synthesis by type 1 fibroblastoid cells in peritubular interstitium of cortex and outer medulla ≈ reduce erythropoiesis
What influence does CKD have on Haemoglobin production?
CKD ≈ myofibroblastoid change of fibroblastoid cells ≈ less erythropoietin production
What are the sites of calcium absorption in the body?
- Bone turnover (resorption)
- Gut (absorption)
- Kidney (filtered and reabsorbed)
What is renal calcium filtration and reabsorption regulated by?
- Vitamin D
- PTH (increased by low calcium ≈ bone reabsorption and vitamin D synthesis)
What influence will hypocalcemia have on PTH and what should occur?
Hypocalcemia ≈ CaSR in PTH detects + triggered ≈ Increase vitamin D synthesis (absorption of calcium) + calcium resorption/liberation ≈ correct Ca:PO4
Case Study… Mr Oliver - 53 Y/o M - Moderate pain - Gross ascites - 3 weeks Hx of ankle swelling - SOBE worsened 1/52 - Unsteady - Smells of alcohol
- PMHx: alcoholic liver disease and cirrhosis
- DHx: Spironolactone 100mg daily, lactulose 20ml BD (reduce hepatic encephalopathy), Maalox
Raised Bilirubin, Alk Phos, GGT; low albumin, increased PT
i) What are the main therapeutic aims for Mr Oliver?
ii) What prescribing considerations are there for Mr. Oliver?
i)
- Relieve ascites/oedema
- Treat any infection
- Prevent complications of alcohol withdrawal
- Prevent VTE
- Provide nutritional support
- Refer patient for alcohol probe
ii)
- Cirrhosis of liver
- Low serum albumin
- Cerebral sensitivity increased
- High risk of VTE despite prolonged PT but also risk of bleeding. Gastric irritation
- increase bleeding tendency
- Caution with nephrotoxics
List 5 common prescribing considerations regarding renal function and status.
- Renal condition/Degree of renal impairment
- Risks associated with prescribing
- Nephrotoxic drugs
- Prescribing in AKI, CKD and dialysis
- Acute/Chronic Kidney Disease
- Proportion of drug renally excreted
- Therapeutic window: narrow or wide
- Renal function markers (eGFR or creatinine clearance)
- Nephrotoxic drugs
- Patient on established renal replacement therapy (dialysis, haemodialysis, peritoneal dialysis)
State 3 risks of prescribing on the kidney.
- Reduced renal excretion of drug and metabolites ≈ toxicity
- Sensitivity increased
- Increased risk of ADRs
- Drugs not effective when renal function reduced
- Drug-induced renal disorders more common in pt with CKD
What type of drug-induced AKI would results from excessive diuretics use?
A. Renal
B. Post-Renal
C. Pre-Renal
D. Peri-Renal
C. Pre-Renal
What type of drug-induced AKI would results from excessive Gentamicin use?
A. Renal
B. Post-Renal
C. Pre-Renal
D. Peri-Renal
A. Renal
What type of drug-induced AKI would results from excessive Ciclosporin use?
A. Renal
B. Post-Renal
C. Pre-Renal
D. Peri-Renal
A. Renal
What type of drug-induced AKI would results from excessive Anticholinergics use?
A. Renal
B. Post-Renal
C. Pre-Renal
D. Peri-Renal
B. Post-Renal
What type of drug-induced AKI would results from excessive cytotoxic chemotherapy use?
A. Renal
B. Post-Renal
C. Pre-Renal
D. Peri-Renal
A. Renal
List 5 potentially nephrotoxic drugs and how they may cause damage.
- ACEi
- ARBs
- NSAIDs: COX-i ≈ reduced PGE2 ≈ afferent arteriole vasoconstriction ≈ renal hypoperfusion ≈ reduced GFR and urine volume
- Diuretics: Water/electrolyte loss, increased catabolism, vascular occlusion ≈ ∆ renal haemodynamics
- Lithium
- Digoxin
- Aminoglycosides (e.g. Gentamicin): Nephrotoxic damage
- Vancomycin
- Metformin: Increased risk of metabolic acidosis; avoid if eGFR < 30mL/min
- Nitrofurantoin: Increased risk of ADRs, peripheral neuropathy, blood dyscrasias; contraindicated if eGFR < 30mL/min unless multi-resistant bugs
- Iodinated contrast media
- Opioids (e.g. Morphine): Active metabolites accumulate ≈ increased ASEs
What are medicine sick day rules?
List 3 drugs affected by the medicine sick day rules.
