Background: Hidradenitis suppurativa (HS) is associated with several comorbidities such as diabetes mellitus and cardiovascular diseases. These comorbidities are also risk factors for chronic kidney disease (CKD), yet little is known about the risk of CKD in HS patients. Objectives: The objective was to study the prevalence of CKD in HS patients. Methods: Cross-sectional population-based study using the United States National Inpatient Sample database between January 1, 2002 and December 31, 2012 was performed. Results: We identified 23,767 hospital admissions for HS patients and 95,068 admissions for age- and gender-matched controls. The prevalence of CKD in HS patients was 6.3% (1,497/23,767) compared to non-HS controls which was 4.3% (4,052/95,068). The association of CKD was strongest in HS patients, who were ≥60 years old, 16.9% (475/2,811), male 7.3% (695/9,556), obese 7.8% (407/5,209), diabetic 12.5% (890/7,105), hyperlipidemic 13.3% (416/3,126), and had cardiovascular diseases 12.5% (631/5,045). The crude odds ratio of CKD in HS patients was 1.5 (95% CI: 1.420–1.605) compared to non-HS patients. The association remained significant after adjusting for important covariates with adjusted odds ratio of CKD in HS patients of 1.1 (95% CI: 1.014–1.176) compared to non-HS patients. Conclusions: Our findings show that there is a possible association of HS with CKD. Any signs of CKD should be assessed by a nephrologist as early diagnosis can hopefully prevent further progression.

Hidradenitis suppurativa (HS) is a recurrent, inflammatory cutaneous disorder usually seen in the intertriginous areas, such as the axillae and genital regions [1]. It is characterized by recurrent tender nodules, abscesses, tunnels, and deforming scars [2]. The pathogenesis is not fully understood; studies propose that it initially starts with follicular occlusion, followed by rupture of the hair follicle, chronic inflammation, and immune dysregulation [3, 4]. HS is a systemic inflammatory disease, with significant comorbidity burden such as inflammatory bowel disease, inflammatory arthritis, diabetes, and all-cause mortality [5‒7]. HS is linked to increased levels of inflammatory cytokines such as tumor necrosis factor-a and interleukin-17 [8‒12]. These cytokines are associated with HS systemic comorbidities [13]. Similarly, psoriasis, which is a chronic inflammatory skin disease, has a higher risk of systemic comorbidities, such as cardiovascular diseases and chronic kidney disease (CKD) [14]. HS-associated comorbidities, such as diabetes and hypertension, are also known risk factors for CKD [15].

CKD is a major global healthcare burden causing considerable morbidity and mortality. There is no effective treatment for CKD; therefore, prevention, early detection, and identification of potential risk factors are essential [15, 16]. HS patients are prone to accelerated atherosclerosis from chronic inflammation, causing damage to endothelial cells, leading to renovascular disease [17]. Also, Th17 lymphocyte, a major cell involved in HSs pathogenesis, can cause inflammation in the kidney by affecting the kidney’s tubular and mesangial cells [18]. HS is a common yet underdiagnosed chronic inflammatory skin disease with a prevalence rate of up to 4%; thus, it could be a significant attributable risk factor for CKD [19].The recent HS comorbidity screening guidelines suggest that there was insufficient evidence to make recommendations for screening for CKD in HS patients [19]. In contrast to the well-known comorbidities, the risk of CKD in HS patients is unclear; hence, our main aim was to investigate the association between HS and CKD.

We conducted a case-control population-based study using the National (nationwide) Inpatient Sample database, a large inpatient USA database, with data of seven million hospital stays. It is part of the healthcare cost and utilization project provided by the Agency for Healthcare Research and Quality. Institutional Review Board (IRB) exemption was approved (log number: 20-645). Data were collected by the use of international classification of diseases, ninth revision, clinical modification codes (ICD-9-CM). We studied all patients who received at least one ICD-9 code (705.83) for HS between January 1, 2002 and December 31, 2012.

