Guest guest Posted September 10, 2009 Report Share Posted September 10, 2009 That's not just fluid retention, that's carb retention. My weight has gone up due to the tumor and my drug regimine. After I begin treatment, I plan to do a low carb diet or the DASH weight reduction to lose about 60 pounds. Bindner Web Directory (links to my sites and blogs): http://www.geocities.com/mikeybdc/index.html http://mikeybdc.blogspot.com >> , do you know why your weight has jumped so dramatically in such a> short time? If it is not from plain over-eating, then that needs to be> investigated.> > Val> > From: hyperaldosteronism> [mailto:hyperaldosteronism] On Behalf Of georgewbill> > > jwwright Are you saying you know more ther Dr Grim dose about Conn's He is> the one that is saying I should try meds for hyperaldo. He has said this> more then once based on what I have in this and other postings. > > > >> > , At the risk of losing my bedside manner award, I'll tell you like> it is.> > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo,> because you do not have the data to indicate that.> > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo.> > I have LREH.> > > > You're problem, according to your data is you are too FAT, as in BMI 44.> That makes you tired and sore.> > > > Get the "Rice Diet Solutions" book.> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 10, 2009 Report Share Posted September 10, 2009 I have seen your postings you say something about carb and conn's. What is the relationship between them. I have see something about aldosterone acting in the liver and in turn doing something with blood sugar. I know in some of my blood work my glucose has been high at times. > > > > > > , At the risk of losing my bedside manner award, I'll tell you like > > it is. > > > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo, > > because you do not have the data to indicate that. > > > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo. > > > I have LREH. > > > > > > You're problem, according to your data is you are too FAT, as in BMI 44. > > That makes you tired and sore. > > > > > > Get the " Rice Diet Solutions " book. > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 10, 2009 Report Share Posted September 10, 2009 All I know is that I lost weight on the carb addicts diet, at least until I added eggs and bread back into my diet. When I went back to work, stress went up and so did weight. When I changed meds to do tests, weight went up - I added a meal, although I have cut down portions and I think I may be stabilizing. The DASH diet takes off weight and I may try that after the AVS on Monday, when I hopefully will be starting Spiro. Hopefully after the tumor is removed the weight will come off more easily, assuming I have Conn's and not BH. Bindner Web Directory (links to my sites and blogs): http://www.geocities.com/mikeybdc/index.html http://mikeybdc.blogspot.com From: georgewbill <georgewbill@...>Subject: Re: How good is the screening tests for Conn's?hyperaldosteronism Date: Thursday, September 10, 2009, 9:20 PM I have seen your postings you say something about carb and conn's. What is the relationship between them. I have see something about aldosterone acting in the liver and in turn doing something with blood sugar. I know in some of my blood work my glucose has been high at times. > > >> > > , At the risk of losing my bedside manner award, I'll tell you like> > it is.> > > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo,> > because you do not have the data to indicate that.> > > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo.> > > I have LREH.> > > > > > You're problem, according to your data is you are too FAT, as in BMI 44.> > That makes you tired and sore.> > > > > > Get the "Rice Diet Solutions" book.> >> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 10, 2009 Report Share Posted September 10, 2009 Set the calories with DASH to 2000 and you will get the weight down. Clarence Grimlowerbp2@... On Sep 10, 2009, at 8:20 PM, georgewbill wrote: I have seen your postings you say something about carb and conn's. What is the relationship between them. I have see something about aldosterone acting in the liver and in turn doing something with blood sugar. I know in some of my blood work my glucose has been high at times. > > > > > > , At the risk of losing my bedside manner award, I'll tell you like > > it is. > > > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo, > > because you do not have the data to indicate that. > > > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo. > > > I have LREH. > > > > > > You're problem, according to your data is you are too FAT, as in BMI 44. > > That makes you tired and sore. > > > > > > Get the "Rice Diet Solutions" book. > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 11, 2009 Report Share Posted September 11, 2009 Awhile back, Dr Grim - you posted that anyone eating 1600 calories each day had to lose weight. I tried that with the Dash plan - and guess what - you were right! Ha! I've lost 7.6 kg in the past month, as I've always been active, I can only say it's the reduction in calories, not increased exercise. My resting heartrate has always been about 55-60, and although I consider myself obese with another 20kg to lose, I had no idea about salt, or the real number of calories to eat to lose -So thanks! SueFrom: Clarence Grim <lowerbp2@...