HOW DO PHYSICIANS TEST YOUR KIDNEY FUNCTION?
A common misconception that people often have is equating urine output to kidney function. Hence, the assumption is that if you are “making urine,” your kidneys are working just fine. However, nothing is further from the truth, and assessing the function of your kidneys requires lab testing and sometimes radiological imaging.
Most people know that getting a stress test is a way to test your heart’s function.
But how do you test your kidney function? You might have heard doctors mention words like “creatinine” or “GFR” when checking how good or bad your kidneys are doing. Although there are a lot of methods by which the kidneys’ performance can be measured, I will explain the ones that are used most often in a clinical setting.
Broadly speaking, you could check kidney function through either:
(1) Blood tests
(2) Urine tests
(3) Radiological imaging
This is the most common and usually the most reliable method. Doctors will often order tests that could be variously worded like “basic metabolic panel (BMP),” “chem 7,” “renal function panel,” “GFR,” etc. Essentially, what they are measuring is the levels of electrolytes and two other chemicals called blood urea nitrogen (BUN) and creatinine.
BUN measures the amount of nitrogen present in your blood in the form of urea, hence the name BUN! In other words, what we are measuring is the urea level in the blood.
Urea, as you might know, is a nitrogen-containing compound present in the urine of mammals and often used as a fertilizer. Before you conclude that there is fertilizer flowing in your blood, let me make emphasize that industrial grade urea that is used in fertilizers is manufactured artificially. In fact, urea was the first “organic“ (that is, found in nature in living organisms) compound that was artificially synthesized in a laboratory when German scientist Friedrich Wohler synthesized ammonium cyanate in 1828.
BUN: An Imperfect Test
So why do we measure the urea level in the blood? That is because the blood urea level, (or BUN!) depends on the balance between processes that increase its blood level vs. the processes that decrease its blood level. Factors that increase the level of urea in the blood include dietary protein intake, the ability of your liver to synthesize urea, and the rate of normal cell breakdown (medically referred to as “catabolism”) that also leads to urea production. Finally, the process that decreases the urea level in the blood is your kidney’s ability to excrete urea in the urine.
Assuming that the factors that increase urea level stay constant on a day to day basis, you could argue that the urea level in the blood would be most dependent on your kidneys’ functioning. Hence, kidney disease could be detected by an increase in the blood level of urea, or BUN. However, please bear in mind that this is a simplistic explanation, and the BUN levels, as you might have guessed, could be influenced by diet, catabolism, and the liver function.
Creatinine Is a Better Alternative
You thus don’t need to be a medical professional to realize that BUN is but an utterly imperfect test of kidneys’ function, subject to the vagaries of a multitude of other non-renal factors.
So let’s talk about the other chemical I mentioned above: creatinine.
The word “creatinine” comes from the Greek word for flesh, and it is a product of muscle breakdown. Since your muscle mass does not change on a daily basis, the rate of creatinine production is also fairly constant. As creatinine level in the blood builds up (from muscle breakdown), the kidneys do a great job of filtering it out of your system. (A very small, and usually insignificant (unlike urea!) amount of creatinine is reabsorbed by the kidneys, which could technically influence its blood level, but for simplicity, let’s disregard that for now).
Hence, assuming a steady muscle mass, the level of creatinine in the blood should only be influenced by the kidney’s ability to filter it out. Therefore, increase in blood level of creatinine usually implies worse kidney function.
The blood’s creatinine level is hence a useful piece of data that can help physicians estimate the rate at which kidneys filter blood using validated formulas and equations (that we obviously don’t need to worry about here). That rate is referred to as Glomerular Filtration Rate or GFR; a term you might hear physicians throw around a lot when talking about your kidney function. For most average sized people, a normal GFR would lie between 60 to 120 ml/min.
Normal Is Normal for Normal People!
GFR estimation is based on a formula that was designed for average sized normal people. Since the calculation depends on the blood creatinine level, which in turn depends on the muscle mass, it may not be applicable in people in extremes of age (kids, people over 70 yrs), or muscle mass (people with muscle wasting, liver failure, etc). In other words, a creatinine level of 1.2 (considered “normal” as per most lab ranges) might be ok for a muscular person like Arnold Schwarzenegger but could reflect significant kidney disease in a 90-year-old woman. Just like the BUN level, a medical professional should be able to tell when to consider creatinine and GFR levels really abnormal.
Testing the urine to look for protein or blood, and its chemical composition may help in indicating the presence of kidney disease. Protein or blood should usually not be detectable in urine and are non-specific markers of kidney disease. A physician should determine whether further specific workup and/or a referral to a nephrologist is warranted.
These techniques entail taking pictures of the kidneys using different methods like ultrasound, CT scan, or MRI. This can help in determining the shape and size of the kidneys. The kidneys are smooth bean-shaped organsapproximately 8-14 cm (3-5.5 inches) in size (depending on the person’s size). Most chronic kidney diseases, with some exceptions, tend to distort the kidneys’ architecture and this can be picked up easily on imaging. One might also be ablfe to pick specific causes of kidney disease/dysfunction like stones, obstructions, hydronephrosis, polycystic kidney disease, etc.
Hall JE, Guyton AC. (2011). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders Elsevier.