Lecture 2-Introduction to Renal Medicine - II
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Transcript of Lecture 2-Introduction to Renal Medicine - II
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Introduction to Renal Medicine - II
Dr Andrew LewingtonConsultant Renal Physician
Clinical Sub DeanLeeds Teaching Hospitals
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Outline of lecture
Consider the endocrine function of the
kidneys
Investigations
Clinical case
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Erythropoietin
Secretion of erythropoietin to stimulate red
blood cell maturation
Stimulatd by hypoxia
Clinical relevance
Patients with kidney failure develop
Anaemia
Recombinant erythropoietin can be prescribed
need for blood transfusions
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Calcium and Phosphate Metabolism
Vitamin D is activated by the kidneys
First stage performed in the liver
Second stage performed in the kidneys
1,25 dihydroxycholecalciferol
Increases absorption of calcium from the gut
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Calcium phosphate metabolism
Clinical relevance
Kidney failure
Decreased activation of vitamin D
Decreased calcium level
Stimulates secretion of parathyroid hormone ( four
glands in the neck)
Secondary hyperparathyroidism
Releases calcium from the bone
Develop bone disease
Renal osteodystrophy
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Blood pressure control
Kidneys intimately linked with blood pressure
control
Kidneys secrete renin
Patients with kidney disease often have high
blood pressure
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Signs and symptoms of chronic
kidney disease
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Glomerular filtration rate
Is an exact measure of kidney function
Accurate measurement requires the injection
of a radioactive tracer
Technetium Tc 99
Performed rarely except
Live kidney donors
Important to determine accurate kidney function prior todonation
Normal range 100-120 mls/min/1.73m2
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Glomerular filtration rate
Alternative is to perform
creatinine clearance
creatinine is released from muscle at a relatively
constant rate
Filtered by the kidneys
Some secretion by the proximal tubule kidneys
Requires blood tests
24-hour urine collection
creatinine clearance is a surrogate marker of GFR
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Glomerular filtration rate
In the clinic Estimated glomerular filtration rate (eGFR)
Requires
Age of patient
Sex of patient
Ethnicity
Serum creatinine
The eGFR roughly correlates with the % of kidney
function
e.g. eGFR=50 = 50% kidney function
Patients will need to commence dialysis if eGFR
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Investigations
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Investigations
Blood tests
Urea and electrolytes
Na
K
Urea
creatinine
Bicarbonate (HCO3) Chloride (Cl)
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Investigations
Arterial blood gases
pH
pO2 (oxygen concentration)
pCO2 (carbon dioxide concentration) BE (base excess)
Bic (bicarbonate) Cl (chloride)
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Investigations
Urine tests
Urinalysis (practical session later this morning)
pH
Haematuria ( blood)
Proteinuria ( protein
Glucose
Nitrites
leucocytes
Midstream urine
Clean catch of urine
Sent if urinary tract infection is suspected
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Investigations
Radiology
Abdominal x-ray
May identify calcification
Renal tract ultrasound
Assesses the size of the kidneys
Identifies any obstruction
CT KUB (kidneys ureter bladder) see next slide
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Investigations
Kidney biopsy
Required to diagnose intrinsic kidney disease
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Normal Focal segmental glomerulosclerosis
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Chronic kidney disease
Chronic kidney disease
Long-standing (> 3 months)
Usually progressive
Reversal unlikely
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Causes of Chronic kidney disease
Diabetes
Hypertension
Glomerulonephritis
Renal vascular disease
Inherited disorders e.g. polycystic
kidney disease Unknown
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Stages of Chronic Kidney Disease
CKD = chronic kidney disease; GFR = glomerular filtration rate.National Kidney Foundation. Am J Kidney Dis. 2003;42(suppl 3):S1-S201.