>hyperaldosteronism Sent: Friday, 11 September, 2009 3:10:41 PMSubject: Re: Re: How good is the screening tests for Conn's? Set the calories with DASH to 2000 and you will get the weight down. Clarence Grimlowerbp2mac (DOT) com On Sep 10, 2009, at 8:20 PM, georgewbill wrote: I have seen your postings you say something about carb and conn's. What is the relationship between them. I have see something about aldosterone acting in the liver and in turn doing something with blood sugar. I know in some of my blood work my glucose has been high at times. > > > > > > , At the risk of losing my bedside manner award, I'll tell you like > > it is. > > > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo, > > because you do not have the data to indicate that. > > > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo. > > > I have LREH. > > > > > > You're problem, according to your data is you are too FAT, as in BMI 44. > > That makes you tired and sore. > > > > > > Get the "Rice Diet Solutions" book. > > > Reading this email at work? Make a change with Xtra Jobs Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 12, 2009 Report Share Posted September 12, 2009 Excellent I also suspect that salt increases appetite in general. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertensionOn Sep 11, 2009, at 8:53 PM, marysue hopper <marysuehopper@...> wrote: Awhile back, Dr Grim - you posted that anyone eating 1600 calories each day had to lose weight. I tried that with the Dash plan - and guess what - you were right! Ha! I've lost 7.6 kg in the past month, as I've always been active, I can only say it's the reduction in calories, not increased exercise. My resting heartrate has always been about 55-60, and although I consider myself obese with another 20kg to lose, I had no idea about salt, or the real number of calories to eat to lose -So thanks! SueFrom: Clarence Grim <lowerbp2mac>hyperaldosteronism Sent: Friday, 11 September, 2009 3:10:41 PMSubject: Re: Re: How good is the screening tests for Conn's? Set the calories with DASH to 2000 and you will get the weight down. Clarence Grimlowerbp2mac (DOT) com On Sep 10, 2009, at 8:20 PM, georgewbill wrote: I have seen your postings you say something about carb and conn's. What is the relationship between them. I have see something about aldosterone acting in the liver and in turn doing something with blood sugar. I know in some of my blood work my glucose has been high at times. > > > > > > , At the risk of losing my bedside manner award, I'll tell you like > > it is. > > > I'm not a DR but if I was, I wouldn't prescribe meds for hyperaldo, > > because you do not have the data to indicate that. > > > My renin is low, 0.2, and aldo 10 in range, and I do NOT have hyper aldo. > > > I have LREH. > > > > > > You're problem, according to your data is you are too FAT, as in BMI 44. > > That makes you tired and sore. > > > > > > Get the "Rice Diet Solutions" book. > > > Reading this email at work? Make a change with Xtra Jobs Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 From what is on here and other things I have read. I would say that in order to the right interpretation of the PRA, your doctor should know what your k is how much salt you have in your urine. So why don't they check this a day or so before doing PRA. Then there is the problem with testing while taking certain meds. Since some meds give a false negative result it is a waste of time and money to be tested on them. Once you are tested on the meds and get a negative result then as far is your doctor goes you don't have Conn's. Even though He doesn't know why your Blood presser in all over the place and your K is low. one on my doctots notes Lightheadedness and volatile BP without definable cause intense concern re health and lications of physiologic changes. K in hospital borderline low and he is not on thiazide. I have been told that the lightheadness I have all the time has nothing to do with conn's. > > > > > > > > > > > > > > > From: georgewbill <georgewbill@> > > > > > Subject: Re: How good is the screening > > tests > > > > for Conn's? > > > > > hyperaldosteronism > > > > > Date: Tuesday, September 8, 2009, 8:50 PM > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > This is from my Darmouth Medical > > > > > > > > > > LAB RESULTS: 00052074-2 03/04/2009 > > > > > > > > > > CO RT MDNITE SAL-MAYO 19* > > > > > (<:100-) > > > > > > > > > > DHEAS <30 L * > > > > > (42-290) > > > > > > > > > > RENIN ACTIVITY-MAYO 0.8* > > > > > (-) > > > > > > > > > > ALDOSTERONE- MAYO 5.5* > > > > > (<=21-) > > > > > > > > > > NORMETANE FREE-MAYO 0.86* > > > > > (<:0.90-) > > > > > > > > > > METANEPHR FREE-MAYO <0.20 * > > > > > ( <:0.50-) > > > > > > > > > > Assessment: > > > > > > > > > > Mr. Bill is a 61 years y.o. M with symptoms of daily > > > > lightheadednass and exartional > > > > > SOB with an incidentally discovered 2.1cm left adrenal mass whom > > > > we saw in our > > > > > Endocrinology Clinic at DHMC on 03/03/2009 for evaluation of the > > > > adrenal mass. > > > > > We felt at the time the pt's symptoms were likely unrelated to > > > > this adrenal > > > > > incidentaloma especially since he has had an extensive negative > > > > work-up in the past. > > > > > However, since most of his previous testing results were not > > > > available to us, and > > > > > the patient would like to be retested, we rechecked levels of: > > > > > midnight salivary cortisol > > > > > renin and aldosterone > > > > > DHEA-S > > > > > serum metanephrine and normetanephrine > > > > > to rule this lesion out as a functioning adenoma. > > > > > The results above show that there is