Discontinue drugs during acute intercurrent illness
Condition: • Vomiting • Diarrhea • Fevers • Sweats • Shaking
Drugs:
• ACEi: Reduced constriction of efferent arteriole ≈ GFR reduced
• NSAIDs: Reduced vasodilation of afferent arteriole ≈ GFR reduced
• ARBs: Reduced constriction of efferent arteriole ≈ GFR reduced
• Diuretics: Fluid loss ≈ hypovolemia ≈ reduced GFR
• Others (blood-pressure lowering): Lower blood pressure and GFR
• Metformin: Accumulation
• Sulfonylurea: Risk of hypoglycaemia
• Trimethoprim: Hyperkalemia risk
List 5 principles of prescribing in renal impairment.
- Check renal function: eGFR, creatinine, U+E
- Baseline trends in renal function
- Consider stopping/withholding nephrotoxic drugs
- Choose non-nephrotoxic drug if possible
- Check resources
- Use therapeutic drug monitoring guide dose/frequency if appropriate
- Continue to monitor patient condition: NEWS + Metabolic profile
Which of the following is not a principle of prescribing in renal impairment?
A. Continue to monitor patient condition: NEWS + Metabolic profile
B. Consider stopping/withholding nephrotoxic drugs
C. Baseline trends in renal function
D. Avoid prescribing any nephrotoxic drugs, even at low dose
D. Avoid prescribing any nephrotoxic drugs, even at low dose
Which of the following is not a principle of prescribing in renal impairment?
A. Check renal function: eGFR, creatinine, U+E
B. Consider stopping/withholding nephrotoxic drugs
C. Never choose a nephrotoxic drug
D. Choose non-nephrotoxic drug if possible
C. Never choose a nephrotoxic drug
Outline the relationship between renal clearance and therapeutic window.
Renal clearance (excretion of active drug/metabolite) and therapeutic window (dose range that is therapeutically safe, not toxic) present trade-off of which action taken is dependent on the combination
List 3 drugs to avoid if low clearance and a narrow therapeutic window.
- Theophyline
- Carbamazepine
- Phenytoin
- Rivaroxaban
- Gabapentin
- Ramipril/ACEi
List 3 prescribing principles for a CKD patient.
- Detect CKD early
- Classify CKD (1 to 5)
- Risk Factor for CVD
- Protect renal function: ACEi + ARBs
- Manage complications: hyperkalemia, anaemia, mineral/bone disorders, hyperphosphataemia
- Manage comorbid conditions
- Watch out for AKI
- Renal replacement therapy: Type of dialysis, Dialyser membrane, blood and dialysate flow rate, drugs removed in dialysis (Consult renal department)
Which of the following is not a prescribing principle in a CKD patient?
A. Detect CKD early
B. Classify CKD (1 to 5)
C. Protect renal function: ACEi + ARBs
D. Check if CVD
• Risk Factor for CVD
No, check if you have risk factors
Which of the following is not a prescribing principle in a CKD patient?
A. Risk Factor for CVD
B. Watch out for AKI
C. Classify CKD from stages 1-3
D. Protect renal function: ACEi + ARBs
C. Classify CKD from stages 1-3
No, classify CKD stages from Stages 1-5
List 3 prescribing principles for a patient regarding their liver.
- Liver function: LFTs
- Drug metabolism
- Hypoproteinaemia
- Clotting factors
- Hepatic encephalopathy signs?
- Fluid balance?
- Hepatotoxic drugs?
List 3 types/categories of drugs that worsen liver disease.
- Constipating drugs
- Medicines causing gastrointestinal ulceration
- Sedating medicines
- Anticoagulants, anti-platelets and medicines causing bleeding
- Medicines affecting fluid-electrolyte balance
- Medicines with high sodium content
- Medicines that are nephrotoxic
What is Drug-Induced Liver disease?
Hepatic dysfunction shown by abnormalities in liver tests due to medications
Outline the two categories of Drug Induced Liver disease.
- Intrinsic drug reactions: Predictable, dose-dependent, rapidly (paracetamol OD)
- Idiosyncratic drug reactions: Unpredictable, dose-independent, longer to develop
Which of the following drugs is not likely to cause acute liver failure?
A. Cyclophosphamide
B. Allopurinol
C. NSAIDs
D. Methotrexate
D. Methotrexate
Causes Fibrosis/Cirrhosis
Which of the following drugs is likely to cause acute liver failure?
A. Phenytoin
B. Allopurinol
C. Azathioprine
D. Methotrexate
B. Allopurinol
Which of the following drugs is likely to cause fibrosis?
