# Acute Interstitial Nephritis and Oxalate Nephropathy After Rapid Pasireotide Response in Treatment-resistant Acromegaly

**Authors:** Annabelle G Hayes, Mark J Penny, Karina Aivazian, Jerry R Greenfield

PMC · DOI: 10.1210/jcemcr/luae071 · JCEM Case Reports · 2024-05-20

## TL;DR

A patient with acromegaly developed kidney damage likely due to oxalate buildup after treatment with pasireotide, which caused pancreatic issues.

## Contribution

Reports a novel case linking pasireotide-induced pancreatic dysfunction to oxalate nephropathy in acromegaly treatment.

## Key findings

- Pasireotide caused acute interstitial nephritis and oxalate nephropathy in a patient with acromegaly.
- Pancreatic exocrine dysfunction led to malabsorption and secondary hyperoxaluria.
- Renal function improved after discontinuing pasireotide and using glucocorticoids.

## Abstract

We report a case of interstitial nephritis, likely secondary to oxalate nephropathy, due to the development of pancreatic exocrine dysfunction after commencement of pasireotide for acromegaly. Pasireotide is known to impair insulin secretion but can also impair pancreatic exocrine function, hypothezised to result from high-affinity binding of somatostatin receptors 1, 2, 3, and 5. This has been an advantage in postoperative tissue anastomoses after pancreatic surgery, but exocrine insufficiency has not been reported when used for the treatment of acromegaly. A 73-year-old woman, diagnosed with acromegaly, was unable to achieve biochemical control despite 2 surgical resections of an invasive mammosomatotroph pituitary tumor and treatment with cabergoline and maximal-dose lanreotide. The tumor expressed somatostatin receptor type 5 but not somatostatin receptor type 2, predicting good response from pasireotide, which was commenced at 40 mg every 4 weeks. IGF-1 rapidly normalized, but the patient presented with nausea, anorexia, and acute kidney injury. Renal biopsy revealed acute-on-chronic interstitial nephritis, with numerous oxalate crystals. Increased fecal fat globules were noted on fat stain (3+), supporting malabsorption as an etiology of secondary enteric hyperoxaluria. Renal function recovered to near baseline over months following pasireotide withdrawal and high-dose glucocorticoids.

## Linked entities

- **Chemicals:** pasireotide (PubChem CID 9941444), cabergoline (PubChem CID 54746), lanreotide (PubChem CID 6918011), oxalate (PubChem CID 71081)
- **Diseases:** acromegaly (MONDO:0019933), interstitial nephritis (MONDO:0001085), malabsorption (MONDO:0020598)

## Full-text entities

- **Genes:** SSTR2 (somatostatin receptor 2) [NCBI Gene 6752] {aka SST2}, SSTR5 (somatostatin receptor 5) [NCBI Gene 6755] {aka SS-5-R, SST5}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}
- **Diseases:** malabsorption (MESH:D008286), acute kidney injury (MESH:D058186), Oxalate Nephropathy (MESH:C563477), tumor (MESH:D009369), Acute Interstitial Nephritis (MESH:D000080203), enteric hyperoxaluria (MESH:D004751), mammosomatotroph pituitary tumor (MESH:D010911), nausea (MESH:D009325), anorexia (MESH:D000855), Acromegaly (MESH:D000172), pancreatic exocrine dysfunction (MESH:C565225), interstitial nephritis (MESH:D009395), exocrine insufficiency (MESH:D010188)
- **Chemicals:** oxalate nephropathy (-), cabergoline (MESH:D000077465), oxalate (MESH:D010070)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11104526/full.md

## References

12 references — full list in the complete paper: https://tomesphere.com/paper/PMC11104526/full.md

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Source: https://tomesphere.com/paper/PMC11104526