Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite the importance of disturbances in plasma volume in nephrotic patients, the only clinically accepted measurement of this value in common use is plasma renin activity. We assessed the usefulness of plasma vasopressin levels as an index of plasma volume in patients with idiopathic nephrotic syndrome. However, since 80% to 90% of arginine vasopressin circulates bound to platelets, we measured vasopressin levels in platelet-rich and platelet-poor plasma. The nephrotic patients (n = 19) had significantly higher vasopressin levels in platelet-poor and platelet-rich plasma compared with controls (3.2 +/- 0.6 vs 1.0 +/- 0.3 pg/mL, and 10.4 +/- 3.6 vs 3.3 +/- 0.6 pg/mL. respectively). The percent binding of vasopressin to platelets was reduced in nephrotic patients compared with controls (50.2% +/- 6% vs 70.4% +/- 2.9%). The values for platelet-poor vasopressin, but not platelet-rich vasopressin, correlated significantly with the plasma renin activity (r = .83). We conclude that in nephrotic patients, platelet-poor vasopressin levels correlate with plasma renin activity and may provide a useful measure of minute-to-minute vasopressin release in response to changes in plasma volume.
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PMID:Platelet vasopressin levels in childhood idiopathic nephrotic syndrome. 305 66

All nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase, and consequently renal functions dependent upon prostaglandin synthesis can be affected. Fortunately, renal function in normal individuals is relatively independent of the PG system, and thus the NSAIDs don't usually produce any renal dysfunction. However, in some circumstances, inhibition of PG dependent renal functions can produce clinically significant effects. When the kidney is in a salt retaining state or when there is renal vascular damage, NSAIDs can reduce renal blood flow and glomerular filtration rate producing acute renal failure that is reversible upon discontinuation of the drug. NSAIDs can also: 1) reduce sodium excretion and blunt the diuretic effect of loop diuretics, thus producing or exacerbating edema, 2) inhibit PG dependent renin secretion occasionally resulting in hyperkalemia, 3) enhance the antidiuretic effects of vasopressin and 4) reduce the antihypertensive efficacy of several drugs. Evidence that any NSAID "spares" renal cyclooxygenase is controversial, and no NSAID is devoid of clinical problems. Syndromes that are less obviously related to inhibition of renal PG synthesis are acute interstitial nephritis with or without the nephrotic syndrome, renal papillary necrosis, and chronic interstitial nephritis. Recently a unique syndrome of flank pain and mild reversible renal dysfunction has been described in healthy individuals receiving suprofen, a uricosuric NSAID. This syndrome may be due to uric acid crystal deposition in the renal tubules and has resulted in the removal of suprofen from the US market.
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PMID:Renal effects of nonsteroidal anti-inflammatory drugs. 314 36

The roles of the antidiuretic hormone arginine-vasopressin (AVP), atrial natriuretic peptide (ANP), renin, aldosterone and catecholamines in the pathogenesis of impaired water excretion were studied in edematous children with nephrotic syndrome. Compared to non-proteinuric children with nephrotic syndrome in remission, edematous children during relapse had lower serum concentrations of sodium and chloride with lower plasma osmolality, but had higher hematocrit values (P less than 0.05, each). Plasma concentration of AVP was higher in edematous children (P less than 0.01). Compared to healthy, normal children, edematous nephrotic children had higher plasma concentrations of AVP, aldosterone, renin, noradrenaline, and adrenaline (P less than 0.01, each), but had similar levels of plasma ANP. Head out water immersion and infusion of 5 ml/kg 20% human serum albumin solution, both procedures known to increase central blood volume, resulted in a reduction of elevated hormone concentrations to near-normal levels and caused a rise in sodium and water excretion. Following albumin infusion, mean ANP rose fivefold, and plasma concentrations of this hormone correlated positively with urine flow (r = 0.64, N = 18, P less than 0.01) and with sodium excretion (r = 0.62, N = 18, P less than 0.01). It is concluded that AVP, renin, aldosterone and catecholamines are stimulated in edematous children with nephrotic syndrome by reduction in effective circulatory blood volume. Central blood volume expansion induced either by water immersion or by infusion of concentrated albumin solution is able to correct elevated hormone levels and to induce salt and water excretion. Plasma ANP appears to trigger the diuretic and natriuretic effects of central volume expansion.
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PMID:Hormonal regulation of water metabolism in children with nephrotic syndrome. 330 10

