Bumpy rashes

Clinical features

Arthropods are responsible for many dermatologic complaints, including bites, stings, and infestations. They can also be vectors for numerous systemic and life-threatening diseases. The clinical manifestations of arthropod bites vary greatly depending on which arthropod is responsible. Because of the scope of this chapter and book, several arthropod reactions will not be covered, including hymenoptera (bees, wasps, hornets), centipedes, millipedes, caterpillars/moths, scorpions, scabies, chiggers, and lice.

Mosquitoes, midges, flies, bed bugs, and fleas are all insects that can cause papular urticaria. These lesions present as discrete, well-demarcated, pink-red, blanching papules at the site of the bite. The usually pruritic papules can last for several days and may not appear until 24 hours after a bite occurred. Occasionally, these lesions can appear papulovesicular or bullous. Often, a central punctum can be identified.

Mosquitoes, midges, and flies tend only to bite exposed sites. Flies (such as the horse fly, deer fly, and greenheads) mostly cause painless bites at first, followed by intense pain. The remaining lesions are often more painful than itchy. Fleas jump and therefore commonly affect the lower legs. Bed bugs tend to bite in groups or lines (the so-called “breakfast, lunch, and dinner” sign).

Mosquitoes can transmit numerous infections, most commonly malaria, worldwide. In the United States, West Nile, Eastern Equine, and Western Equine encephalitis, as well as Zika and chikungunya, are all relevant mosquito borne diseases. Flies do not tend to transmit disease in the United States but can cause myiasis, filariasis, and onchocerciasis elsewhere in the world.

Bed bugs can be a vector for Chagas disease (trypanosomiasis) where the disease is endemic. They may also transmit hepatitis B.

Fleas are vectors for murine typhus, tularemia, bubonic plaque, and tungiasis.

Differential diagnosis

The differential diagnosis for bites from the aforementioned insects includes allergic contact dermatitis (ACD), scabies infestation, lice infestation, and bullous pemphigoid (BP).

• ACD can present with papules; however, this phase tends to result in smaller papules that persist for weeks, as opposed to the 24 to 48 hours these last in bites. The papules in ACD tend to be arranged in a geometric manner and may coalesce into a plaque, unlike papular urticaria, which does not. Patch testing can be performed if there is consideration for ACD. A skin biopsy may be able to distinguish these two entities; however, they have overlapping features.

• Scabies presents as diffuse, whole-body itching from the neck down, often concentrated in the genitals, axillae, and umbilicus, with scaling, crusting, and burrows most often found on the hands. Papules similar to papular urticaria from arthropod bites may be seen in scabies. Scabietic papules, however, tend to cluster in areas like the genitalia, which are rarely involved in arthropod bites. A mineral oil prep of a burrow from the aforementioned anatomic sites could help in the diagnosis of scabies. A skin biopsy may look identical to an arthropod bite, unless a mite or mite eggs or excrement is captured (which is uncommon).

• Lice (pediculosis) can infest the body, scalp, and pubic region, causing diffuse pruritus. They cause lesions identical to the aforementioned arthropods. Unlike the limited nature of those bites, however, lice infestation results in diffuse pruritus, eczematous changes, lichen simplex chronicus, and occasionally crusting related to secondary infection. Finding lice on the body can be challenging and in pediculosis corporis should be looked for in the seams of the clothing. In pediculosis pubis and capitis, on the other hand, nits are usually identified along the hair shafts, and a louse comb may be employed. Skin biopsy would not reliably distinguish lice-induced skin changes from other biting insects.

• BP is an autoimmune pruritic blistering disorder that primarily affects the elderly. In the earliest stages, the eruption can present with small urticarial papules. Tense bullae develop later in the course. Both the initial lesions and bullae in BP can mimic arthropod bites clinically and histopathologically. Therefore referral to a dermatologist for direct immunofluorescence (DIF) testing and other work-up is recommended if there is concern for an autoimmune blistering disease.

• Spiders can bite with a similar reaction to those of the arthropods previously mentioned. Most bites will cause a solitary pruritic or painful red papulonodule that will resolve in days. The brown recluse and black widow spiders, however, do have significant cutaneous and systemic adverse effects. The brown recluse causes a painful swollen bite with hemorrhagic changes, central vesiculation, and resulting necrosis. Systemic reactions include fever, chills, disseminated rashes, hemolysis/disseminated intravascular coagulation, seizures and coma. The black widow bite causes autonomic dysfunction with urinary retention, abdominal pain, diaphoresis, hypertension, and, rarely, death. The clinical differential diagnosis for a brown recluse spider bite includes a methicillin-resistant Staphylococcus aureus (MRSA) abscess/cellulitis, pyoderma gangrenosum, and is-chemia/vascular insufficiency.

