Diabetes insipidus: Polyuria.

Polyuria is defined as the passage of excessive quantities of urine. Pollakauria is defined as urinary frequency; in other words, more trips to the bathroom regardless of urine volume.

Polyuria is arbitrarily defined as the passage of more than 30 mL of urine per kilogram of body weight per day. For the average-sized adult, of 70 kg, greater than 2.1 L per day would be considered polyuria. The body weight calculation is important because small adults and children may not produce tremendous volumes of urine but it will be too much for their body weight. Conversely, very large adults they seem to have excessive amounts of urine that proves to be normal given their body weight.

About 80% to 90% of the water filtered by the kidney is resorbed due to the result of several mechanisms with the most important one being the actions of vasopressin. A lot of different factors influence the amount of urine produced daily. Some of these include the solute (salt and other minerals) load, the need to excrete waste products, and fluid intake. Furthermore, the kidney has to be able to function normally to carefully regulate urine output.

Patients with diabetes insipidus have polyuria as a result of relative or absolute deficiency of vasopressin. Rare patients have a kidney that is insensitive to vasopressin.

The most impressive case of diabetes insipidus I ever encountered was that of a patient who had undergone resection of a craniopharyngioma. The physicians caring for the patient had written through the chart on a daily basis something to the effect of “sodium normal, and thus, no evidence for diabetes insipidus.” Urine outputs and fluid intakes were not recorded in the chart but were, as I determined about an hour later later, available at the bedside. I was consulted because he refused to go home until the medical team sorted out his excessive urination. Upon entering the patient’s hospital room, I found a distraught man standing in the bathroom, urinating in the toilet with his penis in one hand and, with his other hand,drinking water holding a 3 foot piece of surgical tubing that he had connected to the spigot of the sink to facilitate drinking water and urinating at the same time! He explained, between gulps of water, that he had stopped counting his urine output and fluid intake the day before because he couldn’t take the time to write the numbers down. He had not slept in 3 days. I viewed the bedside chart and saw that he had recorded, with the assistance of the nurses who verified, 24 L of urine out daily and 23 L of fluid intake daily. That’s a liter per hour! His serum sodium concentrations were about 142 mEq per liter. Normal. I maintained, however, this is the thirst threshold for his hypothalamus and he was drinking to keep his sodium at his thirst threshold. Of course, he had polyuria….and it was definitely diabetes insipidus! He responded extremely well to dDAVP nasal spray. As soon as his polyuria abated he slept 18 hours….awakened only by the dDAVP having worn off!

I once consulted on a patient who underwent neurological surgery for a rare disorder. Her serum sodium concentrations were elevated at 147 mEq per liter. She was extremely thirsty. The medical team couldn’t make sense of it because they did not think she was polyuric and deemed that she did not have diabetes insipidus. Her urine output averaged 1.7-1.9 L per 24-hour period. Unfortunately, however,her fluid intake was not recorded. She weighed 85 pounds. Calculations showed that polyuria, at this body weight, would be a urine output greater than 1.1 L daily. Thus, she was polyuric! She had diabetes insipidus! And she responded beautifully to dDAVP.

I have learned that most adult patient’s learn to tolerate polyuria. In fact, many are surprised when they have submitted to the exercise of determining their 24-hour urine output, that their urine volumes are 3 liters or more daily. It seems that most adults do not really have a problem until they start to pass more than about 4 L daily. This is not true for everyone. It’s just one of my observations over the course of my practice. I will say, however, that it is important to recognize that the greater the polyuria, the greater the washout of the solutes in the medulla of the kidney, and is the less the concentrating ability of the kidney in response to vasopressin. In other words, polyuria begats polyuria. Bouts of polyuria might explain why some people have a variable sensitivity to vasopressin. There are other potential explanations for this observation, too, and I will cover those at some point in the future when I write about dDAVP therapy.

Visual: Abstract backgrounds by Nicho Design

© 2014, Pituitary World News. All rights reserved.