Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Urea creatinine

4,364 views

Published on

Urea is the major end product of protein metabolism In humans.
Its formed in liver.

Published in: Health & Medicine
  • Be the first to comment

Urea creatinine

  1. 1. Tapeshwar Yadav (Lecturer) BMLT, DNHE, M.Sc. Medical Biochemistry
  2. 2.  Urea is the major end product of protein metabolism In humans.  Its formed in liver.  Urea biosynthesis occurs in four stages: (1) transamination, (2) oxidative deamination of glutamate, (3) ammonia transport, (4) reactions of the urea cycle
  3. 3.  ammonia is produced in various ways by tissues are rapidly removed from circulation by the liver and converted to urea. This is essential, since ammonia is toxic to the central nervous system.  Urea is water soluble ,conversion of ammonia to urea is a kind of detoxification.  This is the importance of urea excretion and its estimation.
  4. 4.  Any defect in any of the enzyme function of urea cycle can lead to various metabolic disorders.  More than 90% of urea is excreted through the kidneys(glomeruli), with losses through GIT and skin in minor fraction.  Determination of blood urea is important not only in many diseases of kidney but in a wide range of conds which r not primarily renal.
  5. 5. Causes of increase in serum urea  Causes r divided in pre-renal , renal and post-renal  PRE-RENAL : dehydration pyloric n intestinal obstruction with vomiting sever n prolonged diarrhea chrn intestinal obstruction without vomiting ulcerative colitis with severe chloride loss diabetic coma
  6. 6. RENAL :  acute glomerulonephritis  malignant hypertension  chronic pyelonephritis  hydronephrosis  congenital cystic kidney  renal tuberculosis  calcium deposition in kidney in hyperthyroidism n hypervitaminosis D.
  7. 7.  POST RENAL: enlargement of prostate stones in urinary tract stricture of the urethra tumors of the bladder affecting the ureter
  8. 8.  Cirrhosis of liver  Acute yellow atrophy of liver  Severe acidosis  Nephritis  Pregnancy
  9. 9.  BLOOD UREA: Diacetyl monoxime method principle when urea is heated with diacetyl(,containing two adjacent carbonyl group) under acidic condition yellow coloured compound is formed.the OD of the colour developed can be read at 420 nm.intensity of the color depends on conc of urea in serum.
  10. 10. additions BLANK STANDARD TEST Protein free filtrate _ _ 1ml Working standard _ 1ml _ Distilled water 1ml _ _ DAM reagent 0.4ml 0.4ml 0.4ml Acid mixture 1.6ml 1.6ml 1.6ml
  11. 11. OD of the test × conc of standard × 100 OD of the standard vol of the test = T/S×100 BUN(blood urea nitrigen): = blood urea level× 28/60 Normal value - 5 -20 mg/dl
  12. 12. Principle: urease hydrolyses urea to ammonia and CO2.the ammonia formed further reacts with a phenolic chromogen and hypo chloride to form a green colored complex. Intensity of colour is directly proportional to the amount of urea present in the sample. addition blank standard test Working reagent 1.0 ml 1.0ml 1.0ml Distilled water 0.01ml - - Urea standard - 0.01ml - sample - - 0.01ml Chorogen reagent 0.2ml 0.2ml 0.2ml
  13. 13. calculation: = T/S × 40 SERUM – 15 to 40mg/dl
  14. 14.  The hypobromite method Principle: the vol of nitrogen liberated by the action of hypobromite on the urea present in the urine is measured. the action is usually though not accurately, expressed URINE - 15 to 30mg/day.
  15. 15.  Urea clearance is less than GFR. Maximum urea clearance: =U × V/P U=mg of urea /ml of urine p=mg of urea/ml of plasma v=mg of urine excreted /minute normal value - 75 ml /mint Standard urea clearance: u × √v/p normal value - 54ml/mint