A. Phenytoin
B. Allopurinol
C. Azathioprine
D. Methotrexate
D. Methotrexate
Which of the following drugs is likely to cause hepatitis?
A. Phenytoin
B. Allopurinol
C. Azathioprine
D. Methotrexate
A. Phenytoin
Which of the following drugs is likely to cause vascular disorders?
A. Phenytoin
B. Allopurinol
C. Azathioprine
D. Methotrexate
C. Azathioprine
Which of the following drugs is likely to cause vascular disorders?
A. Phenytoin
B. Allopurinol
C. OCP
D. Methotrexate
C. OCP
Which 2 of the following drugs is likely to cause Cholestasis?
A. Carbamizole
B. Allopurinol
C. OCP
D. Methotrexate
A. Carbamizole
C. OCP
What should you do if you identify a side effect to a drug with regards to prescribing practice?
A. Report to the Red Card Scheme
B. Report to the Yellow Card Scheme
C. Report to your senior clinician
D. Treat the adverse side effect
B. Report to the Yellow Card Scheme
What is an acute kidney injury (AKI)?
Sudden loss of renal function with consecutive rise in creatinine and BUN as well as reduced urine output (oliguria/anuria) as classified by the KDIGO classification
Outline the three stages of the KDIGO classification of AKI.
- Stage 1
• SCr 1.5-1.9 or > 26umol/L <0.5ml/kg/hour for 12 hours - Stage 2
• SCr 2.0-2.9 or <0.5ml/kg/hour > 12 hours - Stage 3
• SCr 3x or > 354umol/L or Anuria > 12 hours or < 0.3ml/kg/hour > 24 hours
A patient has seen an increase of x1.7 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No pathology
C. Stage 1
A patient has seen an increase of x1.4 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
D. No AKI stage
A patient has seen an increase of x1.9 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
C. Stage 1
A patient has seen an increase of x2.7 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
B. Stage 2
A patient has seen an increase of x2.4 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
B. Stage 2
A patient has seen an increase of x2.8 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
B. Stage 2
A patient has seen an increase of x3.2 his usual SCr, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
A. Stage 3
A patient has seen an increase from his usual Creatinine to 379umol/L, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
A. Stage 3
A patient has seen a reduction in urine output to <0.5ml/kg/hour for 6-12 hours, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
C. Stage 1
A patient has seen a reduction in urine output to <0.5ml/kg/hour for 14 hours, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
B. Stage 2
A patient has seen a reduction in urine output to <0.3ml/kg/hour for 26 hours, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
A. Stage 3
A patient has not passed urine in 12 hours, what stage AKI does he have?
A. Stage 3
B. Stage 2
C. Stage 1
D. No AKI stage
A. Stage 3
List 5 risk factors for an AKI
- Drugs: ACEi/ARB/NSAIDs/Diuretics/Metformin/Azathioprine/Cyclophosphamide
- Comorbidities: Liver disease/CKD/HF/PVD/DM
- Age: > 65 years
- Sepsis
- Underlying kidney disease
- Exposure to nephrotoxins
- Surgery
- Excessive fluid loss
- Haemorrhage
- Recent vascular intervention
- Pancreatitis
- Drug over dose
- Sodium-retaining states: CHF/Cirrhosis/Nephrotic Syndrome)
- Nephrolithiasis
- Hydronephrosis/Pyelonephritis
Which of the following is not a risk factor for AKI?
A. Sepsis
B. Advanced Age
C. Haemorrhage
D. No comorbidities
D. No comorbidities
Which of the following is not a risk factor for AKI?
A. Sepsis
B. Advanced Age
C. Good oral intake
D. Haemorrhage
C. Good oral intake
Which of the following is not a risk factor for AKI?
A. Hydronephrosis
B. Surgery
C. Allergy to house dust mites
D. Haemorrhage
C. Allergy to house dust mites
For each category of AKI, list an example of a disease causing the classification of AKI.
