When the kidney catches a cold: an unusual cause of acute renal failure

Sir,

We report the case of a 51-year-old man with no medical history and no treatment who developed acute renal failure (ARF) after cold water immersion. He was admitted to hospital in August after nearly drowning in a lake while trying to save his dog which was drowning. When he got back to the shore, he was exhausted and fainted briefly. He was transported to the hospital in a warm ambulance. Arriving at the hospital 1 h later, he was conscious but sleepy; his rectal temperature was 35.8°C, his blood pressure 130/70 mmHg and there was no haemodynamic failure during the observation period. Physical examination showed no abnormality. Laboratory studies showed: serum creatinine, 141 µmol/l; urea, 6.8 mmol/l; C-reactive protein <5 mg/l; leukocytosis count, 18 000/mm3, aspartate aminotransferease, 31 UI/l; alanine aminotransferase, 27 UI/l; creatine phosphokinase (CPK), 135 UI/l; ionogram and coagulation functions were normal. An arterial blood gas sample showed moderate metabolic acidosis and hypoxaemia (pH 7.33, 16.6 mmol/l, PCO2 32.6 mmHg and PO2 60 mmHg). Electrocardiogram and chest radiography were normal. The patient was discharged after a 24 h observation period.

He was re-admitted 5 days later, complaining of being tired and anuric. Biological analysis revealed ARF (creatininaemia 1600 µmol/l, urea 38 mmol/l) with hyperkalaemia (6.1 mmol/l), hyperphosphataemia (3.12 mmol/l), normocalcaemia (2.27 mmol/l) and metabolic acidosis (pH 7.34, bicarbonates 18.4 mmol/l). There was no elevation of muscle and hepatic enzymes, no red or white blood count disorder; blood protides and albumin were respectively 61 and 33.7 g/l, and proteinuria was 0.33 g/24 h. There was no infectious or immunological biological abnormality. Urinary analysis showed <1000 red blood cells/ml, 20 000 leukocytes/ml and asterite culture was sterile. Urinary ultrasonography was normal, and Doppler ultrasonography showed no stenosis of the renal arteries. The patient needed three sessions of dialysis over the succeeding 3 days and then renal function recovered spontaneously. Creatininaemia was 652 µmol/l 3 days after the last haemodialysis session, 125 µmol/l 10 days later and 90 µmol/l 7 weeks later. Given the clinical course of this ARF, no renal biopsy was performed and the diagnosis of acute tubular necrosis was retained.

ARF associated with severe hypothermia has been reported widely, but is usually the direct consequence of associated overt haemodynamic failure and/or rhadomyolysis [1]. ARF related to cold water immersion has to our knowledge only been reported once, by Yoshitomi et al. [2], who described the case of a 27-year-old patient who developed histological acute tubular necrosis after nearly drowning in a lake, and then lying on the lake shore for 2 h while the external temperature was –5°C. Interestingly, in our case, the accident occurred in summer when the water temperature was not very cold, and our patient probably experienced only moderate hypothermia as assessed by his central temperature (35.8°C) upon arrival at the emergency room. Thus our observation illustrates that the association of prolonged water immersion with even moderate hypothermia can trigger acute tubular necrosis in a patient not particularly at risk of ARF. The mechanism responsible for the renal hypoperfusion is unclear. Water immersion increases venous return and thereby raises cardiac output, and natriuresis [3]. Conversely, removal from water acutely decreases cardiac ouput. Hypothermia may blunt or delay the normal haemodynamic response that allows maintenance of an adequate renal blood flow in this setting. In an animal experimental model, hypothermia, in contrast, has been shown to prevent ischaemia–reperfusion-induced renal injury [4]. Thus, rather than hypothermia per se, rewarming coincident with renal hypoperfusion after removal from water could be involved in the pathogenesis. Hypoxaemia associated with near drowning could have also played a role in the renal insufficient oxygen delivery. Whatever the mechanism involved, nephrologists should be aware of this rare cause of ARF.

Conflict of interest statement. None declared.

Carine Hottelart, Mirela Diaconita, Béatrice Champtiaux, Fabien Soulis and Jean-Claude Aldigier

Service de Néphrologie Hôpital UniversitaiRe Dupuytren 2, avenue Martin-Luther-King 87042 Limoges cedex France Email: carine.hottelart{at}chu-limoges.fr

References

  1. Kopsa H, Zargornik J, Schmidt P et al. Acute kidney failure in hypothermia. Schweiz Med Wochensch 1977; 107: 942–947[ISI]
  2. Yoshitomi Y, Kojima S, Ogi M, Uramochi M. Acute renal failure in accidental hypothermia of cold water immersion. Am J Kidney Dis 1998; 31: 856–859[ISI][Medline]
  3. Epstein M. Renal effects of head-out water immersion in man: implications for an understanding of volume homeostasis. Physiol Rev 1978; 58: 529–581[Free Full Text]
  4. Zager RA, Gmur DJ, Bredl CR, Eng MJ. Degree and time sequence of hypothermic protection against experimental ischemic acute renal failure. Circ Res 1989; 65: 1263–1269[Abstract]




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