Nephrotic Syndrome: Vasoconstriction and Hypervolemic Types Indicated by Renin-Sodium Profiling

Meltzer, Jay I.; Keim, Hans J.; Laragh, John H.; Sealey, Jean E.; Jan, Kung-Ming; Chien, Shu

doi:10.7326/0003-4819-91-5-688

Cited by 158 publications

(107 citation statements)

References 18 publications

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“…The abnormal water and sodium metabolism typical of the nephrotic state is characterized in part by blunted volume expansion natriuresis, a resistance to the natriuretic actions of ANP, heightened renal sympathetic activity, activation of the renin-angiotensin system [5, 6, 7, 8, 9, 10]and reduced GFR [11]. The mechanisms that underline abnormal water and sodium metabolism, however, are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

“…Nephrotic syndrome (NS), defined as massive proteinuria and hypoalbuminemia, is characterized by water and electrolyte homeostasis disorders. The mechanisms of abnormal sodium metabolism in NS are associated with heightened renal sympathetic nerve activity [5, 6]; activation of the renin-angiotensin system [7, 8]; blunted natriuretic responses to volume expansion and atrial natriuretic peptide (ANP) [9, 10]and a reduced glomerular filtration rate (GFR) [11]. The roles and behavior of uroguanylin in CGN and NS, however, have yet to be clarified.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Plasma and Urine Levels of Uroguanylin, a New Natriuretic Peptide, in Nephrotic Syndrome

Kinoshita

Fujimoto

Fukae

et al. 1999

Nephron

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Uroguanylin, a new natriuretic peptide originally isolated from urine, stimulates the membrane guanylate cyclase C receptor. No information, however, is available on the plasma and urine levels of uroguanylin in nephrotic syndrome (NS), the state associated with sodium and water retention. Using a sensitive radioimmunoassay, we measured the plasma and urine concentrations of immunoreactive (ir-)uroguanylin in NS patients and compared them with those of patients with non-nephrotic glomerulonephritis. Plasma ir-uroguanylin, blood pressure and the cardiothoracic ratio were higher, and urine excretion of ir-uroguanylin was lower in the NS patients. Plasma ir-uroguanylin in the NS patients significantly decreased during remission as compared with findings on admission. There was a significant inverse correlation between the concentration of plasma ir-uroguanylin and that of serum total protein or albumin. Moreover, fluid retention in the NS patients was correlated with the changes in plasma ir-uroguanylin between admission and remission, indicative that the plasma concentration increases with the severity of the nephrotic state. Taking into account its potent natriuretic effect, these findings suggest that uroguanylin may function in the pathophysiological mechanism in NS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma and Urine Levels of Uroguanylin, a New Natriuretic Peptide, in Nephrotic Syndrome

Kinoshita

Fujimoto

Fukae

et al. 1999

Nephron

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“…Higher risks have been reported in men with lower serum albumin and proteinuria, the elderly, and in hypertensive patients [5]. The cause of AKI in nephrotic syndrome remains unclear, but influences include decreases in glomerular permeability [6,7], ischemia-associated tubular injury [3][4][5]8], diuretic administration [9,10], and renal venous thrombosis [11]. In this patient, the presence of an underlying prerenal factor was considered as a potential cause Fig.…”

Section: Discussionmentioning

confidence: 82%

Single low-dose rituximab for the treatment of steroid-resistant nephrotic syndrome with acute kidney injury

Ashikaga¹,

Uda²,

Kamata

et al. 2016

CEN Case Rep

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The efficacy of rituximab for kidney disease, such as frequent relapsing nephrotic syndrome, has been reported recently. Herein, we report a case of a patient with acute kidney injury that was steroid-resistant nephrotic syndrome who responded to a single administration of lowdose rituximab. An 86-year-old Japanese woman with hypertension presented with severe peripheral edema within several days after onset. Due to the patient's age, renal biopsy was not performed, nephrotic syndrome was diagnosed and prednisolone was administered at 40 mg/day on the day after admission. However, anuria developed and hemodialysis was inevitably initiated on the 5th hospital day. The renal function did not recover, and the general condition gradually became aggravated. On the 50th hospital day, 100 mg rituximab was administered, which led to immediate depletion of CD20-positive cells. The urine volume gradually increased from 2-3 weeks after the rituximab administration, and the renal function recovered slightly. After 5 weeks, it became possible to wean the patient from dialysis, which had been applied for 3 months. Rituximab might be an option for the treatment of acute kidney injury due to steroid-resistant nephrotic syndrome.

