# Band keratopathy and conjunctival calcification in end-stage kidney disease: epidemiology, pathophysiology and clinical management

## TL;DR

This paper reviews how kidney disease patients develop eye calcifications and how to manage them.

## Contribution

Proposes a 'two-hit' model explaining the development of ocular calcification in end-stage kidney disease.

## Key findings

- Band keratopathy is a common but overlooked complication in end-stage kidney disease.
- Systemic factors like hyperphosphataemia and local ocular conditions contribute to calcification.
- Deficiencies in calcification inhibitors like fetuin-A and Klotho play a critical role.

## Abstract

Conjunctival and corneal calcification, particularly its severe manifestation, band keratopathy, represents a prevalent yet frequently overlooked form of metastatic calcification in end-stage kidney disease (ESKD). This review integrates current evidence on the epidemiology, pathophysiology and interdisciplinary management of uraemic ocular calcification. The pathogenesis is conceptualized through a ‘two-hit’ model: the systemic ‘first hit’ involves the specific milieu of chronic kidney disease–mineral and bone disorder driven by hyperphosphataemia, calcium load, secondary hyperparathyroidism and a critical deficiency in calcification inhibitors such as fetuin-A and Klotho. The ‘second hit’ comprises local ocular triggers, including tear film instability, inflammation and localized alkalosis, which precipitate mineral deposition in the supersaturated environment.