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PubMed2005

Genetic screening for glucocorticoid-remediable aldosteronism (GRA): experience of three clinical centres in Poland.

Glucocorticoid-remediable aldosteronism (GRA), also known as familial hyperaldosteronism type I (FH-I, OMIM 103900), is a monogenic form of inherited hypertension caused by the presence of a chimaeric gene originating from an unequal cross-over between the CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) genes. The hybrid gene has the CYP11B1 sequence at the 5' end, including the promoter, and the CYP11B2 sequence at the 3' end. The aim of our study was to evaluate the prevalence of GRA in a Polish population of 129 patients with primary hyperaldosteronism (PHA) and 132 patients with essential hypertension (EH), through the use of a PCR-based test revealing the chimaeric gene. None of our PHA or EH patients was positive for the CYP11B1/CYP11B2 chimaeric gene. These data suggest that GRA is unlikely to be a common cause of hypertension in Polish subjects. However, the real prevalence of GRA in Poland, both in the high-risk group of individuals with primary hyperaldosteronism and in the general population, remains to be established.

3' Untranslated Regions↗
PubMed1991

[Various aspects of surgical treatment of vasorenal hypertension].

The results of examination and treatment by surgery of 103 patients with vasorenal hypertension are analysed. Retromboses and restenoses of the reconstructed renal arteries and grafts and uncorrected hyperaldosteronism were the most frequent causes of the poor results. Adequate reconstruction of the renal arteries leads to correction of hyperaldosteronism in patients with normal or high activity of plasma renin. Low-renin secondary hyperaldosteronism in patients with vasorenal hypertension is an indication for simultaneous correction.

Adolescent↗
PubMed1982

[Disorders of kidney function in hepatic coma].

Renal function was evaluated in 80 patients with hepatic coma stage III-IV (24 patients had acute fulminant hepatic failure, 48 patients chronic hepatic failure, 8 patients had a mixed form). Urea, creatinine and electrolytes were measured in plasma and urine as well as creatinine clearance and sodium/potassium ratio in urine. Renal failure was defined as an increase of serum creatinine above 3 mg/dl. In 15 of the 24 patients with fulminant hepatic failure creatinine clearance was reduced; hyperaldosteronism was present in 13 cases; in 2 patients there was necrosis of the tubulus, in 9 patients overt renal failure. In patients with chronic hepatic failure creatinine clearance was pathological in 36 cases, hyperaldosteronism was diagnosed in 23 cases and necrosis of renal tubules in 3 cases; 8 patients had overt renal failure. In the group with the mixed form of hepatic coma creatinine clearance was pathological in 3 cases, in 6 cases hyperaldosteronism was diagnosed; necrosis of the tubules could not be found in this group; 4 patients had overt renal failure. It is suggested that for treatment of this condition dopamine should be given prophylactically as well as intravenous sodium and water substitution.

Acute Kidney Injury↗
PubMed1993

The diagnosis of primary aldosteronism and separation of two major subtypes.

BACKGROUND: To develop a simple screening and diagnostic test for primary aldosteronism and to compare it with established techniques. DESIGN: Comparison of several techniques for screening, diagnosis, and differentiation of primary aldosteronism using normotensive and hypertensive subjects. METHODS: Four hundred thirty-four normotensive subjects, 263 essential hypertensive subjects, 48 subjects with primary aldosteronism due to a unilateral adrenal adenoma, and 14 in whom primary aldosteronism was associated with findings of bilateral hyperaldosteronism were studied. Plasma renin activity and plasma aldosterone were measured in venous blood obtained at 8 AM after 2 hours of ambulation and compared with established suppressive (plasma aldosterone) and stimulatory (plasma renin activity) maneuvers used for the diagnosis of primary aldosteronism. RESULTS: The ratio of plasma aldosterone to plasma renin activity provided complete separation of patients with primary aldosteronism from the normal and essential hypertensive groups. Moreover, based on the use of traditional localizing procedures separating unilateral hyperaldosteronism due to a solitary adenoma from bilateral hyperaldosteronism, confirmed by surgical intervention in the former subgroup, the ratio provided differentiation of these two forms of primary aldosteronism. CONCLUSIONS: The use of the plasma aldosterone to plasma renin activity ratio appears to be useful in the screening, diagnosis, and differentiation of unilateral and bilateral forms of primary aldosteronism. These observations may also be applicable to patients receiving some antihypertensive medications.