This case-cohort identification was validated, with a positive predictive value of 79% (95% CI: 72–85) and a negative predictive value of 100% (95% CI: 98–100) [20]. We included patients aged 18 years or older, having active data in the National Inpatient Sample database from January 1, 2002 to December 31, 2012. We excluded patients who were missing data on age and sex. The control group, with no history of a diagnostic code for HS, was randomly matched based on age and gender with HS case, in a 1:4 ratio. The primary endpoint is the diagnosis of CKD under an ICD-9 code 585, 585.1, 585.2, 585.3, 585.4, 585.5, 585.6, 585.9. We also extracted information on potential confounders including hypertension, diabetes mellitus, cardiovascular diseases, dyslipidemia, obesity, and smoking, each based on its corresponding ICD-9 code.

Statistical Analysis

The analysis included patients above 18 years of age. HS patients were coded as cases and non-HS as controls. Crude ORs were calculated using univariable binary logistic regression analysis, checking the association between HS and CKD for the whole study group and separately for each of the categories of the variables age in years, gender, tobacco smokers, obesity, diabetes mellitus, hypertension, cardiovascular disease, and hyperlipidemia.

Thereafter, multivariable logistic regressions were performed to evaluate HS and renal disease’s relationship while controlling for diabetes, hypertension, cardiovascular diseases, smoking, obesity, and hyperlipidemia in the whole study group. Furthermore, we estimated if HS and CKD risk differ within patient subgroups by using an interaction term for each subgroup variable and HS. The statistical significance level was set at a p value of 0.01 in 2-sided tests. Analyses were done using SPSS software (version 21).

A total of 23,767 hospital admissions for HS patients were matched to 95,068 admissions for controls. The majority of HS patients were female which was 59.8% (14,211/23,767) and in the 18–39 years age group which was 44.3% (10,525/23,767). Demographic characteristics are shown in Table 1. Patients with HS were more likely to be smokers 28.1%, obese 21.9%, have hypertension 30.1%, diabetes mellitus 29.9%, cardiovascular diseases 21.2%, and hyperlipidemia 13.2% compared to controls.

Table 1.

Demographic characteristics hidradenitis suppurativa (HS)

CharacteristicPatients with HS (n = 23,767), N (%)Patients without HS (n = 95,068), N (%)
CKD 1,497 (6.3) 4,052 (4.3) 
Age in years 
 18–39 10,525 (44.3) 42,100 (44.3) 
 40–59 10,431 (43.9) 41,724 (43.9) 
 ≥60 2,811 (11.8) 33,374 (11.8) 
Gender 
 Male 9,556 (40.2) 38,224 (40.2) 
 Female 14,211 (59.8) 56,844 (59.8) 
Tobacco smoker 6,687 (28.1) 13,964 (14.7) 
Obesity 5,209 (21.9) 7,883 (8.3) 
Diabetes mellitus 7,105 (29.9) 15,023 (15.8) 
Hypertension 7,149 (30.1) 22,035 (23.2) 
Cardiovascular disease 5,045 (21.2) 11,871 (12.5) 
Hyperlipidemia 3,126 (13.2) 11,429 (12.0) 
CharacteristicPatients with HS (n = 23,767), N (%)Patients without HS (n = 95,068), N (%)
CKD 1,497 (6.3) 4,052 (4.3) 
Age in years 
 18–39 10,525 (44.3) 42,100 (44.3) 
 40–59 10,431 (43.9) 41,724 (43.9) 
 ≥60 2,811 (11.8) 33,374 (11.8) 
Gender 
 Male 9,556 (40.2) 38,224 (40.2) 
 Female 14,211 (59.8) 56,844 (59.8) 
Tobacco smoker 6,687 (28.1) 13,964 (14.7) 
Obesity 5,209 (21.9) 7,883 (8.3) 
Diabetes mellitus 7,105 (29.9) 15,023 (15.8) 
Hypertension 7,149 (30.1) 22,035 (23.2) 
Cardiovascular disease 5,045 (21.2) 11,871 (12.5) 
Hyperlipidemia 3,126 (13.2) 11,429 (12.0) 

