Robinson Power Kepler water test

The Robinson Power Kepler water test is based on the retention of water in patients with Addison’s disease with increased elimination of chlorides and the relative retention of urea. The test begins at 18 h, when the patient is forbidden to eat and drink. From 22 hours after emptying the bladder, urine is collected until 8 o’clock the next morning. The volume of collected urine is measured, after which the patient is given a certain amount of water to drink for 45 minutes at the rate of 20 ml per 1 kg of body weight. Then, hourly for 4 hours, the amount of urine recovered is determined. In healthy people, the largest volume of the hourly portion of urine is greater than the volume of night urine. In individuals with Addison’s disease, the ratios are inverse. One of the diagnostic tests is the ratio of sodium to potassium in the serum.
In individuals with Addison’s disease, the water sample index is less than 25, and in healthy people it is more than 30.

For the differential diagnosis of primary and secondary adrenal insufficiency, the available and potential reserves of the adrenal cortex (Labhart test) and the level of ACTH in the blood are determined. The content of ACTH in the blood plasma in case of primary insufficiency of the adrenal cortex is increased, and in the case of secondary – it is lowered. To determine the cash and potential reserves of the adrenal cortex, for 2 days, 40 U of ACTH with prolonged 24 hours of intramuscular injection or once 1 mg of synacthen depot are injected intramuscularly. On the first day before the test, 17-ACS in the blood is determined at 16 h, on the 2nd day – at 8 h. At the same time, 17-ACS and in the daily urine are determined. In healthy people after intramuscular administration of ACTH, urinary excretion of 17-ACS on the first day increases by 100% compared to baseline (available reserves of the adrenal cortex), and in the subsequent second and third days it reaches 300% (potential reserves of the adrenal cortex). In case of primary insufficiency of the adrenal cortex, its cash and potential reserves are reduced or absent, and in the case of secondary (hypothalamic-pituitary) cash reserves are preserved, and potential reserves can be reduced.

Diagnosis and differential diagnosis. The diagnosis of Addison’s disease is established on the basis of the characteristic symptoms of the disease (adynamia, hypotension, pigmentation), laboratory data and diagnostic tests.

Melanoderma in Addison’s disease is differentiated from bronze diabetes (hemochromatosis), pellagra, systemic scleroderma, pigment form of toxic goiter, acanthosis nigricans. In some cases, it is differentiated from pigmentation in chronic malaria, pruritic dermatosis, repeated irradiation of the skin with X-rays, chronic lead poisoning, mercury, silver hydrate, arsenic, tan in combination with hypotonic syndrome, as well as racial pigmentation.

Unlike Addison’s disease, the following symptoms are characteristic of bronze diabetes: hepatomegaly, splenomegaly, cirrhosis of the pancreas and other internal organs, combined with diabetes mellitus and deposition of pigment containing iron (hemosiderin) and not containing it (hemophuscin) which gives the skin a slate-gray color.

local_offerevent_note February 11, 2019

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