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Dr. Sanjeev Mehta MDDr. Sanjeev Mehta MD
Ahmedabad, INDIAAhmedabad, INDIA
www.urolab.net
Metabolic Evaluation
&
Stone Analysis
Practical implications
Role of laboratory
• What lab can not tell you, you will not
know.
• What it tells you in error, you will not
correct by using your instincts, your
medical experience or your art.
• Misdirected treatment : unreasonable
expenses.
• The Kidney Stone Handbook; Gail Savitz & co auth.
Stone : Supersaturation of Urine
Stone Promoting and
Inhibiting Factors
PROMOTORS INHIBITORS
Calcium Inorganic : Magnesium
Sodium Phosphorus
Oxalate Citrate
Urate Organic : Nephrocalcin
Cystine Tomm-Horsfall Protein
Low Urine Ph Urinary Prothrombin fragment.
Tomm-Horsfall Protein
Bacterial products
Evaluation of Stone Disease
ROUTINE BLOOD AND URINE TESTS
STONE ANALYSIS.
24 HRS URINE METABOLIC PROFILE
New advances in Stone analysis, Blood and Urinary
Chemical analysis can find out 90-95% cause.
Clinical usefulness
1.Identify treatable metabolic abnormality
2.Identify underlying medical disease that
predisposes to stone formation.
3.Outline a treatment plan.
A. Routine Tests
BLOOD
low K, and HCO3- RTA
High Uric acid - Uric acid
diathesis
High Calcium- pri
hyperparathyroidism
Low phosphorus- renal
phosphorus leak.
Parathyroid ; sos
URINE
pH > 7.5 – infection
lithiasis
pH < 5.5 – Uric acid
lithiasis
Sediments for
crystalluria
Urine culture
Qualitative cystine
Renal Stone Analysis
• Essential step in the examination and initial
treatment of Urolithiasis.
• Yields fundamental information about ;
- Metabolic abnormality.
- Presence of infection.
- Possible artifacts.
- Drug metabolism.
Technique
Integrated
analysis with
Infra-red
spectrometry
Xenthene and
Ca.oxalate
Dihydrite
INTEGRETED
ANALYSIS ;
Mixed Stone
11
Actually up to 65 different chemical
compounds are found in urinary calculi.
Clinical significance of Stone
analysis
• Three categories :
1.Composition and hardness of Renal
Stones.
2.Composition and its predictive value.
3.Composition and related metabolic
abnormalities.
Kourambas J, Aslan P, Teh CL, Mathias BJ, Preminger GM.J Endourol. 2001
Mar;15(2):181-6
Clinical Significance: Hardness
pattern in Stone.
• Useful in describing consistency in individual.
• Formulation of treatment strategies.
- Number of re-treatments.
- Number of Shock waves.
• Energy index (KV x number of shock waves).
Ringdén I, Tiselius HG, Scand J Urol Nephrol. 2007;41(4):316-23
Hardness Factor of Stone
Calcium Oxalate Dihydrate 1.0
Calcium Oxalate Monohydrate 1.3
Hydroxy-peptite 1.1
Brushite 2.2
Uric Acid/ Urate 1.0
Cystine 2.4
Carbonate Apatite 1.3
Struvite 1.0
Mixed Stone 1.0
* Ringden I, Scand J Urol Nephrol.2007;41(4):316-23
Clinical value : Calcium
• Present in approximately 80% stones.
• Combines with phosphate or oxalate or both.
• Risk factors : hypercalciuria,
Hyperoxaluria.
hyperuricosuria.
predominantly acid or alk urine.
hypocitraturia.
low urine volume.
Calcium Stones …..
Pure calcium Stones
• More Acid urine
• Low Urine volume
• High Oxalate
excretion
Mixed Stone formers
• pH is higher
• High Calcium
• High Calcium
excretion
• High recurrence rate
* Schroeppel j Smith et all ; J Am Soc Nephrol
1997;8:568A
Calcium Stone…..
Ca-oxalate Monohydrate
• Hypo- megnesuria
• Acidic Urine
• Low Urine volume
• Hardness +
• Ca-ox Dihydrate
• Hyper-calciuria
• Alkaline Urine
• Hypo-citraturia
• Hardness ; less
Renal tubular acidosis
Carbonate apattite
• Consider RTA
• Increases with amount
• (5-39%)
Brushite Stones
• Consider RTA
Struvite Stone
Magnesium Ammonium Phosphate
• Mixed Stone : Infection.
‘Proteus’
• Strains of staphylococci, pseudomonas and
kelbsiella.
• Rarely; E.coli.
• Urine Ph. Is < 7.5
Ammonium Urate
• Calcium oxalate – containing calculi, may start
hyperuricosuria.