- Pre-Renal: Renal hypoperfusion
• Hypovolemia: Haemorrhage/D+V/Hyperhidrosis/Burns/Diuretics/Dehydration/Acute Pancreatitis
• Hypotension: Sepsis/Dehydration/Cardiogenic Shock/Anaphylactic Shock
• Renal Artery Stenosis (RAS)
• Drugs: NSAIDs/ ACEi/ARBs/Cyclosporine/Tacrolimus - Renal: Direct kidney disease due to damage of renal apparatus by toxin, drug or antibody
• Acute Tubular Necrosis (≈ 85% intrinsic AKIs)**
• Glomerulonephritis
• Vascular: HUS/ TTP/ Malignant hypertension/ Vasculitis
• Tubulointerstitial Nephritis (Drug-induced, infectious, immunological) - Post-Renal: Obstruction of urinary flow from renal pelvis to urethra
-> Classifications: Luminal/Mural/Extramural
• Congenital malformations
• Acquired obstructions: Prostatism/Iatrogenic/Catheter-associated tumours/ Stones/Bleeding
• Neurogenic Bladder: MS/SCL/Peripheral Neuropathy
List 7 potential symptoms or signs of AKI.
• ∆Urine Output: Oliguria/Anuria
Hypovolemic signs: • OH • Reduced skin turgor • Tachycardia • Hypotension
Hypervolaemic signs: • Oedema • Hypertension • Oedema • SOB
Signs of renal obstruction: • Distended bladder • Suprapubic tenderness • Incomplete voiding • Pain in suprapubic region or flanks
Other:
• Confusion
• Seizure or Coma (Severe cases)
• Higher risk of secondary infection throughout all phases
List 5 examples of markers of intrinsic renal causes of AKI.
- Anti-GBM disease (a3 of Type IV collagen)
- ANCA Positive Vasculitis (PR3-ANCA antibodies or MPO-ANCA)
- Immune complexes (SBE/Cryoglobulinaemia)
- Tubular toxins (drugs/contrast/myoglobulin/light chains)
- Streptococcal Group A ß-haemolytic (anti-streptolysin-O antibody)
- Crystals (Uric Acid/CaPO4)
- RPGN (Capillary wall necrosis and cells accumulating in Bowman Space forming crescents)
- AIN (neutrophils and eosinophils infiltrating interstitium of kidney)
- Drug-induced: Gentamicin accumulates in IC lysosomes causing nephrotoxicity when ruptured
- Iatrogenic: Contrast (iodine) ≈ nephrotoxic to proximal tubule causing severe arterial vasoconstriction ≈ reduced eGFR
List 7 investigations in AKI.
• Basic Metabolic Profile (U+E/LFTs): Elevated SCr/High K+/ Metabolic Acidosis/ LFTs (hepatorenal syndrome)
- SCr ≥ 26umol/L or ≥0.3mg/dL in 24 hours or ≥ 1.5 times baseline in 7 days
• FBC: Anaemia/Leukocytosis/Thrombocytopenia
• Venous Blood Gases: Anion gap acidosis (impaired excretion of non-volatile acids)
• Bicarbonate: Low bicarbonate ≈ Acidosis
• CRP: Elevated (infection/vasculitis)
• Blood Culture: Positive for bacterial pathogen
• Serology: ANAANCA/Anti-dsDNA Antibodies
• Urinalysis: RBC/WBC/cellular casts/proteinuria/nitrite/leukocytes
• Urine culture: Bacterial growth with antibiotic sensitivity
• Urine output monitoring: <0.5ml/kg/hour for 6 hours; <0.5ml/kg/hour for 12 hours/anuria or ≤ 0.3ml/kg/hour for 12 hours
- CXR: Infection/Fluid/Cardiomegaly/Haemorrhage
- ECG: Hyperkalemia/Peaked T waves/ Increased PR interval/Widened QRS/Atrial Arrest/Deterioration to Sine Wave Pattern
- Renal-USS: Dilated renal calyces/fat stranding/acoustic shadow/ normal size (rarer cause?)/Reduced corticomedullary differentiation + scarred (CKD)
- CT-abdomen: Stone seen; or not if uric acid stone/calculi
List the common complications of AKI.
- Hyperkalemia ([K+] > 5.5mmol/L)
• Increased risk in CKD/ Metabolic Acidosis/ Drug effects
- Cardiac arrhythmias (> 5.5mmol/L) -> Tented T waves
- Loss of P waves
- Wide QRS complex (> 7.0mmol/L)
- Sine-wave or ventricular fibrillation (> 8.0mmol/L)
Categories of Hyperkalemia:
• Mild: 5.5-5.9mmol/L
• Moderate: 6-6.4mmol/L
• Severe: >6.5mmol/L
Management:
• IV Calcium (10%) 10mL (Ca Gluconate = 2.26mmol or Calcium Chloride = 6.8mmol) Reduce depolarisation effect of elevated K+ on cardiomyocytes
• Insulin: Activate Na+, K+-ATPase
• Salbutamol: Increase efficiency of Na+, K+-ATPase
- Pulmonary Oedema (excess lung fluid)
• Diuretics to fluid deplete individual even if AKI (heart > kidneys)
• Dialysis if anuria - Infection
What are the three categories for hyperkalemia? Give the values and unit of measurement.