The prevalence of CKD in HS patients was 6.3% (1,497/23,767) compared to 4.3% (4,052/95,068) in non-HS controls. The prevalence of CKD was strongest in HS patients, who were ≥60 years old, 16.9% (475/2,811), hyperlipidemic 13.3% (416/3,126), diabetic 12.5% (890/7,105), had cardiovascular diseases 12.5% (631/5,045), obese 7.8% (407/5,209), male 7.3% (695/9,556), non-smoker 7.1% (1,206/17,080). Crude OR of CKD in HS patients was 1.510 (95% CI: 1.420–1.605) compared to non-HS patients. The association between HS and CKD was strongest for younger patients, 18–39 years old (OR 2.109; 95% CI: 1.819–2.444), female, (OR 1.843; 95% CI 1.692–2.007), non-smoker (OR 1.631; 95% CI: 1.525–1.745). We also calculated the adjusted OR controlling for age, diabetes, hypertension, cardiovascular diseases, smoking, obesity, and hyperlipidemia. The adjusted OR of CKD in HS patients was 1.092 (95% CI: 1.014–1.176) compared to non-HS patients. The association was higher in female (OR 1.227; 95% CI: 1.104–1.365), non-smoker (OR 1.126; 95% CI: 1.038–1.222), non-diabetic (OR 1.235; 95% CI: 1.112–1.370), non-hypertensive (OR 1.108; 95% CI: 1.026–1.196), hyperlipidemic (OR 1.103; 95% CI: 0.940–1.294), and patients without cardiovascular disease (OR 1.376; 95% CI: 1.254–1.508) (Table 2).

Table 2.