• Elders : associated with infection.
• Children : May as result of hyperuricosuria,
but No UTI
Brushite : Amm. Calcium
Phosphate
• Sizable stone burden. Increasing trend
• High recurrence rate , 3 yrs
• Familial tendency
• Hypercalciurea and underlying metabolic
abnormality.
• Extreme Alkaline Urine.
J Urol. Oct 2010; 184(4): 1367–1371.
Dahilite ( Carbonate apatite)
• Phosphate stone
• Infection in body.
• May not accompanying sign of disease.
• RTA
• Disorder of phosphate metabolism.
• Rare in pure form ( 2-3%).
Uric Acid
URIC ACID
• Hyperuricemia, hyperuricosuria.
• Low Urine Ph. < 6.2
• Causes:
- Gout.
- Myeloproliferative dis.
- Chemotherapy and
Radiotherapy.
Cystine
CYSTINE
• Cysteinuria.
• Autosomal recessive
disorder.
• Occurs predominantly
in pure form.
• XENTHENE
Most frequent causes:
- Xanthinuria.
- Absence of Xanthene
oxidase.
• Genetic autosomal
hereditary recessive
enzyme disorder.
• Trigger : Allopurinol
Treating Gout.
Urine: Metabolic Evaluation
24 hrs Urine collections: multiple parameters
Stone risk factors : Quantitation
Volume and pH
Calcium
Oxalate
Citrate
Uric acid.
Creatinine
Metabolic Evaluation: 24 hrs
Urine
• Dietary risk factors:
Sodium,
Potassium
Magnesium
Urinary analysts : phosphorus, sulphate, Urea
Children : state sample
Repeat 24 hrs Urine collection 4-6 weeks post
interventi
GOLD STANDARD
Supersaturation
value.
•High risk parameter
can be monitored.
Graphic presentation
Super-saturation : Gold standard….
Conclusion
• Advancement in laboratory can now diagnose
cause of stone formation uo tp 90% cases.
• By appropriate Stone analysis and metabolic
evaluation can effectively treat impact of
Nephrolithiasis and prevent recurrence .
Conclusion: Significance
• Advancement in laboratory can diagnise cause
of Stone disease up to 90%
• Impact mitigated by appropriate metabolic
evaluation.
• Identify risk factor.
• Focused medical treatment
• Significantly reduces recurrence
• Social and financial burden.
• Batter quality of life
Thank you !
For further details
contact:
sanjeev@urolab.net
Phone: +91 79 40380380

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Dr. Sanjeev Mehta MD Stone Analysis and Metabolic Evaluation

  • 1. Dr. Sanjeev Mehta MDDr. Sanjeev Mehta MD Ahmedabad, INDIAAhmedabad, INDIA www.urolab.net Metabolic Evaluation & Stone Analysis Practical implications
  • 2. Role of laboratory • What lab can not tell you, you will not know. • What it tells you in error, you will not correct by using your instincts, your medical experience or your art. • Misdirected treatment : unreasonable expenses. • The Kidney Stone Handbook; Gail Savitz & co auth.
  • 4. Stone Promoting and Inhibiting Factors PROMOTORS INHIBITORS Calcium Inorganic : Magnesium Sodium Phosphorus Oxalate Citrate Urate Organic : Nephrocalcin Cystine Tomm-Horsfall Protein Low Urine Ph Urinary Prothrombin fragment. Tomm-Horsfall Protein Bacterial products
  • 5. Evaluation of Stone Disease ROUTINE BLOOD AND URINE TESTS STONE ANALYSIS. 24 HRS URINE METABOLIC PROFILE New advances in Stone analysis, Blood and Urinary Chemical analysis can find out 90-95% cause.
  • 6. Clinical usefulness 1.Identify treatable metabolic abnormality 2.Identify underlying medical disease that predisposes to stone formation. 3.Outline a treatment plan.
  • 7. A. Routine Tests BLOOD low K, and HCO3- RTA High Uric acid - Uric acid diathesis High Calcium- pri hyperparathyroidism Low phosphorus- renal phosphorus leak. Parathyroid ; sos URINE pH > 7.5 – infection lithiasis pH < 5.5 – Uric acid lithiasis Sediments for crystalluria Urine culture Qualitative cystine
  • 8. Renal Stone Analysis • Essential step in the examination and initial treatment of Urolithiasis. • Yields fundamental information about ; - Metabolic abnormality. - Presence of infection. - Possible artifacts. - Drug metabolism.
  • 11. 11 Actually up to 65 different chemical compounds are found in urinary calculi.
