• When urinary albumin excretion was measured by radioimmunoassay, most diabetics excreted more albumin than nondiabetic subjects. Microalbuminuria was defined as an albumin excretion greater than 30 mg/g of urinary creatinine, more than twice the upper limit of normal. Intermittent microalbuminuria was found in 20% of patients with insulin-dependent diabetes mellitus (IDDM) or non—insulin-dependent diabetes mellitus (NIDDM). Continuous microalbuminuria occurred in a similar percentage of patients with NIDDM, but less frequently in patients with IDDM. Rigorous control of glycemia was followed by cessation of microalbuminuria in nearly half of these patients. Microalbuminuria was associated with an increased incidence of other microvascular complications, as well as a distinctly higher plasma prorenin value in IDDM. Hypertension of 160/100 mm Hg or above was accompanied by increased albumin excretion and lower plasma prorenin values than in normotensive diabetics. (Arch Intern Med1988;148:937-941)

The relative roles of ACTH, angiotensin and potassium in influencing aldosterone secretion in primary aldosteronism were assessed by direct or indirect means. In untreated patients with primary aldosteronism caused either by adrenal adenoma or hyperplasia plasma aldosterone and cortisol concentrations fluctuated in unison and dexamethasone reduced both hormones markedly. Only when renin-angiotensin system was greatly activated and plasma potassium normalized by medical treatment was dexamethasone less successful in lowering plasma aldosterone concentration. Potassium infusion of 10,20 and 30 mEq/hr in patients with adenoma failed to elicit any increase in plasma aldosterone concentration despite significant increases in plasma potassium levels. These results suggest that patients with primary aldosteronism due to adrenal adenoma are relatively more sensitive to small changes in plasma ACTH level than those in plasma angiotensin or potassium levels. In recumbent patients with adrenal hyperplasia ACTH also modulates plasma aldosterone concentration.

Tetrahydrocortisone, tetrahydrocortisol, and allotetrahydrocortisol can be separated by gas—liquid chromatography and quantitated with an argon ionization detector. The retention times of these cortisol metabolites are identical with those of their 17-ketosteroid analogs. This technique has been used to monitor the compostion of fractions from liquid-liquid chromatograms of urine extracts.

s1 April 1963John Phillips Memorial Lecture: Observations on Metabolism of Aldosterone in Man.John A. Luetscher, M.D.John A. Luetscher, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-58-4-719_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe circulating level of aldosterone reflects the balance between rate of secretion by the adrenals and metabolic clearance rate by the liver. Although the concentration of aldosterone in plasma is too low to be measured accurately, the mean plasma level can be calculated. Secretion rate is estimated from measured specific activity of a purified metabolite after injection of labeled aldosterone. In most instances, the quantity released from strongly acidified urine serves as a fair index of secretion rate; but in pregnancy, renal insufficiency, or hepatic cirrhosis, the fraction of secreted aldosterone metabolized to this form is abnormal. Metabolic clearance rate... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: John A. Luetscher, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1963Volume 58, Issue 4Page: 719-719KeywordsAldosteroneAttentionBlood plasmaCirrhosisLiverMetabolitesPregnancyUrine ePublished: 1 December 2008 Issue Published: 1 April 1963 PDF downloadLoading ...

