# ICI Glomerular Disease: Protein and Sediment Change the Question

Proteinuria, kidney function, serologies, and clinical manifestations may recover differently. Follow both renal and oncologic outcomes.

![Infographic: ICI Glomerular Disease: Protein and Sediment Change the Question](https://urinenephrology.org/visual-reference/images/mastery-ici-glomerular.png?v=20261003c)

## A broader immune spectrum

Checkpoint inhibitor-associated kidney disease can include glomerular lesions as well as interstitial inflammation. The lesion determines the treatment framework.

## Spot the glomerular signal

New nephrotic protein loss, glomerular hematuria/RBC casts, or a pulmonary–renal presentation should broaden the diagnosis beyond ICI-AIN. Quantify protein, inspect sediment, and assess complement and targeted serologies. Check for infection and a preexisting glomerular process.

## Investigate targeted pathways

Use urine quantification, serology, complement, monoclonal studies, and infection assessment according to the phenotype. Biopsy often clarifies the mechanism.

## Let biopsy select the framework

A podocytopathy, immune-complex GN, pauci-immune GN, and TMA are not one toxicity syndrome. Use the lesion and severity to guide treatment while oncology assesses cancer benefit and alternatives. Avoid importing the same steroid schedule or rechallenge rule into every pathology.

## Coordinate treatment interruption

Holding, stopping, or restarting an ICI should reflect lesion severity, recovery, alternatives, and patient goals through multidisciplinary review.

## Track lesion-specific response

Proteinuria, kidney function, serologies, and clinical manifestations may recover differently. Follow both renal and oncologic outcomes.

## Source lessons

- [ici glomerular diseases review](https://urinenephrology.org/mastery/onconephrology/ici-glomerular-diseases-review.html)

Read alongside the full lessons; the findings and decisions shown here require the stated clinical context.