Adult↗
PubMed1989

Extrarenal potassium adaptation: the role of aldosterone.

1. Prior adaptation to a high potassium (HK) diet reduces the increment in plasma potassium after nephrectomy and acute potassium loading. Previous work has suggested that this 'extrarenal potassium adaptation' is due to direct stimulation of cellular potassium uptake by chronic hyperaldosteronism. 2. In contrast, we have shown that when dietary potassium is withdrawn from HK rats, large urinary potassium losses persist, resulting in 'paradoxical potassium depletion'. This potassium depletion facilitates cellular potassium uptake and is, at least in part, responsible for extrarenal potassium adaptation. 3. To try to reconcile these observations, we explored further the role of aldosterone in extrarenal potassium adaptation. When dietary potassium was withdrawn from chronically adrenalectomized HK rats, paradoxical potassium depletion was markedly blunted and extrarenal potassium adaptation could not be demonstrated. Similarly, urinary potassium losses and potassium depletion were reduced when acute adrenalectomy was performed concomitantly with dietary potassium withdrawal. 4. We were unable to confirm previous studies showing extrarenal potassium adaptation in the absence of potassium depletion. Thus, extrarenal potassium adaptation did not occur after pretreatment with chronic high-dose mineralocorticoid, after prior adaptation to a sodium-free diet, or after prior adaptation to an extremely HK diet in the absence of dietary potassium withdrawal. 5. We conclude that chronic hyperaldosteronism is important in extrarenal potassium adaptation, but probably not via direct enhancement of cellular potassium uptake. Rather, in HK animals, hyperaldosteronism magnifies urinary potassium losses during fasting and thus promotes potassium depletion, which in turn facilitates the uptake of an acute potassium load.

Adaptation, Physiological↗
PubMed1979

Relation of plasma aldosterone concentration to diuretic treatment in patients with severe heart disease.

To assess the relation of hyperaldosteronism and potassium depletion to the intensity of diuretic therapy we have measured plasma aldosterone by radioimmunoassay and total exchangeable potassium by radioisotope dilution in 24 patients when they were stable at the end of their preparation for cardiac operation. Some patients required intensive frusemide therapy to reach an optimal state for operation and many showed hyperaldosteronism. Plasma aldosterone was significantly related to daily dose of frusemide (r=0.77). Depletion of total exchangeable potassium expressed in terms of predicted weight was significantly related to plasma aldosterone (r= -0.64). The reduction in total exchangeable potassium is interpreted as chiefly related to loss of lean tissue mass from the wasting that leads to cardiac cachexia, but evidence is presented on the basis of measurements of extracellular fluid volume as sulphate space (20 patients) of entry of sodium into the cells which may indicate a true cellular potassium loss. Although plasma potassium is usually easily maintained with oral potassium supplements or aldosterone antagonists, we postulate that intensive diuretic therapy in severe heart disease may provoke hyperaldosteronism which accentuates potassium loss and may contribute to wasting and to intracellular potassium depletion in critical tissue, such as myocardium.

Adult↗
PubMed1971

Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis.

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.

Acidosis, Renal Tubular↗
PubMed1978

Electrolyte economy and its hormonal regulation in congenital chloride diarrhea.

The economy of Cl-, K+, and Mg++, extracellular volume (ECV) and plasma volume, and the role of hyperreninemia and hyperaldosteronism were explored in 22 patients with congenital chloride diarrhea. Stool volume was in significant correlation with its Cl-, Na+ and K+ content, the correlation being significantly better with Cl- content than with the Na+ content. Low fecal Cl- concentrations were seen in chronic hypochloremic contraction, but acute episodes did not cause reduction of fecal Cl- concentration from the basal level of 140--150 mmol/liter. The adequate condition (defined as normal serum electrolyte concentrations and bl;od pH, and presence of Cl- in urine) was associated with high total exchangeable Cl- and ECV. This excess Cl- and ECV roughly equalled the high daily fecal amount of Cl- and volume. Reduced ECV was accompanied by high renin activities and hyperaldosteronism, but in the adequate condition these were normal. Hyperaldosteronism caused a decrease in urinary Na+-K+ ratio and, after the age of 2--6 months, in the fecal Na+-K+ ratio. Total exchangeable K+ was normal in the adequate condition. No Mg++ depletion was present, although the patients lack Mg++ substitution. The adequate condition could be maintained with an oral supplement of NaCl, KCl and water.