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“…1112 Abnormal retention of sodium and fluid is also believed to participate in the pathogenesis of hypertension in these nephropathies, 1315 in which an interaction of sodium-dependent and renin-dependent vasoconstrictor mechanisms is occurring. 16 Indeed, it is likely that there is a change in the prevailing mechanisms at different times during the course of the disease. The significant blood pressure fall in response to the type 1 angiotensin receptor subtype antagonist DuP 753 in both normotensive and hypertensive adriamycin rats in the present experiments indicates that Ang II is activated in this stage of adriamycin nephropathy regardless of actual blood pressure levels.…”

Section: Discussionmentioning

confidence: 99%

Pressor mechanisms in adriamycin-induced nephropathy with hypertension in rats.

Franco

Gut²,

FerrariSpadotto³

et al. 1994

Hypertension

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We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16 ±3 mm Hg) and adriamycin-normotensive (-14±5 mm Hg) groups than the saline-treated controls ( -5 ± 1 mm Hg, P<.05). Vasopressin blockade with either a V,V 2 inhibitor or a selective Vi inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16±4 and -17±2mm Hg, respectively,P<.01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the pressor action of vasopressin contributes to elevated blood pressure in hypertensive animals only. renal failure, with a prevalence reported to vary between 23% and 88%. 1 -2 Moreover, coexistence of hypertension with this condition appears to be a sign of poor prognosis.2 It is usually unrelated to the degree of renal insufficiency 3 or to the presence or absence of nephrotic syndrome or steroid therapy, although remission of this syndrome can be associated with a decrease in blood pressure, 4 and coexistence of the two conditions tends to accelerate the progression of renal insufficiency. 5 The mechanism or mechanisms of high blood pressure maintenance in this setting are still not clearly understood and are believed to involve activation of several neurohumoral vasoactive systems, including the sympathoadrenal system, the renin-angiotensin-aldosterone axis, and vasopressin.Adriamycin is an antineoplastic drug that in rats produces a nephrotic syndrome with mild chronic renal insufficiency within 8 to 10 weeks. 68 We used this model to explore the contribution of two vasopressor hormones -angiotensin II (Ang II) and vasopressin -to the hypertension associated with the nephrotic syndrome. MethodsExperiments were performed on adult, male Wistar rats with initial weights of 250 to 350 g. Adriamycin (2 mg/kg) was administered intravenously from the tail vein to 91 rats twice at 3 weeks apart. All animals had free access to tap water and standard rat chow, were handled humanely, and were killed with an intracardiac injection of sodium pentobarbital at the Correspondence to Haralambos Gavras, MD, Chief, Hypertension and Atherosclerosis, Boston University School of Medicine, Boston, MA 02118. end of the experiment. The rats were studied 8 to 10 weeks after the first injection of adriamycin, when nephropathy with hypertension or normotension developed. Hypertension was defined as baseline mean arterial pressure (MAP) ab...

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Nephrotic Syndrome: Vasoconstriction and Hypervolemic Types Indicated by Renin-Sodium Profiling

Cited by 158 publications

References 18 publications

Plasma and Urine Levels of Uroguanylin, a New Natriuretic Peptide, in Nephrotic Syndrome

Plasma and Urine Levels of Uroguanylin, a New Natriuretic Peptide, in Nephrotic Syndrome

Single low-dose rituximab for the treatment of steroid-resistant nephrotic syndrome with acute kidney injury

Pressor mechanisms in adriamycin-induced nephropathy with hypertension in rats.

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