• MRSA and other infections usually present as solitary, hot, red painful sites on the body. These tend to evolve from cellulitic plaques to abscesses that require drainage. Although brown recluse bites can cause necrosis, they are not commonly purulent. MRSA infections tend to lack the hemorrhagic appearance of brown recluse spider bites. A tissue or routine wound culture can aid in diagnosis. Other bacterial and viral infections can cause a similar picture but normally in the setting of immune compromise or a disseminated infection.

• Pyoderma gangrenosum (PG) is a neutrophilic dermatosis commonly associated with inflammatory bowel disease, rheumatoid arthritis, and hematologic malignancies. It presents as a painful ulcerated plaque with gray, undermined, irregular borders and often has a cribriform appearance. The clinical presentation can be identical to brown recluse spider bites; therefore a careful clinical history is essential. PG is a diagnosis of exclusion and can only be ruled on once infectious causes of ulceration have been excluded.

• Vascular causes of tissue necrosis include thromboembolism, chronic vascular insufficiency, small to medium and large vessel vasculitides, and calciphylaxis. Typically, patients will present with multiple lesions in these scenarios and will have a health history and other physical examination findings suggestive of a systemic process. A skin biopsy may be helpful in the setting of calciphylaxis and possibly vasculitis; however, all of these diseases may have overlapping features histopathologically. Therefore a careful history and comprehensive physical examination will be essential in differentiating them.

• Ticks bite and attach themselves to feed on humans and other animals. Their bite is painless. They can remain attached for days and may be found in an engorged state attached to the skin at presentation. The patient might ask about their new “mole.” Initially, tick bites tend to be red papules. The bites may expand into a patch or plaque of erythema several centimeters large. Necrosis and granuloma formation are less commonly seen. If bitten by an Ixodes tick, there is a risk for Lyme borreliosis. Localized Lyme presents as erythema migrans, which is a red annular plaque that can evolve to the classic target-like lesion that enlarges to be 4 cm in diameter or more. Systemic symptoms, including fever and joint pains, may be present. This eruption may fade without treatment. Nonetheless, treatment is necessary to prevent disseminated Lyme and its complications. Persistent tick bite reactions can form large, purple papulonodules caused by cutaneous lymphoid hyperplasia or pseudolymphoma. These are benign reactions that mimic forms of cutaneous B-cell lymphoma. Other tick-borne diseases include Rocky Mountain spotted fever, ehrlichiosis, and anaplasmosis. The clinical differential diagnosis for tick bites includes gyrate erythema, erythema multiforme (EM), and granuloma annulare (GA).

• Gyrate erythema encompasses a group of inflammatory skin reactions that present as red, blanching, variably scaly annular or arcuate plaques on the extremities or trunk. They can be solitary or multiple. The exact cause is not known; however, infections, drugs, malignancy, and liver disease have been associated with them. The lesions in gyrate erythema tend to be more arcuate than targetoid and have defined central clearing, whereas erythema migrans normally retains central erythema. The lesions may have a classic trailing scale behind the annular edge. Nevertheless, scale may be absent in deeper variants. A skin biopsy, particularly if there is no scale, can have overlapping features with erythema migrans and therefore may not be fully diagnostic. A careful physical examination and clinical history is essential for differentiating these two entities.

• EM is a type IV hypersensitivity reaction caused by drugs or herpes simplex virus (HSV) infection. In contrast to the classic solitary appearance of erythema migrans, EM presents as numerous smaller, red papules that evolve into targetoid plaques that may coalesce. The border tends to be more indurated and urticarial than erythema migrans and lacks significant scale. The central lesion is normally vesicular or bullous. Mucosae may be involved as well. Skin biopsy can differentiate EM from a tick bite/erythema migrans.

• GA is an idiopathic inflammatory reaction pattern in the skin that presents with annular plaques without scale. Normally, the plaques are multiple in nature. The color of the lesions is more purplish-brown as opposed to the bright red seen in erythema migrans. Skin biopsy can differentiate these two entities when a clinical examination is not sufficient.

Work-up

Initial steps in management

Warning signs/common pitfalls

A common pitfall is not taking an adequate history. Asking specific questions about exposures will yield the correct causative type of arthropod most of the time.

