Primary hyperaldosteronism associated with hypertensive emergencies

There is growing awareness of primary hyperaldosteronism as a cause of secondary hypertension. Usually, it manifests as hypertension and hypokalemia, or as resistant hypertension. Much less often, primary hyperaldosteronism may be detected after a hypertensive emergency has developed. We highlight this association by reporting on eight patients with a clinical diagnosis of primary hyperaldosteronism whose course was complicated by a hypertensive crisis. In all patients, an elevated serum aldosterone, was accompanied by a suppressed plasma renin activity despite the presence of a hypertensive crisis. A good outcome was obtained either with laparoscopic adrenalectomy (1 patient) or with an antihypertensive drug regimen that included an antialdosterone agent (7 patients). The differential diagnosis of hypertensive emergencies should include primary hyperaldosteronism.     

Primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. Case report

We present the first report of primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. A 10-year-old white boy with severe hypertension (150/100 mm Hg), hypokalemia (1.4 mEq/liter), and suppressed plasma renin activity (PRA) (less than 0.1 ng/ml/hr) demonstrated fixed PRA and aldosterone (aldo) levels that did not change with alteration of dietary sodium. The paradoxical decrease in serum aldo on assumption of upright posture suggested a tumor. Prolonged ACTH administration produced a continuous rise in blood pressure, but a transient rise in aldo. A minimal decrease in urinary aldo during dexamethasone administration was noted, excluding dexamethasone-suppressible hyperaldosteronism. Blood pressure normalized with spironolactone. Computerized transaxial tomography, iodocholesterol scanning, and adrenal venography were not diagnostic of a discrete adrenal lesion. Although hyperplasia is more common than an adenoma as a cause of hyperaldosteronism in childhood, a tumor was predicted, since adrenal vein hormone sampling with ACTH stimulation lateralized aldosterone secretion unequivocally to the left adrenal gland. However, left adrenalectomy revealed macronodular hyperplasia. Postoperatively, there was reversal of hypertension, hypokalemia, and hyperaldosteronism. Thus, in childhood, unilateral hypersecretion of aldosterone may result from nodular hyperplasia, rather than a discrete adenoma.     

Exudative pericarditis due to secondary kidney amyloidosis--a case report

Non-infective pericarditis in some cases may be caused by secondary amyloidosis. Amyloidosis is a metabolic disorder in which amyloid protein is deposited in various organs and destroys them. The most frequent location of systemic amyloidosis are the kidneys. In this case study we report a 74-year-old man who was admitted to hospital due to very poor condition, generalised oedema and severe dyspnoea. Since 2003 the patient had been hospitalised many times due to pericarditis of unknown aetiology. In this case we diagnosed exudative pericarditis due to nephrotic syndrome caused by secondary kidney amyloidosis which occurs very rarely.     

Pure primary hyperaldosteronism due to adrenal cortical carcinoma

A 47-year-old woman is described who had pure primary hyperaldosteronism due to an adrenal cortical carcinoma. This may represent the first such case in which modern laboratory tests allowed specific diagnosis and exclusion of hypersecretion of other adrenal steroids, and also the first reported case in which modern localizing procedures have been utilized. Other interesting facets of the case include calcification of the tumor, visualization with 131l iodomethylnorcholesterol , metaplastic histologic changes, and coexistent bilateral renal artery fibromuscular disease.     

Relationship between kidney findings and systemic vascular damage in elderly hypertensive patients without overt cardiovascular disease

Few studies have investigated the influence of age on the relationships between systemic vascular damage, kidney dysfunction, and intrarenal hemodynamic changes in patients with hypertension without overt cardiovascular disease. The authors enrolled 126 elderly patients with hypertension (aged ≥65 years) and 350 nonelderly patients with hypertension (aged <65 years). Carotid intima‐media thickness, renal resistive index, and aortic pulse wave velocity were performed in all patients. Elderly patients with hypertension had lower estimated glomerular filtration rates and higher albuminuria, renal resistive index, carotid intima‐media thickness, and aortic pulse wave velocity compared with nonelderly patients with hypertension (P < .001). Carotid intima‐media thickness independently correlated with renal resistive index and estimated glomerular filtration rate in nonelderly patients with hypertension, whereas it was significantly related to renal resistive index only in elderly patients with hypertension. Aortic pulse wave velocity was independently associated with albuminuria in nonelderly patients with hypertension, whereas it did not independently correlate with any indexes of renal damage in elderly patients with hypertension. Age is an important modifier of the relationships between renal function and renal hemodynamics with subclinical vascular involvement in elderly persons without cardiovascular disease.     

