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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cushing's syndrome is characterized by protein wasting secondary to hypergluconeogenesis, which produces thin skin, poor muscle tone, osteoporosis and capillary fragility. These features distinguish patients with true Cushing's syndrome from those who have some of the clinical findings often associated with the syndrome, such as obesity, hypertension, striae and hirsutism. The dexamethasone suppression test helps identify patients with pseudo-Cushing's syndrome.
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PMID:'Not Cushing's syndrome'. 22 Aug 64

The use of plasma renin assays in clinical practice is reviewed and experience with an assay for plasma renin activity (PRA) is reported. In normal subjects, 10am ambulant PRA was significantly related to plasma angiotensin II levels but not related to daily urine sodium exretion in these subjects consuming normal diets. PRA was suppressed in patients with mineralocorticoid hypertension and in a small proportion of patients with essential hypertension. Very high values were observed in patients with untreated primary adrenal insufficiency, treatment of which resulted in a prompt fall of PRA to normal. PRA was usually normal in adrenalectomised patients and those with chronic adrenal insufficiency receiving satisfactory steroid replacement therapy. It is concluded that provided standardised conditions are used for the collection and assay, PRA is helpful in the assessment of hypokalaemic hypertension as well as in the early detection and management of patients with primary adrenal insufficiency or related conditions of salt wasting.
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PMID:Clinical use of plasma renin assays. 27 2

A 2-year-old girl presenting with features of both Bartter's syndrome and renal tubular acidosis was investigated. Hypokalemia, increased plasma renin activity in the absence of hypertension, insensitivity to the pressor effects of angiotensin and a histological picture of juxtaglomerular hyperplasia were characteristic of Bartter's syndrome, but an unusual finding was the presence of metabolic acidosis instead of alkalosis. Functional studies revealed a proximal tubular defect in sodium and bicarbonate reabsorption and a distal defect in sodium reabsorption, urinary acidification and concentrating mechanism. Indomethacin administration was followed by an excellent clinical response and improvement of most functional abnormalities. The defect in distal sodium reabsorption was, however, not corrected by prostaglandin inhibition, and could represent the primary event leading to potassium wasting and secondary hypersecretion of prostaglandins.
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PMID:Bartter's syndrome presenting with features resembling renal tubular acidosis. Improvement of renal tubular defects by indomethacin. 65 58

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.
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PMID:Nephronophthisis. Renal function and histologic studies in a family. 88 91

A patient with primary hyperparathyroidism who presented with hypokalaemia and hypertension is described. Renal potassium wasting was documented and cured by removal of a parathyroid adenoma. Possible mechanisms for this unusual manifestation of hyperparathyroidism are mentioned. Other features of the case were severe anaemia, nephrocalcinosis, pseudogout and postoperative acidosis.
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PMID:An unusual hormonal cause of hypertension and hypokalaemia. 116 32

In the past 30 years 238 cases have been published which describe the nephronophthisiscystic renal medulla complex. Of these, 110 are sufficiently adequate to permit detailed analyses. Both isolated and genetically transmitted cases are reported. The latter include the dominant and recessive modalities, both autosomal, and the former perhaps also X-linked. Renal disease also has been inherited as a recessive trait in association with retinal degeneration. Medullary cysts have been found in 73% of cases in which kidney tissue has been examined directly. Their presence seems to bear no relationship to the ability of involved kidneys to conserve sodium. Salt wasting is described in the presence and absence of medullary cysts. Techniques short of anatomic examination of the kidneys have rarely allowed cysts to be detected and diagnosis continues to rest on a high index of suspicion, aroused in turn by a positive family history for the disease. Arterial hypertension occurs in roughly one third of cases. Aminoaciduria is not a part of the syndrome. A defect in maximum urinary concentrating ability may be the best single early sign of involvement but data are scarce.
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PMID:Juvenile nephronophthisis and renal medullary cystic disease. 126 65

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
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PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

