BMC Nephrology | |
Hyponatremia in a patient with scleroderma renal crisis: a potential role of activated renin-angiotensin system | |
Yoshihide Fujigaki2  Shinsuke Isobe1  Naoko Kinoshita1  Sayaka Ishigaki1  Ryuichi Furuya1  Hirotaka Fukasawa1  | |
[1] Renal Division, Department of Internal Medicine, Iwata City Hospital, 512-3 Ohkubo, Iwata, Shizuoka, 438-8550, Japan;First Department of Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan | |
关键词: Scleroderma renal crisis; Renin-angiotensin system; Hyponatremia; | |
Others : 1083166 DOI : 10.1186/1471-2369-13-47 |
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received in 2012-01-02, accepted in 2012-06-27, 发布年份 2012 | |
【 摘 要 】
Background
Scleroderma renal crisis is an important complication of scleroderma (systemic sclerosis) that is associated with significant morbidity and mortality. On the other hand, hyponatremia has never been reported in patients with scleroderma renal crisis.
Case presentation
A 66-year-old man with scleroderma was admitted to our hospital for an evaluation of renal dysfunction and extreme hypertension. The laboratory evaluation revealed remarkably high plasma renin activity in association with microangiopathic hemolytic anemia, and the anti-RNA polymerase III antibody assessment was positive. The patient was diagnosed with scleroderma renal crisis and was started treatment with enalapril maleate, an angiotensin-converting enzyme inhibitor. During hospitalization, the patient developed symptomatic hyponatremia three times and each laboratory analysis revealed improperly high levels of antidiuretic hormone without signs of extracellular fluid volume depletion as well as remarkably high plasma renin activities and angiotensin levels. However, hyponatremia has not been demonstrated to occur as a result of combined therapy with candesartan cilexetil, an angiotensin II receptor blocker, and aliskiren fumarate, a direct renin inhibitor. The plasma renin activities and angiotensin levels were normalized and the renal function was maintained after treatment.
Conclusions
To our best knowledge, this is the first documented case of scleroderma renal crisis complicated with hyponatremia. This report also suggests that the activated renin-angiotensin system may play a role in the development of hyponatremia and that hyponatremia should be taken into consideration as a rare but possible complication associated with screloderma renal crisis.
【 授权许可】
2012 Fukasawa et al.; licensee BioMed Central Ltd.
【 预 览 】
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20150101011205591.pdf | 247KB | download | |
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Figure 1. | 34KB | Image | download |
【 图 表 】
Figure 1.
Figure 2.
【 参考文献 】
- [1]Traub YM, Shapiro AP, Rodnan GP, Medsger TA, McDonald RH, Steen VD, Osial TA, Tolchin SF: Hypertension and renal failure (scleroderma renal crisis) in progressive systemic sclerosis. Review of a 25-year experience with 68 cases. Medicine (Baltimore) 1983, 62:335-352.
- [2]Lopez-Ovejero JA, Saal SD, D'Angelo WA, Cheigh JS, Stenzel KH, Laragh JH: Reversal of vascular and renal crises of scleroderma by oral angiotensin-converting-enzyme blockade. N Engl J Med 1979, 300:1417-1419.
- [3]Anderson RJ, Chung HM, Kluge R, Schrier RW: Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin. Ann Intern Med 1985, 102:164-168.
- [4]Izzedine H, Fardet L, Launay-Vacher V, Dorent R, Petitclerc T, Deray G: Angiotensin-converting enzyme inhibitor-induced syndrome of inappropriate secretion of antidiuretic hormone: case report and review of the literature. Clin Pharmacol Ther 2002, 71:503-507.
- [5]Wright JW, Harding JW: Regulatory role of brain angiotensins in the control of physiological and behavioral responses. Brain Res Rev 1992, 17:227-262.
- [6]Bader M, Peters J, Baltatu O, Muller DN, Luft FC, Ganten D: Tissue renin-angiotensin systems: new insights from experimental animal models in hypertension research. J Mol Med (Berl) 2001, 79:76-102.
- [7]Ganong WF: Origin of the angiotensin II secreted by cells. Proc Soc Exp Biol Med 1994, 205:213-219.
- [8]Pelisch N, Hosomi N, Ueno M, Masugata H, Murao K, Hitomi H, Nakano D, Kobori H, Nishiyama A, Kohno M: Systemic candesartan reduces brain angiotensin II via downregulation of brain renin-angiotensin system. Hypertens Res 2010, 33:161-164.
- [9]Sink KM, Leng X, Williamson J, Kritchevsky SB, Yaffe K, Kuller L, Yasar S, Atkinson H, Robbins M, Psaty B, Goff DC: Angiotensin-converting enzyme inhibitors and cognitive decline in older adults with hypertension: results from the Cardiovascular Health Study. Arch Intern Med 2009, 169:1195-1202.
- [10]Fitzsimons JT: Angiotensin, thirst, and sodium appetite. Physiol Rev 1998, 78:583-686.
- [11]Thrasher TN, Keil LC: Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis. Am J Physiol 1987, 253:R108-R120.
- [12]Chevillard C, Saavedra JM: Distribution of angiotensin-converting enzyme activity in specific areas of the rat brain stem. J Neurochem 1982, 38:281-284.
- [13]Thunhorst RL, Fitts DA, Simpson JB: Angiotensin-converting enzyme in subfornical organ mediates captopril-induced drinking. Behav Neurosci 1989, 103:1302-1310.