Mmol/L is the most common measurement used in the UK with mg/dL predominantly used in the USA and continental Europe. Mmol/L International standard unit for measuring the concentration of glucose in the blood - also known as millimolar (mM).

• Creatinine Mg Dl To Mmol L
• Creatinine Mmol L To Mg Dl Converter
• Creatinine Mmol L Mg Dl
• Convert Creatinine Mg To Mmol
• Convert Mg Dl To Mmol L
• Mg Dl Mmol L Calculator

To convert mmol/l of glucose to mg/dl, multiply by 18. To convert mg/dl of glucose to mmol/l, divide by 18 or multiply by 0.055. These factors are specific for glucose, because they depend on the mass. Convert Creatinine level to mmol/l, µmol/l, mg/dl, mg/100ml, mg%, mg/l, µg/ml. Clinical laboratory units online conversion from conventional or traditional units to Si units. Table of conversion factors for Creatinine unit conversion to mmol/l, µmol/l, mg/dl, mg/100ml, mg%, mg/l, µg/ml. Creatinine converted to mg/dl: Enter the Creatinine level in the spaces provided above and then click the 'Calculate' button to convert. Use the 'tab' key to move from cell to cell for faster input. Oct 31, 2017  Mmol l this blood sugar converter can convert either from mmol to mg dl. Mmol l is the most common measurement used in uk with mg dl predominantly usa and continental europe. So, if there are 40 grams per mole then it follows that there are 40 mg/mmol 11.5 mg / dL x 1 dL /100 ml x 1000 ml / L x 1 mmol /40 mg = 2.87 mmol/l Or you can use the molarity formula.

Creatinine Mg Dl To Mmol L

Microalbuminuria is a term to describe a moderate increase in the level of urine albumin. It occurs when the kidney leaks small amounts of albumin into the urine, in other words, when an abnormally high permeability for albumin in the glomerulus of the kidney occurs. Normally, the kidneys filter albumin, so if albumin is found in the urine, then it is a marker of kidney disease. The term microalbuminuria is now discouraged by Kidney Disease Improving Global Outcomes^{[citation needed]} and has been replaced by moderately increased albuminuria.

• 1Causes

Causes[edit]

Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria,^[1] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.^[2][3][4]

Associations[edit]

• Marker of vascular endothelial dysfunction
• An important prognostic marker for kidney disease
  • in diabetes mellitus
  • in hypertension
  • in post-streptococcal glomerulonephritis
• Increasing microalbuminuria during the first 48 hours after admission to an intensive care unit predicts elevated risk for acute respiratory failure, multiple organ failure, and overall mortality
• A risk factor for venous thromboembolism^[5]

Microalbuminuria is an important adverse predictor of glycemic outcomes in prediabetes. Prediabetes individuals with increased microalbuminuria even in the so-called normal range is associated with increased progression to diabetes and decreased reversal to normoglycemia. Hence, prediabetes individuals with microalbuminuria warrant more aggressive intervention to prevent diabetes in them.^[6]

Diagnosis[edit]

The level of albumin protein produced by microalbuminuria can be detected by special albumin-specific urine dipsticks, which have a lower detection threshold than standard urine dipsticks. A microalbumin urine test determines the presence of the albumin in urine. In a properly functioning body, albumin is not normally present in urine because it is retained in the bloodstream by the kidneys.

Microalbuminuria can be diagnosed from a 24-hour urine collection (between 30–300 mg/24 hours) or, more commonly, from elevated concentration in a spot sample (20 to 200 mg/l). Both must be measured on at least two of three measurements over a two- to three-month period.^[7]

An albumin level above the upper limit values is called 'macroalbuminuria', or sometimes just albuminuria. Sometimes, the upper limit value is given as one less (such as 300 being given as 299) to mark that the higher value (here 300) is defined as macroalbuminuria.^[8]

To compensate for variations in urine concentration in spot-check samples, comparing the amount of albumin in the sample against its concentration of creatinine is helpful. This is termed the albumin/creatinine ratio (ACR)^[9] and microalbuminuria is defined as ACR ≥3.5 mg/mmol (female) or ≥2.5 mg/mmol (male),^[10] or with both substances measured by mass, as an ACR between 30 and 300 µg albumin/mg creatinine.^[11]For the diagnosis of microalbuminuria, care must be taken when collecting sample for the urine ACR. An early-morning sample is preferred. The patient should refrain from heavy exercises 24 hours before the test. A repeat test should be done 3 to 6 months after the first positive test for microalbuminuria. Lastly, the test is inaccurate in a person with too much or too little muscle mass. This is due to the variation in creatinine level which is produced by the muscle.^[12]