- Mild: 5.5-5.9mmol/L
- Moderate: 6-6.4mmol/L
- Severe: >6.5mmol/L
At a serum potassium level of > 5.5mmol/L what ECG changes may be observed?
A. Depressed T waves
B. Absent T waves
C. Tented T waves
D. Tented Q waves
C. Tented T waves
At a serum potassium level of > 7.5mmol/L what ECG changes may be observed?
A. Depressed QRS complex
B. Widened QRS complex
C. Shortened QRS complex
D. Tented Q waves
B. Widened QRS complex
At a serum potassium level of > 8.5mmol/L what ECG changes may be observed?
A. Ventricular fibrillation
B. Atrial fibrillation
C. Sinus bradycardia
D. Tented Q waves
A. Ventricular fibrillation
Upon noticing tented T waves on an ECG, a sign of hyperkalemia. What should be administered?
A. Calcium Chloride 6.8mmol
B. Calcium Gluconate 3.26mmol
C. Calcium Gluconate 6.8mmol
D. Calcium Chloride 3.26mmol
A. Calcium Chloride 6.8mmol
Which of the following is not used in the management of hyperkalemia secondary to AKI?
A. IV Calcium (10%) 10mL of Calcium gluconate (2.26mmol) or Calcium chloride (6.8mmol
B. Insulin
C. Salbutamol
D. Ivabradine
D. Ivabradine
Which of the following management strategy works through activating the Na+,K+-ATPase?
A. IV Calcium
B. Insulin
C. Salbutamol
D. None of the above
B. Insulin
Which of the following management strategy works through enhancing the Na+,K+-ATPase?
A. IV Calcium
B. Insulin
C. Salbutamol
D. None of the above
C. Salbutamol
Which of the following management strategy works through enhancing the reducing the depolarisation effect of K+ on cardiomyocytes?
A. IV Calcium
B. Insulin
C. Salbutamol
D. None of the above
A. IV Calcium
Outline the stages of AKI recovery, regarding physiology.
- Initiation (Kidney Injury):
• Sx of underlying illness causing AKI
• Hours -> Days - Oliguric/Anuric Phase:
• Reduced urine production: Oliguria cf Anuria
• Urea retention
• Creatinine retention
-> Azotemia
• Complications: Fluid retention/Hyperkalemia/Metabolic acidosis/Uremia/Lethargy/Asterixis
• -> < 2 weeks - Polyuric Phase:
• GFR returns -> Increased urine production (relative to previous)
• Complications: Loss of electrolytes and water/dehydration/hyponatremia/hypokalemia
• -> 3 weeks - Recovery Phase:
• Kidney function and urine production normalize
• -> Up to 2 years
Why is GFR not an accurate measurement of renal function in AKI?
Creatinine not reached steady state (120 hours) of increasing creatinine to reach new steady state ≈ large change in GFR would be required to represent change in creatinine level
What should you do if there is not a reference creatinine available what should you do?
A. Estimate their Creatinine
B. Repeat in 24 hours
C. Use a Creatinine of a similar patient
D. Wait and see based on symptom presentation
B. Repeat in 24 hours
What are sick day rules regarding AKI?
List the drugs to be stopped as part of Sick Day Rules.
What is the evidence for this?
nwell with D+V, stop taking medications listen in Medicine Sick Day Rules for 24-48 hours of eating and drinking normally then continue if condition improves
- ACEi - ARBs - NSAIDs - Diuretics - Metformin
Evidence: D+V ≈ dehydration≈ hypovolemia ≈ renal hypoperfusion ≈ increased % of AKI thus stop drugs already implicated in renal perfusion
What is a urinary cast?
Casts are cylindrical structures composed of mucoprotein (Tamm-Horsfall mucoprotein) secreted by epithelial cells lining renal tubule which indicate haematuria/pyuria is of glomerular or renal tubular origin
What protein are casts made of?
A. Glycoprotein
B. Lipoprotein
C. Tamm-Horsfall mucoprotein
D. Bence-Jones protein
C. Tamm-Horsfall mucoprotein
Where is a RBC cast most likely to be derived from?
A. Medullary interstitium
B. Glomerulus
C. Mesangium
D. Tubules
B. Glomerulus
Where is a WBC cast most likely to be derived from?
