scholarly journals Feline primary hyperaldosteronism: an emerging endocrine disease

2016 ◽  
Vol 46 (4) ◽  
pp. 686-693 ◽  
Author(s):  
Daniel Diola Bento ◽  
Fabíola Soares Zahn ◽  
Laura Carolina Duarte ◽  
Luiz Henrique de Araújo Machado
Keyword(s):  
Water Retention ◽  
Clinical Findings ◽  
Primary Hyperaldosteronism ◽  
Aldosterone Secretion ◽  
Aldosterone Antagonists ◽  
Endocrine Disease ◽  
Potassium Supplementation ◽  
Unilateral Disease ◽  
Appropriate Therapy ◽  
Pendulous Abdomen

ABSTRACT: The primary hyperaldosteronism, an endocrine disease increasingly identified in cats, is characterized by adrenal gland dysfunction that interferes with the renin-angiotensin-aldosterone system, triggering the hypersecretion of aldosterone. Pathophysiological consequences of excessive aldosterone secretion are related to increased sodium and water retention, and increased excretion of potassium, which induce hypertension and severe hypokalemia, respectively. The most common clinical findings in cats include: polydipsia, nocturia, polyuria, generalized weakness, neck ventroflexion, syncope, anorexia, weight loss, pendulous abdomen and blindness. Diagnosis is based on the evidence of hormonal hypersecretion with suppression of renin release, imaging and histopathological evaluation of adrenal glands. Treatment may be curative with adrenalectomy, in cases of unilateral disease, or conservative, through administration of aldosterone antagonists, potassium supplementation and antihypertensives. Prognosis varies from fair to good with the appropriate therapy. This article reviews the main aspects of primary aldosteronism in cats, providing the clinician with important information for the diagnosis of this disease.

Modulation of aldosterone secretion in frusemide-induced hypokalaemia

1984 ◽  
Vol 107 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Masaki Fujimaki ◽  
Shusaku Nagahama ◽  
Hiroko Suzuki ◽  
Ikuo Saito ◽  
Takao Saruta
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Potassium Chloride ◽  
Serum Potassium ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Initial Increase ◽  
Aldosterone Secretion ◽  
Potassium Supplementation ◽  
Secretory Capacity

Abstract. To study the effect of hypokalaemia in the regulation of aldosterone secretion, repeated injections of frusemide (3 mg/kg) plus saline with or without simultaneous infusion of potassium chloride (1 mEq/kg/h) were performed in 24 conscious female rabbits for 7 h. Without potassium supplementation, the plasma renin activity (PRA) remained elevated throughout the study, while an initial increase (1 h to 3 h) in plasma aldosterone (PA) gradually returned to normal with reduction of the serum potassium. In rabbits on potassium supplements to prevent the development of hypokalaemia, both PRA and PA remained elevated. The incremental aldosterone response to administration of potassium chloride, angiotensin II or ACTH, was considerably smaller in potassium-depleted rabbits than in potassium-repleted rabbits. These results suggest that serum potassium modulates the effects of angiotensin II or ACTH on aldosterone secretion, and that a certain level of potassium is necessary to maintain the aldosterone secretory capacity of the adrenal gland.

scholarly journals PROGRESS IN ALDOSTERONISM: A review of the prevalence of primary aldosteronism in pre-hypertension and hypertension

2015 ◽  
Vol 172 (5) ◽  
pp. R191-R203 ◽  
Author(s):  
George Piaditis ◽  
Athina Markou ◽  
Labrini Papanastasiou ◽  
Ioannis I Androulakis ◽  
Gregory Kaltsas
Keyword(s):  
Primary Aldosteronism ◽  
Clinical Phenotype ◽  
Ion Homeostasis ◽  
Genetic Alterations ◽  
Zona Glomerulosa ◽  
Receptor Expression ◽  
Aldosterone Secretion ◽  
Disease Heterogeneity ◽  
Aldosterone Antagonists ◽  
Cardiovascular Morbidity And Mortality