Adolescent↗
PubMed1991

Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects.

Type I pseudohypoaldosteronism (PHA) is a hereditary disease characterized by salt wasting resulting from target organ unresponsiveness to mineralocorticoids. We have studied two kindreds including a total of nine patients with PHA. In kindred I, the propositus presented with renal salt wasting in infancy (vomiting, failure to thrive, short stature, hyponatremia, hyperkalemia) and responded dramatically to a high salt diet (2.5 g/day). Sodium supplementation was discontinued at the age of two. In seven additional family members from three generations, clinical expression of PHA varied from asymptomatic to moderate. In affected members (propositus, mother, and two brothers), hyperaldosteronism persisted over 13 yr; however, the PRA decreased gradually to near normal values. Persistent hyperaldosteronism in the face of a decrease in PRA indicated the development of tertiary hyperaldosteronism due to autonomously functioning zona glomerulosa. The pedigree was consistent with an autosomal dominant mode of transmission with variable expression. In kindred II, the propositus, who was the product of a consanguineous marriage, developed severe renal salt losing at age 9 days. She had also increased salivary and sweat electrolytes consistent with PHA resulting from multiple organ unresponsiveness to mineralocorticoids. Life threatening episodes of salt wasting recurred beyond the age of 2 yr. At 5 yr of age she still requires high amounts of salt supplements (14 g/day). A sister died at 9 days of age with PHA symptoms. Six close relatives (parents, three siblings, maternal uncle) showed no biochemical abnormalities. This pedigree was consistent with an autosomal recessive mode of inheritance. In view of the findings on these two kindreds and the analysis of those in the literature, we conclude that type I PHA includes two clinically and genetically distinct entities with either renal or multiple target organ defects.

Adult↗
PubMed1999

Adrenocortical tumors: recent advances in basic concepts and clinical management.

Adrenocortical masses are among the most common tumors in humans. However, only a small proportion of these tumors cause endocrine diseases (such as primary hyperaldosteronism, hypercortisolism, hyperandrogenism, or hyperestrogenism), and less than 1% are malignant. In recent years, several of the molecular and cellular mechanisms involved in adrenal tumorigenesis have been unraveled. As a result, alterations in intercellular communication, local production of growth factors and cytokines, and aberrant expression of ectopic receptors on adrenal tumor cells have been implicated in adrenal cell growth, hyperplasia, tumor formation, and autonomous hormone production. Genetic and chromosomal abnormalities, including several chromosomal loci and the genes coding for p53, p57, and insulin-like growth factor II, have been reported in adrenal tumors. In addition, chromosomal markers have been identified in several familial syndromes associated with adrenal tumors; these include menin, which is responsible for multiple endocrine neoplasia type I, and the hybrid gene that causes glucocorticoid-remediable hyperaldosteronism. Algorithms for endocrine testing and imaging procedures are now available to codify screening for, confirmation of, and differentiation of causes of primary hyperaldosteronism and the Cushing syndrome. Improved radiologic, computerized radiologic, and magnetic resonance imaging techniques, as well as selective catheterization studies, are useful in localizing adrenal tumors and in distinguishing between benign and malignant lesions and between functional and nonfunctional nodules. Finally, recent refinements in the field of minimally invasive general surgery have made laparoscopic adrenalectomy the method of choice for removing adrenal tumors; this type of surgery allows shorter hospital stays, lower morbidity rates, and faster recovery.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Morphology of the kidneys in arterial hypertension of adrenal genesis (according to biopsy findings)].

67 renal biopsies obtained in the course of adrenalectomy from patients with primary hyperaldosteronism, hypercorticism and pheochromocytoma were studied. Sclerotic affection of the arterioles and renal interstitium were found in long lasting adrenal arterial hypertension. This may cause residual postoperative hypertension. Endocrine nephropathy in primary hyperaldosteronism due to hypopotassemia and alcalosis manifests with vacuolar distrophy and atrophy of the epithelium, dilatation of tubular lumen, intratubular calcinosis and tubulointerstitial nephritis. Primary hyperaldosteronism was characterized by hypoplasia of the juxtaglomerular apparatus (JGA) but in massive spironolacton therapy signs of enhanced renin-secreting function of the glomerular efferent arteriola may be observed. In hypercorticism pyelonephritis is rather frequent. In patients with pheochromocytoma hypercatecholaminemia may result in JGA activation this being particularly evident in renal artery stenosis. Recurrent hypertension after pheochromocytoma removal in the absence of renal pathology may indicate recurrent tumor or missed second tumor.