A. Medullary interstitium
B. Glomerulus
C. Mesangium
D. Tubules
A. Medullary interstitium
Where is a Granular cast most likely to be derived from?
A. Medullary interstitium
B. Glomerulus
C. Mesangium
D. Any region, non-specific
D. Any region, non-specific
Where is a Waxy cast most likely to be derived from?
A. Medullary interstitium
B. Glomerulus
C. Tubules
D. Any region, non-specific
C. Tubules
Where is a Hyaline cast most likely to be derived from?
A. Medullary interstitium
B. Glomerulus
C. Tubules
D. Any region, non-specific
D. Any region, non-specific
Which of the following diseases is most likely to generate a Granular cast?
A. Advanced kidney disease
B. Acute tubular necrosis
C. Pyelonephritis
D. Tumour
B. Acute tubular necrosis
Which of the following diseases is most likely to generate a RBC cast?
A. Advanced kidney disease
B. Glomerulonephritis
C. Pyelonephritis
D. Tumour
B. Glomerulonephritis
Which of the following diseases is most likely to generate a WBC cast?
A. Advanced kidney disease
B. Glomerulonephritis
C. Pyelonephritis
D. Tumour
C. Pyelonephritis
Which of the following is a pre-renal cause of AKI?
A. Glomerulonephritis
B. CAKUT
C. Hydronephrosis
D. Renal Artery Stenosis
D. Renal Artery Stenosis
Which of the following is a pre-renal cause of AKI?
A. Glomerulonephritis
B. CAKUT
C. Hydronephrosis
D. Hypovolemia
D. Hypovolemia
Which of the following is a pre-renal cause of AKI?
A. Glomerulonephritis
B. CAKUT
C. NSAID overuse
D. Hydronephrosis
C. NSAID overuse
Which of the following is a renal cause of AKI?
A. Glomerulonephritis
B. Urothelial tumour
C. NSAID overuse
D. Nephrolithiasis
A. Glomerulonephritis
Which of the following is a renal cause of AKI?
A. Urothelial tumour
B. Acute Tubular Necrosis
C. NSAID overuse
D. Nephrolithiasis
B. Acute Tubular Necrosis
Outline the pathophysiology of Acute Tubular Necrosis.
ABX/PPIs/Immunotherapy agents/Diuretics/H2a/Allopurinol/ Warfarin/Infection/Systemic Diseases/Malignancies/Idiopathic -> antigen-initiated cell-mediated injury ≈ inflammatory cell infiltrate in renal interstitium and tubules ≈ damage to PT + ThAL ≈ cell death –> cast formation ≈ obstruction ≈ reduced GFR ≈ RAAS activation ≈ aldosterone release ≈Na+ reabsorption + H20 ≈ increased urine osmolarity ≈ ADH secretion ≈ H20 + urea resorption
What is the MOA by which tacrolimus causes an AKI?
A. Efferent arteriole vasodilation
B. Afferent arteriole vasoconstriction
C. Renal artery vasoconstriction
D. Reduced cardiac output
B. Afferent arteriole vasoconstriction
What is the MOA by which cyclosporine causes an AKI?
A. Efferent arteriole vasodilation
B. Afferent arteriole vasoconstriction
C. Renal artery vasoconstriction
D. Reduced cardiac output
B. Afferent arteriole vasoconstriction
Which is the primary pathogen causing Haemolytic Uremic Syndrome?
A. Proteus
B. E.Coli
C. Streptococcus Pyogenes
D. Haemophilus influenzae
B. E.Coli
Which of the following biological treatments is used in the management of HUS?
A. Omalizumab
B. Infliximab
C. Etanercept
D. Eculizumab
D. Eculizumab
When is a Red Cell Transfusion indicated in HUS?
A. Hct > 18%
B. Hct < 18%
C. Hb < 18%
D. Hb > 18%
B. Hct < 18%
What type of hypersensitivity reaction is RPGN?
A. Type 1
B. Type 3
C. Type 4
D. Type 2
B. Type 3
or
D. Type 2
What is the definition for Oliguria?
A. < 400mL/24 hours
B. < 40mL/12 hours
C. < 100mL/12 hours
D. < 100mL/24 hours
A. < 400mL/24 hours
What is the definition for Oliguria?
A. < 400mL/24 hours
B. < 40mL/12 hours
C. < 100mL/12 hours
D. < 100mL/24 hours
D. < 100mL/24 hours
Which of the following is not a type of CAKUT?
A. Potters Syndrome
B. Renal Hypoplasia
C. Horseshoe kidney
D. Hydronephrosis
D. Hydronephrosis
Which of the following is not a symptom of Potters Sequence?
