# Situation: A 30-year-old woman with systemic lupus erythematosus (SLE) and lupus nephritis has end-stage kidney disease and receives hemodialysis three times a week through an arteriovenous fistula in her left forearm. She still passes a small amount of urine each day. Her skin rash is currently inactive. She asks why she must keep protecting herself from the sun now that her rash has cleared. Which explanation should the nurse give?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629951  
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> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: A 30-year-old woman with systemic lupus erythematosus (SLE) and lupus nephritis has end-stage kidney disease and receives hemodialysis three times a week through an arteriovenous fistula in her left forearm. She still passes a small amount of urine each day. Her skin rash is currently inactive.

She asks why she must keep protecting herself from the sun now that her rash has cleared. Which explanation should the nurse give?

## 보기

1. Sun exposure affects only the skin, so it may bring the rash back
2. Sunlight can trigger a lupus flare that may involve her organs **✔ 정답**
3. Sunscreen keeps the old rash from leaving dark scars
4. Her dialysis sessions make her skin burn more easily in the sun

**정답: 2**

## 해설

Ultraviolet light is a known trigger of lupus flares, and a flare can affect joints, blood cells, and internal organs as well as the skin. Sun protection with broad-spectrum sunscreen, protective clothing, and avoidance of midday sun is therefore continued even when the rash is quiet.

## 심화 해설

Why sun protection continues even when the rash is quiet

The most accurate explanation is that ultraviolet light is a systemic trigger for lupus, not just a skin irritant. In SLE, UV exposure can provoke a disease flare that extends well beyond the skin to involve joints, blood cells, kidneys, and other internal organs [1][2]. This is why sun protection remains essential even after the visible rash has cleared.

The underlying mechanism involves UV-induced DNA damage and apoptosis in skin cells. When keratinocytes are damaged by sunlight, they release nuclear autoantigens and pro-inflammatory cytokines. In a person with SLE, the immune system recognizes these self-antigens and mounts an exaggerated inflammatory response [3]. This local reaction can then spread systemically through inflammatory cell recruitment and cytokine production, contributing to flare induction in distant organs [3].

Key point! In cutaneous lupus erythematosus, UV radiation provokes acute, nonscarring skin changes or chronic, scarring lesions. In systemic lupus erythematosus, the same UV exposure can trigger flare or progression of systemic involvement [2]. The skin is the entry point, but the disease response is body-wide.

Photosensitivity is remarkably common in this population. Among SLE patients who develop rashes, up to 93% experience photosensitivity [1]. This high prevalence underscores why sun avoidance and sunscreen use are considered the only preventive therapies for photosensitivity in SLE [1]. The absence of an active rash does not mean the underlying immune dysregulation has resolved.

For this patient specifically, several factors reinforce the need for ongoing protection. She has lupus nephritis and end-stage kidney disease, which means her SLE has already demonstrated the capacity for major organ involvement. A UV-triggered systemic flare could threaten her remaining kidney function, worsen hematologic parameters, or cause serositis. The fact that she still passes a small amount of urine indicates some residual renal activity that must be protected.

Watch out! Option 1 is incorrect because it limits sun exposure to a skin-only effect. Option 3 confuses sun protection with scar management, which is not the primary rationale. Option 4 incorrectly attributes photosensitivity to dialysis; hemodialysis does not cause sun sensitivity, though some medications used in SLE (such as hydroxychloroquine or certain antihypertensives) may contribute.

The non-lesional skin of SLE patients already shows early and chronic upregulation of inflammatory pathways even before visible lesions appear . This means the skin is primed for an exaggerated response to UV exposure at all times, not only during active rash periods. Sun protection with broad-spectrum sunscreen, protective clothing, and avoidance of midday sun is therefore a continuous preventive strategy rather than a treatment for existing lesions.

| Comparison | Skin-only effect (incorrect) | Systemic flare trigger (correct) |
| --- | --- | --- |
| Scope of UV impact | Limited to epidermis and dermis | Skin initiates cascade affecting joints, blood cells, kidneys, serosa |
| Relevance when rash is inactive | No protection needed once rash clears | Protection continues because flare risk persists |
| Mechanism | Local irritation only | DNA damage, apoptosis, autoantigen exposure, cytokine release, systemic inflammation [3] |
| Clinical implication | Sunscreen for cosmetic or scar prevention | Sunscreen and sun avoidance as disease-modifying prevention [1] |

The circadian clock may also modulate UV sensitivity in SLE, adding another layer of complexity to how and when sunlight triggers disease activity [3]. While this area requires further research, it reinforces that photosensitivity in SLE is a dynamic, systemic process rather than a static skin condition.

In summary, the nurse should explain that sunlight can reactivate lupus at a systemic level. Even with a clear rash, the immune system remains primed to overreact to UV-induced cellular damage, and that reaction can travel beyond the skin to threaten organs that have already shown vulnerability in this patient.References (research sources)

- [1]Myeloid infiltration and epidermal dysregulation characterize cutaneous photosensitivity in systemic lupus erythematosus.Research articleMaz MP, Zhang L, Ma F, Gharaee-Kermani M, Klein B, Moallemian R, Nguyen N, Cai Y, Loftus SN, Billi AC, Abernathy-Close L, Ma M, Bogle R, Hurst A, Tsoi LC, Gudjonsson JE, Kahlenberg JM. (2026) · DOI: 10.1126/scitranslmed.adw1914

- [2][Ultraviolet radiation in the pathogenesis of lupus erythematosus].Research articleKurz B, Klein B, Berneburg M, Meller S (2024) · DOI: 10.1007/s00105-024-05369-w

- [3]Human and Murine Evidence for Mechanisms Driving Autoimmune Photosensitivity.Research articleWolf SJ, Estadt SN, Gudjonsson JE, Kahlenberg JM (2018) · DOI: 10.3389/fimmu.2018.02430

## 임상 시나리오

Sun Protection in SLEWhy it continues even when the rash is quiet
Ultraviolet light is a systemic trigger for lupus flares, not just a skin irritant. Even when the rash is inactive, UV exposure can provoke disease activity involving joints, blood cells, kidneys, and other internal organs.

UV-induced DNA damage and apoptosis in skin cells release nuclear autoantigens and cytokines. In SLE, this triggers an exaggerated immune response that can spread systemically, making the skin the entry point for body-wide inflammation.

Photosensitivity affects up to 93% of SLE patients who develop rashes. Preventive measures include broad-spectrum sunscreen, protective clothing, and avoidance of midday sun.

CautionSun protection is not only about preventing rash recurrence. A flare may involve internal organs even without visible skin changes, so reinforce sun avoidance at every visit, including for patients on dialysis.

## 핵심 개념

- **Photosensitivity** — An abnormal skin reaction to sunlight, common in SLE, that can trigger local or systemic disease flares.
- **Lupus flare** — A period of increased disease activity in SLE that can involve joints, blood cells, kidneys, and other organs.
- **Ultraviolet light** — A component of sunlight that damages skin cells and can trigger autoimmune responses in lupus.
- **Systemic lupus erythematosus** — A chronic autoimmune disease that can affect multiple organ systems, including skin, joints, and kidneys.
- **Apoptosis** — Programmed cell death; UV-induced apoptosis in skin cells releases autoantigens that may drive lupus flares.

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