Adrenal Gland Neoplasms↗
PubMed1975

Bartter syndrome. Typical facies and normal plasma volume.

Two girls with hypokalemic and hypochloremic metabolic alkalosis and failure to thrive were found to have Bartter syndrome at ages 9 and 6 months. Both had normal blood pressures despite substantial elevation of plasma renin activity and evidence of secondary hyperaldosteronism. A similarity in facial features, including prominent forhead, a large head, triangular facies with drooping mouth, and large eyes and pinnae, was noted in these two infants and in published pictures of other infants with the syndrome. Although the normotension associated with substanital elevation of plasma renin activity and hyperaldosteronism in Bartter syndrome has been considered the effect of hypovolemia, a normal or slightly elevated plasma volume was found in these infants, suggesting that in certain cases an alternate mechanism for the depressed response to renin may be present.

Bartter Syndrome↗
PubMed1984

Hypertension caused by an aldosterone-secreting adenoma. Occurrence in a 7-year-old child.

A 7-year-old girl had hyperaldosteronism due to an adrenal cortical adenoma, a rare, surgically remediable cause of hypertension. Although the plasma potassium concentration was only slightly below normal, and the plasma aldosterone concentration was in a high normal range, the consistently suppressed plasma renin activity suggested primary aldosteronism. This diagnosis was confirmed by the failure of saline infusion to lower the plasma aldosterone concentration. Glucocorticoid-remediable hyperaldosteronism was excluded when dexamethasone did not reduce the high plasma aldosterone concentration. An enlarged left adrenal gland was observed in the computed tomographic scan, and blood from the left adrenal vein contained much more aldosterone than blood from the right adrenal vein. Surgical excision of the left adrenal gland, containing an adenoma, was followed by a return of BP and biochemical measurements to their normal ranges. This case demonstrated the importance of a rational systematic approach in the evaluation of children with sustained unexplained hypertension and the need to obtain plasma renin activity values when either hypokalemia is present or initial investigations fall to provide a diagnosis.

Adenoma↗
PubMed1985

Low-renin hypertension in young infants.

Plasma renin activity (PRA) in neonates is significantly higher than in older infants and children and may increase as a result of numerous physiologic or therapeutic factors. For these reasons, the measurement of PRA is not usually helpful in establishing the cause of hypertension in neonates. In conditions that suppress renin release, however, measurement of PRA can be most useful. Herein, we describe two infants (ages 4 and 5 months, respectively) with sustained hypertension and low PRA secondary to dexamethasone-suppressible hyperaldosteronism. Low PRA was essential in establishing this diagnosis in both patients. Dexamethasone-suppressible hyperaldosteronism should be considered in hypertensive infants who have normal genitalia and low PRA.

Dexamethasone↗
PubMedDate not supplied

A randomized comparison of metoclopramide and domperidone on plasma aldosterone concentration and on spironolactone-induced diuresis in ascitic cirrhotic patients.

The effect of metoclopramide and domperidone, two dopamine antagonists, administered to cirrhotic patients with ascites and secondary hyperaldosteronism, was examined to evaluate the changes in plasma aldosterone levels and in spironolactone-induced diuresis. In 15 patients with ascites and secondary hyperaldosteronism, the intravenous administration of 10 mg metoclopramide significantly increased plasma aldosterone levels (23%, p less than 0.01). This effect was observed when an equivalent dose of domperidone was administered. In 20 ascitic patients treated with spironolactone (300 mg per day), the administration of metoclopramide (20 mg) significantly reduced urinary output (24%, p less than 0.001) and urinary sodium (35%, p less than 0.001) while simultaneously increasing urinary potassium (24%, p less than 0.001) and plasma aldosterone (40%, p less than 0.001). This effect was not observed with domperidone in an equivalent dose. Therefore, it is recommended that metoclopramide should be avoided during diuretic therapy in cirrhotic patients with ascites. In these circumstances, domperidone is preferred.

Adult↗
PubMed1990

Aldosterone-producing tumors (Conn's syndrome).