Primary aldosteronism (PA) secondary to excessive and/or autonomous aldosterone secretion from the renin–angiotensin system accounts for ∼10% of cases of hypertension and is primarily caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenomas (APAs). Although the diagnosis has traditionally been supported by low serum potassium levels, normokalaemic and even normotensive forms of PA have been identified expanding further the clinical phenotype. Moreover, recent evidence has shown that serum aldosterone correlates with increased blood pressure (BP) in the general population and even moderately raised aldosterone levels are linked to increased cardiovascular morbidity and mortality. In addition, aldosterone antagonists are effective in BP control even in patients without evidence of dysregulated aldosterone secretion. These findings indicate a higher prevalence of aldosterone excess among hypertensive patients than previously considered that could be attributed to disease heterogeneity, aldosterone level fluctuations related to an ACTH effect or inadequate sensitivity of current diagnostic means to identify apparent aldosterone excess. In addition, functioning aberrant receptors expressed in the adrenal tissue have been found in a subset of PA cases that could also be related to its pathogenesis. Recently a number of specific genetic alterations, mainly involving ion homeostasis across the membrane of zona glomerulosa, have been detected in ∼50% of patients with APAs. Although specific genotype/phenotype correlations have not been clearly identified, differential expression of these genetic alterations could also account for the wide clinical phenotype, variations in disease prevalence and performance of diagnostic tests. In the present review, we critically analyse the current means used to diagnose PA along with the role that ACTH, aberrant receptor expression and genetic alterations may exert, and provide evidence for an increased prevalence of aldosterone dysregulation in patients with essential hypertension and pre-hypertension.

Adrenalectomy and Caval Thrombectomy in a Cat With Primary Hyperaldosteronism

2007 ◽  
Vol 43 (4) ◽  
pp. 209-214 ◽  
Author(s):  
Scott A. Rose ◽  
Andrew E. Kyles ◽  
Philippe Labelle ◽  
Bruno H. Pypendop ◽  
Jas S. Mattu ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Adrenal Gland ◽  
Laboratory Tests ◽  
Kinase Activity ◽  
Vena Cava ◽  
Clinical Signs ◽  
Creatine Kinase Activity ◽  
Primary Hyperaldosteronism ◽  
Gland Tumor ◽  
Potassium Supplementation

A 13-year-old, castrated male, domestic longhaired cat was diagnosed with primary hyperaldosteronism from an adrenal gland tumor and a thrombus in the caudal vena cava. Clinical signs included cervical ventriflexion, lethargy, weakness, inappetence, and diarrhea. Laboratory tests revealed hypokalemia, normonatremia, hyperglycemia, hypophosphatemia, and elevated creatine kinase activity. Hypokalemia worsened despite oral potassium supplementation. An adrenalectomy and caval thrombectomy were successfully performed utilizing deliberate hypothermia followed by progressive rewarming.

scholarly journals Elizabethkingia meningoseptica –An emerging infection: A case report

2021 ◽  
Vol 8 (8) ◽  
pp. 305-307
Author(s):  
K Favas ◽  
A Bindu
Keyword(s):  
Correct Diagnosis ◽  
Fatal Outcome ◽  
Severe Infection ◽  
Clinical Findings ◽  
Microbiology Laboratory ◽  
Neurological Sequelae ◽  
Elizabethkingia Meningoseptica ◽  
Risk Of Mortality ◽  
Appropriate Therapy

Elizabethkingia meningoseptica are Gram-negative rod bacteria that are commonly found in the environment. The bacteria have also been associated with nosocomial infections, having been isolated on contaminated medical equipment, especially in neonatal wards. Rapid diagnosis and early institution of appropriate therapy for prolonged period are essential for the management of such infections. Here, we report a case of bacteremia due to E. meningoseptica in a neonate who was presented with respiratory distress and seizure episodes. A diagnosis of bacterial meningitis was made based on clinical findings and examination of cerebrospinal fluid. The baby was treated with antibiotics and other supportive measures, that helped to improve the condition. During follow-up, the baby showed developmental delay with hydrocephalus. E. meningoseptica can cause severe infection, with high risk of mortality and neurological sequelae in neonates. Intensive care and multidisciplinary interventions are crucial for the case management. Awareness among clinicians along with correct diagnosis in microbiology laboratory is required to minimize the fatal outcome associated with this infection.