References[edit]

• Abid O, Sun Q, Sugimoto K, Mercan D, Vincent JL (2001). 'Predictive value of microalbuminuria in medical ICU patients: results of a pilot study'. Chest. 120 (6): 1984–8. doi:10.1378/chest.120.6.1984. PMID11742932.
• Andersen S, Blouch K, Bialek J, Deckert M, Parving HH, Myers BD (2000). 'Glomerular permselectivity in early stages of overt diabetic nephropathy'. Kidney Int. 58 (5): 2129–37. doi:10.1111/j.1523-1755.2000.00386.x. PMID11044234.
• Heart Outcomes Prevention Evaluation Study Investigators (2000). 'Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy'. Lancet. 355 (9200): 253–9. doi:10.1016/S0140-6736(99)12323-7. PMID10675071.
• Lemley KV, Abdullah I, Myers BD, et al. (2000). 'Evolution of incipient nephropathy in type 2 diabetes mellitus'. Kidney Int. 58 (3): 1228–37. doi:10.1046/j.1523-1755.2000.00223.x. PMID10972685.
• Lièvre M, Marre M, Chatellier G, et al. (2000). 'The non-insulin-dependent diabetes, hypertension, microalbuminuria or proteinuria, cardiovascular events, and ramipril (DIABHYCAR) study: design, organization, and patient recruitment. DIABHYCAR Study Group'. Controlled Clinical Trials. 21 (4): 383–96. doi:10.1016/S0197-2456(00)00060-X. PMID10913814.
• Parving HH, Lehnert H, Bröchner-Mortensen J, Gomis R, Andersen S, Arner P (2001). 'The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes'. N. Engl. J. Med. 345 (12): 870–8. doi:10.1056/NEJMoa011489. PMID11565519.
• Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney inter., Suppl. 2013; 3: 1-150.

Footnotes[edit]

1. ^Lin, Julie; Hu, Frank B.; Curhan, Gary C. (2010-05-01). 'Associations of diet with albuminuria and kidney function decline'. Clinical Journal of the American Society of Nephrology. 5 (5): 836–843. doi:10.2215/CJN.08001109. ISSN1555-905X. PMC2863979. PMID20299364.
2. ^Lin, Julie; Fung, Teresa T.; Hu, Frank B.; Curhan, Gary C. (2011-02-01). 'Association of dietary patterns with albuminuria and kidney function decline in older white women: a subgroup analysis from the Nurses' Health Study'. American Journal of Kidney Diseases. 57 (2): 245–254. doi:10.1053/j.ajkd.2010.09.027. ISSN1523-6838. PMC3026604. PMID21251540.
3. ^Wiseman, M. J.; Hunt, R.; Goodwin, A.; Gross, J. L.; Keen, H.; Viberti, G. C. (1987-01-01). 'Dietary composition and renal function in healthy subjects'. Nephron. 46 (1): 37–42. ISSN1660-8151. PMID3600911.
4. ^Barsotti, G.; Morelli, E.; Cupisti, A.; Meola, M.; Dani, L.; Giovannetti, S. (1996-01-01). 'A low-nitrogen low-phosphorus Vegan diet for patients with chronic renal failure'. Nephron. 74 (2): 390–394. ISSN1660-8151. PMID8893161.
5. ^Mahmoodi, BK; Gansevoort, RT; Veeger, NJ; Matthews, AG; Navis, G; Hillege, HL; Van Der Meer, J; Prevention of Renal Vascular End-stage Disease (PREVEND) Study Group (2009). 'Microalbuminuria and risk of venous thromboembolism'. JAMA: the Journal of the American Medical Association. 301 (17): 1790–7. doi:10.1001/jama.2009.565. PMID19417196.
6. ^Dutta D, Choudhuri S, Mondal SA, Mukherjee S, Chowdhury S (2014). 'Urinary albumin : creatinine ratio predicts prediabetes progression to diabetes and reversal to normoglycemia: role of associated insulin resistance, inflammatory cytokines and low vitamin D'. Journal of Diabetes. 6 (4): 316–22. doi:10.1111/1753-0407.12112. PMID24251376.
7. ^'Person—microalbumin level (measured), total micrograms per minute N[NNN].N'. Retrieved 2007-07-05.
8. ^ ^abcdeMary Lee (2009-02-26). Basic Skills in Interpreting Laboratory Data. ASHP. pp. 291–. ISBN978-1-58528-274-6.
9. ^Bakker AJ (February 1999). 'Detection of microalbuminuria. Receiver operating characteristic curve analysis favors albumin-to-creatinine ratio over albumin concentration'. Diabetes Care. 22 (2): 307–13. doi:10.2337/diacare.22.2.307. PMID10333950.
10. ^'Proteinuria'. UK Renal Association. December 15, 2005. Archived from the original on August 14, 2007.
11. ^clinlabnavigator.com > Test Interpretations Last Updated on Saturday, 19 June 2010
12. ^Microalbuminura in diabetes
13. ^ ^abPerson—microalbumin level (measured) at Australian Institute of Health and Welfare. 01/03/2005
14. ^ ^abcdefghijk[1]Justesen, T.; Petersen, J.; Ekbom, P.; Damm, P.; Mathiesen, E. (2006). 'Albumin-to-creatinine ratio in random urine samples might replace 24-h urine collections in screening for micro- and macroalbuminuria in pregnant woman with type 1 diabetes'. Diabetes Care. 29 (4): 924–925. doi:10.2337/diacare.29.04.06.dc06-1555. PMID16567839.

