Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of ADH-secretion and transient water diuresis was observed as acute effects of radio-frequency lesions in the septal region of goats. The water diuresis was not compensated for by drinking and therefore rapidly induced pronounced hypernatremia and hypovolemia. The development of hypovolemia was accompanied by a rise in plasma renin activity. Lesions of the same kind, but extending into the preoptic region near the medial portion of the supraoptic nuclei induced the inability to excrete excessive water characteristic of SIADH. Determinations of plasma arginine vasopressin suggested that the lesions causing SIADH did not produce any noticeable increase in basic ADH-secretion. The results suggest that impulses from juxtaventricular receptors regulating ADH-release and water intake to a considerable extent are transmitted via the septal region, and that elimination of this impulse traffic is sufficient to turn water balance to the negative side. However, reflex volumetric inhibition of the ADH-secretion does not seem to be mediated by pathways passing through the septal region.
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PMID:Transient water diuresis and syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by forebrain lesions of different location. 71 63

Seventeen unselected, consecutive patients with intracranial disease and accompanying hyponatraemia were studied. All would previously have been diagnosed as having the syndrome of inappropriate antidiuretic hormone (ADH) secretion on the basis of spot plasma/urinary electrolyte testing with the application to them of existing standard laboratory criteria. Timed urinary collections and matching plasma samples were available in all but three cases for the derivation of creatinine, osmotic and free-water clearances, tubular reabsorbed water, and fractional water and sodium excretions. In a number of patients the plasma renin, aldosterone and ADH levels were also assayed. On the basis of the overall findings, 13 patients were diagnosed as in fact having a salt-wasting state whilst in only four patients was the diagnosis of inappropriate ADH secretion (SIADH) substantiated. It is suggested that obtaining simple derived parameters of sodium and water homeostasis can add significantly in differentiating between these quite opposite syndromes.
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PMID:Hyponatraemia in neurosurgical patients: diagnosis using derived parameters of sodium and water homeostasis. 144 68

1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. 2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow. 3. In normal subjects an inverse relationship exists between plasma ANF values and renin-angiotensin-aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment. 4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures. 5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion. 6. Evidence from low-dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects. 7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.
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PMID:Atrial natriuretic factor in human pathophysiology. 297 38

A 76-year-old woman was admitted to our hospital because of productive cough, fever and anorexia in January 1995. She had suffered from bronchial asthma for 25 years. From 1983, exacerbation of PIE was recorded three times, on which occasions prednisolone and antibiotics were quite effective. On admission, marked leukocytosis (28,000/microliters) and eosinophilia (18,000/microliters) were found. However, plasma IgE level was normal, and specific antigen for eosinophilia was not detected by RAST or the skin allergic reaction test. Chest X-ray film and CT scan revealed extensive bilateral pulmonary infiltration. Increase in eosinophils (33%) was demonstrated in bronchoalveolar lavage. Furthermore, biopsy specimen of the affected lung revealed diffuse infiltration of eosinophils into alveolar septa. On the basis of these findings, the patient was diagnosed as chronic eosinophilic pneumonia (PIE syndrome). Hyponatremia (117 mEq/l) was persistent after the hydration with normal saline. Plasma ADH was not suppressed (2.29 pg/ml) in spite of hypoosmolality of plasma. Laboratory examination showed that renal, adrenal and thyroid function as well as plasma renin activity were normal. Taking these findings together, she was diagnosed as having SIADH. Treatment with prednisolone improved not only the PIE syndrome but also SIADH.
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PMID:[A case of pulmonary infiltration with eosinophilia (PIE) syndrome associated with syndrome of inappropriate secretion of ADH (SIADH) in the elderly patient]. 855 92

Hyponatremia is more frequently observed in elderly patients associated with exaggerated response of ADH release and attenuated response of renin-aldosterone system. Differentiation of SIADH and hyponatremia other than SIADH is essential in anticipating the therapeutic effect of water restriction to correct hyponatremia. Serum concentration of uric acid and urinary excretion of kallikrein are significant parameters in biochemical discrimination index to differentiate these two types of hyponatremia. In addition to sodium replacement, water restriction and mineral corticoid, newly developed non-peptide ADH V2 receptor antagonist, OPC-31260, seems to be a useful tool to correct hyponatremia.
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PMID:SIADH and other hyponatremic disorders: diagnosis and therapeutic problems. 894 Aug 23

