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Clinics and Practice
Volume 8
Issue 4
10.4081/cp.2018.1065
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Clinics and Practice is published by MDPI from Volume 11 Issue 1 (2021). Previous articles were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence, and they are hosted by MDPI on mdpi.com as a courtesy and upon agreement with PAGEPress.
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Case Report

Acute Tubulointerstitial Nephritis and Polyclonal Hypergammaglobulinaemia: Which Is the Culprit?

by
Ana E. Sirvent
1,*,
Ricardo Enríquez
1,
Tania Muci
2,
Francisco Javier Ardoy-Ibañez
3,
Isabel Millán
1,
Amadeo Almiñana
4,
Rosalía Ruiz-Ferrús
1 and
Luis Jiménez del Cerro
1
1
Nephrology Section, Hospital General Universitario de Elche, Spain
2
Pathology Section, Hospital General Universitario de Elche, Spain
3
Diagnostic Radiology Service, Hospital General Universitario de Elche, Spain
4
Ophthalmology Section, Hospital General Universitario de Elche, Spain
*
Author to whom correspondence should be addressed.
Clin. Pract. 2018, 8(4), 1065; https://doi.org/10.4081/cp.2018.1065
Submission received: 29 January 2018 / Revised: 23 October 2018 / Accepted: 2 November 2018 / Published: 7 November 2018

Abstract

Proton pump inhibitors (PPIs) are among the most frequent implicated drugs in acute tubulointerstitial nephritis (ATIN), nevertheless it is important to report cases with atypical profiles. A 80-year-old female, exposed during 34 months to omeprazole, presented with polyclonal hypergammaglobulinaemia and renal failure. After stopping omeprazole there was a partial improvement in serum creatinine and IgG. Renal biopsy revealed ATIN; immunohistochemistry for IgG4 was negative. Treatment with steroids and mycophenolate sodium improved renal function and normalized immunoglobulins. The lack of data of other entities and the patient’s evolution strongly point omeprazole as the culprit. After 27 months of follow-up, she remains clinical and analytically stable. ATIN caused by PPIs may appear after a long period of exposure and may be accompanied by analytical anomalies that simulate a systemic disease.
Keywords: acute tubulointerstitial nephritis; hypergammaglobulinaemia; omeprazole; renal failure acute tubulointerstitial nephritis; hypergammaglobulinaemia; omeprazole; renal failure

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MDPI and ACS Style

Sirvent, A.E.; Enríquez, R.; Muci, T.; Ardoy-Ibañez, F.J.; Millán, I.; Almiñana, A.; Ruiz-Ferrús, R.; del Cerro, L.J. Acute Tubulointerstitial Nephritis and Polyclonal Hypergammaglobulinaemia: Which Is the Culprit? Clin. Pract. 2018, 8, 1065. https://doi.org/10.4081/cp.2018.1065

AMA Style

Sirvent AE, Enríquez R, Muci T, Ardoy-Ibañez FJ, Millán I, Almiñana A, Ruiz-Ferrús R, del Cerro LJ. Acute Tubulointerstitial Nephritis and Polyclonal Hypergammaglobulinaemia: Which Is the Culprit? Clinics and Practice. 2018; 8(4):1065. https://doi.org/10.4081/cp.2018.1065

Chicago/Turabian Style

Sirvent, Ana E., Ricardo Enríquez, Tania Muci, Francisco Javier Ardoy-Ibañez, Isabel Millán, Amadeo Almiñana, Rosalía Ruiz-Ferrús, and Luis Jiménez del Cerro. 2018. "Acute Tubulointerstitial Nephritis and Polyclonal Hypergammaglobulinaemia: Which Is the Culprit?" Clinics and Practice 8, no. 4: 1065. https://doi.org/10.4081/cp.2018.1065

APA Style

Sirvent, A. E., Enríquez, R., Muci, T., Ardoy-Ibañez, F. J., Millán, I., Almiñana, A., Ruiz-Ferrús, R., & del Cerro, L. J. (2018). Acute Tubulointerstitial Nephritis and Polyclonal Hypergammaglobulinaemia: Which Is the Culprit? Clinics and Practice, 8(4), 1065. https://doi.org/10.4081/cp.2018.1065

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