lecture 2-introduction to renal medicine - ii

8/2/2019 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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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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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


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


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

lecture 2-introduction to renal medicine - ii

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