# Proteinuria After Kidney Transplantation

**Authors:** Tomas Seeman, Robert L. Myette, Janusz Feber, Massimiliano Bertacchi, Raja Sekhar Dandamudi, Daniella Levy Erez, Anja Buescher

PMC · DOI: 10.1111/petr.70233 · Pediatric Transplantation · 2025-11-24

## TL;DR

Proteinuria is a common issue after kidney transplants, affecting graft survival, and requires careful monitoring and treatment to manage its causes and reduce risk.

## Contribution

The paper emphasizes the importance of regular proteinuria monitoring and tailored treatment strategies in kidney transplant recipients.

## Key findings

- Proteinuria occurs in 40%-80% of kidney transplant recipients and is often linked to rejection, mTOR inhibitors, or hypertension.
- In children with idiopathic FSGS, daily proteinuria monitoring is recommended post-transplant to detect recurrence early.
- ACE inhibitors and ARBs are primary treatments for proteinuria, with antihypertensive therapy used if initial treatments fail.

## Abstract

Proteinuria is a relatively frequent complication in both adults and children after kidney transplantation (40%–80%). It is usually mild and predominantly of tubular origin and is caused mainly by rejection, mTOR inhibitors, or hypertension; however, proteinuria could also be in the nephrotic range and of glomerular origin if caused by the recurrence of idiopathic FSGS or rejection. Proteinuria is a risk factor impacting graft and patient survival in adults and graft survival in children. Proteinuria should be assessed by protein/creatinine ratio regularly in pediatric kidney transplant recipients. In children with idiopathic FSGS, proteinuria should be assessed daily during the first 2–3 weeks post‐transplant to enable prompt diagnosis of recurrence. The etiology of proteinuria should be identified (recurrence, rejection, mTOR‐inhibitors, hypertension, etc.). If no apparent cause is found, a graft biopsy should be considered. Antiproteinuric therapy is primarily focused on treating the causes of the proteinuria, and this is usually done using Angiotensin‐converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs). The long‐term follow‐up goal should be normalization of proteinuria with a protein/creatinine ratio < 20 mg/mmol (200 mg/g). Because of the role elevated blood pressure may play in exacerbating proteinuria, antihypertensive medications should be used in those who are resistant to initial antiproteinuric therapy to achieve lower BP.

## Linked entities

- **Diseases:** FSGS (MONDO:0100313)

## Full-text entities

- **Genes:** MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}
- **Diseases:** hypertension (MESH:D006973), Proteinuria (MESH:D011507), nephrotic (MESH:D009404)
- **Chemicals:** creatinine (MESH:D003404), antiproteinuric (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12644300/full.md

## References

83 references — full list in the complete paper: https://tomesphere.com/paper/PMC12644300/full.md

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Source: https://tomesphere.com/paper/PMC12644300