On March 7, 1941, Linus Pauling stood before distinguished colleagues prepared to deliver an address in response to his receipt of the prestigious William H. Nichols Gold Medal, presented by the New York chapter of the American Chemical Society.
Before Pauling began his recitation, he spoke candidly to his audience. He thanked the award committee for his selection and expressed gratitude that the acceptance of this award had provided him with an opportunity to reconnect with old friends.
On this rare occasion, however, it was apparent to all in attendance that Pauling’s physical health was suffering. His face was bloated and he reportedly lacked the enthusiasm that he was so well known to exude. Addressing the observations of many of his peers, Pauling joked, “Several of [my old friends] said to me tonight that I appeared to be getting fat. This is not so.”
Just that morning, Pauling had awoken to find his face so bloated that his eyes were nearly swollen shut. His tongue felt enlarged and his voice was flat. Over the previous few weeks, Pauling had been experiencing noticeable swelling, weight gain, and chronic fatigue but he could not identify the cause of his ailments.
With his audience, Pauling half-heartedly pondered over the cause of his puffed-up appearance. He compared the experience to childhood memories of unfortunate encounters with poison oak.
Yesterday I must have bumped into something similar…while I was wondering what the responsible protein could have been, I decided that it was a visitation – that I was being punished for thinking wicked thoughts.
The following evening Linus and Ava Helen had dinner at Alfred Mirsky‘s residence. Pauling was examined by another guest at the dinner party, Dr. Alfred E. Cohen, a cardio specialist from the Rockefeller Medical Institute. After ruling out problems with Pauling’s heart, Dr. Cohen remained perplexed by Pauling’s condition. Nothing appeared to be wrong with the forty-year-old man other than his extreme edema. Concerned by the severity of the swelling however, Dr. Cohen recommended that Pauling come into his office the following day for a more thorough examination and lab work-up.
Adhering to the physician’s recommendation, the Paulings met Dr. Cohen in his office at the Rockefeller Medical Institute the next day. After a battery of lab tests, Pauling was diagnosed with Bright’s disease – a potentially fatal renal disease that results in the degradation of the kidneys. At the time, little was known about Bright’s disease and the majority of the medical community considered it to be a terminal condition.
After receiving this diagnosis, Pauling was fortunately referred to a leading specialist in renal diseases, Dr. Thomas Addis, head of the Clinic for Renal Disease at Stanford. Dr. Addis was a pioneer in the field of nephrology and his treatment plan, at the time, was new and revolutionary. Had Pauling not been referred to Dr. Addis’ care, the treatment he would have received elsewhere would almost surely have killed him.
Under the guidance of Dr. Addis, Pauling’s condition was effectively treated by alternative means – a low-protein, low-sodium diet – rather than the polysaccharide infusions that would have reduced his edema but done little to improve his health. By May, Pauling reported improvements in his overall well-being and by August, the edema had completely disappeared.
Since Pauling’s time of diagnosis, Bright’s disease has been reclassified and redefined. Now it is believed that Pauling was affected by what is currently termed acute glomerulonephritis.
Acute glomerulonephritis is characterized by inflammation of the kidneys due to an immunological response. Damage to the small clusters of capillaries within the kidney, known as glomeruli, results in what can most simply be described as a “leaky kidney.” When the glomeruli are damaged, proteins leak from the bloodstream into the urine through the damaged portions of the kidney. Thus glomerulonephritis consequentially leads to excessive protein loss. Glomerulonephritis profoundly effects the body’s ability to function, because the nephritic kidneys are unable to properly filter the blood.
In his 1941 speech, Pauling had wondered aloud about a protein that was responsible for his swollen condition. The culprit protein can now perhaps be identified as albumin. As proteins leak from the bloodstream into the urine, blood proteins, called albumin, exit the bloodstream. These proteins are known to be essential in the regulation of blood osmotic pressure. Without sufficient albumin in the bloodstream, the body becomes incapable of efficiently extracting excess fluid from the body cavity. This excess fluid then remains trapped in the body and ultimately results in excessive swelling – such as the bloating that Pauling experienced in 1941.
Although the albumin did not cause Pauling’s condition, the loss of this blood protein due to the nephritis appears to have resulted in the symptoms that he was experiencing at his award ceremony. Therefore, contrary to his original speculation, it was the absence, rather than the presence, of a protein that caused his extreme fluid retention.
Over the next series of posts, we’ll explore the details of Pauling’s battle with this frightening disease, and learn more about the people and methods who saved Linus Pauling’s life.