CKD in patients with HS

CharacteristicCKD prevalenceCrude OR [95% CI]ap valueaAdjusted OR [95%CI]bInteraction p valuec
subgroupHSnon-HS
Overall 6.3% (1,497/23,767) 4.3% (4,052/95,068) 1.510 [1.420–1.605] 0.001 1.092 [1.014–1.176]  
Age in years 0.001 
 18–39 2.6% (274/10,525) 1.3% (527/42,100) 2.109 [1.819–2.444] 0.001 1.272 [1.070–1.510]  
 40–59 7.2% (748/10,431) 5.4% (2,270/41,724) 1.343 [1.233–1.463] 0.001 0.928 [0.839–1.027]  
 ≥60 16.9% (475/2,811) 3.8% (1,255/33,374) 1.618 [1.443–1.818] 0.001 1.302 [1.127–1.505]  
Gender 0.001 
 Male 7.3% (695/9,556) 5.9% (2,265/38,224) 1.245 [1.140–1.360] 0.001 0.962 [0.867–1.068]  
 Female 5.6% (802/14,211) 3.1% (1,787/56,844) 1.843 [1.692–2.007] 0.001 1.227 [1.104–1.365]  
Tobacco smoker 0.205 
 Yes 4.4% (291/6,687) 3.2% (442/13,964) 1.392 [1.197–1.619] 0.001 0.909 [0.757–1.091]  
 No 7.1% (1,206/17,080) 4.5% (3,610/81,104) 1.631 [1.525–1.745] 0.001 1.126 [1.038–1.222]  
Obesity 0.001 
 Yes 7.8% (407/5,209) 6.4% (504/7,883) 1.241 [1.084–1.421] 0.002 1.111 [0.933–1.324]  
 No 5.9% (1,090/18,558) 4.1% (3,548/87,185) 1.471 [1.372–1.577] 0.001 1.089 [1.003–1.182]  
Diabetes mellitus 0.001 
 Yes 12.5% (890/7,105) 13.5% (2,026/15,023) 0.919 [0.844–1.000] 0.049 0.949 [0.857–1.052]  
 No 3.6% (607/16,662) 2.5% (2,026/80,045) 1.456 [1.328–1.597] 0.001 1.235 [1.112–1.370]  
Hypertension 0.001 
 Yes 0.5% (35/7,155) 0.7% (152/22,088) 0.708 [0.490–1.024] 0.067 0.654 [0.443–0.968]  
 No 8.8% (1,462/16,612) 5.3% (3,900/72,980) 1.710 [1.606–1.820] 0.001 1.108 [1.026–1.196]  
Cardiovascular disease 0.001 
 Yes 12.5% (631/5,045) 15.6% (1,854/11,871) 0.772 [0.701–0.851] 0.001 0.667 [0.590–0.753]  
 No 4.6% (866/18,722) 2.6% (2,198/83,197) 1.787 [1.649–1.937] 0.001 1.376 [1.254–1.508]  
Hyperlipidemia 0.001 
 Yes 13.3% (416/3,126) 9.7% (1,113/11,429) 1.423 [1.262–1.605] 0.001 1.103 [0.940–1.294]  
 No 5.2% (1,081/20,641) 3.5% (2,939/83,639) 1.518 [1.413–1.630] 0.001 1.069 [0.982–1.163]  
CharacteristicCKD prevalenceCrude OR [95% CI]ap valueaAdjusted OR [95%CI]bInteraction p valuec
subgroupHSnon-HS
Overall 6.3% (1,497/23,767) 4.3% (4,052/95,068) 1.510 [1.420–1.605] 0.001 1.092 [1.014–1.176]  
Age in years 0.001 
 18–39 2.6% (274/10,525) 1.3% (527/42,100) 2.109 [1.819–2.444] 0.001 1.272 [1.070–1.510]  
 40–59 7.2% (748/10,431) 5.4% (2,270/41,724) 1.343 [1.233–1.463] 0.001 0.928 [0.839–1.027]  
 ≥60 16.9% (475/2,811) 3.8% (1,255/33,374) 1.618 [1.443–1.818] 0.001 1.302 [1.127–1.505]  
Gender 0.001 
 Male 7.3% (695/9,556) 5.9% (2,265/38,224) 1.245 [1.140–1.360] 0.001 0.962 [0.867–1.068]  
 Female 5.6% (802/14,211) 3.1% (1,787/56,844) 1.843 [1.692–2.007] 0.001 1.227 [1.104–1.365]  
Tobacco smoker 0.205 
 Yes 4.4% (291/6,687) 3.2% (442/13,964) 1.392 [1.197–1.619] 0.001 0.909 [0.757–1.091]  
 No 7.1% (1,206/17,080) 4.5% (3,610/81,104) 1.631 [1.525–1.745] 0.001 1.126 [1.038–1.222]  
Obesity 0.001 
 Yes 7.8% (407/5,209) 6.4% (504/7,883) 1.241 [1.084–1.421] 0.002 1.111 [0.933–1.324]  
 No 5.9% (1,090/18,558) 4.1% (3,548/87,185) 1.471 [1.372–1.577] 0.001 1.089 [1.003–1.182]  
Diabetes mellitus 0.001 
 Yes 12.5% (890/7,105) 13.5% (2,026/15,023) 0.919 [0.844–1.000] 0.049 0.949 [0.857–1.052]  
 No 3.6% (607/16,662) 2.5% (2,026/80,045) 1.456 [1.328–1.597] 0.001 1.235 [1.112–1.370]  
Hypertension 0.001 
 Yes 0.5% (35/7,155) 0.7% (152/22,088) 0.708 [0.490–1.024] 0.067 0.654 [0.443–0.968]  
 No 8.8% (1,462/16,612) 5.3% (3,900/72,980) 1.710 [1.606–1.820] 0.001 1.108 [1.026–1.196]  
Cardiovascular disease 0.001 
 Yes 12.5% (631/5,045) 15.6% (1,854/11,871) 0.772 [0.701–0.851] 0.001 0.667 [0.590–0.753]  
 No 4.6% (866/18,722) 2.6% (2,198/83,197) 1.787 [1.649–1.937] 0.001 1.376 [1.254–1.508]  
Hyperlipidemia 0.001 
 Yes 13.3% (416/3,126) 9.7% (1,113/11,429) 1.423 [1.262–1.605] 0.001 1.103 [0.940–1.294]  
 No 5.2% (1,081/20,641) 3.5% (2,939/83,639) 1.518 [1.413–1.630] 0.001 1.069 [0.982–1.163]  