Adenomas of the adrenal cortex which produce aldosterone (APA) are among the surgically correctible causes of hypertension accounting for 0.5 to 1.0% of all hypertensive etiologies. The adenomas have a 5:1 predilection for women and generally present with hypertension or profound hypokalemia. A low plasma renin activity completes the triad for primary hyperaldosteronism which could be caused by adrenocortical cancer, a neoplasm with an average diameter of 12 cm, or idiopathic hyperaldosteronism (IHA), a bilateral hyperplasia of the zona glomerulosa of the adrenal cortex which responds poorly to surgical resection. The adenomas are small (2 cm) but can be localized by imaging or selective venous sampling. Resection has a high success rate with minimal morbidity.

Adenoma↗
PubMed1986

Role of aldosterone in the mechanism of renal potassium adaptation.

Chronic potassium loading results in an adaptive change in renal tubular epithelium which increases the capacity for potassium excretion. The present study was performed to evaluate the role of aldosterone in renal potassium adaptation, since hyperaldosteronism stimulates potassium secretion, and potassium loading increases the production of aldosterone. Experiments were performed in animals with intact adrenal glands, and in adrenalectomized animals (Adx) replaced with basal physiologic amounts of corticosterone, which were not replaced with aldosterone, or were chronically infused with aldosterone to achieve either basal plasma levels or elevated levels. Chronic potassium loading in adrenal intact animals was associated with a statistically significant higher rate of urinary potassium excretion (3.57 +/- 0.30 microEq/min/100 g BW) compared to the control rate (2.54 +/- 0.25 microEq/min/100 g BW, p less than 0.05), during acute infusion of KCl. In potassium loaded Adx animals, with selective replacement of adrenal hormones, the maximum rate of potassium excretion was blunted in the absence of aldosterone, compared to potassium loaded animals with intact adrenal glands. In contrast, when Adx animals were infused chronically with aldosterone, to achieve basal or elevated plasma levels, the maximum rate of potassium excretion was not blunted, although at basal aldosterone levels increased potassium excretion was due, at least in part, to hyperkalemia. These results indicate that the induction of renal potassium adaptation after a week or more of chronic potassium loading is dependent on the action of hyperaldosteronism on renal tubular epithelium.

Adaptation, Physiological↗
PubMed1999

Effects of restorative proctocolectomy on renal and adrenal function.

PURPOSE: Restorative proctocolectomy is a standard procedure in the surgical treatment of ulcerative colitis and familial adenomatous polyposis. The radical removal of the colorectum with construction of an ileostomy often results in high stoma losses. These may lead to changes in the electrolyte and acid-base balance and to alterations in renal and suprarenal gland function. METHODS: In this study 33 patients who received an ileoanal pouch before and after proctocolectomy were investigated at different time intervals for electrolyte changes, alteration of the acid-base balance, kidney function, and hormonal changes of the suprarenal glands. Measurements were performed before proctocolectomy, ten days after proctocolectomy with ileal pouch-anal anastomosis under protective loop ileostomy, before ileostomy closure, and 6 to 12 months after ileostomy closure. Neither acute renal failure nor other vital complications were observed. RESULTS: Statistical analysis showed a significant decrease of urine pH to 5.4 +/- 0.22 (before ileostomy closure) and metabolic acidosis (pH 7.32 +/- 0.04; base excess -1.3 +/- 5.6 (before ileostomy closure)). Likewise, we found a decrease in renal clearance to 86 ml/minute (before ileostomy closure) without signs of tubular damage. The most important change during the phase with ileostomy was a functional secondary hyperaldosteronism with aldosterone levels of 63.2 +/- 70.8 ng/dl (before ileostomy closure). In comparison with preoperative levels, there was a ten-fold increase in mineralocorticoid adrenal activity. Additionally, during the period with protective ileostomy, the hepatic synthesis of aldosterone-18-glucuronide was only slightly increased, and the cortisol/cortisone ratio was extremely decreased. CONCLUSIONS: These results show that restorative proctocolectomy with ileal pouch-anal anastomosis and protective loop ileostomy significantly influences fluid, electrolyte, and acid-base balance. Functional secondary hyperaldosteronism is of central importance for subsequent renal recompensation. Approximately one-half year after ileostomy closure, the endogenous hormones with mineralocorticoid effects returned to normal levels.

Acid-Base Equilibrium↗