Journals / Türk Nöroloji Dergisi / 2009 / Cilt: 15 - Sayı: 1

Bilateral basal ganglia lesions associated with lactic acidosis in an end-stage renal failure patient

Son dönem böbrek yetmezlikli hastada laktik asidoza bağlı gelişen bilateral bazal gangliyon lezyonu

Pages
44–49
Publication Date
2022-11-05
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this report bilateral basal ganglia lesions and accompanying signs, which ensued after the use of metformin in a patient with chronic renal failure, are discussed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Although bilateral basal ganglia lesions are common in hypoxic encephalopathy and methanol intoxication, they are a rare finding in end-stage chronic renal failure.
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Key Findings & Data:The pathophysiology of both bilateral and selective involvement of the basal ganglia is unclear, but severe metabolic acidosis is one of the affected processes.
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Conclusion & Impact:In this report bilateral basal ganglia lesions and accompanying signs, which ensued after the use of metformin in a patient with chronic renal failure, are discussed.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Although bilateral basal ganglia lesions are common in hypoxic encephalopathy and methanol intoxication, they are a rare finding in end-stage chronic renal failure. The pathophysiology of both bilateral and selective involvement of the basal ganglia is unclear, but severe metabolic acidosis is one of the affected processes. In this report bilateral basal ganglia lesions and accompanying signs, which ensued after the use of metformin in a patient with chronic renal failure, are discussed.

Özet

Bilateral bazal gangliyon lezyonu, hipoksik ensefalopatilerde ve metanol zehirlenmelerinde sık görülmesine rağmen son dönem böbrek hastalığında nadir görülen bir bulgudur. Bilateral ve seçici tutulumun patofizyolojisi tam bilinmemekle birlikte ağır metabolik asidoz suçlanan süreçlerden bir tanesidir. Bu çalışmada son dönem böbrek hastalığı nedeniyle süregen düzenli hemodiyaliz tedavisi uygulanmakta olan bir hasta, metformin kullanımı sonrası ortaya çıkan bilateral bazal gangliyon lezyonu ve eşlik eden bulguları ile sunulmaktadır.

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Cite This Article

ÜSTÜNDAĞ, S., ÇAKIR, H., YILMAZ, A., GÜLDİKEN, B. (2022). Bilateral basal ganglia lesions associated with lactic acidosis in an end-stage renal failure patient. Türk Nöroloji Dergisi, Cilt: 15 - Sayı: 1, 44–49. https://ajindex.com/articles/637039

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References (18)

  1. Raskin HN, Roberts JK. Böbrek hastalığı. In: Rowland LP (ed). Çeviri Editörü: Baslo B, Gürses C. Merritt’s Neurology
  2. Baskı. Ankara: Öncü Basımevi, 2008:1079-82
  3. Luft FC. Lactic acidosis update for clinical care clinicians. J Am Soc Nephrol 2001;12(Suppl 17):15-9
  4. Fujioka M, Okuchi K, Miyamoto S, Sakaki T, Hiramatsu K, Tominaga M, et al. Changes in the basal ganglia and thalamus following reperfusion after complete cerebral ischaemia. Neuroradiology 1994;36:605-7
  5. Fujioka M, Okuchi K, Sakaki T, Hiramatsu K, Miyamoto S, Iwasaki S. Specific changes in human brain following reperfusion after cardiac arrest. Stroke 1994;25:2091-5
  6. Gaul HP, Wallace CJ, Auer RN, Fong TC. MR findings in methanol intoxication. AJRN Am J Neuroradiol 1995;16:1783-6
  7. Blanco M, Casado R, Vasquez F, Pumar JM. CT and MR imaging findings in methanol intoxication. AJRN Am J Neuroradiol 2006;27:452-4
  8. Kim TK, Seo SI, Kim JH, Lee NJ, Seol HY. Diffusion-weighted magnetic resonance imaging in the syndrome of acute bilateral basal ganglia lesions in diabetic uremia. Mov Disord 2006;21:1267-70
  9. Wang HC, Cheng SJ. The syndrome of acute bilateral basal ganglia lesions in diabetic uremic patients. J Neurol 2003;250:948-55
  10. Li JY, Yong TY, Sebben R, Khoo E, Disney AP. Bilateral basal ganglia lesions in patients with end-stage diabetic nephropathy. Nephrology 2008;13:68-72
  11. Skorecki K, Gren J, Brenner BM. Chronic renal failure. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL (eds). Harrison’s Principles of Internal Medicine. 15th ed. New York: Mc Graw Hill, 2001:1551-62
  12. Raskin NH. Neurological complications of renal failure. In: Aminoff MJ (ed). Neurology and General Medicine. New York: Churchill Livingstone, 1995:303-19
  13. Kanaumi T, Takashima S, Hirose S, Kodama T, Iwasaki H. Neuropathology of methylmalonic acidemia in a child. Pediatr Neurol 2006;34:156-9
  14. Stacpoole PW, Wright EC, Baumgartner TG, Bersin RM, Buchalter S, Curry SH, et al. Natural history and course of ac quired lactic acidosis in adults. DCA-Lactic Acidosis Study Gro up. Am J Med 1994;97:47-54
  15. Stang M, Wysowski DK, Butler-Jones D. Incidence of lactic aci dosis in metformin users. Diabetes Care 1999;22:925-7
  16. Goodman JW, Goldfarb DS. The role of continuous renal repla cement therapy in the treatment of poisoning. Semin Dial 2006;19:402-7
  17. Scheen AJ. Clinical pharmacokinetics of metformin. Clin Pharmacokinet 1996;30:359-71
  18. Weiner DE. Causes and cons