Neurologic Disorders Seen in the Uremic Patient

Tyler, H. Richard

doi:10.1001/archinte.1970.00310110051005

Cited by 47 publications

(4 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1,12 Cross-sectional studies in hemodialysis (HD) patients found cognitive impairment in 30%, with about 10% exhibiting severe impairment. Neurocognitive deficits may have special implications for CKD in early childhood, adversely affecting development of the brain.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Neurologic Complications of Chronic Kidney Disease

Seifter¹,

Samuels²

2010

Comprehensive Clinical Nephrology

View full text Add to dashboard Cite

Section: Clinical Manifestationsmentioning

confidence: 99%

Neurologic Complications of Chronic Kidney Disease

Seifter¹,

Samuels²

2010

Comprehensive Clinical Nephrology

View full text Add to dashboard Cite

“…Neurological manifestations in uraemia are classified as central nervous system (CNS), peripheral nervous system (PNS) and myopathic manifestations [1]. CNS manifestations are the commonest and usually presents as generalised uraemic encephalopathy which is characterised by mental changes, disturbances of consciousness, seizures, asterixis, myoclonus, and electroencephalographic abnormalities [2]. PNS effects manifest as peripheral neuropathy and, myopathy as proximal muscle weakness.…”

Section: Introductionmentioning

confidence: 99%

Uraemic brainstem encephalopathy mimicking ocular myasthenia: a case report

Ruwanpathirana,

Chang

2024

BMC Neurol

View full text Add to dashboard Cite

Background Uraemia causes a generalised encephalopathy as its most common neurological complication. Isolated brainstem uraemic encephalopathy is rare. We report a case of fatigable ptosis and complex ophthalmoplegia in brainstem uraemic encephalopathy. Case presentation A 22-year-old Sri Lankan man with end stage renal failure presented with acute onset diplopia and drooping of eyelids progressively worsening over one week. The patient had not complied with the prescribed renal replacement therapy which was planned to be initiated 5 months previously. On examination, his Glasgow coma scale score was 15/15, He had a fatigable asymmetrical bilateral ptosis. The ice-pack test was negative. There was a complex ophthalmoplegia with bilateral abduction failure and elevation failure of the right eye. The diplopia did not worsen with prolonged stare. The rest of the neurological examination was normal. Serum creatinine on admission was 21.81 mg/dl. The repetitive nerve stimulation did not show a decremental pattern. Magnetic resonance imaging (MRI) of the brain demonstrated diffuse midbrain and pontine oedema with T2 weighted/FLAIR hyperintensities. The patient was haemodialyzed on alternate days and his neurological deficits completely resolved by the end of the second week of dialysis. The follow up brain MRI done two weeks later demonstrated marked improvement of the brainstem oedema with residual T2 weighted/FLAIR hyperintensities in the midbrain. Conclusions Uraemia may rarely cause an isolated brainstem encephalopathy mimicking ocular myasthenia, which resolves with correction of the uraemia.

show abstract

“…Advanced kidney failure impairs mental function. Before the advent of dialysis, patients progressed from fatigue to confusion, somnolence, coma, and death (3,13,29,31,42). Early workers presumed that mental dysfunction in kidney failure was caused, at least in part, by the accumulation of uremic solutes in the brain.…”

Section: Introductionmentioning

confidence: 99%

Accumulation of uremic solutes in the cerebrospinal fluid in experimental acute renal failure

Mair

Nguyen

Huang

et al. 2019

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

The accumulation of uremic solutes in kidney failure may impair mental function. The present study profiled the accumulation of uremic solutes in the cerebrospinal fluid (CSF) in acute renal failure. CSF and plasma ultrafiltrate were obtained from rats at 48 h after sham operation (control; n = 10) or bilateral nephrectomy ( n = 10) and analyzed using an established metabolomic platform. Two hundred forty-eight solutes were identified as uremic based on their accumulation in the plasma ultrafiltrate of nephrectomized compared with control rats. CSF levels of 124 of these solutes were sufficient to allow calculation of CSF-to-plasma ultrafiltrate concentration ratios. Levels of many of the uremic solutes were normally lower in the CSF than in the plasma ultrafiltrate, indicating exclusion of these solutes from the brain. CSF levels of the great majority of the uremic solutes increased in renal failure. The increase in the CSF was, however, relatively less than in the plasma ultrafiltrate for most solutes. In particular, for the 31 uremic solutes with CSF-to-plasma ultrafiltrate ratios of <0.25 in control rats, the average CSF-to-plasma ultrafiltrate ratio decreased from 0.13 ± 0.07 in control rats to 0.09 ± 0.06 in nephrectomized rats, revealing sustained ability to exclude these solutes from the brain. In summary, levels of many uremic solutes are normally kept lower in the CSF than in the plasma ultrafiltrate by the action of the blood-brain and blood-CSF barriers. These barriers remain functional but cannot prevent accumulation of uremic solutes in the CSF when the kidneys fail.

show abstract

Neurologic Disorders Seen in the Uremic Patient

Cited by 47 publications

References 23 publications

Neurologic Complications of Chronic Kidney Disease

Neurologic Complications of Chronic Kidney Disease

Uraemic brainstem encephalopathy mimicking ocular myasthenia: a case report

Accumulation of uremic solutes in the cerebrospinal fluid in experimental acute renal failure

Contact Info

Product

Resources

About