Creatinine and bun relationship tips

Dietary Protein, BUN and Creatinine: What's the Connection? - Kidney Diet Tips

creatinine and bun relationship tips

Blood, urea, nitrogen is used by nephrologists often to determine whether or not the patient is dehydrated. Generally speaking, the relationship between your. If you assumed that only people who workout regularly should be concerned about creatinine, you are wrong. If you feel tired easily and have. Learn how the blood urea nitrogen (BUN) test is used to evaluate kidney function and diagnose disease. Understand when the test is needed.

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 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. 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.

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. For the adult female, with her generally lower muscle mass, the normal range is 0.

Technique 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.

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One system checks the decrease in absorbance at 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. 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. 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. 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. Its primary source is dietary protein.

In the hepatocyte, the amino acids are deaminated and transaminated. The resulting excess nitrogen feeds into the urea cycle to be incorporated into urea. The protein moieties escaping absorption by the small bowel, plus recycled urea, are converted into ammonia by gut flora predominantly in the colon. The ammonia diffuses through the portal circulation into the liver to enter the urea cycle Figure Modified from Raforth and Onstad, The amount of urea produced varies with substrate delivery to the liver and the adequacy of liver function.

creatinine and bun relationship tips

It is increased by a high-protein diet, by gastrointestinal bleeding based on plasma protein level of 7. 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. The bulk of the urea, about 10 gm each day, is excreted by the kidney in a process that begins with glomerular filtration. Low flow, as in urinary tract obstruction, allows more time for reabsorption and is often associated with increases in antidiuretic hormone ADHwhich 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. In a reaction catalyzed by creatine phosphokinase CPKmost of this muscle creatine is phosphorylated to creatine phosphate.

Modified from Dosseter, Thus, creatinine production essentially reflects lean body mass.

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Because this mass changes little from day to day, the production rate is fairly constant. Absolute creatinine production declines with age in line with decreasing muscle mass. Unlike urea, creatinine is largely unaffected by gastrointestinal bleeding or by catabolic factors such as fever and steroids. Blood urea nitrogen and creatinine. Emerg Med Clin North Am ; 4, 2: Jurado R et tal. The decreased serum urea nitrogen-creatinine ratio. Arch Intern Med ; Snook JA et tal. Value of a simple biochemical ratio in distinguishing upper and lower sites of gastrointestinal haemorrhage.

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Gastroenterol Res Pract ; Kim KS et tal. Pediatr Gastroenterol Hepatol Nutr ; 18, 1: Srygley FD et tal. Does this patient have a severe upper gastrointestinal bleed? JAMA ; Pumphrey CW et tal. Raised blood urea concentration indicates considerable blood loss in acute upper gastrointestinal haemorrhage. Br Med J ; Blatchford O et tal. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage. Lancet ; Stevenson J et tal. Validating the Glasgow-Blatchford upper GI bleeding scoring system.

Gut ; 62, 2: Cheng DW et tal. A modified Glasgow Blatchford Score improves risk stratification in upper gastrointestinal bleed: Aliment Pharmacol Ther ; 36, 8: Rahman M et tal. Am Fam Physician ; 86, 7: Pathophysiology of pre-renal azotemia.

creatinine and bun relationship tips

Kidney Int ; 53, 2: Agrawal M et tal. Am Fam Physician ; 61, 7: Uchino S et tal. Clinical Kidney Journal ; 5, 2: Rachoin J et tal. The fallacy of the BUN: Nephrol Dial Transplant ; 27, 6: Beier K et tal. Crit Care Med ; 39, 2: Damman K et tal. The kidney in heart failure: Eur Heart J ; 36, Gotsman I et tal. The significance of serum urea and renal function in patients with heart failure. Medicine Baltimore ; 89, 4: Sood MM et tal.