A. Talipes Equinovarus
B. Oligohydramnios
C. Pulmonary Hypoplasia
D. Ventricular septal defect
D. Ventricular septal defect
Mnemonic: Potters Sequence Pulmonary hypoplasia Oligohydramnios Talipes equinovarus Craniofacial abnormalities
Which of the following is not a symptom of Potters Sequence?
A. Talipes Equinovarus
B. Growth acceleration
C. Craniofacial abnormalities
D. Pulmonary Hypoplasia
B. Growth acceleration
Mnemonic: Potters Sequence Pulmonary hypoplasia Oligohydramnios Talipes equinovarus Craniofacial abnormalities
What type of AKI would Nephrolithiasis cause?
A. Pre-renal
B. Renal
C. Post-renal
D. None of the above
C. Post-renal
What type of AKI would Bilateral Renal Agenesis cause?
A. Pre-renal
B. Renal
C. Post-renal
D. None of the above
C. Post-renal
Which renal calculi is caused by hypercalciuria?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
A. Calcium Oxalate
Which renal calculi is caused by hyperoxaluria?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
A. Calcium Oxalate
Which renal calculi is caused by hypocitruturia?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
A. Calcium Oxalate
Which renal calculi is caused by hyperuricemia?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
B. Uric acid
Which renal calculi is caused by urease-producing bacteria?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
C. Struvite
Which renal calculi is caused by cystinuria?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
D. Cystine
Which renal calculi is caused by hyperparathyroidism?
A. Calcium Oxalate
B. Uric acid
C. Calcium Phosphate
D. Cystine
C. Calcium Phosphate
Which renal calculi has a biconcave dumbbell morphology?
A. Calcium Oxalate
B. Uric acid
C. Calcium Phosphate
D. Cystine
A. Calcium Oxalate
Which renal calculi has a needle-shaped morphology?
A. Calcium Oxalate
B. Uric acid
C. Calcium Phosphate
D. Cystine
B. Uric acid
Which renal calculi has a staghorn morphology?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
C. Struvite
Which renal calculi has a coffin-lid morphology?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Cystine
C. Struvite
Which renal calculi has a wedge-shaped appearance?
A. Calcium Oxalate
B. Uric acid
C. Struvite
D. Calcium Phosphate
D. Calcium Phosphate
Which renal calculi has a hexagon appearance?
A. Calcium Oxalate
B. Uric acid
C. Cystine
D. Calcium Phosphate
C. Cystine
Which renal calculi may not show up on radiological imaging?
A. Calcium Oxalate
B. Uric acid
C. Cystine
D. Calcium Phosphate
B. Uric acid
A 62 year old gentleman comes in presenting with thirst and fatigue. He has no significant past medical history and no family history of kidney disease. His last blood tests in 2015 were unremarkable , you order blood tests (including U+Es) which come back as:
Sodium 139 (135-145mmol/L)
Potassium 6.3 (3.3-5.5mmol/L)
Creatinine 423 (< 90mmol/L)
Urea 24.3 (1.8-7.1mmol/L)
pH 7.2 (7.35-7.45)
Bicarbonate 15.3 (22-28mmol/L)
Lactate 2.1 (0.5-1.8mmol/L)
Looking at these results, what is your initial observations?
Hypercreatinemia (?) - Do not know baseline, could be normal
Hyperkalemia
Uremic
Acidotic
Hypobicarbonatemia
Hyperlactatemia
What mnemonic can be used to remember the management of a patient with a suspected AKI? Outline the steps
Mnemonic RENAL DRS26
Record baseline Serum Creatinine
Exclude obstruction
Nephrotoxic drugs
Assess fluid volume
Losses (output) ± catheterisation
Dipstick test
Review patient
Screen (Acute Renal Screen)
26umol»_space;>
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: On Kardex
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
Which TWO drugs are most likely to contribute
to his haematemesis?
A. Amlodipine 5mg od
B. Aspirin 75mg od
C. Digoxin 125mcg od
D. Ibuprofen 400mg tid
E. Metformin 500mg bd
F. Ramipril 10mg od
G. Senna 15mg od
H. Simvastatin 20mg od
B. Aspirin 75mg od
D. Ibuprofen 400mg tid
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: On Kardex
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
Which TWO drugs might impair renal function?