Hemodynamic and hormonal factors were monitored in nine patients with nephrotic syndrome who were evaluated relative to their capacity to excrete a 20-mL/kg water load (normal greater than 80%). In five "nonexcretor" patients (37% of water load excreted in five hours), as compared to four normal excretors (105% of water load excreted in five hours; P less than .01 v nonexcretors), neither BP (131/88 v 119/79 mm Hg), pulse (74 v 77 beats/min), cardiac index (3.7 v 3.1 L/min/m2), pulmonary wedge pressure (9.3 v 7.3 mm Hg), systemic vascular resistance (1537 v 1254 dynes-sec-cm-5), nor plasma volume (41.3 v 40.1 mL/kg) were different. Similarly, plasma renin activity (2.6 v 3.7 ng/mL/h), plasma aldosterone (12 v 10.9 ng/dL), and plasma norepinephrine (403 v 312 pg/mL) were not different between nonexcretor v excretor patients with nephrotic syndrome. Plasma vasopressin concentrations were also similar both before (3.1 +/- 0.8 v 2.4 +/- 1.2 pg/mL) and during the water load (0.9 +/- 0.3 v 1.0 +/- 0.4 pg/mL). Inulin clearances, however, were lower in the nonexcretor v the excretor nephrotic patients (37 v 78 mL/min/1.73 m2; P less than .02) and correlated with water excretion (r = .68; P less than .05). Head-out water immersion increased sodium (40 to 110 microEq/min; P less than .01) and water excretion (37% to 82%; P less than .025) in the nonexcretors; the improvement correlated with the increase in inulin clearance during immersion (r = .70; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of glomerular filtration rate in the impaired sodium and water excretion of patients with the nephrotic syndrome. 352 75

Decreased free water excretion and the development of interstitial edema are recognized characteristics of preeclampsia. However, the pathophysiology of decreased urine excretion in preeclampsia is presently controversial: diminished glomerular filtration, renal arteriolar spasm, elevated plasma vasopressin levels, and plasma volume contraction have been suggested as etiologies. We studied seven pregnant patients with a diagnosis of mild preeclampsia to assess the role of vasopressin, serum protein, and glomerular function in the renal excretion of water. The ability to excrete a water load was significantly and directly correlated with serum albumin (P less than 0.05) and protein (P less than 0.02) concentrations. Neither plasma vasopressin nor creatinine clearance correlated with water excretion. The similarity of preeclampsia and the nephrotic syndrome with regard to the renal excretion of water is discussed.
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PMID:Water excretion in preeclampsia: behavior as nephrotic syndrome. 405 79

A 59-year-old man was admitted to our hospital because of fever in August 1991. Bone marrow showed normocellularity with 41.5% of CD13, 14, 33 positive blasts, and a diagnosis of AMMoL was made. Laboratory investigation revealed hyponatremia and elevated serum ADH level, indicating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Intensive chemotherapy successfully induced hematological complete remission and his serum sodium level became normal. In February 1992, he developed proteinuria and findings were consistent with nephrotic syndrome (NS). Renal biopsy specimen showed membranous proliferative glomerulonephritis and massive infiltration of macrophages, and his serum interleukin 6 level was elevated. Five months later, he suffered from pancytopenia and elevation of biliary enzymes with increase of hemophagocytic histiocytes in his bone marrow (hemophagocytic syndrome). He transiently responded to low dose chemotherapy but he died due to severe infection. It is interesting that association between macrophages and/or cytokines with these various complications was suggested in AMMoL.
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PMID:[Acute myelomonocytic leukemia complicated with syndrome of inappropriate secretion of antidiuretic hormone, nephrotic syndrome, and hemophagocytic syndrome]. 756 94

