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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 4  |  Page : 668-669
Hypothermia in summer of Saudi Arabia with end stage renal failure suffering from diabetic nephropathy and malnutrition


Department of General Surgery, King Fahd University Hospital, Al Khobar, Saudi Arabia

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Date of Web Publication8-Jul-2009
 

How to cite this article:
Al-wadani H. Hypothermia in summer of Saudi Arabia with end stage renal failure suffering from diabetic nephropathy and malnutrition. Saudi J Kidney Dis Transpl 2009;20:668-9

How to cite this URL:
Al-wadani H. Hypothermia in summer of Saudi Arabia with end stage renal failure suffering from diabetic nephropathy and malnutrition. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2020 Jun 2];20:668-9. Available from: http://www.sjkdt.org/text.asp?2009/20/4/668/53299
To the Editor

Hypothermia is defined as a core temperature below 35°C (95°F), and can be further classified by severity; Mild hypothermia - Core tempera­ture 32 to 35°C (90 to 95°F) Moderate hypo­thermia - Core temperature 28 to 32°C (82 to 90°F) Severe hypothermia - Core temperature below 28°C (82°F). [1] ,[2] Hypothermia causes al­tered cell membrane function, efflux of intra­cellular fluid, enzymatic dysfunction, and elec­trolyte imbalances (including prominent hyper­kalemia). Cell death results from a combination of these injuries and crystallization of intra- and extra-cellular water. [3]

When man is exposed to cold stress, the sti­mulus is transmitted from peripheral cold sen­sitive nerves to the posterior hypothalamus, the sympathetic nerve is activated, and thyrotropin­releasing hormone (TRH) and corticotropin­releasing factor (CRF) secreted through the alpha­adrenergic pathway from the hypothalamus in­duce the secretion of the thyroid and adrenocor­tical hormones from the pituitary gland. Because these hormones act as stress hormones, heat is produced by an increased thermogenesis in mu­scle and adipose tissue. Moreover, when epine­phrine is secreted from the adrenal medulla through alpha adrenergic signals, peripheral va­soconstriction and involuntary constriction of the skeletal muscles (shivering) are induced as means to increase the metabolic rate in a cold environment. [2] Whenever this system is defec­tive, the body response against hypothermia de­clines, such as in hypothyroidism, pituitary in­sufficiency, adrenal insufficiency, sepsis, hypo­glycemia, and diabetic ketoacidosis. [4]

A 70 year old Saudi man on regular peritoneal dialysis because of end-stage renal failure se­condary to diabetic militias, hypertension, and hyperlipidimia was admitted to our hospital on August 2007 with decreased level of conscious­ness and hypothermic temperature 32°C. His medications included furosemide 120 mg bid, amlodipine, atenolol, lisinopril, one alpha vit D3, sevelamer and calcium carbonate, aspirin, and folic acid.

The physical examination revealed a drowsy elderly man with temperature: 32°C, blood pre­ssure 120/80 mmHg, pulse 38, respiratory rate 18 min, O2 saturation 92/min. His weight was 50 Kg, height 177 cm (body mass index 15.6), and urine output: 200 mL per 24 hours. The rest of the physical exam was unremarkable except fundoscopy that revealed stage III diabetic reti­nopathy.

Laboratory investigations included WBC 6.5 × 1000/µL, hemoglobin 11 g/dL, platelet 233 × 1000/µL, BUN 55 mmol/L, Creatinine 7 mg/dL. Na 140 mmol/L, K 4.3 mmol/L, Cl 100 mmol/ L, Co2 28 mmol/L, total bilirubin 0.3 mg/dL, total protein 6.3 g/dL, albumin 3.5 g/dL, alka­line phosphates 300 U/L, phosphorus 5.1 g/dL, and Ca 8.3 g/dL. His hepatitis profile C and B and HIV were non reactive. The measured intraabdominal pressure was 19. Urinalysis and culture and blood culture and PD fluid analysis and culture were negative. His chest X-ray was within normal limits, and ECG showed brady­cardia. No abnormality was detected in the thy­roid, pituitary, and adrenal glands. The patient was treated with oxygen, external rewarming by heated blankets, and warmed glucose in saline infusion. The hypothermia and level of con­sciousness dramatically improved, and the pa­tient was discharge home next day with tem­perature 36.7°C.

Our patient's main problem was hypothermia in the absence of any obviously associated di­sease. Cryogenic substance (endogenous cryo­gen) has been reported to induce falls in the bo­dy temperature accompanied by peripheral va­sodilation and suppression of the shivering me­tabolism. In patients with end stage renal fai­lure, this decline in temperature has been repor­ted to improve when endogenous cryogen is removed by hemodialysis. [5] However, since hy­pothermia generally does not occur in cases suf­fering from renal failure alone, it is difficult to attribute the condition solely to endogenous cryogen.

The thermoregulatory responses to cold ex­posure are mediated by the shivering of skeletal muscle and the non-shivering of brown adipose tissue (BAT). Recent reports revealed that mito­chondrial uncoupling proteins (UCPs) play an important role as mediators of non-shivering thermogenesis. UCP-1 mRNA is exclusively upregulated by cold stress, [6] while UCP-2 and UCP-3 mRNA are upregulated by fasting, exer­cise training, and thyroid hormone. [7] In our case, hypothermia may have occurred because shive­ring thermogenesis could not fully act on acute cold stress due to the dramatically reduced muscle mass. [8] We should always keep in mind that older malnourished diabetic patients can easily suffer from impairments of the ther­moregulatory system.


   Acknowledgment Top


The author would like to thank Dr. Abdullah Al-Hweish and all the staff in peritoneal dia­lysis Unit at King Fahad University hospital for their valuable help and cooperation.

 
   References Top

1.Vidal-Puig A, Solanes G, Grujic D, et al. UCP3: an uncoupling protein homologue expressed preferentially and abundantly in skeletal muscle and brown adipose tissue. Biochem Biophys Res Commun, 1997;235:79-82.  Back to cited text no. 1    
2.Gimeno RE, Dembski M, Weng X, et al. Cloning and characterization of an uncoupling protein homolog: a potential molecular mediator of human thermo genesis. Diabetes 1997;46: 900-6.  Back to cited text no. 2  [PUBMED]  
3.Gong DW, He Y, Karas M et al. Uncoupling protein-3 is a mediator of thermo genesis regulated by thyroid hormone, beta3 adrenergic agonists, and leptin. J Biol Chem 1997;272: 24129 -32.  Back to cited text no. 3    
4.Morrison RC. Hypothermia in the elderly. Int Anesthesia Clin 1988;26:124-33.  Back to cited text no. 4    
5.Kluger MJ, Turnbull AJ, Cranston WI. Endo­genous cryogen excreted by the kidneys. Am J Physiol 1981;241:R271-6.  Back to cited text no. 5    
6.Boss O, Samec S, Dulloo A, et al. Tissue­dependent upregulation of rat uncoupling protein-2 expression in response to fasting or cold. FEBS Lett 1997;412:111-4.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Fleury C, Neverova M, Collins S, et al. Un­coupling protein-2: a novel gene linked to obesity and hyperinsulinemia. Nat Genet 1997; 15:269-72.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Mansell PI, Fellows IW, Macdonald IA, et al. Defect thermoregulation in malnutrition re­versed weight gain. Physiological mechanism and clinical importance. Q J Med 1990;76:817­29.  Back to cited text no. 8    

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Correspondence Address:
Hamed Al-wadani
Department of General Surgery, King Fahd University Hospital, Al Khobar
Saudi Arabia
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PMID: 19587515

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