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Clinical Biochemistry and Renal Disease

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Clinical Biochemistry and Renal Disease. Dr Vivion Crowley Consultant Chemical Pathologist St James’s Hospital. What are the primary functions of the Kidney. Excretion of waste – urea, creatinine, urate Water and electrolyte balance Acid-base balance

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slide1

Clinical Biochemistry and Renal Disease

Dr Vivion Crowley

Consultant Chemical Pathologist

St James’s Hospital

slide2

What are the primary functions of the Kidney

  • Excretion of waste – urea, creatinine, urate
  • Water and electrolyte balance
  • Acid-base balance
  • Regulation of systemic circulation – Renin and Aldosterone
  • Production of hormones – Vit D, Erythropoietin
  • Participates in gluconeogenesis
slide3

What is the primary functional unit of the Kidney

  • Nephron
  • Proximal tubule – Na, K, H20, HCO3, PO4, aminoacids
  • Loop of Henle – Countercurrent multiplier system
  • Distal tubule – Na, K, Acid-base balance
  • Collecting duct – Osmoregulation
slide4

How do we assess Renal Function?

  • Glomerular filtration rate (GFR)
  • key measure of functioning renal mass
  • the sum of filtration rate of functioning nephrons
  • Normal GFR 120-130ml/min/1.73 m2 in young adults
  • -decreases with age
  • (consider GFR as approximately 100ml/min)
slide5

Are there plasma markers of GFR?

  • Plasma Urea
  • Breakdown product of protein metabolism
  • Produced in liver
  • Plasma Creatinine
  • Derived from creatine in muscle
  • Related to muscle mass
slide8

Caveats in the interpretation of PUrea and Creatinine

  • Increases in Urea and Creatinine above the upper
  • reference range are evident only when GFR is reduced
  • by 50% or normal
  • A normal urea and crea may not reflect a normal GFR
  • Consider other causes of elevations in Urea and Crea
slide9

Urinary clearance of filtration markers is

used to estimate GFR

  • Ideal filtration marker
  • Neither secreted nor absorbed by kidney tubule
  • Exogenous
  • Inulin
  • IV infusion
  • Difficult to assay
  • Other markers include Cr51-EDTA, I125-iothalamate
slide10

Endogenous filtration markers of GFR

  • Urinary urea as a filtration marker
  • easy to measure
  • Freely filtered at glomerulus
  • Reabsorbed in proximal and sistal tubule
  • Significantly Underestimates GFR
  • Urinary creatinine as a filtration marker
  • Most commonly used
  • Freely filtered at glomerulus
  • Secreted in renal tubule
  • Overestimates GFR by 10-20ml/min
  • Requires 24h urine collection
  • Problematic for patients
  • Over or under collection
slide11

Equations using serum creatinine can

be used to estimate GFR

  • Cockcroft–Gault equation
  • -Uses age, wt, gender, plasma creatinine
  • Really an estimation of creatinine clearance
  • MDRD equation for eGFR
  • Estimate of GFR rather than Creatinine clearance
  • 4 variable eqn.
  • Plasma crea, age, gender, ethnicity
  • Increasingly used to classify Chronic kidney Disease (CKD)
slide12

Equations used to estimate GFR

Cockcroft–Gault equation

MDRD equation for eGFR

slide14

Other potential markers of GFR

  • Plasma Cystatin C
  • Cysteine protease inhibitor
  • Freely filterd by gloerulus
  • Almost completelyReabsorbed and catbolised by tubules
  • Plasma levels correlate with GFR
  • Expensive test
  • Not routinely available
slide15

What is Renal Failure?

A deterioration in renal function leading to a

complex of symptoms and signs

Azotaemia

– increase in nitrogenous substances e.g. urea, crea

Uraemia

– symptoms of confusion etc. associated with azotaemia

slide16

How is Renal Failure classified?

  • Time of onset
  • Acute renal failure
  • An abrupt reduction in GFR
  • Usually over hours or days
  • Oliguria <400ml/day, anuria <100ml/day, polyuria>3L/day
  • Chronic Renal Failure
slide18

What are the causes of acute renal failure (ARF)

  • Prerenal
  • Volume depletion e.g. vomiting, diarrhoea, fistulae, renal Na wasting
  • Sepsis
  • Cirrhosis
  • Renal artery stenosis
  • Intrarenal
  • Vascular
  • Glomerular
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis
  • Postrenal
  • Ureteral obstruction
  • Bladder obstruction
slide19

What is the biochemical profile associated

with pre-renal failure?

  • 53y old male
  • 3/7 hx of vomiting and diarrhoea
slide21

What is the biochemical profile associated

with established ARF e.g. ATN?

slide22

What are the causes of CRF?