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39

In this work we analyze the renal and systemic factors involved in the sodium retention in two conditions: in extracellular volume depletion and in edema forming states, particularly liver cirrhosis with ascitis. In this paper we accept that the volume loss of body fluids stimulates the "effective arterial blood volume" (VAE). This term results from a decrease in the arterial blood volume secondary to a fall in cardiac output or a peripheral arterial vasodilatation. The reduction in the VAE stimulates: the high pressure baroreceptors (carotid sinus and aortic arch); the intrarrenal mechanisms, such as the yuxtaglomerular apparatus and the renin angiotensin aldosterone system; the sympathetic adrenergic system; the non osmotic release of antidiuretic hormone; prostaglandins (PGE1, Tromboxane) and endothelin; and inhibits the atrial natriuretic peptide. We also describe the sodium transport mechanisms along the nephron during physiological conditions and after volume depletion, and in edema formation states, specially hepatic cirrhosis with ascitis. We speculate that the intrarenal mechanisms are more important and persistent than the systemic mechanisms. It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. The clonation and structural characterization of the different sodium transports may help us to establish, more precisely, the intracellular tubular mechanisms responsible for the tendency of the body to retain sodium. The amount of information generated in the future may help us to demonstrate, with more precision, the mechanisms responsible for the sodium retention and excretion in normal and pathological conditions, particularly the edema forming states such as cardiac failure, nephrotic syndrome and hepatic cirrhosis with ascitis.
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PMID:[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites]. 777 18

Nephrotic syndrome is characterized by water and sodium retention, which leads to edema formation. The nonosmotic stimulation of arginine vasopressin (AVP) release from the pituitary gland has been implicated to be one of the important factors of abnormal water retention in patients with nephrotic syndrome. It is not known, however, whether nephrotic syndrome is associated with stimulation of hypothalamic vasopressin gene expression. Puromycin aminonucleoside is known to cause altered glomerular permeability, which results in experimental nephrotic syndrome in rats. In the present study, therefore, AVP gene expression has been studied in the hypothalamus of rats with puromycin aminonucleoside-induced nephrotic syndrome (PNS). Nephrotic syndrome was induced by a single intravenous injection of puromycin aminonucleoside (50 mg/kg body weight). Nephrotic syndrome was confirmed by urinary protein excretion (control 20.8 +/- 3.5 mg/24 hr v PNS 273.9 +/- 41.4 mg/24 hr; P < 0.0001, n = 6) and serum albumin concentrations (control 4.52 +/- 0.07 g/dL v PNS 2.96 +/- 0.22 g/dL; P < 0.001, n = 6). In PNS rats, plasma AVP was significantly higher than in control rats (control 0.77 +/- 0.10 pg/mL v PNS 2.13 +/- 0.42 pg/mL; P < 0.005, n = 12), even though there were no differences in plasma osmolality (control 292.0 +/- 2.0 mOsm/kg H2O v PNS 290.3 +/- 2.5 mOsm/kg H2O; P = NS, n = 12) or serum sodium concentration (control 142.7 +/- 0.7 v PNS 142.1 +/- 1.1; PNS, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine vasopressin gene expression in rats with puromycin-induced nephrotic syndrome. 781 May 34

Considerable controversy exists in regard to the state of arterial circulatory integrity in patients with the nephrotic syndrome. Increased sympathetic nervous system activity, along with activation of the renin-angiotensin-aldosterone system and the nonosmotic release of vasopressin, is seen in other states of arterial underfilling. Thus, in the present study, sympathetic nervous system activity was assessed by determining plasma norepinephrine secretion and clearance rates using a whole-body steady-state radionuclide tracer method in 6 edematous patients with the nephrotic syndrome of various parenchymal etiologies and 6 normal control subjects in the supine position. Patients were withdrawn from all medications 7 days prior to study. Mean creatinine clearances and serum creatinine concentrations were normal in both the nephrotic syndrome patients and controls (99 +/- 13 vs. 112 +/- 15 ml/min, p = NS, 1.1 +/- 0.1 vs. 0.8 +/- 0.0 mg/dl, p = 0.03, respectively). However, the nephrotic syndrome patients exhibited significant hypoalbuminemia (2.0 +/- 0.4 vs. 3.8 +/- 0.1 g/dl, p < 0.01). The supine plasma norepinephrine level was elevated in the patients with the nephrotic syndrome as compared with controls (240 +/- 58 vs. 119 +/- 22 pg/ml, p = 0.07). More significantly, the secretion rate of norepinephrine was markedly increased in nephrotic patients (0.30 +/- 0.07 vs. 0.13 +/- 0.02 micrograms/m2/min, p < 0.05), whereas the clearance rate of norepinephrine was similar in the two groups (2.60 +/- 0.29 vs. 2.26 +/- 0.27 l/min, p = NS). Plasma renin activity and plasma aldosterone, arginine vasopressin and atrial natriuretic peptide concentrations were not different in nephrotic syndrome patients compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased norepinephrine secretion in patients with the nephrotic syndrome and normal glomerular filtration rates: evidence for primary sympathetic activation. 826 24


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