# Always Consider a Repeat Kidney Biopsy: Acute Interstitial Nephritis Soon After Membranous Nephropathy

**Authors:** Jarrad Hopkins, James Nolan, Maleeka Ladhani, Chiang Lee

PMC · DOI: 10.1155/crin/2277958 · 2026-01-31

## TL;DR

A patient with membranous nephropathy later developed acute interstitial nephritis, showing the need for repeat kidney biopsies when kidney function worsens.

## Contribution

Highlights the importance of repeat kidney biopsies in diagnosing acute interstitial nephritis superimposed on membranous nephropathy.

## Key findings

- A second kidney biopsy revealed acute interstitial nephritis in a patient with membranous nephropathy.
- Withdrawing suspected drugs and restarting corticosteroids improved renal function significantly.
- Timely repeat biopsy prevented the need for dialysis in this case.

## Abstract

The heterogeneity of membranous nephropathy is well described in the literature, and its clinical course and response to treatment vary. Similarly, acute interstitial nephritis (AIN) can present in unexpected and unusual ways and should always be considered within the differential diagnosis of worsening renal function. This case study describes the cross‐section of these two disease entities.

A 68‐year‐old male with a history of hypertension, chronic obstructive pulmonary disease (COPD), hyperlipidaemia, gout and treated prostate cancer presented with bilateral lower limb swelling and progressive renal dysfunction. Initial laboratory findings demonstrated nephrotic syndrome with impaired renal function. A positive phospholipase A2 receptor (PLA2R) antibody confirmed primary membranous nephropathy. Renal biopsy showed typical findings of membranous nephropathy. Treatment with prednisolone and cyclophosphamide improved renal function initially. However, as prednisolone was tapered, creatinine levels rapidly worsened, leading to a second biopsy. The second biopsy demonstrated AIN superimposed on chronic membranous nephropathy. A drug‐induced aetiology was suspected, with pantoprazole, trimethoprim–sulfamethoxazole and frusemide identified as the most likely contributors. Following withdrawal of these agents and reinitiation of high‐dose corticosteroids, the patient’s renal function improved markedly, obviating the need for dialysis.

This case highlights the importance of considering AIN and the need for timely repeat renal biopsy in cases of deteriorating renal function.

## Linked entities

- **Chemicals:** pantoprazole (PubChem CID 4679), trimethoprim–sulfamethoxazole (PubChem CID 358641), frusemide (PubChem CID 3440), prednisolone (PubChem CID 5755), cyclophosphamide (PubChem CID 2907)
- **Diseases:** membranous nephropathy (MONDO:0005376), nephrotic syndrome (MONDO:0005377), chronic obstructive pulmonary disease (MONDO:0005002), hyperlipidaemia (MONDO:0001336), gout (MONDO:0005393), prostate cancer (MONDO:0005159)

## Full-text entities

- **Genes:** PLA2R1 (phospholipase A2 receptor 1) [NCBI Gene 22925] {aka CLEC13C, PLA2-R, PLA2G1R, PLA2IR, PLA2R}
- **Diseases:** Membranous Nephropathy (MESH:D015433), AIN (MESH:D000080203), hypertension (MESH:D006973), lower limb swelling (MESH:D038061), impaired renal function (MESH:D007674), nephrotic syndrome (MESH:D009404), COPD (MESH:D029424), gout (MESH:D006073), prostate cancer (MESH:D011471), Interstitial Nephritis (MESH:D009395)
- **Chemicals:** pantoprazole (MESH:D000077402), creatinine (MESH:D003404), trimethoprim-sulfamethoxazole (MESH:D015662), prednisolone (MESH:D011239), cyclophosphamide (MESH:D003520), frusemide (MESH:D005665)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12860571/full.md

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Source: https://tomesphere.com/paper/PMC12860571