Development of structural kidney damage in spontaneously hypertensive rats

The spontaneously hypertensive rat (SHR) is one of the major models of hypertension. This article describes the current state of knowledge about the mechanism behind kidney damage in SHR in the context of human hypertension and hypertensive kidney disease. It will argue that hypertensive damage in the SHR is pressure-dependent and shows how initial vascular damage leads to a loss of autoregulation and arterial hypertrophy in the juxtamedullary cortex while the outer cortical structures are relatively protected. Progressive arteriolar media hypertrophy then leads to the collapse of some glomeruli followed by tubular atrophy. The reduced glomerular filtration, thus, leads to compensatory hyperfiltration in another population of glomeruli which develop proteinuria and glomerulosclerosis. This model provides some important questions for future research. The regulation of media hypertrophy will be of great interest, as it might slow nephron loss and interstitial fibrosis. Finally, the mechanism by which reduced tubular flow leads to tubular atrophy is another important area for future research. Initial findings indicate that cilia activation may be of major importance for maintaining tubular structure.     

Primary and secondary prevention of chronic kidney disease

The incidence and prevalence of chronic kidney disease (CKD) is on the rise worldwide. End-stage renal disease (ESRD) is the most advanced form of CKD, requiring some form of renal replacement therapy to ensure survival. Interventions to prevent or slow the progression of CKD, irrespective of the original cause, are thus of significant importance. The most effective of these interventions is based on the inhibition of the renin-angiotensin system (RAS) and is the main focus of this review.     

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats

We studied the effects of regular diet (0.35% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4 +/- 0.8, 4.1 +/- 0.9, and 5.2 +/- 1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7 +/- 3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3 +/- 3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1 +/- 2.9 ng/ml/hr) or in the regular diet (7.8 +/- 4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI = 79 +/- 14) than in the high NaCl/high potassium (RVDI = 40 +/- 11) and regular diet (RVDI = 7.8 +/- 4.6) groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevalence of primary hyperaldosteronism in mild to moderate hypertension without hypokalaemia

Screening for primary hyperaldosteronism (PHA) is often indicated in individuals with resistant hypertension or hypokalaemia. However, in the far larger subset of the hypertensive population who do not fit into these criteria, the evidence for screening is conflicting and dependent on the disease prevalence. The purpose of this study was to examine the prevalence of PHA in a large population with mild to moderate hypertension and without hypokalaemia using a carefully controlled study protocol including a normotensive control population. Hypertensive subjects underwent medication washout and both hypertensive and normotensive subjects placed on a high-sodium diet prior to biochemical and haemodynamic testing. Study specific cutoff values were based on results from the normotensive population studied under identical conditions. A screening test (serum aldosterone/PRA ratio [ARR]>25 with a serum aldosterone level >8 ng/dl) was followed by a confirmatory test (urine aldosterone excretion rate [AER] >17 microg/24 h) to demonstrate evidence of PHA. An elevated ARR with a concomitant elevated serum aldosterone was present in 26 (7.5%) individuals. Of these, 11 (3.2%) had an elevated AER, consistent with evidence of PHA. Individuals with PHA had higher blood pressure and lower serum potassium levels while on a high-sodium diet. Sodium restriction neutralized these differences between PHA and essential hypertensives. The prevalence of PHA in this mild to moderate hypertensive population without hypokalaemia is at most 3.2%, a rate that might lead to excessive false positives with random screening in comparable populations. Hyperaldosteronism, when present, is responsive to sodium restriction.     

Duodenal polyposis secondary to portal hypertensive duodenopathy

Portal hypertensive duodenopathy(PHD) is a recognized, but uncommon finding of portal hypertension in cirrhotic patients. Lesions associated with PHD include erythema, erosions, ulcers, telangiectasia, exaggerated villous pattern and duodenal varices. However, duodenal polyposis as a manifestation of PHD is rare. We report a case of a 52-year-old man who underwent esophagogastroduodenoscopy and was found with multiple small duodenal polyps ranging in size from 1-8 mm. Biopsy of the representative polyps revealed polypoid fragments of duodenal mucosa with villiform hyperplasia lined by reactive duodenal/gastric foveolar epithelium and underlying lamina propria showed proliferating ectatic and congested capillaries. The features were diagnostic of polyps arising in the setting of PHD.