Another pitfall is not counseling the patient appropriately about risks and procedures in the setting of home infestations. Many patients are concerned about added costs and are reluctant to pursue veterinary or exterminator appointments as needed.

Counseling

Your skin lesions are small inflammatory reactions to the bite of an insect. These bites are usually very itchy. They can persist for several days or, rarely, weeks. You may not recall being bitten, and bites can take 1 to 2 days to appear. Most insect bites are caused by insects that live outside, such as mosquitoes, flies, or midges. These can be prevented by wearing clothing and applying insect repellent sprays. Most bite more frequently at twilight, so it is best to move indoors at that time. Avoid areas of standing water because these are places where most of them breed.

If you do not recall being outside at a time of year when insect bites are common, then you may have been exposed to insects that can live inside.

Fleas are common causes of insect bites and can infest pets and humans. They live in your home and are small insects that can be pulled from your involved pet’s coat. They tend to cause bites on the lower legs.

Bed bugs can also cause bites. These insects infest homes and are extremely hard to detect except by trained professional exterminators. They live in walls, floorboards, bed frames, and other areas. They can be acquired by staying in an infested home or hotel room and may travel in your luggage. They only feed during a brief period in the night and leave small pinpoint bloodstains on the sheets. Without an exterminator, the infestation will persist.

These types of insect bites can be easily treated with topical steroids applied twice daily for 5 to 7 days.

If you notice blistering at your bite site, or if there is persistent pain or skin breakdown, you may have been bitten by a spider. You may need to have your home investigated for an infestation.

If you have pulled an insect off of you that seemed attached to your skin, it was almost certainly a tick. These bites can cause red target like rashes on the skin. We may need to treat you with an oral antibiotic for several weeks to treat any potential Lyme disease.

Clinical features

Grover disease (GD), also known as “transient acantholytic dermatosis,” is an acquired condition usually seen in middle-aged Caucasian men. The etiology is poorly understood, but GD has been associated with heat, sweating, sun exposure, radiation, and certain medications. Although benign and potentially self-resolving, the rash may become chronic with fluctuating symptoms that can last for several months or even years.

• Patients who complain about their lesions often endorse a history of intense pruritus in the affected areas; however, GD may also be asymptomatic, in which case it is frequently identified with a full-body skin examination.

• It typically presents as pruritic, erythematous, scaly papules on the trunk with occasional vesicles, crusting, and erosions ( Fig. 6.1 ).

  

• Factors that increase sweating, such as fever, heat, sun exposure, or prolonged immobility, may predispose patients to the development of GD-related pruritus.

Work-up

GD is typically a clinical diagnosis based on the findings of a pruritic papulosquamous eruption on the abdomen and lower back of an older adult. Clues in the patient history, such as symptomatic exacerbation with sweating/overheating, can be helpful in securing the diagnosis. Rarely, a punch biopsy of lesional skin is required to confirm the diagnosis.

Initial steps in management

There are no disease-specific therapies for GD, and treatment is directed toward symptom management.

• Patients should avoid excessive heat and sun exposure because this may exacerbate the condition.

• Moisturizers and emollients containing camphor or menthol can be applied to help reduce pruritus and prevent xerosis, which may worsen the condition. These can be stored in the refrigerator to further enhance the cooling sensation when applied to the skin.

• Mid-potency topical steroid creams or ointments (such as triamcinolone 0.1%) can be applied twice daily for up to 2 weeks to the affected areas to alleviate pruritus. Patients should be counseled on the risk for skin atrophy, striae, and dyspigmentation associated with the long-term use of steroids.

• Calcipotriene 0.005% (a vitamin D analog) cream applied twice daily to affected areas can help manage symptoms and function as a steroid-sparing agent.

• Oral antihistamines (diphenhydramine 25–50 mg every 6 hours as needed, cetirizine 5–10 mg daily as needed, or hydroxyzine 10–25 mg every 6 hours as needed) can provide temporary symptomatic relief.

For GD that is refractory to topical steroids and supportive therapies, other treatment options may be considered.

• Narrowband ultraviolet B (NBUVB) radiation has been shown to improve GD but may initially exacerbate the condition before an improvement is seen.

• Systemic medications, such as oral retinoids (acitretin or isotretinoin) and methotrexate, may also be prescribed for severe and recalcitrant GD; however, these should only be prescribed by practitioners experienced with these medications because of the risk for potential side effects and the need for close monitoring.

