The Relationship of Cardiovascular and Renal Hemodynamic Function to Sodium Excretion in Patients With Severe Heart Disease but Without Edema 12

Hollander, William; Judson, Walter E.

doi:10.1172/jci103357

Cited by 45 publications

(6 citation statements)

References 7 publications

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“…In the group receiving the normal-sodium diet, only nine patients were readmitted during the follow-up period compared with 30 patient in the group receiving the low-sodium diet. These findings are in contrast with results from previous studies in which untreated and conventionally treated patients with CHF have been shown to accumulate excess sodium and water during dietary sodium loading [24][25][26][27][28]. In view of these clinical results, we hypothesized that normal sodium intake maintains a suitable arterial blood volume that inhibits the neurohormonal activation observed during a low-sodium diet, and improves both renal and hormonal alterations.…”

Section: Discussioncontrasting

confidence: 70%

Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

et al. 2008

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The aim of the present study was to evaluate the effects of a normal-sodium (120 mmol sodium) diet compared with a low-sodium diet (80 mmol sodium) on readmissions for CHF (congestive heart failure) during 180 days of follow-up in compensated patients with CHF. A total of 232 compensated CHF patients (88 female and 144 male; New York Heart Association class II-IV; 55-83 years of age, ejection fraction <35% and serum creatinine <2 mg/dl) were randomized into two groups: group 1 contained 118 patients (45 females and 73 males) receiving a normal-sodium diet plus oral furosemide [250-500 mg, b.i.d. (twice a day)]; and group 2 contained 114 patients (43 females and 71 males) receiving a low-sodium diet plus oral furosemide (250-500 mg, b.i.d.). The treatment was given at 30 days after discharge and for 180 days, in association with a fluid intake of 1000 ml per day. Signs of CHF, body weight, blood pressure, heart rate, laboratory parameters, ECG, echocardiogram, levels of BNP (brain natriuretic peptide) and aldosterone levels, and PRA (plasma renin activity) were examined at baseline (30 days after discharge) and after 180 days. The normal-sodium group had a significant reduction (P<0.05) in readmissions. BNP values were lower in the normal-sodium group compared with the low sodium group (685+/-255 compared with 425+/-125 pg/ml respectively; P<0.0001). Significant (P<0.0001) increases in aldosterone and PRA were observed in the low-sodium group during follow-up, whereas the normal-sodium group had a small significant reduction (P=0.039) in aldosterone levels and no significant difference in PRA. After 180 days of follow-up, aldosterone levels and PRA were significantly (P<0.0001) higher in the low-sodium group. The normal-sodium group had a lower incidence of rehospitalization during follow-up and a significant decrease in plasma BNP and aldosterone levels, and PRA. The results of the present study show that a normal-sodium diet improves outcome, and sodium depletion has detrimental renal and neurohormonal effects with worse clinical outcome in compensated CHF patients. Further studies are required to determine if this is due to a high dose of diuretic or the low-sodium diet.

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Section: Discussioncontrasting

confidence: 70%

Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

et al. 2008

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“…An elevated radiosulfate space has likewise been observed by Walser, Duffy and Griffin in mild heart failure without peripheral edema (16). The present and previous studies indicate that these alterations in body composition may also occur without a demonstrable impairment in sodium excretory capacity (18)(19)(20). In view of these observations it is possible that the increases in body sodium and extracellular fluid volume found by Ross in a group of subjects with severe hypertension might have been due to complicating subclinical heart failure.…”

supporting

confidence: 76%

Body Fluid and Electrolyte Composition in Arterial Hypertension. I. Studies in Essential, Renal and Malignant Hypertension*

