# Pharmacologic management of renal involvement in monogenic autoinflammatory diseases

**Authors:** Ahmed Fayed, Mohamed Tharwat Hegazy, Jurgen Sota, Carla Gaggiano, Gaafar Ragab

PMC · DOI: 10.1186/s40001-026-03936-6 · European Journal of Medical Research · 2026-02-12

## TL;DR

This review discusses how to manage kidney issues in rare genetic inflammatory diseases using medications, focusing on safety and effectiveness.

## Contribution

The paper provides a focused review on pharmacologic strategies for renal involvement in monogenic autoinflammatory diseases.

## Key findings

- Kidney damage in monogenic AIDs can result from both inflammation and drug toxicity.
- Tailoring therapy to individual phenotypes is essential for improving patient outcomes.
- Preventing drug-induced nephrotoxicity is crucial for safe treatment of these disorders.

## Abstract

Kidney involvement represents one of the main targets of the systemic inflammatory process and is underscored by a heterogeneous pathology ranging from amyloidosis to non-amyloid-related damage rooted in inflammasome activation. A thorough approach to monogenic autoinflammatory disorders (AIDs) includes identifying phenotypic patterns, comprehending pathophysiology, and customizing therapy to improve patients' quality of life. In this review, we will discuss some pharmacological aspects focusing on the kidney as a target in AIDs. A special emphasis will be placed on medications used for AIDs cases with renal impairment, as well as drug-induced nephrotoxicity in monogenic AIDs. Understanding the mechanisms of drug-induced nephrotoxicity and applying preventive measures are critical for safely managing monogenic AIDs with renal involvement.

## Linked entities

- **Diseases:** amyloidosis (MONDO:0019065)

## Full-text entities

- **Diseases:** AIDs (MESH:D056660), renal involvement (MESH:C565423), renal impairment (MESH:D007674), amyloidosis (MESH:D000686), inflammatory (MESH:D007249), amyloid (MESH:C000718787)
- **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/PMC12930578/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12930578/full.md

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Source: https://tomesphere.com/paper/PMC12930578