External links[edit]

• Microalbumin and Urine Albumin/Creatinine Ratio – Lab Tests Online

In medicine, the BUN-to-creatinine ratio is the ratio of two serum laboratory values, the blood urea nitrogen (BUN) (mg/dL) and serum creatinine (Cr) (mg/dL). Outside the United States, particularly in Canada and Europe, the truncated term urea is used (though it is still the same blood chemical) and the units are different (mmol/L). The units of creatinine are also different (μmol/L), and this value is termed the urea-to-creatinine ratio. The ratio may be used to determine the cause of acute kidney injury or dehydration.

The principle behind this ratio is the fact that both urea (BUN) and creatinine are freely filtered by the glomerulus; however, urea reabsorbed by the tubules can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption).

• 4Specific causes of elevation

Definition[edit]

Urea and creatinine are nitrogenous end products of metabolism.^[1] Urea is the primary metabolite derived from dietary protein and tissue protein turnover. Creatinine is the product of muscle creatine catabolism. Both are relatively small molecules (60 and 113 daltons, respectively) that distribute throughout total body water. In Europe, the whole urea molecule is assayed, whereas in the United States only the nitrogen component of urea (the blood or serum urea nitrogen, i.e., BUN or SUN) is measured. The BUN, then, is roughly one-half (7/15 or 0.466) of the blood urea.

The normal range of urea nitrogen in blood or serum is 5 to 20 mg/dl, or 1.8 to 7.1 mmol urea per liter. The range is wide because of normal variations due to protein intake, endogenous protein catabolism, state of hydration, hepatic urea synthesis, and renal urea excretion. A BUN of 15 mg/dl would represent significantly impaired function for a woman in the thirtieth week of gestation. Her higher glomerular filtration rate (GFR), expanded extracellular fluid volume, and anabolism in the developing fetus contribute to her relatively low BUN of 5 to 7 mg/dl. In contrast, the rugged rancher who eats in excess of 125 g protein each day may have a normal BUN of 20 mg/dl.

The normal serum creatinine (sCr) varies with the subject's body muscle mass and with the technique used to measure it. For the adult male, the normal range is 0.6 to 1.2 mg/dl, or 53 to 106 μmol/L by the kinetic or enzymatic method, and 0.8 to 1.5 mg/dl, or 70 to 133 μmol/L by the older manual Jaffé reaction. For the adult female, with her generally lower muscle mass, the normal range is 0.5 to 1.1 mg/dl, or 44 to 97 μmol/L by the enzymatic method.

Technique[edit]

Multiple methods for analysis of BUN and creatinine have evolved over the years. Most of those in current use are automated and give clinically reliable and reproducible results.