no evidence that this > > adenoma > > > > is producing any > > > > > excess adrenal hormones. > > > > > > > > > > Plan/Instructions: > > > > > Pt was counselled and reassured that this likely represents a > > > > benign finding, > > > > > especially since the lesion has been stable over time and an > > > > extensive work-up in > > > > > the past has been negative as well. However, pt was asked to > > > > coordinate with his > > > > > PCP if he develops any new signs/symptoms or change in his > > present > > > > signs/symptoms. > > > > > Tharsan Sivakumar MD > > > > > Endocrinology Fellow > > > > > I am being supervised by TURCO MD,JOHN H Endocrinology > > > > > Electronically signed by: SIVAKUMAR MD, THARSAN 03/13/ 2009 > > 09:32 > > > > > + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + + > > + + > > > > + + + + + > > > > > MULTI-AUTHOR NOTE > > > > > I agree with these recommendations. > > > > > Jack Turco, M.D. > > > > > Electronically signed by: TURCO MD, JOHN H 03/18/2009 17:01 > > > > > > > > > > Reason for Consultation: > > > > > symptoms of lightheadedness, SOB with incidentally discovered > > > > adrenal > > > > > lesion > > > > > Referred by: > > > > > self > > > > > BPI: > > > > > Francis B. Bill is a 61 years y.o. M with PMH as below has had > > > > symptoms of all-day > > > > > lightheadedness and exertional shortness of breath for 3 years, > > > > which had been > > > > > worked up at the VA with CT, echo, Holter, and other studies > > which > > > > did not yield any > > > > > etiology for these symptoms. Pt presented to the ER for these > > > > symptoms several > > > > > times as well. > > > > > CT scan of the chest performed in 2006 to evaluate for the SOB > > > > showed a well defined > > > > > 7mm right lower lung lobe nodule. A left 2.1cm adrenal nodule > > was > > > > found as well > > > > > with soft tissue attenuation likely representing an adenoma. > > > > According DHMC > > > > > Emergency Medicine notes, these have been stable over time. > > > > > > > > > > PMSH: > > > > > hypertension, and dyslipidemia. > > > > > appendectomy, tonsil/adenoidectom y > > > > > > > > > > Medications: > > > > > AMBULATORY MEDICATIONS· Last charted on· 03/03/2009 > > > > > DRUG DOSE/ROUTE FREQUENCY > > > > > Aspirin 325 mg Tablet 650 MG = 2 Tablet(s) / PRN > > > > > Oral > > > > > Multivitamin Tablet 1 Tablet (s) / Oral Once daily > > > > > Furosemide 20 mg Tablet 60 MG = 3 Tablet(s) / Once daily > > > > > Oral > > > > > Potassium Chloride 10 mEg 20 MEQ = 2 Capsule(s) / Once daily > > > > > Capsule, Sustained Oral > > > > > Release > > > > > Atenolol 25 mg Tablet 25 MG = 1 Tablet (s) / Once daily > > > > > Oral > > > > > Triamterene 50 mg Capsule 50 MG = 1 Capsule (s) / Once daily > > > > > Oral > > > > > > > > > > Allergies: > > > > > ADR/ALLERGIES: Last charted on: 03/03/2009 > > > > > ADR/ALLERGY REACTION SEVERITY > > > > > Sulfonamides > > > > > > > > > > Social. history: > > > > > Very brief smoking history during teenage years > > > > > Asbestos exposure 15 years in a boiler room > > > > > Denies ETOH > > > > > never married > > > > > no children > > > > > > > > > > Famil.y Hx: > > > > > Thyroid dysfunction: Mother, sister > > > > > Thyroid cancer: No > > > > > Diabetes mellitus: No > > > > > Other auto-immune diseases: No > > > > > Vitiligo: No > > > > > > > > > > Physical Exam > > > > > Vitals: > > > > > VITAL SIGNS (03/03/2009 @ 14·44) > > > > > Heart Rate 96 > > > > > Systolic BP 156 > > > > > Diastolic BP 91 > > > > > Mean BP 112.67 > > > > > Weight (kg) 137.16 > > > > > Height (cm) 176.9 > > > > > Body Surface Area (m2 ) 2.6 > > > > > BMI (kg/m 2 ) 43.83 > > > > > Pain Scale 0 > > > > > Smoking > > > > > Smoke History Remote > > > > > General: NAD, morbidly obese > > > > > HEENT: EOMI, anicteric, PERRL, moist mucous membranes, full > > visual > > > > fundi > > > > > Neck: No LAD, no thyromegaly, no tenderness > > > > > CV: Sl S2, RRR > > > > > Lungs: CTAB > > > > > Abd: soft, NT, obese > > > > > Neuro: reflexes difficult to elicit > > > > > Extremities: trace ankle edema > > > > > Integumentary: Skin warm/dry/intact; no hyperpigmentation of > > hand > > > > creases or > > > > > gumline/ rash > > > > > 06/06 > > > > > K 4.0 > > > > > 08/06 > > > > > TSH 2.34 > > > > > cortisol 14:38 pm 12.0 ug/dL > > > > > 03/2007 > > > > > VMA 6.4 (ref 2.0-10.0) > > > > > Assessment and Plan: > > > > > Mr. Bill is a 61 years y.o. M as above with symptoms of daily > > > > lightheadedness and > > > > > exertional SOB with an incidentally discovered 2.1cm left > > adrenal > > > > mass. > > > > > Pt's symptoms are likely unrelated to this adrenal incidentaloma > > > > especially since he > > > > > has had an extensive negative work-up in the past. However, > > since > > > > most of these > > > > > results are not available to us, and the patient would like to > > be > > > > retested, we will > > > > > check levels of: > > > > > midnight salivary cortisol > > > > > renin and aldosterone > > > > > DHEA-S > > > > > serum metanephrine and normetanephrine > > > > > to rule this lesion out as a functioning adenoma. > > > > > Pt was counselled and reassured that this likely represents a > > > > benign finding, > > > > > especially since the lesion has been stable over time. > > However, pt > > > > was asked to > > > > > coordinate with his PCP if he develops any new signs/symptoms or > > > > change in his > > > > > present signs/symptoms. > > > > > We have reviewed our plan outlined above with the patient and > > Mr. > > > > Bill verbalized > > > > > understanding. All questions were answered. > > > > > Tharsan Sivakumar, MD > > > > > Endocrinology Fellow > > > > > I am being supervised by TURCO MD,JOHN H Endocrinology > > > > > Electronically signed by: SIVAKUMAR MD, THARSAN 03/03/2009 15:58 > > > > > > > > > > MULTI-AUTHOR NOTE > > > > > I have interviewed and examined this patient along with Dr. > > > > Sivakumar and agree with > > > > > this note and also these recommendations. The patient will be > > > > contacted with final > > > > > recommendations when results of testing are complete. > > > > > >50% of the 60 minute appointment was spent in face to face > > > > counseling the patient > > > > > about the possible significance and evaluation of his adrenal > > > > abnormality. > > > > > Jack Turco, M.D. > > > > > Communication sent to: L. Durand 03/03/2009 17:28 > > > > > Electronically signed by: TURCO MD, JOHN H 03/03/2009 17:28 > > > > > > > > > > DARTMOUTH-HITCHCOCK MEDICAL CENTER > > > > > ENCOUNTER DATE: 08/06/ 2009 > > > > > OFFICE NOTES > > > > > BILL,FRANCIS H > > > > > > > > > > Nephrology Clinic New Patient Visit > > > > > Francis H. Bill > > > > > > > > > > August 6, 2009 > > > > > ID: 62 years old male seen at the request of Dr. Mogielnicki > > for? > > > > Conns Syndrome. > > > > > Past Medical History: > > > > > HTN diagnosed about 5 yrs ago > > > > > Chronic Fatigue Syndrome > > > > > Chronic dyspnea > > > > > Chronic dizziness > > > > > s/p appendectomy in Dec 2008 > > > > > Multiple granulomas in the Lungs > > > > > Exophytic cyst Lt kidney > > > > > > > > > > History of Present Illness: > > > > > Mr Bill presents today for a second opinion regarding whether he > > > > might have Conns > > > > > Syndrome. In 2006, he underwent w/u for SOB. He had a CT scan of > > > > the chest which > > > > > showed a 2.1 cm soft tisuue mass in the Lt adrenal gland. > > > > Subsequent tests showed > > > > > that the adenoma was non secretory. He has since undergone > > several > > > > chest CT and the > > > > > adrenal mass has not grown is size. In March 2009, he was seen > > by > > > > endocrinology at > > > > > DHMC. He again underwent testing including cortisol, PRA, > > > > aldosterone, metanephrines > > > > > etc, all of which were within normal limits. Patient was > > reassured > > > > that this likely > > > > > represents an incidentaloma. > > > > > Over the past 3-4 yrs, he has had chronic SOB and dizziness . He > > > > has undergone > > > > > extensive testing for both including EKG, stress tests, > > > > echocardiograms, Holter > > > > > montior, MRI brain (to r/o acoustic neuroma), sleep studies, > > PFTs > > > > etc all of which > > > > > have not identified an abnormality. > > > > > In Dec 2008, he presented with abd pain and was found to have > > > > appendicitis on CT > > > > > scan. It also showed an exophytic mass in the L kidney for which > > > > he unerwent an > > > > > ultrasound. He was told by his PCP that he needs f /u CT scan > > for > > > > the lesion. I do > > > > > not have records relating to this issue today. > > > > > He has normal renal fucnti on ( Cr from VA records has ranged > > from > > > > 0.8-1.1 in the > > > > > past 3 yrs) . > > > > > AMBULATORY MEDICATIONS· Last charted on· 08/06/2009 > > > > > DRUG DOSE/ROUTE FREQUENCY > > > > > Aspirin 325 mg Tablet 650 MG = 2 Tablet(s) / PRN > > > > > Oral > > > > > Furosemide 20 mg Tablet 60 MG = 3 Tablet(s) / Once daily > > > > > Oral > > > > > Potassium Chloride 10 mEq 20 MEQ = 2 Capsule(s) / Once daily > > > > > Capsule, Sustained Oral > > > > > Release > > > > > Atenolol 25 mg Tablet 25 MG = 1 Tablet(s) / Once daily > > > > > Triamterene 50 mg Capsule 50 MG = 1 Capsule (s) / Once daily > > > > > Oral > > > > > Multivitamin Tablet 1 Tablet (s) / Oral > > > > > ADR/ALLERGIES: Last charted on: 08/06/2009 > > > > > ADR/ALLERGY REACTION SEVERITY > > > > > Sulfonamides > > > > > > > > > > Family History: > > > > > No family h/o renal disease. He denies family h/o DM and CAD. > > > > > Social History: > > > > > Lives in Enfield NH. Vietnam war vet, now on disability 2 to > > > > chronic fatigue > > > > > syndrme. Quit smoking 40 yrs ago, denies ETOH ot illicit drug > > use. > > > > > > > > > > Review of Systems: > > > > > System Abnormalities > > > > > Constitutional gained 40 Ibs over the past 3-4 yrs, + cheonic > > > > fatigue > > > > > Eye denies visual changes > > > > > ENT denies sorethroay, odynophagia > > > > > CV denies CP, palp > > > > > Resp + SOB, + DOE, denies cough, PND or orthopnea > > > > > GI denies loss appetite, change in bowel habit > > > > > GU denies hematuria, dysuria, voiding difficulties > > > > > Skin denies rash, hype rp igment at ion > > > > > Allergy > > > > > Endocrine no h/o DM, denies exessive sweating, heat or cold > > > > intolerance > > > > > Neurologic denies h/o seizures, headahces > > > > > Musculoskeletal denies muscle aches, joint swelling > > > > > Lymph > > > > > Psych denies depression > > > > > All other systems reviewed and negative. > > > > > > > > > > Physical Examination: > > > > > VITAL SIGNS (08/06/2009 @ 13:28) > > > > > Temperature © 36.61 > > > > > Route Oral > > > > > Heart Rate 82 > > > > > Rhythm Regular > > > > > Method Radial > > > > > Systolic BP 149 > > > > > Diastolic BP 72 > > > > > Patient Position Sitting > > > > > Extremity Left Arm > > > > > Method NIBP > > > > > Mean BP 97.67 > > > > > Weight (kg) 140.61 > > > > > Height (cm) 177.8 > > > > > Body Surface Area (m2 ) 2.64 > > > > > BMI (kg/m 2 ) 44.48 > > > > > > > > > > General: elderly