Distal Renal Tubular Acidosis that Became Exacerbated by Proton Pump Inhibitor Use

Okamoto, Natsumi; Nambu, Takuo; Matsuda, Yuki; Matsuo, Koji; Osaki, Keisuke; Kanai, Yugo; Ogawa, Yoshihisa; Yonemitsu, Shin; Kita, Ryuichi; Muro, Seiji; Sugawara, Akira; Oki, Shogo

doi:10.2169/internalmedicine.51.7981

Cited by 5 publications

(7 citation statements)

References 21 publications

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“…There is little to no data with regards to metabolic acidosis and hypokalemia as presenting cause of PPI-associated AIN. We found one case report suggesting that PPI can worsen acidosis and hypokalemia [8]. The PPIs mechanism of action is inhibiting the H, K ATPase in the stomach for treatment of gastroesophageal reflux disease.…”

Section: Discussionmentioning

confidence: 99%

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Kidney biopsy for renal tubular acidosis: when tissue diagnosis makes a difference

Humayun¹,

Sánchez²,

Norris³

et al. 2015

CNCS

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Renal tubular acidosis (RTA) is a disorder with variable presentations and oftentimes a nebulous underlying primary diagnosis. We describe a rare cause of RTA as an unusual complication of proton pump inhibitor (PPI) therapy. We report a case of a 33-year-old male with history of hypertension, acid reflux, allergic rhinitis, and low testosterone admitted with complaints of fatigue, weight loss, and unexplained acidosis for ~ 2 months. His medications prior to admission included losartan, omeprazole, potassium chloride, sildenafil, and testosterone propionate injections. His physical exam was unremarkable with a blood pressure of 120/80 mmHg. Initial lab work showed a nonanion gap metabolic acidosis with serum bicarbonate level of 16 mM/L and potassium 3 mM/L. Urine studies showed urine pH of 6.5 and a positive urine anion gap. The serum creatinine was within normal range(1.13 mg/dL). He required massive doses of bicarbonate and potassium supplementation with minimal improvement of serum chemistries achieved. The cause of apparent distal RTA remained elusive despite extensive blood, urine, and imaging testing. Ultimately a renal biopsy was obtained showing mild to moderate tubule-interstitial inflammation with 5% fibrosis. PPI therapy (omeprazole) was stopped, and he was started on prednisone 60 mg per day. Two weeks later, his RTA findings resolved, and he no longer required bicarbonate and potassium supplementation. Our case highlights the importance of recognizing a unique complication of RTA following PPI therapy. It also underscores the possible need for considering a kidney biopsy in the setting of nondiagnostic laboratory work up to uncover the underlying etiology of RTA and suspected allergic interstitial nephritis (AIN).

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Section: Discussionmentioning

confidence: 99%

“…Therefore, a PPI is extremely unlikely to explain metabolic acidosis based on the “pharmacologic” effect of the medication. There is only a single case report describing a correlation of PPI with worsening metabolic acidosis and hypokalemia [8]. …”

Section: Discussionmentioning

confidence: 99%

Kidney biopsy for renal tubular acidosis: when tissue diagnosis makes a difference

Humayun¹,

Sánchez²,

Norris³

et al. 2015

CNCS

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“…While the primary site of action for PPIs are the H + /K + ATPases in the gastric parietal cell, PPIs may also affect H + /K + ATPases in the kidney 22 and osteoclasts in bone. 23 For example, PPI administration has been reported to induce renal tubular acidosis with subsequent hypokalemia and hypomagnesemia.…”

Section: Discussionmentioning

confidence: 99%

Retrospective analysis of the effect of acid-suppressant therapy on clinicopathologic parameters of cats with chronic kidney disease

Gould

Kłos

Price

et al. 2017

Journal of Feline Medicine and Surgery

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Objectives The aim was to retrospectively evaluate the effects of acid-suppressant therapy in a population of cats with chronic kidney disease (CKD). The study objectives were to evaluate the effects of acid-suppressant therapy on clinicopathologic variables and progression of CKD over time. Methods The databases of two institutions were searched over an 11 year time span for cats fitting inclusion criteria for CKD. A total of 89 cats met the criteria for inclusion and were grouped according to either early (ie, stages 1-2) or advanced (ie, stages 3-4) CKD. Variables were statistically analyzed before and after treatment with either: (1) proton pump inhibitors (PPIs; n = 17), (2) histamine-2 receptor antagonists (H2RAs; n = 30), (3) combined acid-suppressant therapy (PPI + H2RA; n = 6) or (4) no acid-suppressant therapy (n = 36). Shapiro-Wilk testing and Q-Q plots were used to assess normality and variance, respectively. A complete randomized design with a mixed-effects repeated measures ANOVA was used to evaluate for differences in stage, treatment and time, as well as the interaction between these effects. Results A significant increase in blood creatinine concentration was found over time independent of severity of CKD and treatment group ( P = 0.0087). A significant increase in blood sodium concentration (change of 3.12 mmol/l) was found independent of stage in cats receiving PPI therapy ( P = 0.0109). A significant decrease in total blood magnesium (change of 0.15 mmol/l) was detected in two cats with early CKD receiving combined acid suppressants ( P = 0.0025). Conclusions and relevance Results of this retrospective study suggest that cats with CKD receiving PPI therapy may develop alterations in blood sodium concentrations but do not experience more rapid progression of CKD.

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“…Absence of H + ‐ATPase and autoantibodies to intercalated cells in the distal nephron has been described, suggesting a defect in distal H + secretion . Similarly, proton pump inhibitors, which block H + ‐K + ‐ATPase, have been reported to exacerbate type 1 RTA . Interstitial inflammation is often found in renal biopsies but other than case reports, there is no consensus on steroid treatment for RTA .…”

Section: Useful Equations In the Assessment Of Suspected Renal Tubulamentioning

confidence: 99%

“…Interstitial inflammation is often found in renal biopsies but other than case reports, there is no consensus on steroid treatment for RTA . Type 1 RTA is less commonly reported with systemic lupus erythematosus, primary biliary cirrhosis, autoimmune hepatitis and autoimmune thyroiditis . Rarely, it is said to occur with fibrosing alveolitis, polyarteritisnodosa and cryoglobulinaemia .…”

Section: Useful Equations In the Assessment Of Suspected Renal Tubulamentioning

confidence: 99%

Distal renal tubular acidosis associated with Sjogren syndrome

Lim

Choi

2013

Internal Medicine Journal

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Renal tubular acidosis is a common cause of normal anion gap metabolic acidosis but these disorders can be easily missed or misdiagnosed. We highlight the approach to assessing renal tubular acidosis by discussing a case study with a temporal data set collected over more than 5 weeks. We highlight the principles and the necessary information required for a diagnosis of classic distal renal tubular acidosis. We also briefly review several aspects of type 1 renal tubular acidosis related to autoimmune disease, drugs and thyroid disorders.

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Distal Renal Tubular Acidosis that Became Exacerbated by Proton Pump Inhibitor Use

Cited by 5 publications

References 21 publications

Kidney biopsy for renal tubular acidosis: when tissue diagnosis makes a difference

Kidney biopsy for renal tubular acidosis: when tissue diagnosis makes a difference

Retrospective analysis of the effect of acid-suppressant therapy on clinicopathologic parameters of cats with chronic kidney disease

Distal renal tubular acidosis associated with Sjogren syndrome

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