# Treatment of glomerular and tubular proteinuria in the nephrotic range in a female cat: case report

**Authors:** Maria Vitória dos Santos Pascoal, Guilherme Sena, Stephanie Favato de Azevedo, Juliana de Moraes Intrieri, Heloísa Justen Moreira de Souza

PMC · DOI: 10.29374/2527-2179.bjvm012825 · 2026-03-19

## TL;DR

A female cat with severe kidney disease showed significant improvement after treatment, including medication and dietary changes.

## Contribution

This case report presents a successful treatment approach for a cat with mixed-origin nephrotic-range proteinuria.

## Key findings

- The cat showed progressive clinical improvement with resolution of anasarca by day 21.
- Albumin levels normalized by day 37, and proteinuria decreased by 93.85% after nine months.
- The patient remained stable with no recurrence of symptoms during follow-up.

## Abstract

The objective is to serve as a descriptive and educational report regarding the case of an eight-year-old spayed mixed-breed cat with nephrotic-range tubular and glomerular lesion, with no history of prior medication use or comorbidities, the main complaint being prostration and sudden weight gain. Physical examination revealed anasarca, moderate dyspnea and paradoxical breathing. Imaging tests revealed bicavitary effusion and subcutaneous edema. Laboratory analyses revealed serum creatinine equal to 3.0 mg/dL, severe hypoalbuminemia of 0.8g/dL, urine specific gravity equal to 1.020 and intense proteinuria (UPC ratio= 13.09). Urinary electrophoresis confirmed proteinuria with both glomerular and tubular involvement. This led to the suspicion of nephrotic syndrome with mixed-origin lesions. Treatment included furosemide, dexamethasone, benazepril, omega-3 fatty acid, mirtazapine and renal diet, in addition to procedures such as paracentesis for drainage. Progressive clinical improvement was observed, with resolution of anasarca by day 21, normalization of albumin by day 37 and a reduction of up to 93.85% in proteinuria nine months after the end of treatment. The patient remained stable, with no recurrence of symptoms. The therapeutic conclusions are limited by the single-case design, although continuous clinical and laboratory monitoring was implemented, aiming to adjust therapeutic management.

## Linked entities

- **Chemicals:** furosemide (PubChem CID 3440), dexamethasone (PubChem CID 5743), benazepril (PubChem CID 5362124), mirtazapine (PubChem CID 4205)
- **Diseases:** nephrotic syndrome (MONDO:0005377)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** proteinuria (MESH:D011507), weight gain (MESH:D015430), anasarca (MESH:D004487), bicavitary effusion (MESH:D000080324), hypoalbuminemia (MESH:D034141), range tubular and glomerular lesion (MESH:D007674), nephrotic (MESH:D009404), dyspnea (MESH:D004417)
- **Chemicals:** furosemide (MESH:D005665), mirtazapine (MESH:D000078785), creatinine (MESH:D003404), omega-3 fatty acid (MESH:D015525), benazepril (MESH:C044946), dexamethasone (MESH:D003907)
- **Species:** Felis catus (cat, species) [taxon 9685], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13003675/full.md

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Source: https://tomesphere.com/paper/PMC13003675