Warning signs/common pitfalls

• A high degree of suspicion should be maintained for GD in any mature patient with a chronic, pruritic papulosquamous eruption on the abdomen and lower back because this condition is very bothersome to many individuals.

• Many patients have symptoms out of proportion to their physical examination findings. These patients, who frequently have sleep disturbances, require aggressive management with systemic medications to achieve satisfactory disease control.

Counseling

You have a condition called Grover disease, which is not dangerous to your health but can be challenging to treat. It is important to avoid any known triggers, such as excessive heat, sweating, and sun exposure, because these can exacerbate the rash.

The course of the condition can be unpredictable with fluctuating symptoms, and it may last anywhere between a few weeks to a few years. There is no cure for your condition, but certain over-the-counter (OTC) and prescription medications can help reduce your symptoms. Moisturizers, topical steroids, and antihistamines can help alleviate the itching and may be used as instructed by your physician. Other systemic medications and therapies can be prescribed if your rash is persistent. These medications can be discussed if your symptoms do not improve with the use of creams.

The itching you experience may become severe. Let your physician know if it begins to negatively affect your quality of life so that your treatment plan can be adjusted accordingly.

Clinical features

Prurigo nodularis (PN) is a chronic skin condition caused by repetitive scratching, rubbing, or picking ( Fig. 6.2 ). It is more commonly seen in middle-aged women, who often have an underlying condition that may be dermatologic or psychiatric. Less commonly, it can be seen in the pediatric population secondary to concomitant atopic dermatitis (AD). Early recognition is important to halt this cosmetically disfiguring process, which can be extremely distressing for the patient, and to address any underlying conditions that may be contributing to this disease.

• Patients are often unaware of or unwilling to admit that they are scratching or picking. The most common complaint is pruritus, which may be exacerbated by heat, sweating, or irritation from friction. Nevertheless, the patients may insist that the areas are asymptomatic, which can confuse the clinical picture.

• On examination, lesions often appear as multiple, firm, dome-shaped papules or nodules that can be hyperpigmented. The lesions may have overlying central scale or crust with an erosion or ulcer from manipulation of the area. These nodules are usually symmetrically distributed on the extensor surfaces of the extremities with classic sparing of the midback, which is known as the “butterfly sign” because patients are not able to reach that area. These lesions are rarely found on the face, palms, or soles. Although the pathophysiology is similar to lichen simplex chronicus, lichenification of the lesions is not usually present.

• Underlying conditions, such as xerosis, AD, chronic kidney or liver disease, thyroid issues, HIV infection, psychiatric conditions, parasitic infestations, and malignancy may be present because these can be associated with pruritus.

• PN is often associated with sleep disturbances, anxiety, and depression, leading to a decreased quality of life for the patient.

Differential diagnosis

The differential diagnosis for PN includes keloids, acquired perforating dermatoses, pemphigoid nodularis, nodular scabies, hypertrophic lichen planus (LP), multiple keratoacanthomas, and epidermolysis bullosa pruriginosa.

• Keloids can be difficult to distinguish from PN because they can also present as pruritic, firm, hyperpigmented papules or plaques. History may be helpful in this case because the patient often relates a history of trauma or inflammation (i.e., acne) in those areas. Keloids are typically treated with topical or intralesional steroids for symptomatic relief.

• Acquired perforating dermatoses can be associated with chronic renal failure and diabetes. They usually present as multiple, flesh-colored papules with a central keratotic plug at trauma-prone sites, such as the hands and knees. These lesions often regress spontaneously; however, treatment of the underlying disease is important.

• Pemphigoid nodularis is a rare variant of BP, an autoimmune blistering disorder. It is classically seen more frequently in the elderly population. The lesions typically present as pruritic hyperkeratotic nodules that clinically resemble those found in PN. These two conditions may be distinguished through skin biopsy and DIF analysis. Pemphigoid nodularis often requires systemic treatment with steroids or immunomodulators.

• Nodular scabies is most commonly localized to the groin, buttocks, and axillae, with increased nighttime pruritus. More characteristic signs such as linear burrows, excoriations, and interdigital web space involvement may also be present on physical exam, which can help with the diagnosis. Microscopic examination of a burrow’s contents may reveal the mites, eggs, or feces. Nodular scabies is typically treated with permethrin or oral ivermectin.

• Hypertrophic LP is characterized by pruritic, pink to purple hyperkeratotic or verrucous plaques that are usually localized to the anterior lower extremities. This can be a challenging diagnosis to make, and a referral to a dermatologist is recommended because a biopsy may need to be performed to establish a diagnosis.

