The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism
Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 μg of 1–38 PTH in patients with PsH type I ( n = 8) and PsH ty...
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creator | Stone, M.D. Hosking, D.J. Garcia-Himmelstine, C. White, D.A. Rosenblum, D. Worth, H.G. |
description | Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 μg of 1–38 PTH in patients with PsH type I (
n = 8) and PsH type II (
n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (ΔcAMP) was lower (
p < 0.001) in the PsH type I (175 ± 6.4 nmol/l glomerular filtrate) than in the HP group (3251 ± 515 nmol/l glomerular filtrate). ΔcAMP in the PsH type I subjects was dependent on endogenous PTH concentrations (
r = − 0.76;
p = 0.046) and serum calcium (
r = 0.74;
p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO
4/ glomerular filtration rate) were lower (
p = 0.013) in the PsH type I (28.8 ± 3.75) compared with those of the HP patients (43 ± 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH (
r = 0.94;
p < 0.001) and serum calcium levels (
r = 0.94;
p < 0.001) so that the responses of subjects with normal or low PTH levels were no different (
p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH.
These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH. |
doi_str_mv | 10.1016/8756-3282(93)90204-N |
format | Article |
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n = 8) and PsH type II (
n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (ΔcAMP) was lower (
p < 0.001) in the PsH type I (175 ± 6.4 nmol/l glomerular filtrate) than in the HP group (3251 ± 515 nmol/l glomerular filtrate). ΔcAMP in the PsH type I subjects was dependent on endogenous PTH concentrations (
r = − 0.76;
p = 0.046) and serum calcium (
r = 0.74;
p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO
4/ glomerular filtration rate) were lower (
p = 0.013) in the PsH type I (28.8 ± 3.75) compared with those of the HP patients (43 ± 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH (
r = 0.94;
p < 0.001) and serum calcium levels (
r = 0.94;
p < 0.001) so that the responses of subjects with normal or low PTH levels were no different (
p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH.
These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/8756-3282(93)90204-N</identifier><identifier>PMID: 8268047</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Biological and medical sciences ; Calcium - blood ; Calcium - urine ; Cyclic AMP - urine ; Endocrinopathies ; Female ; Glomerular Filtration Rate - drug effects ; Humans ; Hypoparathyroidism - drug therapy ; Hypoparathyroidism - metabolism ; Hypoparathyroidism - physiopathology ; Kidney Tubules - drug effects ; Kidney Tubules - physiopathology ; Male ; Medical sciences ; Middle Aged ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Parathyroid hormone ; Parathyroid Hormone - administration & dosage ; Parathyroid Hormone - blood ; Parathyroid Hormone - pharmacology ; Parathyroid Hormone - therapeutic use ; Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases) ; Peptide Fragments - administration & dosage ; Peptide Fragments - pharmacology ; Peptide Fragments - therapeutic use ; Phosphates - urine ; Pseudohypoparathyroidism ; Pseudohypoparathyroidism - drug therapy ; Pseudohypoparathyroidism - metabolism ; Pseudohypoparathyroidism - physiopathology ; Renal response ; Sodium - urine</subject><ispartof>Bone (New York, N.Y.), 1993-09, Vol.14 (5), p.727-735</ispartof><rights>1993</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-334950c8058dfcc79530f8eb6e1f83074273f92552d24b63dfeecfe005482d463</citedby><cites>FETCH-LOGICAL-c417t-334950c8058dfcc79530f8eb6e1f83074273f92552d24b63dfeecfe005482d463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/8756-3282(93)90204-N$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3753186$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8268047$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stone, M.D.</creatorcontrib><creatorcontrib>Hosking, D.J.</creatorcontrib><creatorcontrib>Garcia-Himmelstine, C.</creatorcontrib><creatorcontrib>White, D.A.</creatorcontrib><creatorcontrib>Rosenblum, D.</creatorcontrib><creatorcontrib>Worth, H.G.</creatorcontrib><title>The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 μg of 1–38 PTH in patients with PsH type I (
n = 8) and PsH type II (
n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (ΔcAMP) was lower (
p < 0.001) in the PsH type I (175 ± 6.4 nmol/l glomerular filtrate) than in the HP group (3251 ± 515 nmol/l glomerular filtrate). ΔcAMP in the PsH type I subjects was dependent on endogenous PTH concentrations (
r = − 0.76;
p = 0.046) and serum calcium (
r = 0.74;
p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO
4/ glomerular filtration rate) were lower (
p = 0.013) in the PsH type I (28.8 ± 3.75) compared with those of the HP patients (43 ± 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH (
r = 0.94;
p < 0.001) and serum calcium levels (
r = 0.94;
p < 0.001) so that the responses of subjects with normal or low PTH levels were no different (
p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH.
