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      Focal Segmental Glomerular Sclerosis in Two Patients with Addison’s Disease: Any More than Fortuitous Development of Glomerular Disease?

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          Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison’s disease. We report the clinical and biological conditions of 2 patients with Addison’s disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison’s disease.

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          Association of hypotension with hyperreninemic hypoaldosteronism in the critically ill patient.

          Paradoxical suppression of plasma aldosterone (PA) despite increased plasma renin activity (PRA) has recently been noted in some critically ill patients. To determine the prevalence of this entity and to identify possible etiologic factors, we studied 100 consecutive patients admitted to a medical intensive care unit (ICU). Twenty-two of 100 ICU patients had hyperreninemia and inappropriately reduced PA concentrations, with a PA to PRA ratio less than the 98th percentile of the control population. Comparison of clinical data of these 22 patients with the other hyperreninemic ICU patients revealed no differences in electrolyte concentrations, nutrition, medications, or survival. However, persistent hypotension was much more frequent (91% v 53%). Thus, impaired aldosterone response to hyperreninemia has a high prevalence among critically ill patients and may be related to adrenal damage from persistent hypotension.
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            Nephrotic Syndrome, Hyperreninemia and Multiple Transplant Renal Arterial Stenoses in a Patient with Diabetes

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              Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

              A 24-year-old Japanese woman with IgA nephropathy exhibited a decreased serum aldosterone level with normal plasma renin activity after toxemia of pregnancy. Our studies revealed selective hypoaldosteronism with normal adrenoglucocorticoid functions. Levels of serum corticosterone and deoxycorticosterone were normal. Resting plasma renin activity was normal, and plasma levels of total and inactive renin were increased. Rapid ACTH administration failed to stimulate any secretion of aldosterone, whereas it adequately increased serum cortisol, deoxycorticosterone, and corticosterone concentrations. Responses of both plasma renin activity and serum aldosterone level to the furosemide-posture challenge were blunted. Angiotensin II also failed to stimulate any secretion of aldosterone despite a progressive rise in blood pressure and an appropriate increase in serum corticosterone. These results suggest that combined defects of the conversion from inactive renin to active renin and aldosterone biosynthesis are the causes of selective hypoaldosteronism in our patient.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                August 2002
                02 August 2002
                : 22
                : 4
                : 389-393
                Services of aNephrology, bPathology, and cEndocrinology, Hospital Clínic, Institut d’Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain
                65234 Am J Nephrol 2002;22:389–393
                © 2002 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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                Figures: 3, References: 20, Pages: 5
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