Autonomic Insufficiency in Uremia as a Cause of Hemodialysis-Induced Hypotension

Es, Kersh; Sj, Kronfield; Unger, Allan M.; Rw, Popper; Cantor, Stephen A.; Cohn, Keith

doi:10.1056/nejm197403212901203

Cited by 273 publications

(105 citation statements)

References 14 publications

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“…279 CKD may lead to sleep apnea by autonomic nerve damage, effected by generalized uremic neuropathy, interfering with baroreceptor activity, pharyngeal narrowing due to fluid overload, and accumulation of uremic toxins. [279][280][281][282][283][284] Sleep apnea likely causes CKD through numerous mechanisms that promote renal hypoxia. 285,286 The most obvious mechanism is that apnea causes insufficient or absent ventilation, compromised gas exchange, and, thus, intermittent nocturnal hypoxia.…”

Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

125

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

125

111

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“…These include defective function of sweat glands (Hennessy & Siemsen, 1968), abnormal response to the Valsalva manoeuvre (Ewing & Winney, 1975;Campese, Romoff, Levitan, Lane & Massry, 1981), vagal neuropathy (Burgess, 1982;Endre, Perl, Kraegen, Charlesworth & Macdonald, 1982) and reduced pressor response to sustained hand grip exercise (Ewing & Winney, 1975;Campese et al, 1981). Impairment of autonomic function has also been implicated in haemodialysis-induced hypotension (Kersh, Kronfield, Unger, Popper, Cantor & Cohn, 1974); although the importance of any defect in the autonomic nervous system in this disorder has been disputed (Naik, Mathias, Wilson, Reid & Warren, 1981).…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular responses in rats with glycerol‐induced acute renal failure

Bowmer¹,

Warren²,

Yates³

1983

British J Pharmacology

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“…Investigations of the sympathetic nervous system are limited and have either failed to localize an autonomic lesion or neglected any possible relationship of the aforementioned defect with clinical behavior on hemodialysis (5)(6)(7)(8)(9). The results of two investigations suggest that severe hypotension during hemodialysis may be related to autonomic neuropathy, reduction in central blood volume, or lower plasma oncotic pressure (5,7). There was no obvious localization of the autonomic defect and no description of blood pressure patterns before and after hemodialysis treatment.…”

Section: Introductionmentioning

confidence: 99%

“…Inhalation of amyl nitrite appears to be a useful way to determine the function of the visceral afferent and efferent limbs of the cardiopulmonary or baroreceptor reflex arcs (5). The early hemodynamic response to immersion of one hand in ice water (cold pressor test) is a proposed index of visceral efferent adrenergic activity or vascular integrity (10).…”

Section: Introductionmentioning

confidence: 99%

Adrenergic regulation of blood pressure in chronic renal failure.

Lilley¹,

Golden²,

Stone³

1976

J. Clin. Invest.

168

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A B S T R A C T Previous investigations have suggested that significant hypotension during hemodialysis may result from abnormalities of sympathetic nervous system activity. To further evaluate these phenomena, plasma dopamine 8-hydroxylase (D3H) and cold pressor test (proposed indexes of efferent sympathetic nervous system activity) and amyl nitrite inhalation (an index of the entire baroreceptor reflex arc) were studied in two groups of patients: group I, patients exhibiting a mean arterial pressure decrease to less than 70 mm Hg during less than 10% of dialyses; group II (hemodialysis hypotension), patients with a mean arterial pressure decrease to less than 70 mm Hg during more than 90% of dialyses. The groups were similar with respect to plasma renin activity, renin response to ultrafiltration, age, duration of dialysis, nerve conduction velocity, plasma protein concentration, hematocrit, dialysis weight change, resting heart rate, sex, race, blood pressure and heart rate response to cold pressor test, and 1"I-albumin plasma volume. Supine mean arterial pressure was higher in patients with hemodialysis hypotension than in patients without hemodialysis hypotension (group I) both before and after dialysis. Plasma D#3H activity was significantly higher in patients with hemodialysis hypotension (group II) than in group I both before and after dialysis. Amyl nitrite inhalation, expressed as change in AR-R interval/mean arterial pressure decrease, was less in hemodialysis hypotension patients.These results suggest that hemodialysis hypotension may result from a lesion in the baroreceptors, cardiopulmonary receptors, or visceral afferent nerves. Furthermore, elevated mean arterial pressure in patients with hemodialysis hypotension may be neurogenic in origin, as reflected by plasma Dj8H activity, and appears similar to the hypertension that follows baroreceptor deafferentation of experimental animals.

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Autonomic Insufficiency in Uremia as a Cause of Hemodialysis-Induced Hypotension

Cited by 273 publications

References 14 publications

Hypoxia: The Force that Drives Chronic Kidney Disease

Hypoxia: The Force that Drives Chronic Kidney Disease

Cardiovascular responses in rats with glycerol‐induced acute renal failure

Adrenergic regulation of blood pressure in chronic renal failure.

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