HomeCirculationVol. 25, No. 6SYMPOSIUM ON THE ROLE OF HORMONES IN HEART FAILURE Free AccessResearch ArticlePDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBSYMPOSIUM ON THE ROLE OF HORMONES IN HEART FAILURE Introduction JOHN A. LUETSCHER JOHN A. LUETSCHERJOHN A. LUETSCHER GUEST EDITOR Search for more papers by this author Originally published1 Jun 1962https://doi.org/10.1161/01.CIR.25.6.1001Circulation. 1962;25:1001"SYMPOSIUM ON THE ROLE OF HORMONES IN HEART FAILURE ." Circulation, 25(6), p. 1001 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Genth-Zotz S, Zotz R, Sigmund M, Hanrath P, Hartmann D, Böhm M, Waagstein F, Treese N, Meyer J and Darius H (2012) MIC trial: metoprolol in patients with mild to moderate heart failure: effects on ventricular function and cardiopulmonary exercise testing, European Journal of Heart Failure, 10.1016/S1388-9842(00)00078-7, 2:2, (175-181), Online publication date: 1-Jun-2000. June 1, 1962Vol 25, Issue 6 Advertisement Article InformationMetrics © 1962 American Heart Association, Inc.https://doi.org/10.1161/01.CIR.25.6.1001 Originally publishedJune 1, 1962 PDF download Advertisement

Patients complaining of an insidious onset of edema and showing heavy proteinuria, a low serum albumin concentration, and high blood fats and cholesterol present the cardinal manifestations of the nephrotic syndrome, or lipemic nephrosis. Current ideas on the etiology, pathology, and treatment of this syndrome have been summarized in recent reviews.* The underlying pathology is in the kidneys, and the first aim of treatment is to promote the healing of the renal lesion, on which the ultimate outcome depends. During the course of the disease, numerous secondary manifestations may appear. In the early stages we commonly see oliguria, retention of sodium and water with edema, and alterations in the concentration of sodium, potassium, or calcium in the blood. Later, especially in those patients with destructive renal lesions, there is progressive azotemia, with acidosis, anemia, and hypertension.† Today we are to consider the disturbances of water and electrolytes in the nephrotic

Patients complaining of an insidious onset of edema and showing heavy proteinuria, a low serum albumin concentration, and high blood fats and cholesterol present the cardinal manifestations of the nephrotic syndrome, or lipemic nephrosis. Current ideas on the etiology, pathology, and treatment of this syndrome have been summarized in recent reviews.* The underlying pathology is in the kidneys, and the first aim of treatment is to promote the healing of the renal lesion, on which the ultimate outcome depends. During the course of the disease, numerous secondary manifestations may appear. In the early stages we commonly see oliguria, retention of sodium and water with edema, and alterations in the concentration of sodium, potassium, or calcium in the blood. Later, especially in those patients with destructive renal lesions, there is progressive azotemia, with acidosis, anemia, and hypertension.† Today we are to consider the disturbances of water and electrolytes in the nephrotic

re- present results on normal urine show sodium- retaining activity less than that found in earlier but definite sodium-retaining effect of the injected and a less satisfactory method of estimating dosage

This chapter contains section titled: References Discussion

An assay for desoxycortieoster-one-like activity in biological fluids is presented, having a sensitivity in the order of 10 y of DOCA. The critical nature of solvent vehicle choice and of time-dosage of urinary extracts is presented and discussed. Urinary extracts from some edematous patients with heart failure and nephrosis show a sodium-retaining activity greater than that observed in normals and in non-edematous controls.

The administration of concentrated human se- rum albumin to patients with the nephrotic syn- drome is followed by an effective diuresis in approximately one-half of the treated cases (1-4).Previous reports (3, 5) indicate that the injected albumin is diluted by extracellular fluid to ap- proximately the original level of plasma protein concentration until diuresis occurs.Replacement of the normal total amount of circulating albumin does not regularly ensure a return to normal con- ditions.The plasma proteins can be concentrated to normal levels only after elimination of most of the edema.These observations suggest that the inability of the kidneys to excrete normal quantities of so- dium and water in nephrosis (6-8) may be a cause, not a consequence, of the edema, and may help to maintain a low plasma protein concentra- tion.In the present study, certain aspects of the renal control of sodium and water excretion are examined, as well as some circulatory and hor- monal factors which influence this control. METHODSThe 13 patients were adults with the characteristic fea- tures of the nephrotic syndrome, without significant hy-

WEASK the reader's indulgence for some liberties in the selection and presentation of recent developments in renal disease. The literature on the kidney is too large to permit any complete description in these few pages. We have therefore chosen a few subjects of current interest for discussion. These include some studies of the earlier stages of glomerular nephritis and a glimpse of the gradually evolving cardiovascular-renal relations. The curious effects of large doses of vitamin D on the kidney are mentioned. The acute renal tubular injury that accompanies many types of bodily injury is now recognized as one of the . . .