  16. 16.  Values below 75% is abnormal  Values fall progressively with increasing renal failure  Clearance values r the early indicator then plasma value  creatinine clearance is more preferred  Neither urea clearance nor blood urea r used as index of kidney function today
  17. 17.  Creatine constitutes about 0.5% of total muscle weight.  Its synthesized from 3 amino acids Glycine , Arginine & Methionine. glycine arginine (occurs in mitochondia of kidney n pancreas) Guanidoacetic acid ornithine SAM (in liver) SAH Creatine creatine phosphate (ck is pesent in muscle brain n liver) creatinine
  18. 18. CREATINE creatine kinase PHOSPHOCREATINE SPONTANEOUS SPONTANEOUS H₂O Pi CREATININE
  19. 19.  Stored creatine phosphate which is a high energy compound, stored in the muscle, serves as an immediate store of energy.  Inter conversion of phosphocreatine & creatine is an indicator of metabolic process of muscle contraction.  A particular proportion of muscle creatine is converted to creatinine spontaneously everyday.  So amount of creatinine produced in body is related to muscle mass .  Conc. Of creatinine in blood is mostly constant.  Diet may influence the value with high meat intake.  Its freely filtrated by glomerulus.  Its an indicator of renal function.
  20. 20. Increased conc of creatine  Muscular disorders  Myasthenia gravis  Different myositis  Starvation  High fever  Diabetes mellitus  Hyperthyroidism
  21. 21. Causes of increase in serum Creatinine  Causes are divided in pre-renal , renal and post-renal  PRE-RENAL :  Dehydration  Pyloric & intestinal obstruction with vomiting  Severe n prolonged diarrhea  Chronic intestinal obstruction without vomiting  Ulcerative colitis with severe chloride loss  Diabetic coma
  22. 22. RENAL :  Acute glomerulonephritis  Malignant hypertension  Chronic pyelonephritis  Hydronephrosis  Congenital cystic kidney  Renal tuberculosis  Calcium deposition in kidney in hyperthyroidism & hyper-vitaminosis D .
  23. 23.  POST RENAL: Enlargement of prostate Stones in urinary tract Stricture of the urethra Tumors of the bladder effecting the ureter
  24. 24. Increased conc of creatinine  Conditions r same as increased urea conc.  But in renal causes creatinine increases more than the pre-renal causes.
  25. 25. Jaffe`s method (in urine) principle: creatinine in urine reacts with picric acid in presence of NaOH to give orange colored compound.creatinine- picrate color read at 500 nm. addition BLANK STANDARD TEST Distilled water 3ml - - Working standard - 3ml - Diluted urine - - 3ml Picric acid 1ml 1ml 1ml 0.75 N NaOH 1ml 1ml 1ml
  26. 26. calculation: =gms of creatinine /lt =T/S×0.03/1000×1000/0.03 =T/S gm/lt Normal value – 1 - 1.5gm/lt
  27. 27. Modified jaffe`s reaction: principle: cretinine reacts with alkaline picrate to produce a reddish color. Absorbance of the color is directly proportional to creatinine conc in plasma n its measured in 500-520nm. addition blank standard sample Working reagent - 1000ùl 1000ùl Standard - 100ùl - serum - - 100ùl
  28. 28. Calculation: =T/S ×conc of standard(mg/lt)(2mg/dl) normal value – 0.7 -1.4mg/dl (male) 0.6 – 1.2 mg/dl (female)
  29. 29. Uncorrected clearance =(u/p)× v U=urinary creatinine conc. p=plasma creatinine conc v=urine flow in ml/min Corrected clearance =u×v×1.73 p×A
  30. 30. Normal value: 85-125 ml/min (male) 80-115 ml/min (female) Clinical importance  decreased creatinine clearance is an sensitive indicator of GFR.  UPTO 75% is nornal.  Early detection of renal impairment  Long term monitoring of renal patients  Creatinine clearance is altered by body muscle mass ,drugs,age,sex

×