1/4. Renovascular hypertension: a rare cause of neonatal salt loss.We report a case of severe hypertension in the newborn period due to obstruction of the right renal artery. The baby presented with polyuria leading to dehydration and was found to have hyponatraemia and severe renal salt loss. When sudden malignant hypertension is induced in experimental conditions, a high pressure diuresis and increased angiotensin ii production are found. These findings could explain the renal salt loss, notwithstanding the effects of secondary hyperaldosteronism and hyper-reninaemia.- - - - - - - - - - ranking = 1keywords = hyperaldosteronism (Clic here for more details about this article) |
2/4. cystic fibrosis presenting with chronic electrolyte depletion, metabolic alkalosis and hyperaldosteronism.A five month old infant who presented with failure to thrive and was found to have severe electrolyte depletion, metabolic alkalosis and hyperaldosteronism is described. The diagnosis of cystic fibrosis was made by demonstrating abnormal sweat electrolytes and pancreatic insufficiency. It is important to exclude cystic fibrosis in any infant presenting with this biochemical abnormality.- - - - - - - - - - ranking = 5keywords = hyperaldosteronism (Clic here for more details about this article) |
3/4. Metabolic complications of the use of stomach for urinary reconstruction.A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.- - - - - - - - - - ranking = 1keywords = hyperaldosteronism (Clic here for more details about this article) |
4/4. Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide--a new clinical syndrome.A state of normokalemic renal sodium wasting associated with an apparently inappropriate secretion of atrial natriuretic peptide (ANP) has not been previously recognized. We here report an 11-year-old boy who presented with a chronic "salt-losing" nephropathy manifested by normonatremic or mildly hyponatremic extracellular fluid volume depletion, hypodipsia, absence of salt appetite, normokalemic metabolic alkalosis, hyper-reninemic hyperaldosteronism, hypertrophy of the juxtaglomerular apparatus, and highly conserved capacities for concentrating diluting the urine. plasma ANP values were paradoxically elevated (between 10 and 47 fmol/ml), despite the coexistence of intravascular volume depletion and increased plasma levels of renin and aldosterone. Although the patient had some clinical similarities to Bartter's syndrome, fractional sodium chloride (NaCl) reabsorption during hypotonic saline diuresis was normal and no clinical amelioration was observed while on indomethacin therapy. Neither a tumor nor cardiac or cerebral abnormalities, which could be responsible for the increased ANP secretion, were detected. These clinical, biochemical, and histological features have not been previously described together and may represent a new clinical syndrome. The pathophysiology of this entity remains unknown, but an attractive, although unproven, hypothesis is that the renal defect in NaCl reabsorption in this patient could be related to an inappropriate and unregulated secretion of ANP.- - - - - - - - - - ranking = 1keywords = hyperaldosteronism (Clic here for more details about this article) |