Oliguric ARF occurred in 0.5% of battle casualties who reached the field medical care system and raised their mortality expectancy from less than 5% to nearly 90%, due primarily to fluid volume overload and/or myocardial potassium intoxication. For their effective treatment the Renal Insufficiency Center with laboratory and a Brigham-Kolff rotating drum dialyzer began operations in 1952, as depicted in a videotape prepared for this presentation from motion picture footage filmed in early 1953. Our Surgical Research Team's major findings relevant to ARF were: (1) Renal function was depressed in most battle casualties in proportion to the severity of their wounds and blood loss. (2) Among the more severely wounded some developed nonoliguric; others, oliguric ARF. (3) Oliguria lasted from 3 days to 3 weeks without a discernible peak frequency of beginning diuresis at 10 days. (4) During oliguria, posttraumatic catabolism greatly accelerated extracellular accumulations of nitrogen, potassium, phosphate, and hydrogen ion with rapid, concurrent clinical deterioration. (5) Dialysis "on indication" produced an oscillating clinical and chemical course. (6) ARF was then revealed as a wasting disease complicated by infections, poor wound healing until diuresis occurred, anemia and bleeding, and hypertension during dialyses and in early diuresis. (7) The overall mortality rate was reduced.
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PMID:Acute renal failure during the Korean War. 150 54

We report oligohydramnios and renal dysgenesis in one of identical twins, which might have resulted from in utero exposure to early, prolonged high-dose indomethacin. The proposita was the second of twin girls born at 36 weeks of gestation. Pregnancy was complicated initially by polyhydramnios in both amniotic sacs and premature uterine contractions. After administration of indomethacin and terbutaline from 16 to 30 weeks' gestation, serial prenatal ultrasound examinations ultimately showed oligohydramnios in twin B and resolution of polyhydramnios in twin A. On day 5 twin B developed hematuria, hypertension, renal failure, hyponatremia, hyperkalemia, metabolic acidosis, sodium wasting and severe, transient inability to excrete potassium. Renal sonography showed enlarged, hyperechoic kidneys with almost no corticomedullary differentiation. Renal biopsy revealed immature glomeruli, dilated Bowman's spaces, dilated tubules, and interstitial fibrosis. The liver was histologically normal. Indomethacin may induce oligohydramnios and transient renal insufficiency in humans and renal dysgenesis in fetal monkeys; it might have induced the abnormalities in this patient.
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PMID:Renal dysgenesis in a monozygotic twin: association with in utero exposure to indomethacin. 148 12

Patients with apparent mineralocorticoid excess (AME) have low or absent activity of the enzyme 11 beta OH steroid dehydrogenase (11SD), and inappropriately high intrarenal levels of cortisol resulting in Na+ retention and hypertension. Pseudohypoaldosteronism (PHA), in contrast, is characterized by salt wasting despite hyperaldosteronemia, reflecting low or absent mineralocorticoid receptors (MR). Although AME is presumed to reflect inappropriate cortisol occupancy of MR, several features also suggest inappropriate occupancy of glucocorticoid receptors (GR). To test this possibility, we administered carbenoxolone, which is known to block 11SD, to four patients with PHA, and observed marked mineralocorticoid effects, e.g., antinatriuresis and elevated plasma bicarbonate. To further test the possibility that occupancy of renal GR may induce a classical mineralocorticoid response, we administered the highly specific glucocorticoid RU 28362 to adrenalectomized rats and showed that it has profound antinatriuretic effects. Finally, by selectively blocking MR with RU 28318 or GR with RU 38486, we have shown that corticosterone, the physiologic glucocorticoid in rats, has an antinatriuretic effect in adrenalectomized rats via either MR or GR occupancy. Previous studies have clearly shown that MR are inherently nonselective and have equivalent intrinsic affinity for aldosterone, corticosterone, and cortisol. The present studies suggest that this nonselectivity includes the nuclear response element to which either MR or GR may bind to elicit a mineralocorticoid effect, and further underscore the importance of the enzyme 11SD in the specific mineralocorticoid action of aldosterone.
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PMID:Apparent mineralocorticoid excess, pseudohypoaldosteronism, and urinary electrolyte excretion: toward a redefinition of mineralocorticoid action. 217 62


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