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Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. In recent years, the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in man, it has been found that the nonosmotic release of vasopressin is consistently associated with the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and in the activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context, neither total extracellular-fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade, or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae, and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV). initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

Twenty-two patients with definite or classical rheumatoid arthritis (RA) who were diagnosed as amyloidosis by biopsy or at autopsy were investigated. The average duration of RA prior to the diagnosis of amyloidosis was 16.5 +/- 12.5 years. The symptoms that led to the diagnosis of amyloidosis were renal symptoms in 11 cases and gastrointestinal symptoms in 5 cases. Urinary protein was positive in 16 cases (73%). The degree of proteinuria varied in each case. Nephrotic syndrome was observed in 5 cases. Azotemia (Cr greater than 1.5 mg/dl) was present in 18 cases (82%). The period from the diagnosis of amyloidosis to death was 3.0 +/- 2.2 years. The causes of death were uremia in 10 cases, heart failure in 2 cases, malignancy in 2 cases, sepsis in 2 cases and others in 2 cases. Thirteen patients were autopsied and the frequency of amyloidosis complicated with RA was 22.0% in autopsied rheumatoid patients. Although nephropathy was present in most cases of amyloidosis complicated with RA, proteinuria and azotemia greatly varied in both degree and course.
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PMID:Clinical studies on amyloidosis complicated with rheumatoid arthritis--with particular reference to nephropathy. 227 6

Ultrasonic dopplerography revealed development of the hypodynamia syndrome in the III term of physiological pregnancy. Disorders of the pumping function of the heart were revealed in the nephrotic syndrome of chronic nephritis and severe pregnancy nephropathy. Hypertension deteriorates the functional cardiac insufficiency. Correction of contractile function of the myocardium is necessary in these cases.
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PMID:[Myocardial contractile function in pregnant women with kidney diseases]. 228 65

A 57-year-old patient presented with periorbital and lower limb edema. The physical examination revealed no signs of cardiac insufficiency or chronic liver disease. Initial laboratory values showed significant hypoproteinemia and hyperlipidemia. Renal function was normal. Urinary protein excretion was 5.5 g/d. Thus, the patient was diagnosed to have nephrotic syndrome. The patient's history, the physical examination and further laboratory work-up suggested a primary glomerulopathy. Percutaneous renal biopsy was performed. The biopsy was diagnostic of minimal change glomerulonephritis. A therapy with steroids was initiated which induced a complete remission of the nephrotic syndrome. The patient has been relapse-free for the entire follow-up period.
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PMID:[Eyelid and ankle edema]. 231 82

Recovery of renal function was observed in 10 out of 300 patients (3.3%) treated by CAPD. These 10 patients presented the following primary renal diseases: 4 nephroangiosclerosis, 4 interstitial nephropathies, 1 diabetic nephropathy, 1 unknown nephropathy, and were treated by CAPD for a mean period of 10.2 +/- 5.5 months. CAPD was discontinued when residual renal function reached 12 ml/min. After recovery 8 patients were still alive, including 1 patient who returned to dialysis. 2 patients died. When risk factors such as uncontrolled hypertension, cardiac failure, severe nephrotic syndrome, rapidly progressive renal failure, analgesics or non steroidal anti-inflammatory drug treatments or abuses, chronic urinary obstruction, cholesterol emboli were associated with end stage renal failure, CAPD should be the dialysis treatment of choice, expecting the preservation of the kidney capacities and further a recovery of renal function.
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PMID:Recovery of renal function in patients treated by CAPD. 257 29

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Pathophysiology of vasopressin in edematous disorders. 269 4

We use the unexpected results of five kidney biopsies to discuss how early biopsy in renal disease can change the therapy and correct the diagnosis of the disease. The first patient was a 73 year-old male diabetic who had osteomyelitis and developed rapidly progressive glomerulonephritis. The next patient was a 72 year-old man who was treated for cardiac failure and increasing serum creatinine. The kidney biopsy revealed rapidly progressive glomerulonephritis. The third patient developed acute renal failure after an episode with vomiting. Here the histological diagnosis was acute renal failure and parenchymatous renal disease could be ruled out. The next patient was a 13 year-old girl. She had proteinuria (5-6 g/d) and hypertension (200/140 mm Hg). After four months, serum creatinine was 200 mumol/l. She was then biopsied, and we found membranoproliferative glomerulonephritis type 1. After the diagnosis was established she was treated with immunosuppression and her condition improved. The last patient was a 55 year-old male diabetic. He developed nephrotic syndrome and the histological diagnosis of the kidney biopsy was membranous glomerulonephritis stage 1. Six months after the kidney biopsy we found carcinoma of the lung. This underlines the importance of the fact that 10% of membranous glomerulonephritides are tumour associated.
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PMID:[Clinical significance of early kidney biopsy]. 281 89

This article has analyzed the pathogenesis of sodium and water retention in several circumstances. The initiator of retention has been proposed to be either a fall in cardiac output (e.g., low-output cardiac failure and vasoconstrictor hypovolemic nephrotic syndrome) or peripheral arterial vasodilatation (e.g., high-output cardiac failure, cirrhosis, arteriovenous fistula, and pregnancy). In the only state discussed, in which the kidney is diseased and not merely responding to extrarenal reflexes--i.e., nephrotic syndrome--intrarenal mechanisms may predominate and lead to expansion of the arterial vascular tree and suppression of the renin-angiotensin-aldosterone system (i.e., hypervolemic nephrotic syndrome). Otherwise, when kidneys are healthy, either a fall in cardiac output or peripheral arterial vasodilatation may diminish arterial vascular filling and thereby initiate a series of hemodynamic and hormonal events that result in renal sodium and water retention (Fig. 7). Finally, the approach presented in this article should be considered to be a vantage point from which to evaluate states of sodium and water retention, but not to be an exclusive position.
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PMID:Pathogenesis of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy (2) 272 90

Sodium retention frequently occurs in the critically ill patient. Sodium retention states include cardiac failure, liver failure, nephrotic syndrome, and hypoalbuminemic states. A clear understanding of the pathophysiology and the mechanism of sodium retention are essential for the proper care of these patients.
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PMID:Disordered sodium metabolism: sodium retention states. 333 24

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.
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PMID:Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model. 346 7


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