man, NAD, dishevelled > > > > > Eye: no scleral icterus, EOM intact > > > > > ENT: no pharyngeal erythema or thrush, poor dentition > > > > > Neck: no JVD, no thyromegaly > > > > > CV: sl s2 reg, no murmur > > > > > Resp: CTAB > > > > > Abd: + BS, NT/NO, obese > > > > > Lymph: no cervical adenopathy > > > > > Ext: no LE Edema > > > > > Skin: no rash, hyperpigmentation > > > > > Neuro: no focal motor deficit, sensations intact > > > > > Psych: alert and oriented. affect appropriate > > > > > Labs: > > > > > LAB RESULTS: 00052074-2 03/04/2009 > > > > > > > > > > CO RT MDNITE SAL-MAYO 19* > > > > > (<:100-) > > > > > > > > > > DHEAS <30 L * > > > > > (42-290) > > > > > > > > > > RENIN ACTIVITY-MAYO 0.8* > > > > > (-) > > > > > > > > > > ALDOSTERONE- MAYO 5.5* > > > > > (<=21-) > > > > > > > > > > NORMETANE FREE-MAYO 0.86* > > > > > (<:0.90-) > > > > > > > > > > METANEPHR FREE-MAYO <0.20 * > > > > > ( <:0.50-) > > > > > > > > > > Records from WRJVA reviewed and will be scanned into CIS. > > > > > AlP: > > > > > 62 M with chronic fatigue, > > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 You are correct about sodium affecting PRA. My renin was 0.5 and 0.9 on normal/low sodium. On ultra-low sodium, it rose to 1.85. My urinary sodium at that time was too low to quantitate. The PRA assumes " normal " sodium and thus, becomes worthless if one's urinary sodium is too low to measure. Of course, the Mayo doc who saw that exclaimed that he'd never before seen such low sodium. Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Francis Bill From what is on here and other things I have read. I would say that in order to the right interpretation of the PRA, your doctor should know what your k is how much salt you have in your urine. So why don't they check this a day or so before doing PRA. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 Actually the lower the ENa the better. The problem is getting most to such a low intake. Therefore even Mayo does not hAve normAls at thatow of an ENa. We need to teach most Endos about this concept. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertensionOn Sep 22, 2009, at 3:27 PM, Valarie <val@...> wrote: You are correct about sodium affecting PRA. My renin was 0.5 and 0.9 on normal/low sodium. On ultra-low sodium, it rose to 1.85. My urinary sodium at that time was too low to quantitate. The PRA assumes "normal" sodium and thus, becomes worthless if one's urinary sodium is too low to measure. Of course, the Mayo doc who saw that exclaimed that he'd never before seen such low sodium. Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Francis Bill From what is on here and other things I have read. I would say that in order to the right interpretation of the PRA, your doctor should know what your k is how much salt you have in your urine. So why don't they check this a day or so before doing PRA. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 Dr Grim do you use mayo lab? If so do you do as they say or do you stop meds that you know will affect the tests. I know you do stop the meds. Here is what they say to do. Renin - Aldosterone Studies A. Renin-Angiotensin-Aldosterone System: 1. Renin is secreted by the juxtaglomerular cells of the kidneys in response to changes in plasma volume. An increase in renin normally produces an increase in aldosterone through angiotensin intermediates. Renin's physiological effects are manifested mainly through its changes on aldosterone production. Aldosterone is produced by the adrenal glands and fluctuates normally with changes in renin levels. With aldosterone-producing tumors, the serum aldosterone level is elevated even though renin is suppressed. Aldosterone production results in retention of sodium and excretion of potassium. B. Usual Laboratory Test Findings in Renin—Aldosterone Disorders: 1. Renal disease, such as unilateral renal artery stenosis, results in elevated renin and aldosterone levels. Renal venous catheterization may be helpful. A positive test is a renal venous renin ratio (affected/normal) >1.5. 2. Primary aldosteronism is manifested by low renin and elevated aldosterone levels. The aldosterone level will not be suppressed by a high salt intake, whereas in normals it will. An elevated urinary aldosterone excretion rate and increased levels of serum aldosterone associated with low plasma renin activity is presumptive evidence for primary aldosteronism. C. Preparation of Patient for Plasma Renin Activity Determination: 1. When screening for primary aldosteronism, no preparation is required. The plasma renin activity cannot be interpreted if the patient is being treated with spironolactone (Aldactone®). Spironolactone should be discontinued for 4 to 6 weeks before testing. 2. When performing renal vein renins to investigate renovascular hypertension, the angiotensin converting enzyme (ACE) inhibition protocol may be used. It has been shown that acute administration of drugs which block the action of ACE will enhance renin lateralization. Surprisingly, the effect is not seen if 3 drugs are given chronically. An advantage of this protocol is that the inhibiting effects of other drugs can be eliminated, and it is unnecessary to allow a washout period to pass. Captopril (Capoten®—Squibb) is available as a converting enzyme inhibitor. Reports of renal toxicity by a variety of mechanisms are known. It would appear, however, that a single dose for testing purposes is relatively innocuous. Administer captopril 25 mg by mouth 30 minutes prior to the procedure. Caution should be taken to guard against orthostatic hypotension. D. Preparation of Patient and Specimens for Primary Aldosteronism Study: 1. Screening testing—the serum aldosterone to plasma renin activity (SA/PRA) ratio a. No salt depletion is necessary. b. Collect a simultaneous blood specimen for plasma aldosterone and plasma renin activity before 10 a.m. No special posture instructions are needed. Blood should be drawn in the seated position. The SA/PRA ratio may be performed while the patient is on antihypertensive medications. Spironolactone is the only medication that will absolutely interfere with interpretation of the ratio. ACE inhibitors have the potential to " falsely elevate " PRA. Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low SA/PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor. A high ratio of SA (in ng/dL) to PRA (in ng/mL/hour) is a positive screening test result, a finding that warrants further testing. An SA/PRA ratio m20 and SA m15 ng/dL indicates probable primary aldosteronism. 2. Confirmatory testing—aldosterone suppression testing An elevated SA/PRA ratio is not diagnostic by itself, and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion. The list of drugs and hormones capable of affecting the renin-angiotensin-aldosterone axis is extensive; and frequently in patients with severe hypertension, a " medication-contaminated " evaluation is unavoidable. Calcium channel blockers, a1-adrenergic receptor blockers, and ß-adrenergic receptor blockers do not affect the diagnostic accuracy in most cases. It is impossible to interpret data obtained from patients receiving treatment with spironolactone. Therefore, spironolactone treatment should not be initiated until the evaluation is completed and the final decisions about treatment are made. If primary aldosteronism is suspected in a patient receiving treatment with spironolactone, the treatment should be discontinued for at least 6 weeks. Aldosterone suppression testing can be performed with orally administered sodium chloride and measurement of urinary aldosterone or with intravenous sodium chloride loading and measurement of SA. Our practice has been oral salt loading over 3 days. After hypertension and hypokalemia are controlled, patients should receive a high sodium diet (supplemented with sodium chloride tablets if needed) for 3 days. The risk of increasing dietary sodium in patients with severe hypertension must be assessed in each case. Because the high salt diet can increase kaliuresis and hypokalemia, vigorous replacement of potassium chloride should be prescribed. On the third day of the high sodium diet, a 24-hour urine specimen is collected for measurement of aldosterone, sodium, and potassium. The 24-hour urinary sodium excretion should exceed 200 mEq to document adequate sodium repletion. Urinary aldosterone excretion >12 mg/24 hours in this setting is consistent with hyperaldosteronism. > > > You are correct about sodium affecting PRA. My renin was 0.5 and > > 0.9 on normal/low sodium. On ultra-low sodium, it rose to 1.85. My > > urinary sodium at that time was too low to quantitate. The PRA > > assumes " normal " sodium and thus, becomes worthless if one's urinary > > sodium is too low to measure. Of course, the Mayo doc who saw that > > exclaimed that he'd never before seen such low sodium. > > > > > > > > Val > > > > > > > > From: hyperaldosteronism > > [mailto:hyperaldosteronism ] On Behalf Of Francis Bill > > > > > > From what is on here and other things I have read. I would say that > > in order to the right interpretation of the PRA, your doctor should > > know what your k is how much salt you have in your urine. So why > > don't they check this a day or so before doing PRA. > > > > > > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 I need to find a new doc. I visited my endo in late August and she said she couldn't do anything more for me. She concluded that Dr. Young at Mayo said I didn't have PA. That's not what he said but she wasn't interested in pursuing and I'm not interested in seeing her again either. She has my record computerized and couldn't find it in the system. I don't think she's teachable. She gave me a year's spiro and K. I feel a little better when I take 10 mEq K/day. I'm seeing the Lyme doc in CA again in October. My tests are still equivocal. Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Clarence Grim Actually the lower the ENa the better. The problem is getting most to such a low intake. Therefore even Mayo does not hAve normAls at thatow of an ENa. We need to teach most Endos about this concept. On Sep 22, 2009, at 3:27 PM, Valarie <val@...> wrote: The PRA assumes " normal " sodium and thus, becomes worthless if one's urinary sodium is too low to measure. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 If you don't have a copy of your records you need to get them It is your right to have them. You may have to pay a fee to get them but it is worth it. Not that that it will help you with any doctors. You need to know every thing there is in them. > The PRA assumes " normal " sodium and thus, becomes worthless if one's urinary > sodium is too low to measure. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 Did u ever try inspra again?Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertensionOn Sep 22, 2009, at 7:30 PM, Francis Bill <georgewbill@...