No, it's not just a Beatles song.
I went to the endo yesterday. Nothing has changed for me. Nothing will. He wants me to take more cortef. I don't want to gain weight again. He looked up Provigil and it's not indicated for panhypopituitarism. So he won't prescribe it. My kidney surgeon probably won't let me take, anyway, but it was worth a try.
He did take more blood than usual. One tube was ACTH, another renin. I don't know what the other tube was for. Probably just general metabolic.
I don't think I've ever had renin levels tested before. When I looked that up, there's a lot of kidney stuff. I sure hope that there's nothing wrong with my kidney. I've been so careful.
He did mention that in "only" 2.5 years maybe I can go back on growth hormone. I don't want to live like this another year let alone 2.5. But then, when I was on GH before it didn't help me like it helps most everyone else.
I'm tired of catering to a kidney that may or may not fail sometime anyway, tired of being so exhausted all the time. I feel like I've lost nearly half my life to this Cushing's stuff already.
A bit about rennin levels from http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/ency/plasma_renin_activity.jsp
Definition
Renin is an enzyme released by the kidney to help control the body's sodium-potassium balance, fluid volume, and blood pressure.
Purpose
Plasma renin activity (PRA), also called plasma renin assay, may be used to screen for high blood pressure (hypertension) of kidney origin, and may help plan treatment of essential hypertension, a genetic disease often aggravated by excess sodium intake. PRA is also used to further evaluate a diagnosis of excess aldosterone, a hormone secreted by the adrenal cortex, in a condition called Conn's syndrome.
Precautions
Patients taking diuretics, antihypertensives, vasodilators, oral contraceptives, and licorice should discontinue use of these substances for two to four weeks before the test. It should be noted that renin is increased in pregnancy and in diets with reduced salt intake. Also, since renin is affected by body position, as well as by diurnal (daily) variation, blood samples should be drawn in the morning, and the position of the patient (sitting or lying down) should be noted.
Description
When the kidneys release the enzyme renin in response to certain conditions (high blood potassium, low blood sodium, decreased blood volume), it is the first step in what is called the renin-angiotensin-aldosterone cycle. This cycle includes the conversion of angiotensinogen to angiotensin I, which in turn is converted to angiotensin II, in the lung. Angiotensin II is a powerful blood vessel constrictor, and its action stimulates the release of aldosterone from an area of the adrenal glands called the adrenal cortex. Together, angiotensin and aldosterone increase the blood volume, the blood pressure, and the blood sodium to re-establish the body's sodium-potassium and fluid volume balance. Primary aldosteronism, the symptoms of which include hypertension and low blood potassium (hypokalemia), is considered "low-renin aldosteronism."
Renin itself is not actually measured in the PRA test, because renin can be measured only with great difficulty even in research laboratories. In the most commonly used renin assay, the test actually determines, by a procedure called radioimmunoassay, the rate of angiotensin I generation per unit time, while the PRC (plasma renin concentration) measures the maximum renin effect.
Both the PRA and the PRC are extremely difficult to perform. Not only is renin itself unstable, but the patient's body position and the time of day affect the results. Also, the sample must be collected properly: drawn into a chilled syringe and collection tube, placed on ice, and sent to the performing laboratory immediately. Even if all these procedures are followed, results can vary significantly.
A determination of the PRA and a measurement of the plasma aldosterone level are used in the differential diagnosis of primary and secondary hyperaldosteronism. Patients with primary hyperaldosteronism (caused by an adrenal tumor that overproduces aldosterone) will have an increased aldosterone level with decreased renin activity. Conversely, patients with secondary hyperaldosteronism (caused by certain types of kidney disease) will have increased levels of renin.
Conn syndrome? I don't want that, either! I just want a normal, healthy life for a few years. AARRGGHH.
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