Stage Description
GFR(mL/min/1.73 m2)
1
2
3
4
5
Kidney damage withnormal or GFRKidney damage withmild GFRModerate GFRSevere GFRKidney failure
90
60-89
30-59
15-29
15 or dialysis
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Acute kidney injury
Previously known as acute renal failure
Abrupt deterioration in kidney function
occurring over a period of days or weeks
Many different causes
Potential to recover BUT
Not in all cases
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Acute kidney injury
AKI is diagnosed when
serum creatinine rises by 26mol/L from the
baseline value within 48 hours or
serum creatinine rises 1.5 fold from the baseline
value which is known or presumed to have
occurred within one week or
urine output is < 0.5ml/kg/hr for >6 consecutive
hours
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Acute kidney injury
after establishing a diagnosis of AKI the
severity of AKI can be staged
staging can be performed using serum
creatinine or urine output criteria
patients should be staged according to the
criteria that gives them the highest stage
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AKI stage Serum Creatinine criteria Urine output criteria
1 SCr increase 26 mol/L
or
SCr increase 1.5-2 fold from
baseline
< 0.5 mL/kg/hr for 6
consecutive hrs
2 SCr increase 2-3 fold frombaseline
< 0.5 mL/kg/hr for 12 hr
3 SCr increase 3 fold from
baseline
or
SCr increase 354 mol/L
or
initiated on RRT (irrespective of
stage at time of initiation)
< 0.3 mL/kg/hr for 24 hr
or
anuria for 12 hr
AKI Staging
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ACUTE KIDNEY INJURY
PRERENAL INTRINSIC POSTRENAL
ACUTE TUBULAR INTERSTITIAL ACUTE
INJURY NEPHRITIS GLOMERULONEPHRITIS
(10%) ( 5%)
ISCHAEMIA /SEPSIS TOXINS
ll
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Post-renal
renal calculiretroperitoneal
fibrosisprostatic
hypertrophycervical Caurethral
strictureobstructed
urinary catheter
intra-abdominal
hypertension
Pre-renal
Hypovolaemia
vomiting and
diarrhoeahaemorrhage
in effective
circulating
volumecardiac failure
septic shock
cirrhosis
DrugsACE inhibitors
Intrinsic
Glomerularglomerulonephritis
Tubularacute tubular injury/
necrosisrhabdomyolysismyeloma
Interstitial
interstitial nephritis
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Case presentation
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Case Presentation
71-year-old male
Admitted to outside hospital
Presenting Complaint cellulitis of legs (infection of legs)
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Case Presentation
Past medical history
hypertension
baseline blood pressure 150/90
Hypercholesterolaemia
Chronic kidney disease
Medications
angiotensin converting enzyme inhibitor (antihypertensive
medication) Statin (lower cholesterol)
Aspirin (antiplatelet medication)
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Case Presentation
on examination fever
BP 110/60 (lower than usual blood pressure)
cellulitis of legs
investigations
Hb 14.8 g/dl (normal)
WBC 16
albumin 30 SCr 125mol/L
eGFR 55 mls/min/1.73m2 (CKD stage 3)
CRP 140 (< 5) (inflammatory marker)
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Case Presentation
management
intravenous antibiotics
no fluid balance chart
96 hrs later
clinical assessment on ward round
BP 135/50
JVP not assessed
lungs clear
bilateral pitting ankle oedema
Furosemide (loop diuretic) prescribed
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Case Presentation
later that day
Na 144 mmol/L (135-145)
K 4.3 mmol/L (3.5-5.0)
Ur 32 mmol/L (3-5)
SCr 434 mol/L (
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Case presentation
diagnosis
acute kidney injury
Hypovolaemia (insufficient fluid in the
intravascular space)
Sepsis (infection leading to vasodilatation
and further lowering of blood pressure)
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Case Presentation
management plandecision not to give furosemide
iv fluids
0.9% sodium chloride
fluid balance chart
daily U&Es
renal tract ultrasound
small kidneys
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Case Presentation
48 hrs later 8 litres 0.9% sodium chloride
BP
Oliguric (decreased urine output) investigations
Na 151 mmol/L
K 4.4 mmol/L
Ur 23.8 mmol/L
Cl 125 mmol/L
SCr 476 mol/L
no bicarbonate measured
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Case Presentation
Diagnosis acute kidney injury (oliguric)
pulmonary oedema
Referred to renal unit
transfer to renal unit
8L positive fluid balance
pulmonary oedema
significant peripheral oedema of trunk and limbs
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What investigations would you
perform?
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Case Presentation
Investigations
Arterial blood gases
pH 7.04 (7.35-7.45)
pO2 12
pCO2 3.02 BE -13 (-2-2)
Bic 8 (22-30)
Cl 125 (98-107)
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Case Presentation
Metabolic acidosis
what type of metabolic abnormality?
Hyperchloraemic metabolic acidosis
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Case Presentation
Cause for acute kidney injury (AKI)?
pre-renal AKI
Hypovolaemia/hypotension
progressed to intrinsic AKI prolonged hypotension and ischaemia
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Case Presentation
Management
intermittent haemodialysis
4hrs with bicarbonate buffer
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Case Presentation
required dialysis for 4 weeks
recovered kidney function
SCr 135 mol/L
But not back to previous level
Left with worse chronic kidney disease
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Thank you
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Any Questions