> wrote: If you don't have a copy of your records you need to get them It is your right to have them. You may have to pay a fee to get them but it is worth it. Not that that it will help you with any doctors. You need to know every thing there is in them. > The PRA assumes "normal" sodium and thus, becomes worthless if one's urinary > sodium is too low to measure. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 I have everything for many years back. Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Francis Bill If you don't have a copy of your records you need to get them It is your right to have them. You may have to pay a fee to get them but it is worth it. Not that that it will help you with any doctors. You need to know every thing there is in them. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 I never tried Inspra since the first time in March 2008. It made me very nauseous then so I would have to gradually exchange spiro for Inspra. Do you think Inspra would do any better for me? Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Clarence Grim Did u ever try inspra again? Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 22, 2009 Report Share Posted September 22, 2009 As they note many drugs will interfere with renin and Aldo. Therefore ideally one should test without any drugs on board. This has been my approach for about 45 years. More later. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertensionOn Sep 22, 2009, at 5:33 PM, Francis Bill <georgewbill@...> wrote: Dr Grim do you use mayo lab? If so do you do as they say or do you stop meds that you know will affect the tests. I know you do stop the meds. Here is what they say to do. Renin - Aldosterone Studies A. Renin-Angiotensin-Aldosterone System: 1. Renin is secreted by the juxtaglomerular cells of the kidneys in response to changes in plasma volume. An increase in renin normally produces an increase in aldosterone through angiotensin intermediates. Renin's physiological effects are manifested mainly through its changes on aldosterone production. Aldosterone is produced by the adrenal glands and fluctuates normally with changes in renin levels. With aldosterone-producing tumors, the serum aldosterone level is elevated even though renin is suppressed. Aldosterone production results in retention of sodium and excretion of potassium. B. Usual Laboratory Test Findings in Renin—Aldosterone Disorders: 1. Renal disease, such as unilateral renal artery stenosis, results in elevated renin and aldosterone levels. Renal venous catheterization may be helpful. A positive test is a renal venous renin ratio (affected/normal) >1.5. 2. Primary aldosteronism is manifested by low renin and elevated aldosterone levels. The aldosterone level will not be suppressed by a high salt intake, whereas in normals it will. An elevated urinary aldosterone excretion rate and increased levels of serum aldosterone associated with low plasma renin activity is presumptive evidence for primary aldosteronism. C. Preparation of Patient for Plasma Renin Activity Determination: 1. When screening for primary aldosteronism, no preparation is required. The plasma renin activity cannot be interpreted if the patient is being treated with spironolactone (Aldactone®). Spironolactone should be discontinued for 4 to 6 weeks before testing. 2. When performing renal vein renins to investigate renovascular hypertension, the angiotensin converting enzyme (ACE) inhibition protocol may be used. It has been shown that acute administration of drugs which block the action of ACE will enhance renin lateralization. Surprisingly, the effect is not seen if 3 drugs are given chronically. An advantage of this protocol is that the inhibiting effects of other drugs can be eliminated, and it is unnecessary to allow a washout period to pass. Captopril (Capoten®—Squibb) is available as a converting enzyme inhibitor. Reports of renal toxicity by a variety of mechanisms are known. It would appear, however, that a single dose for testing purposes is relatively innocuous. Administer captopril 25 mg by mouth 30 minutes prior to the procedure. Caution should be taken to guard against orthostatic hypotension. D. Preparation of Patient and Specimens for Primary Aldosteronism Study: 1. Screening testing—the serum aldosterone to plasma renin activity (SA/PRA) ratio a. No salt depletion is necessary. b. Collect a simultaneous blood specimen for plasma aldosterone and plasma renin activity before 10 a.m. No special posture instructions are needed. Blood should be drawn in the seated position. The SA/PRA ratio may be performed while the patient is on antihypertensive medications. Spironolactone is the only medication that will absolutely interfere with interpretation of the ratio. ACE inhibitors have the potential to "falsely elevate" PRA. Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low SA/PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor. A high ratio of SA (in ng/dL) to PRA (in ng/mL/hour) is a positive screening test result, a finding that warrants further testing. An SA/PRA ratio m20 and SA m15 ng/dL indicates probable primary aldosteronism. 