Questions and Answers
In patients with CKD, GH levels are typically decreased after a glucose challenge.
False
Cabergoline is a somatostatin analogue used to treat acromegaly.
False
Pegvisomant is a GH-receptor agonist used to treat acromegaly.
False
Surgery is usually the second-line treatment for acromegaly in CKD.
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IGF-1 levels are typically increased in patients with CKD and acromegaly.
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Pasireotide is a dopamine agonist used to treat acromegaly in CKD.
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Somatostatin analogues target GH receptors in pituitary tumors.
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There is a wealth of literature on the medical treatment of acromegaly in patients with CKD.
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Cabergoline is effective in controlling acromegaly in approximately two-thirds of patients.
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IGF-1 level is not a reliable diagnostic criterion for acromegaly in patients with CKD.
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Pasireotide LAR is a short-acting somatostatin analogue.
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Dose adjustment of cabergoline is necessary in patients with CKD.
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Octreotide LAR is a long-acting somatostatin analogue used to control acromegaly.
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Lanreotide depot is a somatostatin analogue used to treat prolactin disorders.
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AVP and copeptin are secreted in a 2:1 ratio upon stimulation by an increase in serum osmolarity.
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Intramuscular injection of octreotide LAR depot has no effect on GH and IGF-1 levels in patients with acromegaly and CKD.
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Cabergoline is FDA approved for the treatment of Cushing's disease in the United States.
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Mifepristone is primarily used to target the adrenal gland in the treatment of Cushing's disease.
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Etomidate requires a higher dose in patients with renal insufficiency.
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Pasireotide targets the adrenal gland in the treatment of Cushing's disease.
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Mitotane is FDA approved for the treatment of Cushing's disease in the United States.
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Somatostatin receptor agonists, such as pasireotide, are used to treat acromegaly.
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An MRI with intravenous contrast is usually required to confirm the presence of a pituitary lesion in patients with acromegaly.
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Ketoconazole requires a dose adjustment in patients with renal impairment.
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Copeptin levels are decreased in patients with CKD.
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Measurement of AVP is less exacting than measurement of copeptin.
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Lanreotide depot requires dose adjustment in patients with normal renal function.
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Pasireotide is a somatostatin analogue used to treat acromegaly in CKD.
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Cabergoline is used to target GH receptors in pituitary tumors.
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The increase in copeptin in CKD is similar to that of AVP.
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Neurophysin II is a product of proteolytic cleavage of AVP.
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The peptide content in secretory vesicles accounts for the faint signal observed on the T1-weighted MRI of the neurohypophysis.
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In patients with CKD, the diagnosis of acromegaly is facilitated by the typical decrease in growth hormone after an oral glucose load.
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Arginine vasopressin levels are decreased in patients with renal impairment due to increased clearance.
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Diabetes insipidus can be diagnosed early in patients with advanced kidney disease.
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Hypothalamic dopamine stimulates the secretion of prolactin.
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Prolactin levels are typically decreased in patients with chronic kidney disease (CKD).
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Surgery is the first-line treatment for acromegaly in patients with CKD.
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PRL levels follow a circadian rhythm with higher levels during the daytime and lower levels during sleep.
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The diagnosis of the syndrome of inappropriate antidiuretic hormone is similar in patients with advanced kidney disease as in normal subjects.
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What is the effect of V2R activation in vascular endothelial cells?
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What is the primary site of action for V1a receptors?
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What is the reason for increased AVP levels in patients on HD?
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Which receptor is responsible for the stimulatory effect of AVP on ACTH secretion?
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What is the site of arginine vasopressin synthesis?
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What is the primary metabolic pathway for pasireotide LAR?
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What is the recommended dosage adjustment for octreotide in acromegalic patients with CKD?
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What is the function of V2Rs in the kidney?
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What is the primary mechanism of V2R activation by AVP?
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What is co-secreted with AVP in equimolar amounts?
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Which somatostatin analogue does not require dose adjustment in patients with CKD?
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What is the effect of AVP on the kidney in patients with CKD?
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What is the primary site of action for V2 receptors?
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What is the recommended dosage adjustment for oral octreotide in acromegalic patients with CKD?
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What is a possible effect of ineffective deactivation of cortisol by 11 beta-hydroxysteroid dehydrogenase 2 in patients with CKD?
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Which of the following medications has a shortened half-life in patients with CKD?
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What is a potential consequence of CKD on the metabolism of exogenous glucocorticoids?
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Which of the following medications is used to treat nausea in patients with CKD?