• Keratoacanthomas, a well-differentiated subtype of squamous cell carcinoma (SCC), can also present as flesh-colored, dome-shaped nodules with a central keratotic plug on the extremities. Significant tenderness, a history of bleeding, ulceration, recurrence, or a history of immunosuppression should raise the clinical suspicion for a malignancy.

• Epidermolysis bullosa pruriginosa is a rare subtype of dystrophic epidermolysis bullosa. It can present as chronic pruritic hypertrophic plaques, usually on the lower extremities with sparing of the face. They are often lichenified with a linear configuration, which can help distinguish them from PN. Treatment can be challenging, but topical and intralesional steroids are often used, with more refractory disease requiring systemic therapy.

Work-up

Patients with suspected PN should be referred to a dermatologist for further evaluation and treatment. PN is usually a clinical diagnosis made by the dermatologist based on the patient’s history and physical examination.

• If the history and clinical findings do not clearly indicate a diagnosis of PN, then the dermatologist can perform a skin biopsy for further evaluation.

• Diagnostic testing to identify systemic diseases that may precipitate pruritus should be considered, including a complete blood count (CBC), liver function test (LFT), basic metabolic panel (BMP), thyroid-stimulating hormone (TSH), HIV testing, urinalysis, and stool examination for ova or parasites.

• If there is any uncertainty in the diagnosis, the patient should be referred to a dermatologist.

Initial steps in management

The most important step in management is to communicate expectations with the patient because PN can be a challenging condition to treat. The patients are often anxious and become easily frustrated by the lack of improvement. Helping to control the pruritus and urge to scratch or pick at the areas is of the utmost importance to stop the repetitive itch-scratch cycle. Based on the complexity and possible reactions to the treatments, a referral to dermatology is advised.

• Recommend that the patient maintain short nails, wear gloves when sleeping, and cover the lesions with bandages to reduce further injury from scratching.

• Gentle skin care, including the use of fragrance-free soaps and emollients, may help because xerosis is a common cause of pruritus.

• Recommend OTC soothing lotions that may be applied to the skin as needed. These include creams containing calamine, menthol, or camphor, which can be stored in the fridge, because this can further enhance the cooling sensation when applied. Topical capsaicin cream is also available over the counter and can be used to help with pruritus, but some patients may not be able to tolerate the burning sensation initially felt when the cream is applied.

• If the lesions look secondarily infected, a course of antibiotics may be warranted.

Warning signs/common pitfalls

• There should be a low threshold for referral to a dermatologist because this condition can mimic other diseases, and there is a wide differential that has to be considered. In addition, the early involvement of a dermatologist can be helpful to guide management.

• Work-up for underlying systemic diseases, including CBC, LFT, BMP, TSH, HIV testing, urinalysis, and a stool sample, should be considered when clinically indicated.

• Patients should be routinely screened for anxiety, depression, and psychological distress so that supportive therapy can be provided.

Counseling

You have a condition called “prurigo nodularis,” which refers to nodules (bumps) on your skin that are the result of long-term scratching, rubbing, or picking. They are often itchy, which can lead to a vicious itch-scratch cycle that may worsen your condition. The main treatment goal is to control this itching and prevent further injury to the skin. We recommend keeping your nails short, wearing gloves to bed, and keeping the areas covered with bandages to reduce further damage. You should avoid excessive heat exposure and tight garments because sweating and skin irritation from clothing may exacerbate your itching. We recommend gentle cleansers and emollients to keep the skin moisturized while avoiding any harsh scrubs or cleansing agents. Treatment of this condition depends on the number and severity of the lesions. Antihistamines and topical steroids can be helpful in this condition. For severe cases, other treatments, such as phototherapy, steroid injections, or immunomodulators, may be considered. In some cases, a biopsy (skin sample) may be necessary to determine a diagnosis.

Inform your physician if you are experiencing any stress, anxiety, depression, or sleepless nights. Psychological support and/or medication to manage these symptoms can be offered to you if appropriate.

Clinical features

Renal pruritus develops in patients with end-stage renal disease (ESRD) who are undergoing hemodialysis, with a prevalence of 20% to 60% in this population. Although the exact cause of renal pruritus is not known, it is potentially caused by stimulation of itch neurons from (1) a build-up of poorly dialyzed metabolic toxins, (2) opioid receptor derangements, and (3) systemic inflammation. As expected, dialysis patients are more likely to develop pruritus after inadequate dialysis and in cases where they have persistently elevated serum calcium, phosphorus, and magnesium levels.