These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Calcium - blood</subject><subject>Calcium - urine</subject><subject>Cyclic AMP - urine</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Humans</subject><subject>Hypoparathyroidism - drug therapy</subject><subject>Hypoparathyroidism - metabolism</subject><subject>Hypoparathyroidism - physiopathology</subject><subject>Kidney Tubules - drug effects</subject><subject>Kidney Tubules - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Parathyroid hormone</subject><subject>Parathyroid Hormone - administration & dosage</subject><subject>Parathyroid Hormone - blood</subject><subject>Parathyroid Hormone - pharmacology</subject><subject>Parathyroid Hormone - therapeutic use</subject><subject>Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptide Fragments - therapeutic use</subject><subject>Phosphates - urine</subject><subject>Pseudohypoparathyroidism</subject><subject>Pseudohypoparathyroidism - drug therapy</subject><subject>Pseudohypoparathyroidism - metabolism</subject><subject>Pseudohypoparathyroidism - physiopathology</subject><subject>Renal response</subject><subject>Sodium - urine</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1rGzEQhkVJcZ20_6CBPYSSHLbVt7SXQDH9gpBeXHoUsjSKFXZXG2kd6n_f3dqYntrLzGGed5h5EHpL8HuCifyglZA1o5peN-ymwRTz-v4FWhKtWE2VZGdoeUJeofNSHjHGrFFkgRaaSo25WqKf6y1UGXrbTrUMqS9QjamCX-kB-rQr1WCzHbf7nKKvtil3qYcq9tWYwY7gq6HAzqftfkh_gbF0r9HLYNsCb479Av34_Gm9-lrfff_ybfXxrnacqLFmjDcCO42F9sE51QiGg4aNBBI0w4pTxUJDhaCe8o1kPgC4ABgLrqnnkl2gd4e9Q05POyij6WJx0La2h-l8oyQhc_6_IJFSMEHxBPID6HIqJUMwQ46dzXtDsJnFm9mqma2ahpk_4s39FLs87t9tOvCn0NH0NL86zm1xtg3Z9i6WE8aUYETP_9weMJikPUfIprgIvQMfM7jR-BT_fcdvHZWgDw</recordid><startdate>19930901</startdate><enddate>19930901</enddate><creator>Stone, M.D.</creator><creator>Hosking, D.J.</creator><creator>Garcia-Himmelstine, C.</creator><creator>White, D.A.</creator><creator>Rosenblum, D.</creator><creator>Worth, H.G.</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7X8</scope></search><sort><creationdate>19930901</creationdate><title>The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism</title><author>Stone, M.D. ; Hosking, D.J. ; Garcia-Himmelstine, C. ; White, D.A. ; Rosenblum, D. ; Worth, H.G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-334950c8058dfcc79530f8eb6e1f83074273f92552d24b63dfeecfe005482d463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Calcium - blood</topic><topic>Calcium - urine</topic><topic>Cyclic AMP - urine</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Humans</topic><topic>Hypoparathyroidism - drug therapy</topic><topic>Hypoparathyroidism - metabolism</topic><topic>Hypoparathyroidism - physiopathology</topic><topic>Kidney Tubules - drug effects</topic><topic>Kidney Tubules - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Parathyroid hormone</topic><topic>Parathyroid Hormone - administration & dosage</topic><topic>Parathyroid Hormone - blood</topic><topic>Parathyroid Hormone - pharmacology</topic><topic>Parathyroid Hormone - therapeutic use</topic><topic>Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptide Fragments - therapeutic use</topic><topic>Phosphates - urine</topic><topic>Pseudohypoparathyroidism</topic><topic>Pseudohypoparathyroidism - drug therapy</topic><topic>Pseudohypoparathyroidism - metabolism</topic><topic>Pseudohypoparathyroidism - physiopathology</topic><topic>Renal response</topic><topic>Sodium - urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stone, M.D.</creatorcontrib><creatorcontrib>Hosking, D.J.</creatorcontrib><creatorcontrib>Garcia-Himmelstine, C.</creatorcontrib><creatorcontrib>White, D.A.</creatorcontrib><creatorcontrib>Rosenblum, D.</creatorcontrib><creatorcontrib>Worth, H.G.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Bone (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stone, M.D.</au><au>Hosking, D.J.</au><au>Garcia-Himmelstine, C.</au><au>White, D.A.</au><au>Rosenblum, D.</au><au>Worth, H.G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism</atitle><jtitle>Bone (New York, N.Y.)</jtitle><addtitle>Bone</addtitle><date>1993-09-01</date><risdate>1993</risdate><volume>14</volume><issue>5</issue><spage>727</spage><epage>735</epage><pages>727-735</pages><issn>8756-3282</issn><eissn>1873-2763</eissn><abstract>Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 μg of 1–38 PTH in patients with PsH type I (
n = 8) and PsH type II (
n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (ΔcAMP) was lower (
p < 0.001) in the PsH type I (175 ± 6.4 nmol/l glomerular filtrate) than in the HP group (3251 ± 515 nmol/l glomerular filtrate). ΔcAMP in the PsH type I subjects was dependent on endogenous PTH concentrations (
r = − 0.76;
p = 0.046) and serum calcium (
r = 0.74;
p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO
4/ glomerular filtration rate) were lower (
p = 0.013) in the PsH type I (28.8 ± 3.75) compared with those of the HP patients (43 ± 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH (
r = 0.94;
p < 0.001) and serum calcium levels (
r = 0.94;
p < 0.001) so that the responses of subjects with normal or low PTH levels were no different (
p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH.
These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8268047</pmid><doi>10.1016/8756-3282(93)90204-N</doi><tpages>9</tpages></addata></record> |
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subjects | Adult Biological and medical sciences Calcium - blood Calcium - urine Cyclic AMP - urine Endocrinopathies Female Glomerular Filtration Rate - drug effects Humans Hypoparathyroidism - drug therapy Hypoparathyroidism - metabolism Hypoparathyroidism - physiopathology Kidney Tubules - drug effects Kidney Tubules - physiopathology Male Medical sciences Middle Aged Non tumoral diseases. Target tissue resistance. Benign neoplasms Parathyroid hormone Parathyroid Hormone - administration & dosage Parathyroid Hormone - blood Parathyroid Hormone - pharmacology Parathyroid Hormone - therapeutic use Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases) Peptide Fragments - administration & dosage Peptide Fragments - pharmacology Peptide Fragments - therapeutic use Phosphates - urine Pseudohypoparathyroidism Pseudohypoparathyroidism - drug therapy Pseudohypoparathyroidism - metabolism Pseudohypoparathyroidism - physiopathology Renal response Sodium - urine |
title | The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism |
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