Microalbuminuria in Insulin Sensitivity in Patients with Growth Hormone-Secreting Pituitary Tumor

Baldelli, Roberto; Marinis, Laura De; Bianchi, Antonio; Pivonello, Rosario; Gasco, Valentina; Auriemma, Renata S.; Pasimeni, Giuseppe; Cimino, Vincenzo; Appetecchia, Marialuisa; Maccario, Mauro; Lombardi, Gaetano; Pontecorvi, Alfredo; Colao, Annamaria; Grottoli, Silvia

doi:10.1210/jc.2007-1197

Cited by 25 publications

(9 citation statements)

References 23 publications

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“…Children with ESRD have an increased number of secretory bursts of GH compared to children with normal renal function [Tonshoff et al, ]. Definite evidence for a causal role of GH in nephropathy has come from acromegalic subjects wherein excess GH levels were associated with significant structural and functional changes in the kidney and albuminuria [Baldelli et al, ; Manelli et al, ]. In case of mice transgenic for bovine GH, glomeruli was disproportionately enlarged paralleled with glomerulosclerosis and increased albumin: creatinine ratio [Doi et al, ].…”

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confidence: 99%

Growth Hormone Induces Transforming Growth Factor‐Beta‐Induced Protein in Podocytes: Implications for Podocyte Depletion and Proteinuria

Chitra

Swathi

Sahay

et al. 2015

J of Cellular Biochemistry

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The glomerular podocytes form a major size selective barrier for the filtration of serum proteins and reduced podocyte number is a critical event in the pathogenesis of proteinuria during diabetic nephropathy (DN). An elevated level of growth hormone (GH) is implicated as a causative factor in the development of nephropathy in patients with type 1 diabetes mellitus. We have previously shown that podocytes express GH receptor and are a target for GH action. To elucidate the molecular basis for the effects of GH on podocyte depletion, we conducted PCR-array analyses for extracellular matrix and adhesion molecules in podocytes. Our studies reveal that GH increases expression of a gene that encodes transforming growth factor-beta-induced protein (TGFBIp) expression. Similarly, microarray data retrieved from the Nephromine database revealed elevation of TGFBIp in patients with DN. Treatment with GH results in increased secretion of extracellular TGFBIp by podocytes. Both GH and TGFBIp induced apoptosis and epithelial mesenchymal transition (EMT) of podocytes. Exposure of podocytes to GH and TGFBIp resulted in increased migration of cells and altered podocyte permeability to albumin across podocyte monolayer. Administration of GH to rats induced EMT and apoptosis in the glomerular fraction of the kidney. Therefore, we conclude that the GH-dependent increase in TGFBIp in the podocyte is one of the mechanisms responsible for podocyte depletion in DN.

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confidence: 99%

Growth Hormone Induces Transforming Growth Factor‐Beta‐Induced Protein in Podocytes: Implications for Podocyte Depletion and Proteinuria

Chitra

Swathi

Sahay

et al. 2015

J of Cellular Biochemistry

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“…Microalbuminuria has been associated with an increased risk of cardiovascular events in diabetic patients (31), as well as in non-diabetic patients (32). There are data showing increased levels of albuminuria in acromegaly (33). There is evidence that acromegaly has a major effect on the kidneys, more exactly on glomerular filtration and renal plasma flow (34), and this effect is a consequence of IGF-1 activity (35).…”

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confidence: 99%

Hypertension-related factors in patients with active and inactive acromegaly

Fedrizzi

Rodrigues

Costenaro

et al. 2011

Arq Bras Endocrinol Metab

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Introduction: There are several complications of the cardiovascular system caused by acromegaly, especially hypertension. Objectives: To evaluate hypertension characteristics in patients with cured/controlled acromegaly and with the active disease. Patients and methods: Cross-sectional study of the follow-up of forty-four patients with acromegaly submitted to clinical evaluation, laboratory tests and cardiac ultrasound. Patients with cured and controlled disease were evaluated as one group, and individuals with active disease as second one. Results: Forty-seven percent of the patients had active acromegaly, and these patients were younger and had lower blood pressure levels than subjects with controlled/cured disease. Hypertension was detected in 50% of patients. Subjects with active disease showed a positive correlation between IGF-1 and systolic and diastolic blood pressure levels (r = 0.48, p = 0.03; and r = 0.42, p = 0.07, respectively), and a positive correlation between IGF-1 and urinary albumin excretion (UAE) rates. In patients with active disease, IGF-1 was a predictor of systolic blood pressure, although it was not independent of UAE rate. For individuals with cured/controlled disease, waist circumference and triglycerides were the predictors associated with systolic and diastolic blood pressure. Conclusions: Our findings suggest that blood pressure levels in patients with active acromegaly are very similar, and depend on excess GH. However, once the disease becomes controlled and IGF-1 levels decrease, their blood pressure levels will depend on the other cardiovascular risk factors. Arq Bras Endocrinol Metab. 2011;55(7):468-74

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“…Patients commonly experience abnormal growth of bone and soft tissue (3,4) and have dysregulated glucose metabolism (5,6) with increased risk for cardiovascular disease (7), all of which may impact mortality risk (8). Treatment of patients with acromegaly is aimed at controlling excess GH and/or IGF-I levels, but signs and symptoms of the disease often persist despite achievement of biochemical control (1,9,10).…”

Section: Introductionmentioning

confidence: 99%

A Consensus on the Diagnosis and Treatment of Acromegaly Comorbidities: An Update

Giustina

Barkan

Beckers

et al. 2019

The Journal of Clinical Endocrinology &Amp; Metabolism

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197

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Objective The aim of the Acromegaly Consensus Group was to revise and update the consensus on diagnosis and treatment of acromegaly comorbidities last published in 2013. Participants The Consensus Group, convened by 11 Steering Committee members, consisted of 45 experts in the medical and surgical management of acromegaly. The authors received no corporate funding or remuneration. Evidence This evidence-based consensus was developed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to describe both the strength of recommendations and the quality of evidence following critical discussion of the current literature on the diagnosis and treatment of acromegaly comorbidities. Consensus Process Acromegaly Consensus Group participants conducted comprehensive literature searches for English-language papers on selected topics, reviewed brief presentations on each topic, and discussed current practice and recommendations in breakout groups. Consensus recommendations were developed based on all presentations and discussions. Members of the Scientific Committee graded the quality of the supporting evidence and the consensus recommendations using the GRADE system. Conclusions Evidence-based approach consensus recommendations address important clinical issues regarding multidisciplinary management of acromegaly-related cardiovascular, endocrine, metabolic, and oncologic comorbidities, sleep apnea, and bone and joint disorders and their sequelae, as well as their effects on quality of life and mortality.

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Microalbuminuria in Insulin Sensitivity in Patients with Growth Hormone-Secreting Pituitary Tumor

Abstract: Impairment of glucose tolerance in acromegaly is associated with high levels of microalbuminuria. For this reason, microalbuminuria should be part of cardiovascular risk assessment in these patients.

Cited by 25 publications

References 23 publications

Growth Hormone Induces Transforming Growth Factor‐Beta‐Induced Protein in Podocytes: Implications for Podocyte Depletion and Proteinuria

Growth Hormone Induces Transforming Growth Factor‐Beta‐Induced Protein in Podocytes: Implications for Podocyte Depletion and Proteinuria

Hypertension-related factors in patients with active and inactive acromegaly

A Consensus on the Diagnosis and Treatment of Acromegaly Comorbidities: An Update

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