Creatinine and bun relationship test

BUN and Creatinine - Clinical Methods - NCBI Bookshelf

creatinine and bun relationship test

Urea and creatinine are nitrogenous end products of metabolism. Even though the test is now performed mostly on serum, the term BUN is still retained by . due to their parabolic relationship and to the wide range of normal (Figure ). Creatinine and urea blood levels reflect glomerular filtration rate (GFR) and for this reason is the preferred test for assessment of kidney function [3],[4]. (of the order ) because of the difference between urea and urea nitrogen, and is . Creatinine blood test is a test that measures kidney function. Learn what Blood urea nitrogen (BUN) level is another indicator of kidney function. Urea is also a.

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.

Understanding Renal Function Tests: The BUN/Creatine Ratio

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. 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. However, the ingestion of cooked meat can raise the sCr because cooking converts the creatine in meat to creatinine.

Certain drugs, notably the psychoactive phenacemide, can increase the production rate. Like urea, creatinine distributes throughout total body water.

Its concentration in serum is a function of the usually constant production and excretion rates. It may be slightly higher in the evening than in the morning, due most likely to dietary meat intake by day. In normal subjects, creatinine is excreted primarily by the kidneys. There is minimal extrarenal disposal or demonstrable metabolism. As a small molecule molecular weight of daltonsit is freely filtered by the glomerulus.

Urea and creatinine concentration, the urea:creatinine ratio

Unlike urea, it is not reabsorbed or affected by urine flow rate. Excretion of both urea and creatinine is increased during exercise without producing significant change in serum concentration. The amount excreted has been used as a rough index of the completeness of daily urine collection. Measurement of urine creatinine excretion is used in calculating the creatinine clearance cCr. Short of the more precise but technically impractical inulin clearance, the cCr is the standard clinical tool for estimating GFR, especially in the early stages of renal disease.

In contrast, the cCr has the major disadvantage of inaccuracies in urine collection, especially during short-term clearances or in patients with low urine volumes. For this reason, hour clearances are preferred for general use, because the usually larger volumes will minimize errors of collection.

The concentration of creatinine in the serum and urine is determined, and with careful attention to the units of measurement, the cCr is calculated as follows: The result may then be standardized to 1. The subject's BSA is related to weight and height and is usually obtained from a nomogram.

Several shortcuts to estimate the cCr without collecting urine have been proposed. The earliest and probably the least accurate ignores the subject's age and weight, and simply divides by the sCr. The Cockcroft-Gault formula is the one usually recommended for use in calculating dosage of drugs especially nephrotoxic antibiotics. It takes into account the well-documented fall in GRF with age as follows: In advanced renal failure, net creatinine excretion decreases significantly.

Further, there is measurable creatinine metabolism by gut flora and, in some patients, decreased creatinine synthesis. Thus cCr is unreliable and often overestimates GFR in chronic renal failure and in cirrhosis. Certain drugs may affect cCr without changing GFR. Salicylates, cimetidine, and trimethoprim interfere with tubular secretion of creatinine and cause a spuriously low cCr. Because they are handled primarily by glomerular filtration with little or no renal regulation or adaptation in the course of declining renal function, they essentially reflect GFR.

Unfortunately, their relation to GRF is not a straight line but rather a parabolic curve Figure Within that range, however, a doubling of the values e.

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Therefore, in the early stages of renal disease, these tests could create a false sense of security. Random values above the midrange of normal should be corroborated by a normal cCr before one can confidently tell a patient that his or her kidney function is normal. At the other end of the curve, small changes in kidney function can produce large increments in BUN and sCr.

Here, these tests are generally adequate to follow a patient's course. Indeed, the reciprocal of the sCr plotted against time shows a straight-line progression of renal disease in each individual patient, and can be used to predict the advent of end-stage renal disease. At all stages of renal insufficiency, the sCr is a much more reliable indicator of renal function than the BUN because the BUN is far more likely to be affected by dietary and physiologic conditions not related to renal function Table The stages of renal failure have been defined according to the sCr as follows: With so many limitations on the usefulness of the BUN, one wonders why the test survives.

Creatinine test - Mayo Clinic

When taken with the sCr, it is a very useful clue to the presence of a prerenal or postrenal component to azotemia. Other factors being normal, a patient with an sCr of 5. Note that this 10 to 1 ratio applies best in moderate to advanced renal failure.

Attention to these reversible complications of uremia can give a patient a reprieve from an untimely sentence of end-stage renal disease. The BUN survives and is finding wide application in the nutritional management of critically ill patients. 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.

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creatinine and bun relationship test

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.

creatinine and bun relationship test

The significance of serum urea and renal function in patients with heart failure. Medicine Baltimore ; 89, 4: Sood MM et tal. The urea-to-creatinine ratio is predictive of worsening kidney function in ambulatory heart failure patients. J Card Fail ; 21, 5: Takaya Y et tal. Circ J ; 79, 7: Aronson D et tal. Elevated blood urea nitrogen level as a predictor of mortality in patients admitted for decompensated heart failure.

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creatinine and bun relationship test

Prediction of severity in acute pancreatitis: Lancet ; 2, Wu BU et tal. Blood urea nitrogen in the early assessment of acute pancreatitis: Arch Intern Med ;7: Haemodialysis — clinical standards and targets Chapter 3 In: Treatment of Adults and Children with Renal Failure: Standards and Audit Measures: Royal College of Physicians of London;