  • Diabetic nephropathy
  • Glomerulonephritis
  • Hypertensive nephropathy
  • Tubulointerstitial disease
  • Polycystic kidney disease
  • Reflux nephropathy
  • In many instances cause is unknown
slide23

What are the metabolic consequences of CRF

  • Na handling
  • - reduced Na excretory capacity – oedema, HT
  • H2O handling
  • Urine becomes isosmotic – inability to dilute or conc urine
  • Hyperkalaemia
  • Acidosis – RTA and high anion gap
  • Bone disease
  • Hypocalcaemia
  • Hyperphosphataemia
  • Secondary hyperparathyroidism
  • Acidosis
  • Anaemia – reduced erythropoietin
  • Dyslipidaemia
  • Endocrine – hyperprolactinaemia, hypogonadism
slide25

What is the biochemical profile associated with ESRD

65y old male

C/O malaise, tiredness, nocturia

O/E BP 182/110, pale

slide27

Causes of Tubulointerstitial Disease

  • Immunologic – SLE, Amyloidosis, Sjoogren’s syndrome, MM
  • Drugs – NSAIDs, Chemotherapy
  • Heavy metals- lead, cadmium, mercury
  • Sickle cell disease
  • Lymphoma
  • Pyelonephritis
  • Sarcoidosis
  • Hyepruricaemia (Gout)
slide29

How do you check for proteinuria?

  • Urine dipstick
  • Protein – detects albumin >200-300mg/L
  • Does not detect Bence-Jones protein (Ig light chains)
  • pH, Glucose, Hb, Bilirubin, Urobilinogen
  • Nitrite, Leukocyte esterase
  • Timed urine collection
  • 24h urine
  • First morning voided urine – Albumin:creatinine ratio
  • used in detecting microalbuminuria in DM
slide30

How is proteinuria classified?

  • Time:
  • Transient – exercise-related, acute illness
  • Persistent – requires further investigation
  • Cause:
  • UTI
  • Overflow proteinuria
  • - Bence-Jones, Amylase, Hb, Myoglobin, lysozyme
  • Orthostatic proteinuria
  • No proteinuria in first morning urine
  • Proteinuria detectable when patient ambulant
  • Glomerular
  • - Leaky glomerulus – glomerulonephritis
  • Tubular
  • - Tubulointerstitial disease
slide32

What is nephrotic syndrome?

  • Nephrotic range proteinuria >3.5g/24h
  • Hypoalbuminaemia
  • Oedema – periorbital, dependent
  • Hyperlipidaemia – marked hypercholesterolaemia
  • Causes
  • Primary renal disease – glomerulonephritis
  • Systemic disease – DM, amyloidosis, SLE
  • Multiple Myeloma
  • Infection – HepB, HIV, TB
  • Malignancy
  • Drugs – Gold, Penicillamine
  • Pre-eclampsia
slide33

Biochmeical investigation of Proteinuria should include:

  • Urine dipstick
  • Urine protein/creatinine ratio ( random urine sample)

>40mg/mmol suggests underlying proteinuria

24 hour urine collection for protein

> 300mg/24hr suggests proteinuria

slide34

What are the most common kidney stones?

  • Calcium Oxalate and Phosphate – 40%
  • Calcium Oxalate – 30%
  • Calcium Phosphate – 10%
  • Struvite (MgNH4PO4)– 10%
  • Urate – 7%
  • Cystine – 2%
  • Miscellaneous – Xanthine etc.- 1%
slide35

What factors predispose to nephrolithiasis?

  • Idiopathic Hypercalciuria
  • Primary hyperparathyrodism
  • Hyperoxaluria
  • 1o Autsomal recessive
  • 2o Small bowel resection, bypass or inflammation
  • Hyperuricosuria – associated with gout
  • Renal tubular acidosis
  • Cystinuria – cystinosis
  • UTI
  • Hypocitraturia
  • Idiopathic nephrolithiasis
  • Most likely a genetic predisposition
slide36

What is idipopathic hypercalciuria (IH)?

  • Hypercalciuria - Urine Ca > 10mmol/24h
  • IH
  • - affects 10% of population
  • 40% of renal stone formers
  • Absoprtive hypercalciuria
  • Intestinal calcium hyperabsorption
  • ? Increased sensivity to VitD
  • Renal phosphate leak
  • Renal hypercalciuria
slide37

How would you investigate a patient with Nephrolithiasis?

Plasma

Na, K, Urea, Creatinine, HCO3, Ca, PO4, Urate, PTH, VITD

Urine

- Dipstick for pH, protein

- 24 h urine collection

Ca, PO4, Mg, Urate

Occasionally – Oxalate, Citrate, Cystine, Xanthine

Direct stone analysis

Nonbiochemical investigation

- microbiology, radiology

slide38

Remember

Read Your Clinical Biochemistry Books!

slide39

Recommended Reading

Lecture Notes in Clinical Biochmesitry 7th Edition

G Beckett, S Walker, P Rae, P Ashby (Blackwell publishing)

Clinical Chemistry 5th Edition

W J Marshall, S K Bangert (Pubslished by Mosby)

An illustrated Colour text - Clinical Biochmeistry 3rd edition

Alan Gaw et al (Churchill Livingston)

Handbook of Clinical biochmeistry 1st Edition

R Swaminathan (Oxford University Press)

Clinical Chemistry in diagnosis and treatment

Philip Mayne (Edward Arnold)

A Guide to Diagnostic Clinical Chemistry 3rd Edition

Walmsely & White (Blackwell)

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