Authors deal in detail with the pathophysiology of the osmolal regulation. Besides hyperosmolality the secretion of antidiuretic hormone (ADH) in increased by hypovolemia and hypotension. Secretion of ADH is lowered in hypoosmolal states. All other mechanisms are preferebly volume regulating and they influence mainly retention and excretion of sodium. Authors discuss homeostatic effects of the renin-angiotensin-aldosteron system, effects of renal failure with prevailing glomerular or tubular function disorder, impact of diuretics, natriuretic peptides, digitalis-like hormone, urodilantin and influence of the other solutes. Disorders of the effective osmolality regulation are frequent in the cerebral affections that originate from trauma, vascular disease, inflammation or tumors. Hypoosmolality and hyponatremia are presented in two different conditions: Inappropriate Vasopressin Secretion Syndrome (IADHS) and Cerebral Salt Wasting Syndrome (CSWS). Quick differential diagnose is important because the treatment of both syndromes is essentially different. Typical cause of hypernatremia is central diabetes insipidus (DI). The group of available calculated renal function parameters is applied in the differential diagnosis of these syndromes. They are creatinin clearance, excretion fraction of water and sodium, electrolyte clearance and electrolyte free water clearance. Investigation of ADH and natriuretic peptide could be even misleading. Pathophysiologic consequence of the state given by inappropriate elevation of one hormone can be the elevation of the second one.
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PMID:[Disturbances of effective osmolality regulation in disorders of the central nervous system and possible methods of monitoring]. 974 51

We evaluated in 110 consecutive elderly hyponatremic patients the value of traditional clinical and biochemical data and the place of a test infusion of 2 liters isotonic saline over 24 hours, in establishing the etiology of the hyponatremia. The causes of hyponatremia were as follows: 31% SIADH patients, 23% patients with hyponatremia due to diuretics, 18% potomania patients, 15% salt depleted patients, 5% salt depleted SIADH patients, 5% patients with a salt loosing syndrome and 3% patients with hyponatremia of unknown origin. Several salt depleted (SD) and SIADH patients could be confounded. Usually, adults with SIADH show plasma uric acid values <4 mg/dL. In our elderly population, 41% of SD patients presented plasma uric acid <4 mg/dL, while 27% of SIADH patients showed plasma uric acid >4 mg/dL. Eighty-two percent of SD patients appeared to have plasma urea levels >30 mg/dL, but this was also the case in 21% of SIADH patients. Twenty-nine of the SD patients presented a urinary sodium >30 mEq/L, but all had fractional sodium excretion (FENa) lower than 0.5%. However, in SIADH, 42% of the patients presented also FENa <0.5%. Fractional excretion of urea (FE urea) below 50% was encountered in 82% of SD patients and FE urea above 50% in only 52% of the SIADH patients. Plasma renin and aldosterone values were poorly discriminative. A test infusion with 2 liters isotonic saline over 24 hours allowed a correct classification of all the patients. In about 2/3 of the population, administration of isotonic saline could be considered as useful (SD, most diuretic patients, potomania patients, salt loosing syndrome patients and some SD SIADH patients). A plasma sodium (PNa) increase of at least 5 mEq/L 24 hours after saline infusion has been suggested as highly suggestive of SD. Nevertheless, 29% of our SD patients did not increase their PNa level by 5 mEq/L or more, while 30% of our SIADH patients did. PNa improved after 2 liters isotonic saline over 24 hours in 90 patients (85%) as opposed to 12 others (9 SIADH and 3 diuretic patients), decreasing their plasma sodium. The isotonic saline infusion test, only allows a reliable classification of hyponatremia, as far as both PNa and sodium excretion were taken into account. In the SIADH group, 6 patients (5%) presented initially manifest solute depletion and retained the 2 liters isotonic saline before developping inappropriate natriuresis. Six patients showed a transient salt loosing syndrome with high fractional potassium excretion (FEK) and high calciuria, which differentiates them from thiazide patients presenting also high FEK, but low calciuria. These patients were also polyuric at admission. The saline infusion was well tolerated in all but 2 patients, developing mild pulmonary congestion at the end of the test infusion.
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PMID:Utility and limitations of biochemical parameters in the evaluation of hyponatremia in the elderly. 1158 74