Article1 May 1943SEVERE INJURY TO KIDNEYS AND BRAIN FOLLOWING SULFATHIAZOLE ADMINISTRATION: HIGH SERUM SODIUM AND CHLORIDE LEVELS AND PERSISTENT CEREBRAL DAMAGEJOHN A. LUETSCHER JR., SAM S. BLACKMAN JR.JOHN A. LUETSCHER JR., SAM S. BLACKMAN JR.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-18-5-741 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFive patients with a history of recent sulfonamide medication have developed an unusual type of renal insufficiency, as well as evidence of injury to the brain. The patients presented a temporary, severe disturbance of serum sodium and chloride concentration, which was responsible, at least in part, for the death of two patients. In all cases there were signs of injury to the central nervous system, which persisted in two patients despite return of the blood chemistry to normal.Case 1. This 25 year old colored laborer was brought to the hospital because of vomiting and delirium. His past health had...Bibliography1. PETERSVAN SLYKE JPDD: Quantitative clinical chemistry, 1931, The Williams and Wilkins Company, Baltimore, l, 761. Google Scholar2. PETERSWAKEMANEISENMANLEE JPAMAJC: Total acid-base equilibrium of plasma in health and disease. X. The acidosis of nephritis, Jr. Clin. Invest., 1929, vi, 517. CrossrefGoogle Scholar3. PETERSWAKEMANEISENMANLEE JPAMAJC: Total acid-base equilibrium of plasma in health and disease. XII. A study of renal edema, Jr. Clin. Invest., 1929, vi, 577. CrossrefGoogle Scholar4. PETERSWAKEMANLEE JPAMC: Total acid-base equilibrium of plasma in health and disease. XI. Hypochloremia and total salt deficiency in nephritis, Jr. Clin. Invest., 1929, vi, 551. CrossrefGoogle Scholar5. BUTLERWILSONFARBER AMJLS: Dehydration and acidosis with calcification at the renal tubules, Jr. Pediat., 1936, viii, 489. CrossrefGoogle Scholar6. ALBRIGHTCONSOLAZIOCOOMBSSULKOWITCHTALBOT FWVFSHWJH: Metabolic studies and therapy in a case of nephrocalcinosis with rickets and dwarfism, Bull. Johns Hopkins Hosp., 1940, lxvi, 7. Google Scholar7. CLIMENKOWRIGHT DRAW: Effects of continued administration of sulfathiazole and sulfapyridine in monkeys, Arch. Path., 1941, xxxii, 794. Google Scholar8. MAISELMCSWAINGLENN BBF: Lesions produced with sulfadiazine, Proc. Soc. Exper. Biol. and Med., 1942, xlix, 715. CrossrefGoogle Scholar9. DUNNGILLESPIENIVEN JMJS: Renal lesions in two cases of crush syndrome, Lancet, 1941, ii, 549. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Baltimore, Maryland*Received for publication March 13, 1943.From the Chemical Division, Department of Medicine, and the Department of Pathology, Johns Hopkins University and Hospital, Baltimore, Maryland. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCase 8-1967Postoperative management of fluid volumes and electrolytesHypokalemia and Hypertension A Presentation of Four Cases Including a Case of Primary AldosteronismDIABETIC COMA WITHOUT KETOACIDOSISHypernatraemia in cerebral disordersZellosmolarit�t und ZellwassergehaltProblems in fluid replacement and cerebral edema in the management of surgical lesions of the central nervous systemClinical and Experimental Interrelations of Sodium and the Central Nervous System*Chronische Hyperosmolarit�t bei Hirnsch�den an Hand eines Falles von CyklopenventrikelAn evaluation of intermittent peritoneal lavageSERUM HYPERTONICITY SECONDARY TO CEREBRAL DISEASE*MARVIN F. LEVITT, M.D., MARVIN BELSKY, M.D., DEMETRA POLIMEROS, B.S.Funktionelle Orthologie und Pathologie der NierenausscheidungHyperosmolarity in adults: A critical reviewHypernatremia, azotemia and acidosis after cerebral injuryHypernatraemia in Extrarenal UraemiaHYPERNATRÆMIA AND HYPERCHLORÆMIA IN BULBAR POLIOMYELITISTherapy of acute and chronic glomerulonephritisSulfonamideSulfonamideLower nephron nephrosisPOST-TRAUMATIC ACUTE RENAL INSUFFICIENCY COMPLICATED BY HYPERNATREMIA*PAUL D. DOOLAN, CHRISTOPHER C. SHAW, WALTON W. SHREEVE, HAROLD A. HARPER, Ph.D.Dehydration with hypernatremia, hyperchloremia and azotemia complicating nasogastric tube feedingElectrolyte abnormalities in epidemic hemorrhagic feverElectrolyte Disturbances in Cerebral LesionsHyperosmolarity of the extracellular fluid in encephalitisChronic hyperosmolarity of the body fluids with a cerebral lesion causing diabetes insipidus and anterior pitutiary insufficiencyDisorders of Electrolyte and Water Metabolism Following Brain SurgerySOME ASPECTS OF RENAL INSUFFICIENCY IN OBSTETRIC PRACTICECONSERVATIVE TREATMENT OF TUBULAR NECROSIS (LOWER NEPHRON NEPHROSIS)METABOLIC DISORDERS IN HEAD INJURY HYPERCHLORÆMIA AND HYPOCHLORURIAAcute Renal Insufficiency Due to Lower-Nephron NephrosisRenal DiseaseTreatment of Renal InsufficiencyKidney Complications during Sulphonamide Therapy1Renal damage resulting from idiosyncrasy to neoarsphenamineBiochemical Abnormalities during Renal InsufficiencySpecific Therapy in Acute Hemorrhagic NephritisManagement of the Patient with Chronic Diffuse Glomerulonephritis 1 May 1943Volume 18, Issue 5Page: 741-756KeywordsBlood chemistryBrainCentral nervous systemChloridesDeliriumHospital medicineKidneysSodiumSulfonamideVomiting ePublished: 1 December 2008 Issue Published: 1 May 1943 PDF downloadLoading ...