CKD, chronic kidney disease; CI, confidence interval; HS, hidradenitis suppurativa; OR, odds ratio.

aResults from the univariate analysis models.

bResults from the multivariate analysis models adjusting for confounders (diabetes, hypertension, cardiovascular diseases, smoking, obesity, and hyperlipidemia).

cResults from the logistic regression models with the interaction of HS and each subgroup variable.

This study of 23,767 hospital admissions for HS patients showed that the prevalence of CKD in HS patients is 6.3% with a significant association between HS and CKD aOR 1.1 (95% CI: 1.014–1.176). There are several hypotheses to explain this association. First, most HS-associated comorbidities, such as diabetes, hypertension, obesity, and cardiovascular diseases, are known risk factors for CKD [16, 21, 22]. Second, type 1 and type 17 helper T lymphocytes (Th17) are significant cells involved in the pathogenesis of HS [3]; studies have shown that Th17 lymphocytes can affect tubular and mesangial cells of the kidney [18]. Third, HS is associated with a structural impairment in the basement membrane zone in the skin; it has been hypothesized that a similar defect could affect the basement membrane in other tissues, including the kidneys [23]. This may increase glomerular hyperfiltration, leading to changes in eGFR and proteinuria [23‒25]. Fourth, CKD, as an immunosuppressive state, could result in alteration in the skin microbiota, which is also associated with HS [26, 27]. Another possible mechanistic link is an altered gut microbiome in both diseases [28].

Fifth, chronic inflammatory skin disorders such as HS and psoriasis can result in glomerular impairment. Studies showed that psoriasis, which shares some inflammatory pathways with HS, has increased glomerulonephritis incidence, specifically mesangial proliferative glomerulonephritis. This type of glomerulonephritis is commonly seen in autoimmune diseases [29]. In addition to glomerulonephritis, amyloidosis is another potential mechanism of CKD. Several cases reported patients with chronic HS developing secondary renal amyloidosis [30‒34]. The possible explanation is that chronic inflammation can lead to deposition of acute phase protein such as amyloid A.

Studies examining the association of kidney disease and HS have been scarce [23, 24, 35].

A Recent UK study reports the prevalence of several chronic inflammatory skin diseases, including HS, in a large population of CKD patients. Adjusted OR for HS in CKD patients was 1.49 (99% CI: 1.19–1.85) [35]. Miller et al. used a population- and hospital-based cross-sectional study, 32 hospitalized HS patients, 430 outpatients with HS, and 20,780 controls without HS. They found an elevated eGFR in the hospitalized HS patients compared to controls, with an eGFR difference of 6.81 (1.27–12.35) mL/min/1.73 m2 [23]. Major limitations of this study were relying on a survey to identify HS patients and lack of assessment of other measures of renal impairment beyond eGFR. Also, the method of estimating GFR was based on the CKD epidemiology collaboration equation which can underestimate eGFR in obese patients, and obesity is commonly seen in HS patients [23]. Kimball et al. [36] used several severity indicators such as biologic drugs, surgery, and emergency department visits, to stratify HS patients into mild or severe. HS patients who had one of these severity indicators were classified as severe HS. They reported a higher percentage of kidney disease in severe HS (3.1%) than mild HS (1.5%). Kidney diseases were also more prevalent in severe HS (3.1%) than non-HS controls (0.5%) [36]. Andersen et al. [37] studied the temporal disease trajectories in HS patients using ICD-10 codes, which did not find an association with CKD in the Danish population.