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Why may hyperkalemia occur in patients with advanced CKD?
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What is a potential side effect of glucocorticoid therapy in patients with CKD?
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Which of the following medications is NOT used to treat gastrointestinal motility disorders in patients with CKD?
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What is a difference in the metabolism of exogenous steroids in CKD?
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Study Notes
Acromegaly Diagnosis in CKD
- Acromegaly diagnosis is challenging in patients with CKD due to changes in GH and IGF-1 metabolism.
- Typical facial and acral features are often considered in patients without CKD.
- Biochemical diagnosis of acromegaly is established with an increased IGF-1 level and nonsuppressed GH levels after a glucose challenge.
- In patients with CKD, GH levels increase but IGF-1 levels remain normal.
- Paradoxical increase in GH after a glucose challenge can be seen in patients with CKD, making diagnosis more difficult.
Treatment of Acromegaly in CKD
- Surgery is usually the treatment of choice for acromegaly.
- Medical treatment is recommended if surgery is not curative or the patient is ineligible.
- Medical treatments target pituitary tumors using dopamine agonists like cabergoline and/or somatostatin analogues.
- Cabergoline is a plausible choice in patients with modest increases of postoperative GH and IGF-1 levels, but it is effective in only approximately one-third of patients.
- No dose adjustment of cabergoline is needed in patients with CKD.
- Long-acting somatostatin analogues (octreotide LAR, lanreotide depot, and pasireotide LAR) are the mainstay for controlling acromegaly.
Treatment of Cushing's Disease in CKD
- Medications used to treat Cushing's disease include cabergoline, pasireotide, etomidate, osilodrostat, ketoconazole, metyrapone, and mitotane.
- Some medications require dose adjustments in patients with renal disease.
Arginine Vasopressin (AVP) and Copeptin
- AVP is secreted in response to various stimuli, including increased serum osmolarity, decreased intravascular volume, stress, and nausea.
- Copeptin is secreted in equimolar amounts with AVP and is proposed as a surrogate marker of AVP secretion.
- Measurement of AVP is difficult, while copeptin measurement is less exacting.
- Copeptin levels are increased in patients with CKD or on chronic hemodialysis.
Hyperprolactinemia
- Prolactin is synthesized and secreted from the lactotrophs in the anterior pituitary.
- Hypothalamic dopamine exerts tonic inhibition of prolactin secretion.
- In patients with CKD, there is an increase in prolactin levels.
Renal Hyperfiltration and Medications
- There are no reports of the use of octreotide LAR or lanreotide depot in patients with CKD, and their package inserts do not contain dose adjustments for renal impairment.
- The manufacturer recommends a lower starting dose of oral octreotide in acromegalic patients with CKD.
- Pasireotide LAR is metabolized mainly in the liver, with a small fraction excreted via the kidney, and its package insert does not recommend dose adjustments for CKD.
- There is one case report of pasireotide LAR use in a patient with acromegaly and CKD requiring hemodialysis.
Arginine Vasopressin (AVP) and Kidney Disease
- AVP is secreted by magnocellular neurons in the hypothalamus and exerts its action at multiple tissues through activation of its various receptors (V1a, V1b, and V2R).
- V1a receptors are found in smooth muscles of arterioles, leading to constriction and increased systemic circulatory resistance and blood pressure.
- V1b receptors are located in the anterior pituitary and are responsible for the stimulatory effect of AVP on ACTH secretion.
- V2R activation results in urinary concentration through the insertion of aquaporin 2 molecules into the apical membrane of principal cells in the kidney.
- V2Rs are also found in extrarenal tissues, including vascular endothelial cells, where they cause release of coagulation factor VIII and von Willebrand factor.
AVP and Hemodialysis
- AVP levels are increased in patients on hemodialysis due to decreased metabolic clearance rate and impermeability of AVP molecules by dialysis membranes.
- Copeptin, co-secreted with AVP, is also increased in patients with CKD.
Other Hormonal Changes in CKD
- In CKD, there is ineffective deactivation of cortisol by 11β-hydroxysteroid dehydrogenase 2, leading to exaggerated activation of mineralocorticoid receptors and hypertension.
- Altered metabolism of exogenous glucocorticoids in CKD results in prolonged half-life of hydrocortisone and prednisolone, but shortened half-life of dexamethasone.
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Description
This quiz covers the diagnosis and treatment of Acromegaly in patients with Chronic Kidney Disease (CKD). It includes the signs and symptoms, hormone levels, and surgical treatment options.