The amino acid content of fasting human blood appears to be quite constant. Extensive surveys (1) have revealed only a few diseases in which the blood amino acid level is modified significantly. Acute yellow atrophy of the liver is associated with a rise in amino acids in the blood, whereas hypoaminoacidemia has been reported in patients with nephrosis and in pneumococcal pneumonia (2). Concerning the fasting amino acid level in diabetes mellitus there is little agreement. Several investigators (la, 3) have observed elevated amino acid levels in a few of their diabetic subjects. Greene, Sandiford and Ross (lb) studied 116 diabetics and observed that the average amino acid level was within normal limits. No accurate data on the condition or treatment of these patients were given. On the other hand, a high blood amino acid content has been reported in dogs with experimentally induced diabetes (4). Luck, Morrison and Wilbur (5) observed that insulin lowered the amino acid content of blood in both experimental animals and normal human subjects. These results have been confirmed by several investigators (6) using the Folin colorimetric method and by Farr and Alpert (7) using Van Slyke and MacFadyen's manometric ninhydrin method (8). Luck also studied two diabetic patients under insulin treatment and observed low normal fasting amino acid levels. The lack of agreement of existing data on the blood amino acid content in human diabetes mellitus, together with the paucity of data on the clinical condition and therapy of the patients, suggested the present study.