Erythrodermic Psoriasis Causing Uric Acid Crystal Nephropathy.


Journal

Case reports in medicine
ISSN: 1687-9627
Titre abrégé: Case Rep Med
Pays: United States
ID NLM: 101512910

Informations de publication

Date de publication:
2019
Historique:
received: 18 09 2018
accepted: 11 02 2019
entrez: 30 4 2019
pubmed: 30 4 2019
medline: 30 4 2019
Statut: epublish

Résumé

Erythrodermic psoriasis is a rare and severe variant of psoriasis. It is characterized by widespread skin erythema, scaling, pustules, or exfoliation of more than 75% of the body's surface area. This condition has life-threatening complications to include hemodynamic, metabolic, immunologic, and thermoregulatory disturbances. One metabolic complication, hyperuricemia, occurs from rapid keratinocyte differentiation and infiltration of inflammatory cells into psoriatic lesions. Although renal injury caused by shunting of blood to the skin has been reported, there are no reports of erythrodermic psoriasis causing crystal-induced nephropathy. We present a case of erythrodermic psoriasis and hyperuricemia complicated by uric acid crystal nephropathy. A 57-year-old male with long-standing psoriatic arthritis presented with diffuse scaling of his skin. He was being treated with adalimumab, leflunomide, and topical clobetasol, but had recently stopped taking his medications. Physical exam revealed yellow scaling covering his entire body with underlying erythema and tenderness without mucosal involvement. Labs were notable for a creatinine of 3.3 mg/dL, with no prior history of renal disease, and uric acid of 12.7 mg/dL. He was admitted to the intensive care unit given >80% of body surface area involvement and acute renal failure. Despite aggressive fluid resuscitation, renal function did not improve, and creatinine peaked at 4.61 mg/dL. Urine microscopy showed diffuse polymorphic uric acid crystals, consistent with uric acid crystal-induced nephropathy. He was started on rasburicase, urinary alkalinization, and fluids. His renal function improved dramatically; urine output, uric acid, and electrolytes normalized. He was discharged on topical clobetasol and leflunomide and started on secukinumab with little to no skin involvement. This case presents the rare complication of crystal-induced nephropathy in a patient with erythrodermic psoriasis. Uric acid crystal nephropathy is well described in diseases with rapid cell turnover such as tumor lysis syndrome. It is thought that rapid keratinocyte differentiation and inflammatory infiltration of psoriatic lesions produced life-threatening electrolyte abnormalities similar to tumor lysis syndrome. Early recognition of this rare complication is critical, and aggressive fluid resuscitation, urine alkalinization, and uric acid lowering agents should be administered immediately.

Sections du résumé

BACKGROUND BACKGROUND
Erythrodermic psoriasis is a rare and severe variant of psoriasis. It is characterized by widespread skin erythema, scaling, pustules, or exfoliation of more than 75% of the body's surface area. This condition has life-threatening complications to include hemodynamic, metabolic, immunologic, and thermoregulatory disturbances. One metabolic complication, hyperuricemia, occurs from rapid keratinocyte differentiation and infiltration of inflammatory cells into psoriatic lesions. Although renal injury caused by shunting of blood to the skin has been reported, there are no reports of erythrodermic psoriasis causing crystal-induced nephropathy. We present a case of erythrodermic psoriasis and hyperuricemia complicated by uric acid crystal nephropathy.
CASE PRESENTATION METHODS
A 57-year-old male with long-standing psoriatic arthritis presented with diffuse scaling of his skin. He was being treated with adalimumab, leflunomide, and topical clobetasol, but had recently stopped taking his medications. Physical exam revealed yellow scaling covering his entire body with underlying erythema and tenderness without mucosal involvement. Labs were notable for a creatinine of 3.3 mg/dL, with no prior history of renal disease, and uric acid of 12.7 mg/dL. He was admitted to the intensive care unit given >80% of body surface area involvement and acute renal failure. Despite aggressive fluid resuscitation, renal function did not improve, and creatinine peaked at 4.61 mg/dL. Urine microscopy showed diffuse polymorphic uric acid crystals, consistent with uric acid crystal-induced nephropathy. He was started on rasburicase, urinary alkalinization, and fluids. His renal function improved dramatically; urine output, uric acid, and electrolytes normalized. He was discharged on topical clobetasol and leflunomide and started on secukinumab with little to no skin involvement.
CONCLUSION CONCLUSIONS
This case presents the rare complication of crystal-induced nephropathy in a patient with erythrodermic psoriasis. Uric acid crystal nephropathy is well described in diseases with rapid cell turnover such as tumor lysis syndrome. It is thought that rapid keratinocyte differentiation and inflammatory infiltration of psoriatic lesions produced life-threatening electrolyte abnormalities similar to tumor lysis syndrome. Early recognition of this rare complication is critical, and aggressive fluid resuscitation, urine alkalinization, and uric acid lowering agents should be administered immediately.

Identifiants

pubmed: 31031815
doi: 10.1155/2019/8165808
pmc: PMC6458895
doi:

Types de publication

Case Reports

Langues

eng

Pagination

8165808

Références

Blood. 2001 May 15;97(10):2998-3003
pubmed: 11342423
J Clin Invest. 1961 Aug;40:1486-94
pubmed: 13726168
Am J Med. 1992 Feb;92(2):141-6
pubmed: 1543197
Ren Fail. 2005;27(1):123-7
pubmed: 15717645
Clin Exp Dermatol. 2007 Mar;32(2):176-9
pubmed: 17176269
J Dermatolog Treat. 2009;20(1):67-9
pubmed: 18651300
J Am Acad Dermatol. 2010 Apr;62(4):655-62
pubmed: 19665821
J Am Acad Dermatol. 2012 Nov;67(5):e179-85
pubmed: 21752492
Clin Rev Bone Miner Metab. 2011 Dec;9(3-4):207-217
pubmed: 25045326
J Am Acad Dermatol. 1989 Nov;21(5 Pt 1):985-91
pubmed: 2530253
NDT Plus. 2008 Oct;1(5):307-9
pubmed: 25983919
Medicine (Baltimore). 2016 May;95(19):e3676
pubmed: 27175702
JAAD Case Rep. 2017 Dec 18;4(1):22-23
pubmed: 29296644
J Am Acad Dermatol. 1996 May;34(5 Pt 2):911-4
pubmed: 8621827
Dermatol Clin. 1995 Oct;13(4):757-70
pubmed: 8785881

Auteurs

John Ellis (J)

Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.

Jeffrey Lew (J)

Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.

Sumir Brahmbhatt (S)

Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.

Sarah Gordon (S)

Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.
Nephrology Service, Tripler Army Medical Center, Honolulu, HI, USA.

Troy Denunzio (T)

Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.
Nephrology Service, Tripler Army Medical Center, Honolulu, HI, USA.

Classifications MeSH