Importantly, the majority of patients with ESRD develop comorbid xerosis ( Chapter 3 , Body Dermatitis section “Dry Skin”). Xerosis contributes to itch in these patients and also should be addressed. Renal pruritus has been identified as a key research priority by patients with ESRD because of its distressing impact and potential association with poor sleep quality, worsened quality of life, and depression. Renal pruritus typically exhibits a chronic course and, once present, generally remains for months to years and can often remain indefinitely.

Renal pruritus is characterized by the development of intense, generalized pruritus in the absence of primary skin lesions.

• The itch most frequently occurs on the back, arms, head, and abdomen, but it can also be widespread across the body.

• Only secondary skin changes, such as excoriations, and prurigo nodules are seen on examination.

• Pruritus can be constant or intermittent, but it is generally worse during the evening hours and frequently impedes adequate sleep.

• Patients may demonstrate elevated serum blood urea nitrogen (BUN), phosphate, calcium, magnesium, and parathyroid hormone (PTH) levels; however, these findings are not needed to make the diagnosis nor are they specific for the diagnosis because they are also present in many patients with ESRD who lack renal pruritus.

Differential diagnosis

In a patient with suspected renal pruritus with secondary skin changes, the main differential diagnosis is an acquired perforating dermatosis (APD).

• The development of secondary skin changes in renal pruritus, such as excoriations, erosions, and prurigo nodules, can be confused with APD (e.g., acquired reactive perforating collagenosis, acquired perforating folliculitis), especially because these conditions are all common in patients with ESRD and are incited in part by epidermal irritation. Nevertheless, prurigo nodules in renal pruritus are more often dome-shaped, firm, and flesh-colored, whereas the hallmark of APD is umbilicated papules with a hyperkeratotic central plug.

  • In clinical practice, renal pruritus with prurigo nodules can be difficult to distinguish from APD and, regardless of the exact diagnosis, antipruritic therapies are indicated for improvement of both classes of disorders.

In the absence of skin findings, generalized causes of isolated pruritus, such as primary biliary cholangitis, lymphoma, and polycythemia vera, should be considered.

• Patients with primary biliary cholangitis may also demonstrate significant pruritus in the absence of skin findings; however, they are likely to further exhibit jaundice and fatigue, and laboratory findings will be significant for elevated serum liver enzyme and bilirubin levels.

• Several lymphoma subtypes, including Hodgkin lymphoma and mycosis fungoides, commonly pre-sent with pruritus that may precede the development of other symptoms.

  • In the case of Hodgkin lymphoma, pruritus is generally localized to the lower extremities, and patients may have associated so-called “B symptoms” (e.g., fevers, night sweats, weight loss).

  • Although it can be isolated, pruritus from mycosis fungoides is more likely to occur in association with numerous scaly skin plaques and diffuse erythroderma.

• Pruritus from polycythemia vera is typically elicited by contact with water (aquagenic pruritus) and is further associated with tingling or burning sensations.

Work-up

The diagnosis of renal pruritus is relatively straightforward given the high likelihood in a patient undergoing hemodialysis. As always, a careful evaluation of patient history and clinical examination is essential in solidifying the diagnosis.

• When considering patient history, it is important to assess for the temporal relationship between dialysis onset/significant decline in renal function and symptom presentation.

• A full-body skin examination is warranted to rule out the presence of a primary dermatosis that can have associated pruritus (e.g., ACD or irritant contact dermatitis, psoriasis).

  • If skin lesions are identified, they should be carefully evaluated because they may represent either prurigo nodules in the context of renal pruritus or a perforating disorder.

• Laboratory testing that indicates elevated calcium, phosphate, magnesium, BUN, or PTH levels is further supportive of a diagnosis of renal pruritus.

Initial steps in management

Warning signs/common pitfalls

• It is important to consider and address the day-to-day implications of renal pruritus on patients’ lives. Pruritus can become particularly severe at night, which can adversely affect a patient’s sleep. In these cases, treatments targeted at promoting sleep, such as melatonin, may be considered.

• In a patient not currently undergoing dialysis therapy (especially those with stages 1 to 3 of chronic kidney disease), renal pruritus is a very unlikely cause of pruritus and other potential differential diagnoses should be considered.

• Antiinflammatory medications, such as corticosteroids and tacrolimus, have not been shown to benefit individuals with renal pruritus and are typically not considered as potential treatments.