Hollander¹,

Chobanian²,

Burrows³

1961

J. Clin. Invest.

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In previous studies in this laboratory it was found that the capacity to excrete sodium as indicated by the rate of excretion of an intravenously administered sodium load was significantly increased in essential and renal hypertension (1, 2). Sodium excretory capacity was reduced by antihypertensive therapy and was correlated significantly with the level of arterial pressure. However, the absence of a high degree of correlation, together with the ability of dietary sodium intake to influence the renal capacity to excrete sodiun-m, suggested that in addition to an elevated blood pressure other factors such as an increase in body sodium and fluid volume might enhance sodium excretion in hypertensive individuals.Studies in Cushing's syndrome and Addison's disease by other workers suggest that the level of adrenal cortical activity may influence not only the renal capacity to excrete sodium but also the arterial pressure as well as the body's content of fluids and electrolytes (3, 4). In line with these observations are recent relports indicating that an increase in aldosterone activity occurs in certain groups of hypertensive subjects (5-7). tions in primary aldosteronism are presented in a separate report (9). CLTNTCAL MATERTAL AND METHODSRadioisotope dilution studies were performed in untreated ambulatory hypertensive patients and normal subjects who were paired as to age, sex, height, weight and body build. The dietary intake of salt as indicated by history and urinary sodium excretion over a 24 hour period was "unrestricted" and comparable in the hypertensive and the control subjects.The 20 subjects with essential hypertension had sustained elevations of blood pressure with grade I to III retinopathy (Keith-Wagener) but without complicating nitrogen retention or congestive heart failure. However, 8 of these subjects were found to have enlarged left ventricles on roentgenographic examination.The 10 subjects designated as having "renal hypertension" had a history of kidney disease which antedated the onset of the hypertension. Included in the group were 5 subjects with bilateral chronic pyelonephritis, 2 with polycystic kidney disease and 3 with glomerulonephritis. Their fundi showed grade I to III retinopathy whereas their blood urea nitrogen levels were normal except in 2 subjects. The left ventricle was enlarged in 5 subjects but no patient had complicating congestive heart failure.The 7 hypertensive subjects with complicating heart failure bad enlargement of the left ventricle with symptoms and signs of pulmonary congestion but without clinically detectable peripheral edema. The decholin circulation time was prolonged in all subjects but only 1 had a definite elevation of venous pressure. Two of the subjects had nitrogen retention and all showed grade II to III hypertensive retinopathy.All 10 subjects who had malignant hypertension had grade IV retinopathy (papilledema) as well as marked elevation of blood pressure. In the group there were 4 subjects with chronic bilateral pyelonephritis, 3 with essential hyp...

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“…In humans with valvular heart disease, the only hemodynamic variable differentiating patients with and without edema was high right ventricular end‐diastolic pressure in those with edema …”

Section: Discussionmentioning

confidence: 99%

Cardiorenal syndrome in renal transplant recipients — It’s the fistula at fault: A case series

Samarendra

Mohan

Sharma

et al. 2018

Clinical Transplantation

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Not much is known about the impact of high flow functional AVF in kidney transplant recipients. As such, there is no consensus regarding management of AVF after renal transplantation. High-flow AVF (>2 L/min) can cause cardiovascular dysfunction 1-3 due to high output state and renal allograft dysfunction through high venous pressure. We report an observational study of renal transplant recipients presenting with a constellation of clinical features, viz., edematous state, dyspnea, high pulmonary pressure, and allograft dysfunction.We draw attention to the hemodynamic effect of high-flow AVF, resulting in a syndrome consistent with Cardio-Renal Syndrome Type 5 (CRS-5). | MATERIAL S & ME THODSThirteen renal transplant recipients, average age of 60 years, including three African-Americans (two men, one woman) were identified with the above syndrome. Eleven had functioning allografts, while in two, allograft failure necessitated hemodialysis. Clinical examination of these patients predominantly showed features of high output state with right heart failure.Investigations included transthoracic echocardiography, where heart chamber sizes, stroke volume, tricuspid annulus (TA), and inferior vena cava (IVC) sizes were measured with quantification of tricuspid regurgitation (TR), and pulmonary systolic pressure in standard manner. All transplant recipients underwent allograft ultrasound.Nine of the thirteen patients underwent right heart catheterization (RHC). RHC in patient # 11 was done 6 months after initial presentation, when treatment with increasing dose of diuretic (Bumetanide 4 mg twice daily) to maintain euvolemia resulted in worsening renal parameters (Table 1 shows RHC results and AVF flow rate).Patient # 1 underwent Transesophageal echocardiography and cardiac MRI. Allograft rejection was ruled out in all cases with appropriate investigations. All management decisions were exclusively taken by the treating physicians.Lack of satisfactory response to diuretics and a strong suspicion of pathogenic role of AVF led to ligation in five patients (# 1-5) and partial closure with banding in Patient # 6. In Patients # 7-9, the AVF flow (Qa) spontaneously decreased to <2 L/min during follow-up. AbstractComplications arising from a functional arteriovenous fistula (AVF) in successful kidney transplant recipients (KT) have been overlooked despite some reports of its deleterious effect on heart, lungs, and kidney allograft. As such, there is no consensus regarding management of AVF after renal transplantation. We report Cardio-Renal Syndrome Type 5 in kidney transplant recipients who presented with a clinical syndrome of shortness of breath, edematous state, kidney allograft dysfunction, and high pulmonary pressure 3-8 months after successful transplantation. Investigations showed this to be due to high flow functioning AVF (>2 L/min) behaving like a systemic shunt causing high output heart failure, along with pulmonary and venous hypertension. This led to allograft dysfunction of fluid homeostasis. Symptoms resolved with...

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The Relationship of Cardiovascular and Renal Hemodynamic Function to Sodium Excretion in Patients With Severe Heart Disease but Without Edema 12

Cited by 45 publications

References 7 publications

Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend?

Body Fluid and Electrolyte Composition in Arterial Hypertension. I. Studies in Essential, Renal and Malignant Hypertension*

Cardiorenal syndrome in renal transplant recipients — It’s the fistula at fault: A case series

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