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Acquired pincer nail deformity associated with end stage renal disease secondary to diabetes

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Acquired pincer nail deformity associated with end stage renal disease secondary to diabetes
C Ryan Kirkland MD1, Pranav Sheth MD2
Dermatology Online Journal 15 (4): 17

1. Dermatology Resident
2. Professor
Department of Dermatology, University Hospital Cincinnati, Cincinnati, Ohio.


Pincer nail deformity has been described in association with several diseases and medications, but the mechanism of its development remains unknown. We report a woman with a rapid and severe decline in renal function that coincided with the development of pincer nails.


Pincer Nail deformity (also referred to as omega nail deformity or trumpet nail deformity) is a relatively rare condition in which there is a transverse over-curvature of the nail plate. Pincer nail deformity may either be inherited or acquired. Etiology, pathogenesis, and mechanism of inheritance are unknown [1]. Acquired pincer nail deformity has been reported to occur in association with medications, secondary to psoriasis, onychomycosis, tumors of the nail apparatus, as well as due to underlying systemic disease such as systemic lupus erythematosus, Kawasaki disease and malignancy [2-7]. This condition has not yet been reported with the onset of end stage renal disease. We present a case of acquired pincer nail deformity involving all twenty nails associated with declining renal function and the onset of end stage renal disease secondary to diabetes.

Report of a Case

A 55-year-old woman presented with a two-year history of progressive nail deformity involving all 20 nails. She was concerned with the appearance of her nails (she was a former hand model) and the associated subungual pain and tenderness. Her past medical history was significant for chronic renal insufficiency secondary to insulin dependent type II diabetes, coronary artery disease, hyperlipidemia, and hypertension. She was on multiple stable medications including furosemide, gemfibrozil, clopidogrel, metoprolol, isosorbide, losartan, humilin, and clonidine.

The patient initially noted the nail changes coincidental with the timing of a dramatic reduction in renal function prior to her presentation to us. Before the onset of her pincer nail deformity, the patient's glomerular filtration rate was 41 ml/min/1.73 m² consistent with stage III renal disease (correlates to moderately reduced kidney function and a filtration rate of 30-59 ml/min/1.73 m²). During the time of development of her nail deformities, her glomerular filtration rate progressed from stage III renal disease to stage V renal disease (kidney failure less than 15 ml/min/1.73 m²) and she was awaiting peritoneal dialysis. During the same time, there was no decline in her cardiac function and her diabetes remained moderately well controlled with hemoglobin A1c levels ranging from 6.5 to 8.2 over these two years.

Figure 1Figure 2

On examination, there was a moderate transverse over-curvature of all 20 finger and toenail plates with nail bed elevation and entrapment of the nail bed within the over-curvature (Figs. 1 & 2). Fungal culture obtained from nail clippings was unremarkable for dermatophyte.

She was prescribed urea 40 percent gel to be applied daily after soaking her nails. One week later she underwent trimming of the nails to the hyponychium. Although the patient still complains of an over-curvature, she reports much less pain and is satisfied with the results of the trimming.


Chronic renal insufficiency may cause nail changes including the absence of a lunula, splinter hemorrhages and half-and-half nails [8]. A direct relationship to pincer nail deformity has not been previously described.

Acquired pincer nail deformity has been reported in association with many systemic diseases including Kawasaki disease, psoriasis, and gastrointestinal malignancies [3, 5, 6]. Majeski et al. recently reported a case of pincer nail deformity associated with systemic lupus erythematosus. In their case, the underlying pathogenesis was hypothesized to be altered nail keratinization because of vasculitis and subsequent fibrous deposits around the distal interphalangeal joints [5]. Pincer nail deformity has also been reported in patients with pseudo-Kaposi sarcoma after arterio-venous fistula placement. The development of pincer nails was unilateral and on the side of the fistula. Moreover, the deformity resolved with ligation of the fistula and subsequent decrease of venous pressure in the affected arm [4].

There have been several reported cases of pincer nail deformity with the initiation of beta blockers. Nail changes were noted to appear within approximately six months of treatment. These patients experienced subsequent return to normal nail plate structure after cessation of the medication [2, 9, 10]. Although our patient reports taking a beta blocker, its initiation was greater than ten years before the development of her pincer nails making it an unlikely cause.

The simultaneous occurrence of pincer nail deformity of all twenty nails and the progressive deterioration of the patient's renal function to end stage renal disease, as well as the stability of her other medical conditions and medications, suggests a relation with end stage renal disease. Although there is no data that a significant change in renal function can affect the nail matrix or underlying microvasculature, it has been reported that chronic renal insufficiency in association with diabetes causes endothelial dysfunction and impaired microcirculatory function in humans [11, 12]. It is possible that in our case, her diabetes and renal disease could have contributed to the nail changes perhaps due to microvascular changes in the nail bed. Observation for reversal of the deformity after long term dialysis or renal transplant may better confirm the hypothetical link of the renal function and acquired pincer nail deformity.


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