A recent study showed that many patients with HS have a high Charlson Comorbidity Index (CCI), a validated measure of global comorbidity formed of 17 components. One of the scoring criteria for the CCI is CKD. It categorizes patients’ comorbidities using International Classification of Diseases codes and predicts 1-year mortality based on comorbidities. HS patients had a CCI of at least 5, which is associated with increased 5-year mortality. They, therefore, suggested a multidisciplinary approach of screening and close monitoring for early detection of comorbidity [5].

A recent meta-analysis suggests that smoking is an independent risk factor for CKD [38]. Some studies point to a relationship between smoking, HS severity, and failure to respond to treatment [3]. In contrast, other studies have not found an association with HS. Regardless, quitting smoking is advisable to reduce many adverse health statuses and potentially improve HS [3].

Mahé et al. [39] studied the cutaneous side effect of 80 renal transplant patients on sirolimus, prednisolone, and mycophenolate mofetil and showed that 12% developed HS lesions. In contrast, Arnadottir et al. reported a case of HS patient who underwent a kidney transplant and was on immunosuppressive medication, including prednisolone, tacrolimus, and mycophenolate mofetil. The HS lesions improved and continued to have no signs of disease activity in the 1-year observation [40]. Dauden et al. [41], in their recommendations for the management of HS comorbidities, recommend ordering renal function test to screen for renal diseases in HS patients. It is important for clinicians who treat HS patients to know about this possible association to avoid factors that can cause further damage to the kidney, such as tetracycline which are contraindicated in kidney disease [20]. Chronic use of NSAIDs to control pain could have a nephrotoxic effect [20]. For these patients, alternative treatment modalities with less potential for nephrotoxicity should be considered [21, 22].

Our study has several limitations. As a cross-sectional study, we could not clarify the temporal relationship between HS and CKD. While we adjusted for major risk factors for CKD, the database lacked information on other CKD risk factors, such as the use of medications and herbal supplements. Similarly, any database is prone to mislabeling and misdiagnosis from inaccurate coding of HS, which is based on ICD-codes. In addition, reporting bias of smoking using ICD-9 codes as there could be patient groups where smoking is more well-registered, e.g., HS patients compared to other diagnoses.

Finally, we could not assess the severity of HS. However, as this database only represents hospitalized HS patients, these findings are more likely to be relevant to moderate-severe HS. These results could potentially be applicable to moderate-severe HS in an outpatient setting in which the majority of HS patients are treated. However, the findings cannot be generalized to all HS patients.

Our study showed a possible association between HS and CKD. HS patients have the morbidity of CKD since comorbidities are similar. Therefore, patients with HS, even if they do not yet have the comorbidities that predispose to CKD, should be monitored for later developing comorbidities and thereof CKD. HS may be seen as yet another comorbidity that should alert the physician to assess kidney function, analogous to hypertension and diabetes. We recommend screening for renal disease with urinalysis for proteinuria and hematuria, serum creatinine, GFR, and blood urea nitrogen in patients with HS. Any abnormal investigation should be assessed by a nephrologist. Early diagnosis and early intervention can prevent further progression and complications in this high-risk group.

Our findings show that there is an association of hidradenitis suppurativa with chronic kidney disease.

We would like to thank Priscilla Gikandi, Bsc, MPH for her assistance with the data analysis.

Ethics approval exemption was approved by Second Health Cluster at King Fahad Medical City Institutional Review Board (log number: 20-645). Patients consent’s was not required as this study was based on publicly available data. The need for informed consent was waived by the Institutional Review Board at King Fahad Medical City.

The authors have no conflicts of interest to declare.

This research received no grant from any funding agency.