  • 12. Clinical significance of Stone analysis • Three categories : 1.Composition and hardness of Renal Stones. 2.Composition and its predictive value. 3.Composition and related metabolic abnormalities. Kourambas J, Aslan P, Teh CL, Mathias BJ, Preminger GM.J Endourol. 2001 Mar;15(2):181-6
  • 13. Clinical Significance: Hardness pattern in Stone. • Useful in describing consistency in individual. • Formulation of treatment strategies. - Number of re-treatments. - Number of Shock waves. • Energy index (KV x number of shock waves). Ringdén I, Tiselius HG, Scand J Urol Nephrol. 2007;41(4):316-23
  • 14. Hardness Factor of Stone Calcium Oxalate Dihydrate 1.0 Calcium Oxalate Monohydrate 1.3 Hydroxy-peptite 1.1 Brushite 2.2 Uric Acid/ Urate 1.0 Cystine 2.4 Carbonate Apatite 1.3 Struvite 1.0 Mixed Stone 1.0 * Ringden I, Scand J Urol Nephrol.2007;41(4):316-23
  • 15. Clinical value : Calcium • Present in approximately 80% stones. • Combines with phosphate or oxalate or both. • Risk factors : hypercalciuria, Hyperoxaluria. hyperuricosuria. predominantly acid or alk urine. hypocitraturia. low urine volume.
  • 16. Calcium Stones ….. Pure calcium Stones • More Acid urine • Low Urine volume • High Oxalate excretion Mixed Stone formers • pH is higher • High Calcium • High Calcium excretion • High recurrence rate * Schroeppel j Smith et all ; J Am Soc Nephrol 1997;8:568A
  • 17. Calcium Stone….. Ca-oxalate Monohydrate • Hypo- megnesuria • Acidic Urine • Low Urine volume • Hardness + • Ca-ox Dihydrate • Hyper-calciuria • Alkaline Urine • Hypo-citraturia • Hardness ; less
  • 18. Renal tubular acidosis Carbonate apattite • Consider RTA • Increases with amount • (5-39%) Brushite Stones • Consider RTA
  • 19. Struvite Stone Magnesium Ammonium Phosphate • Mixed Stone : Infection. ‘Proteus’ • Strains of staphylococci, pseudomonas and kelbsiella. • Rarely; E.coli. • Urine Ph. Is < 7.5
  • 20. Ammonium Urate • Calcium oxalate – containing calculi, may start hyperuricosuria. • Elders : associated with infection. • Children : May as result of hyperuricosuria, but No UTI
  • 21. Brushite : Amm. Calcium Phosphate • Sizable stone burden. Increasing trend • High recurrence rate , 3 yrs • Familial tendency • Hypercalciurea and underlying metabolic abnormality. • Extreme Alkaline Urine. J Urol. Oct 2010; 184(4): 1367–1371.
  • 22. Dahilite ( Carbonate apatite) • Phosphate stone • Infection in body. • May not accompanying sign of disease. • RTA • Disorder of phosphate metabolism. • Rare in pure form ( 2-3%).
  • 23. Uric Acid URIC ACID • Hyperuricemia, hyperuricosuria. • Low Urine Ph. < 6.2 • Causes: - Gout. - Myeloproliferative dis. - Chemotherapy and Radiotherapy.
  • 24. Cystine CYSTINE • Cysteinuria. • Autosomal recessive disorder. • Occurs predominantly in pure form. • XENTHENE Most frequent causes: - Xanthinuria. - Absence of Xanthene oxidase. • Genetic autosomal hereditary recessive enzyme disorder. • Trigger : Allopurinol Treating Gout.
  • 25. Urine: Metabolic Evaluation 24 hrs Urine collections: multiple parameters Stone risk factors : Quantitation Volume and pH Calcium Oxalate Citrate Uric acid. Creatinine
  • 26. Metabolic Evaluation: 24 hrs Urine • Dietary risk factors: Sodium, Potassium Magnesium Urinary analysts : phosphorus, sulphate, Urea Children : state sample Repeat 24 hrs Urine collection 4-6 weeks post interventi
  • 27. GOLD STANDARD Supersaturation value. •High risk parameter can be monitored. Graphic presentation
  • 28. Super-saturation : Gold standard….
  • 29.
  • 30. Conclusion • Advancement in laboratory can now diagnose cause of stone formation uo tp 90% cases. • By appropriate Stone analysis and metabolic evaluation can effectively treat impact of Nephrolithiasis and prevent recurrence .
  • 31. Conclusion: Significance • Advancement in laboratory can diagnise cause of Stone disease up to 90% • Impact mitigated by appropriate metabolic evaluation. • Identify risk factor. • Focused medical treatment • Significantly reduces recurrence • Social and financial burden. • Batter quality of life
  • 32. Thank you ! For further details contact: sanjeev@urolab.net Phone: +91 79 40380380