There are two general methods for the measurement of urea nitrogen. The diacetyl, or Fearon, reaction develops a yellow chromogen with urea, and this is quantified by photometry. It has been modified for use in autoanalyzers and generally gives relatively accurate results. It still has limited specificity, however, as illustrated by spurious elevations with sulfonylurea compounds, and by colorimetric interference from hemoglobin when whole blood is used.

In the more specific enzymatic methods, the enzyme urease converts urea to ammonia and carbonic acid. These products, which are proportional to the concentration of urea in the sample, are assayed in a variety of systems, some of which are automated. One system checks the decrease in absorbance at 340 mm when the ammonia reacts with alpha-ketoglutaric acid. The Astra system measures the rate of increase in conductivity of the solution in which urea is hydrolyzed.

Creatinine Mmol L To Mg Dl Converter

Even though the test is now performed mostly on serum, the term BUN is still retained by convention. The specimen should not be collected in tubes containing sodium fluoride because the fluoride inhibits urease. Also chloral hydrate and guanethidine have been observed to increase BUN values.

The 1886 Jaffé reaction, in which creatinine is treated with an alkaline picrate solution to yield a red complex, is still the basis of most commonly used methods for measuring creatinine. This reaction is nonspecific and subject to interference from many noncreatinine chromogens, including acetone, acetoacetate, pyruvate, ascorbic acid, glucose, cephalosporins, barbiturates, and protein. It is also sensitive to pH and temperature changes. One or another of the many modifications designed to nullify these sources of error is used in most clinical laboratories today. For example, the recent kinetic-rate modification, which isolates the brief time interval during which only true creatinine contributes to total color formation, is the basis of the Astra modular system.

More specific, non-Jaffé assays have also been developed. One of these, an automated dry-slide enzymatic method, measures ammonia generated when creatinine is hydrolyzed by creatinine iminohydrolase. Its simplicity, precision, and speed highly recommend it for routine use in the clinical laboratory. Only 5-fluorocytosine interferes significantly with the test.

Creatinine must be determined in plasma or serum and not whole blood because erythrocytes contain considerable amounts of noncreatinine chromogens. To minimize the conversion of creatine to creatinine, specimens must be as fresh as possible and maintained at pH 7 during storage.

The amount of urea produced varies with substrate delivery to the liver and the adequacy of liver function. It is increased by a high-protein diet, by gastrointestinal bleeding (based on plasma protein level of 7.5 g/dl and a hemoglobin of 15 g/dl, 500 ml of whole blood is equivalent to 100 g protein), by catabolic processes such as fever or infection, and by antianabolic drugs such as tetracyclines (except doxycycline) or glucocorticoids. It is decreased by low-protein diet, malnutrition or starvation, and by impaired metabolic activity in the liver due to parenchymal liver disease or, rarely, to congenital deficiency of urea cycle enzymes. The normal subject on a 70 g protein diet produces about 12 g of urea each day.

This newly synthesized urea distributes throughout total body water. Some of it is recycled through the enterohepatic circulation. Usually, a small amount (less than 0.5 g/day) is lost through the gastrointestinal tract, lungs, and skin; during exercise, a substantial fraction may be excreted in sweat. The bulk of the urea, about 10 g each day, is excreted by the kidney in a process that begins with glomerular filtration. At high urine flow rates (greater than 2 ml/min), 40% of the filtered load is reabsorbed, and at flow rates lower than 2 ml/min, reabsorption may increase to 60%. Low flow, as in urinary tract obstruction, allows more time for reabsorption and is often associated with increases in antidiuretic hormone (ADH), which increases the permeability of the terminal collecting tubule to urea. During ADH-induced antidiuresis, urea secretion contributes to the intratubular concentration of urea. The subsequent buildup of urea in the inner medulla is critical to the process of urinary concentration. Reabsorption is also increased by volume contraction, reduced renal plasma flow as in congestive heart failure, and decreased glomerular filtration.

Creatinine formation begins with the transamidination from arginine to glycine to form glycocyamine or guanidoacetic acid (GAA). This reaction occurs primarily in the kidneys, but also in the mucosa of the small intestine and the pancreas. The GAA is transported to the liver where it is methylated by S-adenosyl methionine (SAM) to form creatine. Creatine enters the circulation, and 90% of it is taken up and stored by muscle tissue.^[1]

Interpretation[edit]

Normal serum values

Creatinine Mmol L Mg Dl

Serum Ratios

An elevated BUN:Cr due to a low or low-normal creatinine and a BUN within the reference range is unlikely to be of clinical significance.