2. Confirmatory testing—aldosterone suppression testing An elevated SA/PRA ratio is not diagnostic by itself, and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion. The list of drugs and hormones capable of affecting the renin-angiotensin-aldosterone axis is extensive; and frequently in patients with severe hypertension, a "medication-contaminated" evaluation is unavoidable. Calcium channel blockers, a1-adrenergic receptor blockers, and ß-adrenergic receptor blockers do not affect the diagnostic accuracy in most cases. It is impossible to interpret data obtained from patients receiving treatment with spironolactone. Therefore, spironolactone treatment should not be initiated until the evaluation is completed and the final decisions about treatment are made. If primary aldosteronism is suspected in a patient receiving treatment with spironolactone, the treatment should be discontinued for at least 6 weeks. Aldosterone suppression testing can be performed with orally administered sodium chloride and measurement of urinary aldosterone or with intravenous sodium chloride loading and measurement of SA. Our practice has been oral salt loading over 3 days. After hypertension and hypokalemia are controlled, patients should receive a high sodium diet (supplemented with sodium chloride tablets if needed) for 3 days. The risk of increasing dietary sodium in patients with severe hypertension must be assessed in each case. Because the high salt diet can increase kaliuresis and hypokalemia, vigorous replacement of potassium chloride should be prescribed. On the third day of the high sodium diet, a 24-hour urine specimen is collected for measurement of aldosterone, sodium, and potassium. The 24-hour urinary sodium excretion should exceed 200 mEq to document adequate sodium repletion. Urinary aldosterone excretion >12 mg/24 hours in this setting is consistent with hyperaldosteronism. > > > You are correct about sodium affecting PRA. My renin was 0.5 and > > 0.9 on normal/low sodium. On ultra-low sodium, it rose to 1.85. My > > urinary sodium at that time was too low to quantitate. The PRA > > assumes "normal" sodium and thus, becomes worthless if one's urinary > > sodium is too low to measure. Of course, the Mayo doc who saw that > > exclaimed that he'd never before seen such low sodium. > > > > > > > > Val > > > > > > > > From: hyperaldosteronism > > [mailto:hyperaldosteronism ] On Behalf Of Francis Bill > > > > > > From what is on here and other things I have read. I would say that > > in order to the right interpretation of the PRA, your doctor should > > know what your k is how much salt you have in your urine. So why > > don't they check this a day or so before doing PRA. > > > > > > > Messages in this topic (37) Reply (via web post) | Start a new topic Recent Activity 4 New Members 1 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 23, 2009 Report Share Posted September 23, 2009 If you do as they say here you don't need to stop most meds. The SA/PRA ratio may be performed while the patient is on antihypertensive medications. Spironolactone is the only medication that will absolutely interfere with interpretation of the ratio. ACE inhibitors have the potential to " falsely elevate " PRA. Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low SA/PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor. > > > > > > > You are correct about sodium affecting PRA. My renin was 0.5 and > > > > 0.9 on normal/low sodium. On ultra-low sodium, it rose to 1.85. My > > > > urinary sodium at that time was too low to quantitate. The PRA > > > > assumes " normal " sodium and thus, becomes worthless if one's > > urinary > > > > sodium is too low to measure. Of course, the Mayo doc who saw that > > > > exclaimed that he'd never before seen such low sodium. > > > > > > > > > > > > > > > > Val > > > > > > > > > > > > > > > > From: hyperaldosteronism > > > > [mailto:hyperaldosteronism ] On Behalf Of Francis > > Bill > > > > > > > > > > > > From what is on here and other things I have read. I would say > > that > > > > in order to the right interpretation of the PRA, your doctor > > should > > > > know what your k is how much salt you have in your urine. So why > > > > don't they check this a day or so before doing PRA. > > > > > > > > > > > > > > > > > > > > > Messages in this topic (37) Reply (via web post) | Start a new topic > > Messages | Files | Photos | Links | Database | Polls | Members | > > Calendar > > > > Change settings via the Web ( ID required) > > Change settings via email: Switch delivery to Daily Digest | Switch > > format to Traditional > > Visit Your Group | Terms of Use | Unsubscribe > > RECENT ACTIVITY > > 4 > > New Members > > 1 > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 23, 2009 Report Share Posted September 23, 2009 Do you have them scaned into your computer? Again this may be something you may want to pay someone to do. They should be scaned so you can search them. > > I have everything for many years back. > > Val > > From: hyperaldosteronism > [mailto:hyperaldosteronism ] On Behalf Of Francis Bill > > > If you don't have a copy of your records you need to get them It is your > right to have them. You may have to pay a fee to get them but it is worth > it. Not that that it will help you with any doctors. You need to know every > thing there is in them. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted September 23, 2009 Report Share Posted September 23, 2009 It might be worth a try again. Maybe small dose and work up as you decrease spiro. Clarence Grimlowerbp2@... On Sep 22, 2009, at 11:01 PM, Valarie wrote: I never tried Inspra since the first time in March 2008. It made me very nauseous then so I would have to gradually exchange spiro for Inspra. Do you think Inspra would do any better for me? Val From: hyperaldosteronism [mailto:hyperaldosteronism ] On Behalf Of Clarence Grim Did u ever try inspra again? Quote Link to comment Share on other sites More sharing options...
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