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism

1982 ◽  
Vol 101 (1) ◽  
pp. 66-71 ◽  
Author(s):  
C. Beretta-Piccoli ◽  
P. Weidmann ◽  
J. J. Brown ◽  
R. Fraser ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Primary Hyperaldosteronism ◽  
Oral Glucose ◽  
Aldosterone Secretion ◽  
Glucose Loading ◽  
Glucose Ingestion

Abstract. The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Glucose-induced changes in plasma aldosterone correlated significantly (P < 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

scholarly journals SAT-196 The Use of 11C-metomidate PET-CT to Detect Unilateral Primary Hyperaldosteronism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sumitro Harjanto ◽  
Aye Chan Maung ◽  
Troy Puar ◽  
Daphne Gardner
Keyword(s):  
Blood Pressure ◽  
Adrenal Gland ◽  
Primary Hyperaldosteronism ◽  
Left Adrenal Gland ◽  
Active Renin ◽  
Potassium Supplementation ◽  
Serum Aldosterone ◽  
Pet Ct ◽  
History Of ◽  
The Right

Abstract Background Identifying causative adrenal lesions presents a significant diagnostic burden for physicians and radiologists. We describe the use of radiolabelled metomidate to lateralise primary hyperaldosteronism. Case presentation A 52-year old Chinese man with a 5-year history of hypertension was referred for hypokalemia [K 2.7 mmol/L (3.6 - 5.0)]. He had been on Telmisartan 80 mg and Amlodipine 10 mg daily and blood pressure at home ranged 110-120 / 70-80 mmHg. There was no history of poor oral intake, persistent diarrhea or vomiting, and he was not on any other prescription or alternative medications. There was no significant family history of hypertension or sudden cardiac death. Clinic blood pressure was 140/84 mmHg. There were no features suggestive of Cushing’s syndrome. Repeat biochemical tests confirmed hypokalemia (K 3.1 mmol/L), and associated raised bicarbonate 37.3 mmol/L [19 - 29]. Magnesium and creatinine were normal. Aldosterone-renin Ratio was elevated at 8.1 (serum Aldosterone 611 pmol/L [97.3 - 834.0], active renin 2.7 pg/ml [1.8 – 59.4]). Post-saline infusion, non-suppressible serum aldosterone levels of 1137 pmol/L was demonstrated, consistent with autonomous aldosterone production. A computed tomography of the adrenal revealed a 2.3 cm x 1.9 cm nodule on the left adrenal gland consistent with lipid rich adenoma. Adrenal vein sampling (AVS) under continuous synacthen infusion was performed. Adrenal to peripheral cortisol ratio was ≥10 for either adrenal veins, confirming cannulation of the adrenal veins. Aldosterone-cortisol ratios showed lateralization to the left adrenal gland (lateralization ratio of 10.35). There was contralateral suppression of the right adrenal gland with ratio of 0.41. 11C-Metomidate PET-CT scan demonstrated a maximum standardised uptake value (SUVmax) of 26.8 over the left adrenal nodule, while the SUVmax of the right adrenal gland was 16.2. Ratio of the left to right adrenal gland SUVmax was 1.65 (above the threshold of 1.25); and was concordant with AVS. This confirmed that the patient had a left functional adrenal adenoma responsible for hyperaldosteronism. Our patient underwent a left adrenalectomy, and histology was consistent with adrenal cortical adenoma. Prior to surgery he required 72 mmol/l of potassium supplementation daily to maintain K levels of 3.3 – 4.0 mmol/L. Two weeks post-operatively, he was normokalemic (K 4.9 mmol/L) without potassium supplementation. Serum aldosterone normalized to 159.3 pmol/L (active renin 9.3 pg/ml). Blood pressure is well controlled on amlodipine 5mg daily. Conclusion Targeted molecular imaging such as 11C-Metomidate PET-CT could aid localisation of functional adrenal disease to guide definitive surgical management. In the future, this could obviate the need for invasive and technically complex procedures like AVS.

Aldosterone Secretion in Experimental Congestive Heart Failure

1957 ◽  
Vol 191 (1) ◽  
pp. 140-144 ◽  
Author(s):  
Thomas E. Driscol ◽  
Maxie M. Maultsby ◽  
Gordon L. Farrell ◽  
Robert M. Berne
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Water Retention ◽  
Urine Samples ◽  
Adrenal Vein ◽  
Blood Levels ◽  
Aldosterone Secretion ◽  
Initial Salt ◽  
Secretion Rates

Adrenal vein blood levels of aldosterone were measured in six dogs with experimental congestive heart failure and compared with secretion rates in 19 normal and 2 sham-operated animals. No significant differences in adrenal aldosterone secretion were found. Aldosterone was not detected by chromatography or bioassay in pooled 3-day urine samples from three dogs before or after heart failure was present. The results suggest that in dogs with congestive heart failure (1) increased secretion of aldosterone is not necessary for the initial salt and water retention, and (2) heart failure can exist in the presence of normal secretory rates of aldosterone as determined by analysis of adrenal vein blood.

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