Nouf Almuhanna and Raed Alhusayen have made contributions to conception and design. Nouf Almuhanna, Raed Alhusayen, and Sheldon Tobe have made contributions to acquisition of data, analysis, interpretation of data, drafting the the manuscript, revising the manuscript critically, and gave the final approval of the manuscript to be published. Nouf Almuhanna agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All authors have read and approved the final manuscript and agreed on the order in which their names will be listed in the manuscript.

Publicly available datasets were used in this study. These can be found in Healthcare Cost and Utilization Project (HCUP) at https://www.hcup-us.ahrq.gov/db/nation/nis/nisdbdocumentation.jsp. For additional information contact the corresponding author: Nouf Almuhanna.

1.
Phan
K
,
Charlton
O
,
Smith
SD
.
Hidradenitis suppurativa and diabetes mellitus: updated systematic review and adjusted meta-analysis
.
Clin Exp Dermatol
.
2019
;
44
(
4
):
e126
32
.
2.
Oskardmay
AN
,
Miles
JA
,
Sayed
CJ
.
Determining the optimal dose of infliximab for treatment of hidradenitis suppurativa
.
J Am Acad Dermatol
.
2019
;
81
(
3
):
702
8
.
3.
Alikhan
A
,
Sayed
C
,
Alavi
A
,
Alhusayen
R
,
Brassard
A
,
Burkhart
C
.
North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations – Part I – diagnosis, evaluation, and the use of complementary and procedural management
.
J Am Acad Dermatol
.
2019
;
81
(
1
):
76
90
.
4.
Goldburg
SR
,
Strober
BE
,
Payette
MJ
.
Hidradenitis suppurativa: epidemiology, clinical presentation, and pathogenesis
.
J Am Acad Dermatol
.
2020
;
82
(
5
):
1045
58
.
5.
Reddy
S
,
Strunk
A
,
Garg
A
.
Comparative overall comorbidity burden among patients with hidradenitis suppurativa
.
JAMA Dermatol
.
2019
;
155
(
7
):
797
802
.
6.
Egeberg
A
,
Gislason
GH
,
Hansen
PR
.
Risk of major adverse cardiovascular events and all-cause mortality in patients with hidradenitis suppurativa
.
JAMA Dermatol
.
2016
;
152
(
4
):
429
34
.
7.
Sampogna
F
,
Fania
L
,
Mazzanti
C
,
Caggiati
A
,
Pallotta
S
,
Panebianco
A
.
The broad-spectrum impact of hidradenitis suppurativa on quality of life: a comparison with psoriasis
.
Dermatology
.
2019
;
235
(
4
):
308
14
.
8.
Van der Zee
HH
,
de Ruiter
L
,
van den Broecke
DG
,
Dik
WA
,
Laman
JD
,
Prens
EP
.
Elevated levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-10 in hidradenitis suppurativa skin: a rationale for targeting TNF-α and IL-1β
.
Br J Dermatol
.
2011
;
164
(
6
):
1292
8
.
9.
Moran
B
,
Sweeney
CM
,
Hughes
R
,
Malara
A
,
Kirthi
S
,
Tobin
AM
.
Hidradenitis suppurativa is characterized by dysregulation of the Th17:treg cell Axis, which is corrected by anti-TNF therapy
.
J Invest Dermatol
.
2017
;
137
(
11
):
2389
95
.
10.
Frew
JW
,
Hawkes
JE
,
Krueger
JG
.
A systematic review and critical evaluation of inflammatory cytokine associations in hidradenitis suppurativa
.
Res
.
2018
;
7
:
1930
.
11.
Jiménez-Gallo
D
,
de la Varga-Martínez
R
,
