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Case Reports
. 2019 May;8(2):83-88.
doi: 10.1007/s13730-018-0371-9. Epub 2018 Nov 19.

Adrenal crisis presented as acute onset of hypercalcemia and hyponatremia triggered by acute pyelonephritis in a patient with partial hypopituitarism and pre-dialysis chronic kidney disease

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Case Reports

Adrenal crisis presented as acute onset of hypercalcemia and hyponatremia triggered by acute pyelonephritis in a patient with partial hypopituitarism and pre-dialysis chronic kidney disease

Shunsuke Yamada et al. CEN Case Rep. 2019 May.

Abstract

A 57-year-old woman with pre-dialysis chronic kidney disease (CKD) was hospitalized because of fever and fatigue. On admission, increased inflammatory response and pyuria with bacteriuria were observed. Pyelonephritis was successfully treated with antibiotics, whereas her fatigue continued and she developed progressive hypercalcemia and hyponatremia; serum sodium level, 116 mEq/L and corrected serum calcium level, 13.4 mg/dL. Plasma concentrations of adrenocorticotropic hormone and cortisol and serum luteinizing hormone were under the detection level. Although the reaction of other anterior pituitary hormones and the serum antidiuretic hormone (ADH) was preserved, the response of serum luteinizing hormone to administration of luteinizing hormone releasing hormone was impaired. Magnetic resonance imaging showed no structural abnormality in the thalamus, hypothalamus, and pituitary gland. She was diagnosed with adrenal insufficiency caused by partial hypopituitarism in concomitant with pyelonephritis. After starting hydrocortisone replacement, serum levels of sodium and calcium were rapidly normalized. This case highlights the importance of adrenal insufficiency as a differential diagnosis of hypercalcemia in patients with pre-dialysis CKD, especially when hyponatremia was concomitantly observed. Besides, infection should be considered as an important trigger for the development of latent adrenal insufficiency since it could increase the physiological demand of corticosteroid in the body. Also, CKD may enhance the magnitude of hypercalcemia since CKD patients have decreased capacity to increase urinary calcium excretion.

Keywords: Adrenal insufficiency; Chronic kidney disease; Hypercalcemia; Hyponatremia; Partial hypopituitarism.

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Conflict of interest statement

Conflict of interest

All the authors declare no competing interest.

Human and animal rights

This article does not contain any studies with human participants or animals performed by any of the authors.

Informed consent

A written informed consent was obtained from the patient included in this case study.

Figures

Fig. 1
Fig. 1
Serial changes in surrogates of kidney function and serum mineral markers before admission. BUN blood urea nitrogen, Ca calcium, Cr creatinine, Na sodium, P phosphate
Fig. 2
Fig. 2
Clinical course during hospitalization. After initiation of levofloxacin treatment, serum CRP level decreased, whereas serum sodium level began to decrease and serum calcium level began to increase. CRH test and provocation test were then performed, because the presence of adrenal insufficiency was highly suspected. After the diagnosis of adrenal insufficiency, intravenous administration of hydrocortisone followed by oral hydrocortisone replacement was initiated. Soon after the replacement of hydrocortisone, the sensation of fatigue rapidly disappeared. Furthermore, hypercalcemia and hyponatremia were normalized. Ca calcium, CRH corticotropin-releasing hormone, CRP C-reactive protein, iv intravenous, Na sodium

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References

    1. Assadi F. Hypercalcemia: an evidence-based approach to clinical cases. UJKD. 2009;3:71–79. - PubMed
    1. Carroll R, Matfin G. Endocrine and metabolic emergencies: hypercalcaemia. Ther Adv Endocrinol Metab. 2010;1:225–234. doi: 10.1177/2042018810390260. - DOI - PMC - PubMed
    1. Ziegler R. Hypercalcemic crisis. J Am Soc Nephrol. 2001;12(Suppl 17):3–9. - PubMed
    1. Martin KJ, González EA. Prevention and control of phosphate retention/hyperphosphatemia in CKD-MBD: what is normal, when to start, and how to treat? Clin J Am Soc Nephrol. 2011;6:440–446. doi: 10.2215/CJN.05130610. - DOI - PubMed
    1. Goldsmith DJ, Massy ZA, Brandenburg V. The uses and abuses of vitamin D compounds in chronic kidney disease-mineral bone disease (CKD-MBD) Semin Nephrol. 2014;34:660–668. doi: 10.1016/j.semnephrol.2014.10.002. - DOI - PubMed

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