A. Amlodipine 5mg od
B. Aspirin 75mg od
C. Digoxin 125mcg od
D. Ibuprofen 400mg tid
E. Metformin 500mg bd
F. Ramipril 10mg od
G. Senna 15mg od
H. Simvastatin 20mg od
B. Aspirin 75mg od
D. Ibuprofen 400mg tid
E. Metformin 500mg bd
F. Ramipril 10mg od
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: On Kardex
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
Which TWO drugs should be prescribed at
night?
A. Amlodipine 5mg od
B. Aspirin 75mg od
C. Digoxin 125mcg od
D. Ibuprofen 400mg tid
E. Metformin 500mg bd
F. Ramipril 10mg od
G. Senna 15mg od
H. Simvastatin 20mg od
G. Senna 15mg od
H. Simvastatin 20mg od
OR
E. Metformin 500mg bd
(taken in evening)
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: On Kardex
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
Which TWO drugs might require dose review?
A. Amlodipine 5mg od
B. Aspirin 75mg od
C. Digoxin 125mcg od
D. Ibuprofen 400mg tid
E. Metformin 500mg bd
F. Ramipril 10mg od
G. Senna 15mg od
H. Simvastatin 20mg od
A. Amlodipine 5mg od
B. Aspirin 75mg od
C. Digoxin 125mcg od
D. Ibuprofen 400mg tid
F. Ramipril 10mg od
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: On Kardex
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
When considering the cause of the haematemesis what aspect of the history would be important?
A. Alcohol
B. Close contact with H.pylori
C. Smoking
D. Spicy foods
E. Stress
A. Alcohol
B. Close contact with H.pylori
C. Smoking
A 65 year old man is admitted to the medical ward for investigation of two episodes of haematemesis in the previous month.
PMHx: HTN, T2Dm, AF
DHx: Amlodipine; Metformin; Digoxin; Aspirin; Ibuprofen, Ramipril
Investigations: Na+ 142mmol/L (137-144); K+ 4.6mmol/L (3.5-4.9); U 7.6mmol/L (2.5-7.0); Cr 180 umol/L (60-110)
List all possible causes of this patient’s renal impairment.
- NSAIDs
- Metformin
- Alcoholism
- Digoxin
- Ramipril
- Age
- Idiopathic/ Autoimmune
A 75 year old man is admitted to hospital with worsening shortness of breath and cough with increased sputum production which is coloured green. Previous medical history – hypertension and COPD
Drug history – amlodipine, aclidinium/formoterol combination inhaler
Social history – longstanding smoker
O/E:
Temp 36.8Oc, HR 96/min, regular rhythm, BP 165/90 mmHg, RR 22/min, O2 sats 90% breathing air. Respiratory exam reveals widespread expiratory wheeze.
Investigations – CXR shows hyper-expansion of the lung fields and some old scarring at the left apex
What is your differential diagnosis?
Diagnosis –infective exacerbation of COPD.
What class of drug is amlodipine and how does it work in management of hypertension?
- CCB (DHP)
- Act on vasculature to reduce HTN
List 2 common side-effects of amlodipine
- Headaches
- Ankle edema
- Nausea
A 75 year old man is admitted to hospital with worsening shortness of breath and cough with increased sputum production which is coloured green. Previous medical history – hypertension and COPD
Drug history – amlodipine, aclidinium/formoterol combination inhaler
Social history – longstanding smoker
O/E:
Temp 36.8Oc, HR 96/min, regular rhythm, BP 165/90 mmHg, RR 22/min, O2 sats 90% breathing air. Respiratory exam reveals widespread expiratory wheeze.
Investigations – CXR shows hyper-expansion of the lung fields and some old scarring at the left apex
Apart from what the patient came in on, name 4 other drug treatment options suitable at this stage?
- Ramipril
- Losartan/Candesartan
- Furosemide
- Inhaled corticosteroid e.g. Butenone?
- ABX: Amoxicillin
There are risks associated with prescribing in renal impairment. Which of the following drugs will most likely require review in patients with moderate to severe renal impairment?
A. paracetamol
B. Montelukast
C. Ibuprofen
D. amoxicillin
E. omeprazole
C. Ibuprofen
What are the three terms used for the different reasons for administering intravenous fluids?
- Maintenance
- Replacement
- Resuscitation
O/E BP 90/54mmHg, HR 110/min, CRT 4secs,
chest clear
A. 5%Glucose500mls@75mls/hr
B. 0.9%Saline500mls@ 2000mls/hr
C. 0.45% saline 4%glucose 500mls @ 75mls/hour
D. Hartmann’s 500mls @ 2000mls/hour
E. 10% Dextrose 200mls @ 800mls/hour
B. 0.9%Saline500mls@ 2000mls/hr