We report a 47-year-old man with multiple sclerosis (MS) with previous history of recurrent sensorimotor disturbance and visual deficit. The patient developed bilateral motor weakness in the upper limbs, and systemic malaise. An administration of 20 mg/day of prednisolone was ineffective for his symptoms and he complained dyspnea a week later. On admission, his clinical findings included brainstem dysfunction with optic nerve atrophy, motor disturbance in the bilateral upper limbs, hyperreflexia, and superficial sensory disturbance. Biochemical examination revealed marked reduction in serum Na (117 mEq/l) and C1 (85 mEq/l) with increased urinary Na excretion. Although his plasma osmotic pressure decreased to 233 mOsm/kg, urinary osmotic pressure increased to 409 mOsm/kg. Serum antidiuretic hormone (ADH) concentration was 26.1 pg/ml and plasma renin activity was 0.1 ng/ml/ hour. Renal function and adrenal function were normal. Cerebrospinal fluid contained increased protein concentration, IgG, and myelin basic protein. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with MS was diagnosed. Intravenous Na infusion with restricted supplemental fluid and serial administration of methylprednisolone (1,000 mg/day for three days) improved his neurological abnormalities and normalized his serum serum Na level and plasma osmotic pressure. This suggests that demyelinating lesions in the hypothalamus due to MS may cause the transient increased ADH secretion.
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PMID:[Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with relapsing multiple sclerosis]. 1578 1

Acute hyponatremia, following neurosurgery, results from inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW). CSW is due to abnormally high atrial or brain natriuretic peptides (ANP, BNP), which block all stimulators of zona glomerulosa steroidogenesis, resulting in mineralocorticoid deficiency. A 3 year-old girl presented CSW at day 4, after resection of craniopharyngioma and hypophysectomy. Hyponatremia, hyperkalemia and high natriuresis occurred on day 8, with low renin and aldosterone and elevated BNP 120.3 ng/ml (undetectable before surgery). Fludrocortisone 100 microg/day controlled natriuresis and restored electrolytes within 24 hours. A 5 year-old boy presented CSW at day 6 after partial resection of optic glioma. Fludocortisone 100 microg/day restored electrolytes within 8 hours. ANP was elevated, 60.6 ng/l, aldosterone and renin were low. Fludrocortisone supplementation should be considered in CSW, as excessive natriuresis is controlled, and electrolytes are easily restored, avoiding life-threatening complications of this complex disorder.
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PMID:Mineralocorticoid deficiency in post-operative cerebral salt wasting. 1805 34

We herein describe a rare case of hyponatremia that was aggravated by a burn injury. The patient was also found to have hypothyroidism, followed by SIADH, and finally CSWS, which showed complicated clinical features. A 68-year-old man was admitted for evaluation and treatment of a thermal burn. On admission, the patient was dehydrated, which was evidenced by physical signs. The patient had hyponatremia (serum Na 123 mmol/L) with high excretion of urinary sodium. Plasma AVP levels related to plasma osmolality were high. Plasma levels of renin and aldosterone were low, while the plasma ANP level was normal. However, there was no deficiency of mineralocorticoid or glucocorticoid. After admission, the hyponatremia worsened, and edema with hypoproteinemia developed. The patient was found to have hypothyroidism due to chronic thyroiditis. However, hyponatremia was not completely recovered with replacement of thyroid hormone. The hyponatremia was normalized by administration of DMC. The skin injury was treated with a skin graft. After DMC was discontinued, hyponatremia developed once again. However, this time, there was no inappropriate antidiuresis and the hyponatremia was normalized with the administration of fludrocortisone. These findings revealed that the hyponatremia in this patient may have been primarily due to CSWS. It was most likely exacerbated by hypothyroidism, burn injury, and SIADH caused by the infection. The patient showed physical signs of dehydration and edema. Furthermore, biochemical laboratory data were unable to distinguish between hypovolemia and non-hypovolemia. These complicated features were explained by multiple disorders
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PMID:Hyponatremia secondary to multiple etiologies: a case report. 1808 71


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