Renal Failure Obfuscates the Diagnosis of Cushing’s Disease

Sharp, Nina A.; Devlin, John T.; Rimmer, Jeffrey M.

doi:10.1016/s0022-5347(17)44258-3

Cited by 2 publications

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“…This result suggests that the patients with nonsuppressible plasma cortisol after 1 mg Dex seem not to have hyperadrenocorticism. It has been reported that the diagnosis of Cushing's syndrome in hemodialysis patients is complicated because of lack of the simple methods for the evaluation of hyperadrenocorticism [12]. Urinary 17-OHCS is not applicable, and plasma cortisol is often nonsuppressible with overnight or low-dose Dex [2,[10][11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

Determination of 17-Hydroxycorticosteroids in Dialysate Solution as a Measure of Adrenocortical Function in Hemodialysis Patients

Kohda¹,

Hiramatsu²,

Kuwahara³

et al. 1994

Nephron

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Dialysate contents of 17-hydroxycorticosteroids (17-OHCS) in hemodialysis patients were studied as a potential measure of adrenocortical function. Dialysate 17-OHCS contents after a 2-day interval of hemodialysis in 15 hemodialysis patients were determined. Dialysate 17-OHCS increased after intravenous injection of cortisol the evening prior to hemodialysis (n = 4). Dialysate 17-OHCS content was suppressed, as was plasma cortisol, after a standard dexamethasone (Dex) suppression test (n = 1). Their plasma cortisol was suppressible or nonsuppressible by an overnight Dex suppression test, as reported previously. However, basal dialysate 17-OHCS contents were not different between them, indicating that the nonsuppressible patients with overnight Dex seem not to have hypercortisolism. We conclude that determination of dialysate 17-OHCS seems a useful noninvasive technique for the evaluation of adrenocortical function in hemodialysis patients.

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Section: Discussionmentioning

confidence: 99%

Determination of 17-Hydroxycorticosteroids in Dialysate Solution as a Measure of Adrenocortical Function in Hemodialysis Patients

Kohda¹,

Hiramatsu²,

Kuwahara³

et al. 1994

Nephron

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“…In humans, the combination of Cushing's disease and renal failure is considered to be very rare [186,187]. However, one case-control study reported a decreased GFR in a group Cushing's patients mainly with cured disease; 4 out of 18 patients had CKD, which was defined as a GFR < 60 mL/min/1.73 m 2 .…”

Section: Chronic Kidney Diseasementioning

confidence: 99%

Endocrine Hypertension and Chronic Kidney Disease

Koch

Pamporaki

Kantorovich

2014

Chronic Kidney Disease and Hypertension

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IntroductionEndocrine forms of secondary hypertension (HTN) have traditionally included syndromes of mineralocorticoid excess with primary aldosteronism (PA) representing the most common etiology, followed by Cushing's syndrome (CS), and pheochromocytoma. Besides these conditions of hormonal excess, there are also other rare conditions such as congenital adrenal hyperplasia (11β-hydroxylase, 17α-hydroxylase deficiency), apparent mineralocorticoid excess, Geller syndrome (mineralocorticoid receptor (MR) activation), Liddle syndrome, pseudohypoaldosteronism type 2, and Chrousos syndrome that can cause HTN [1-4] (see Fig. 16.1).When considering the current obesity epidemic, with its many hormonal derangements (e.g., deficiencies of testosterone, vitamin D, growth hormone), the hitherto estimated prevalence rates of approximately 10 % for endocrine HTN are likely to be an underestimate. Potential nonadrenal causes of endocrine HTN include excess production of growth hormone (acromegaly), thyroid hormone, and parathyroid hormone, as well as insulin resistance, hypothyroidism, and overstimulation of central MRs [1,. These "nontraditional" forms of endocrine HTN will not be discussed in detail in this chapter.Cutoffs of systolic and diastolic blood pressure (BP) for defining HTN along with reference ranges for hormonal assays among various patient populations are 186 C. A. Koch et al. all important to consider when applying existing or emerging data to clinical patient scenarios. HTN guidelines by various societies have been recently revisited [41][42][43][44][45][46]. The American Society of Hypertension/International Society of Hypertension (ASH/ISH) guidelines reaffirm the traditional threshold of 140/90 mmHg as a cutoff for defining an elevated BP and state that individuals with a BP of 140-159/90-99 mmHg and no other risk factors are considered at low risk. On the other hand, the Joint National Committee (JNC 8) suggests a systolic blood pressure (SBP) of 150 mmHg as a worrisome threshold, especially for those 80 years and older. For the diastolic BP goal, both the ASH/ISH and JNC 8 guidelines view 90 mmHg as the cutoff; the exception are diabetic hypertensives for whom the cutoff is 85 mmHg. From epidemiologic studies and drug trials, there appears no sound evidence to continue recommending a BP of 140/90 mmHg as the cutoff to initiate antihypertensive treatment; moreover, any increased benefit from additional antihypertensive medications can be nonexistent or negligible, particularly in the face of increased likelihood of adverse effects. .1 Inherited endocrine condition related to mineralocorticoid excess. The picture shows the molecular pathways involved in dysregulation of NaCl homeostasis located in the distalrenal tubules. AME apparent mineralocorticoid excess; GRA glucocorticoid-remediable aldosteronism; PHA2 pseudohypoaldosteronism type 2; MR mineralocorticoid receptor; WNK with-no-lysine ( K) kinase 1,4; ROMK renal outer medullary potassium channel; ENaC epithelial sodium channel; KLHL3 kelch-like 3; C...

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Renal Failure Obfuscates the Diagnosis of Cushing’s Disease

Cited by 2 publications

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Determination of 17-Hydroxycorticosteroids in Dialysate Solution as a Measure of Adrenocortical Function in Hemodialysis Patients

Determination of 17-Hydroxycorticosteroids in Dialysate Solution as a Measure of Adrenocortical Function in Hemodialysis Patients

Endocrine Hypertension and Chronic Kidney Disease

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