Specific causes of elevation[edit]

Acute kidney injury (previously termed acute renal failure)[edit]

The ratio is predictive of prerenal injury when BUN:Cr exceeds 20^[2] or when urea:Cr exceeds 100.^[3] In prerenal injury, urea increases disproportionately to creatinine due to enhanced proximal tubular reabsorption that follows the enhanced transport of sodium and water.

Gastrointestinal bleeding[edit]

The ratio is useful for the diagnosis of bleeding from the gastrointestinal (GI) tract in patients who do not present with overt vomiting of blood.^[4] In children, a BUN:Cr ratio of 30 or greater has a sensitivity of 68.8% and a specificity of 98% for upper gastrointestinal bleeding.^[5]

A common assumption is that the ratio is elevated because of amino acid digestion, since blood (excluding water) consists largely of the proteinhemoglobin and is broken down by digestive enzymes of the upper GI tract into amino acids, which are then reabsorbed in the GI tract and broken down into urea. However, elevated BUN:Cr ratios are not observed when other high protein loads (e.g., steak) are consumed.^{[citation needed]} Renal hypoperfusion secondary to the blood lost from the GI bleed has been postulated to explain the elevated BUN:Cr ratio. However, other research has found that renal hypoperfusion cannot fully explain the elevation.^[6]

Convert Creatinine Mg To Mmol

Convert Mg Dl To Mmol L

Advanced age[edit]

Because of decreased muscle mass, elderly patients may have an elevated BUN:Cr at baseline.^[7]

Other causes[edit]

Mg Dl Mmol L Calculator

Hypercatabolic states, high-dose glucocorticoids, and resorption of large hematomas have all been cited as causes of a disproportionate rise in BUN relative to the creatinine.^[8]

References[edit]

1. ^ ^abHosten, Adrian O. (11 November 1990). Walker, H. Kenneth; Hall, W. Dallas; Hurst, J. Willis (eds.). Clinical Methods: The History, Physical, and Laboratory Examinations. Butterworths. PMID21250147 – via PubMed.
2. ^Morgan DB, Carver ME, Payne RB (October 1977). 'Plasma creatinine and urea: creatinine ratio in patients with raised plasma urea'. Br Med J. 2 (6092): 929–32. doi:10.1136/bmj.2.6092.929. PMC1631607. PMID912370.
3. ^'Acute renal failure: urea:creatinine ratio was not very helpful in diagnosing prerenal failure'. Evidence-Based On-Call database. Archived from the original on 2006-09-26.
4. ^Witting MD, Magder L, Heins AE, Mattu A, Granja CA, Baumgarten M (May 2006). 'ED predictors of upper gastrointestinal tract bleeding in patients without hematemesis'. Am J Emerg Med. 24 (3): 280–5. doi:10.1016/j.ajem.2005.11.005. PMID16635697.
5. ^Urashima M, Toyoda S, Nakano T, et al. (July 1992). 'BUN/Cr ratio as an index of gastrointestinal bleeding mass in children'. J. Pediatr. Gastroenterol. Nutr. 15 (1): 89–92. doi:10.1097/00005176-199207000-00014. PMID1403455.
6. ^Mortensen PB, Nøhr M, Møller-Petersen JF, Balslev I (April 1994). 'The diagnostic value of serum urea/creatinine ratio in distinguishing between upper and lower gastrointestinal bleeding. A prospective study'. Danish Medical Bulletin.
7. ^Feinfeld DA, Bargouthi H, Niaz Q, Carvounis CP (2002). 'Massive and disproportionate elevation of blood urea nitrogen in acute azotemia'(PDF). Int Urol Nephrol. 34 (1): 143–5. doi:10.1023/A:1021346401701. PMID12549657.
8. ^Irwin, RS.; Rippe, JM. (2008). Irwin and Rippe's Intensive Care Medicine. Philadelphia: Lippincott Williams & Wilkins. ISBN978-0781791533.

External links[edit]

• Agrawal M, Swartz R (April 2000). 'Acute renal failure'. Am Fam Physician. 61 (7): 2077–88. PMID10779250.