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12.10: Guest Lecturer

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    Guest Lecturer: Robert S. Swenson, MD

    Notes of a Nephrologist

    A physician trained in the medical management of kidney disease is called a nephrologist. Surgery of the kidney, ureters, bladder, prostate, etc., is performed by urologists, whereas vascular surgeons and transplant surgeons provide the techniques used to manage kidney disease and kidney failure.

    The kidneys are paired organs located at the back of the abdomen. In size and shape they resemble small adult fists, averaging 4 inches in length. Each kidney contains 1 million nephrons (the Greek nephros means kidney). Each nephron consists of a blood filter followed by a long, complex tubule in which water and substances dissolved in it (solutes) are absorbed and/or secreted. The nephrons empty into the part of the kidney that leads to the ureter, the tube that carries the urine from each kidney to the bladder.

    Two normal kidneys can filter 100 milliliters of water from the blood per minute—144 quarts per day. Fortunately, the amount of urine we excrete is less than 1% of this filtered volume. More than 99% of filtered water and solutes are reabsorbed within the tubule of the nephron back into the bloodstream. The amount of materials being filtered is breathtaking: the 144 quarts—one day’s filtrate—contains about 900 grams of sodium chloride (almost 2 pounds of table salt) and about 320 grams of sodium bicarbonate (the content of a box of baking soda)! Most of these sodium salts are reabsorbed back into the bloodstream, leaving only 10-30 grams of sodium salts being excreted daily in the urine. Very importantly, our kidneys also filter out substances that would be toxic if retained.

    When kidneys are severely diseased, the person suffers signs and symptoms of uremic toxicity, which are nonspecific (e.g., nausea, easy fatigue, itching, easy bruising, edema) and occur even when urine output is normal.

    It follows that our kidneys provide a large degree of flexibility even when both kidneys are diseased. People born with only one kidney can lead normal lives, which is the reason why kidney transplantation works for both the donor and the recipient.

    The kidney has many functions (e.g. synthesis of vitamin D precursors, and breakdown of blood-filtered compounds, such as insulin), but its most obvious function is to produce a pale yellow, slightly aromatic liquid called urine. The volume of urine excreted in health varies as a function of the water (food and drink) ingested.

    Normal daily urine output ranges from a pint to several quarts, generally reflecting the water in your food and drink.

    In health, 75-90% of an acute water load is excreted as urine within four hours. Taking in a lot of salt, however, can delay the excretion of an acute water load by hours to days. One result of kidney failure is a loss of the ability to concentrate and/or dilute urine. As such, urine volume doesn’t respond as easily to your intake of water or salt.

    People who are in kidney, liver, or heart failure may retain sodium, resulting in salt-water retention (edema) and weight gain. If they retain urea in their blood, the diagnosis is uremia, indicating acute or chronic kidney failure.

    The normal pigment of urine is urochrome, a normal breakdown product of hemoglobin. Large urine volumes obviously dilute urochrome, and therefore produce a paler yellow urine. Urinary urochrome may be overwhelmed by other pigments. Eating a lot of carrots may result in an orange hue (carotemia). Similarly, eating a lot of beets can produce a red urine (beeturia).

    Changes in urine color are as likely to be from drug-induced causes as from food pigments. An orange color can result from taking Pyridium (a urinary antiseptic), rifampin (an antibiotic), or large amounts of oral vitamins. Red urine can follow administration of Ex-Lax, or phenothiazines. Blue urine follows ingestion of methylene blue, once considered a college prank. A brown or black hue may also reflect Ex-Lax or dietary intake of rhubarb or fava beans. These new colors may alarm, but are rarely clinically significant.

    A common complaint is a change in the smell of one’s own or one’s partner’s urine. This may be due to changes in diet, or taking in less water, resulting in a smaller volume of more concentrated urine. It is commonly thought that a smelly urine is a sign of urinary tract infection. However, most urinary tract infections are not associated with a change in urine’s smell.

    A really smelly urine can follow eating asparagus, the whiff of which is thought to be due to the excretion of mercaptan (a sulfur compound, akin to the smell of rotten eggs). “Asparagus urine” has three components: 1) intake of asparagus even in small quantities, 2) an autosomal dominant inheritance of urinary excretion of the smelly substance, and 3) most interestingly an inherited ability to smell it. This means that some individuals (who me?) may be unaware that they are excreting a vile-smelling urine.

    Garlic also is smelly, and some believe its odor on eating may permeate urine. However, it’s more likely that the garlic permeates exhaled breath, and body perspiration. Dinner parties heavy in asparagus and garlic may have predictable results that affect hosts and guests alike. 

    Dr. Swenson, as faculty in the Nephrology Division of Stanford Medical School, taught clinical renal disease and urinalysis to medical students and postgraduate fellows for more than 20 years. His clinical activities included renal transplantation and acute and chronic dialysis. He was later Chief of Staff of Livermore’s VA Medical Center, a teaching hospital of Stanford.


    This page titled 12.10: Guest Lecturer is shared under a CC BY-NC-SA 4.0 license and was authored, remixed, and/or curated by Judi S. Morrill via source content that was edited to the style and standards of the LibreTexts platform.

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