Ossorio-García
L
,
Collantes-Rodríguez
C
,
Rodríguez
C
,
Linares-Barrios
M
.
Effects of adalimumab on T-helper-17 lymphocyte- and neutrophil-related inflammatory serum markers in patients with moderate-to-severe hidradenitis suppurativa
.
Cytokine
.
2018
;
103
:
20
4
.
12.
Matusiak
Ł
,
Szczęch
J
,
Bieniek
A
,
Nowicka-Suszko
D
,
Szepietowski
JC
.
Increased interleukin (IL)-17 serum levels in patients with hidradenitis suppurativa: implications for treatment with anti-IL-17 agents
.
J Am Acad Dermatol
.
2017
;
76
(
4
):
670
5
.
13.
Ingram
JR
,
Collier
F
,
Brown
D
,
Burton
T
,
Burton
J
,
Chin
MF
.
British Association of Dermatologists guidelines for the management of hidradenitis suppurativa (acne inversa) 2018
.
Br J Dermatol
.
2019
;
180
(
5
):
1009
17
.
14.
Ungprasert
P
,
Raksasuk
S
.
Psoriasis and risk of incident chronic kidney disease and end-stage renal disease: a systematic review and meta-analysis
.
Int Urol Nephrol
.
2018
;
50
(
7
):
1277
83
.
15.
Shlipak
MG
,
Tummalapalli
SL
,
Boulware
LE
,
Grams
ME
,
Ix
JH
,
Jha
V
.
The case for early identification and intervention of chronic kidney disease: conclusions from a Kidney Disease: improving Global Outcomes (KDIGO) Controversies Conference
.
Kidney Int
.
2021
;
99
(
1
):
34
47
.
16.
Kazancioğlu
R
.
Risk factors for chronic kidney disease: an update
.
Kidney Int Suppl
.
2011
2013
;
3
(
4
):
368
71
.
17.
Libby
P
,
Ridker
PM
,
Maseri
A
.
Inflammation and atherosclerosis
.
Circulation
.
2002
;
105
(
9
):
1135
43
.
18.
Turner
JE
,
Paust
HJ
,
Steinmetz
OM
,
Panzer
U
.
The Th17 immune response in renal inflammation
.
Kidney Int
.
2010
;
77
(
12
):
1070
5
.
19.
Garg
A
,
Malviya
N
,
Strunk
A
,
Wright
S
,
Alavi
A
,
Alhusayen
R
.
Comorbidity screening in hidradenitis suppurativa: evidence-based recommendations from the US and Canadian hidradenitis suppurativa foundations
.
J Am Acad Dermatol
.
2022
;
86
(
5
):
1092
101
.
20.
Strunk
A
,
Midura
M
,
Papagermanos
V
,
Alloo
A
,
Garg
A
.
Validation of a case-finding algorithm for hidradenitis suppurativa using administrative coding from a clinical database
.
Dermatology
.
2017
;
233
(
1
):
53
7
.
21.
Gulliver
W
,
Zouboulis
CC
,
Prens
E
,
Jemec
GBE
,
Tzellos
T
.
Evidence-based approach to the treatment of hidradenitis suppurativa/acne inversa, based on the European guidelines for hidradenitis suppurativa
.
Rev Endocr Metab Disord
.
2016
;
17
(
3
):
343
51
.
22.
Maarouf
M
,
Clark
AK
,
Lee
DE
,
Shi
VY
.
Targeted treatments for hidradenitis suppurativa: a review of the current literature and ongoing clinical trials
.
J Dermatolog Treat
.
2018
;
29
(
5
):
441
9
.
23.
Miller
IM
,
Carlson
N
,
Mogensen
UB
,
Ellervik
C
,
Jemec
GBE
.
A population- and hospital-based cross-sectional study of renal function in hidradenitis suppurativa
.
Acta Derm Venereol
.
2016
;
96
(
1
):
68
71
.
24.
Jemec
GBE
,
Chen
K
,
Chen
N
,
Skup
M
.
Association and risk of renal disease for patients with Hidradenitis Suppurativa
.
Exp Dermatol
.
2017
;
26
:
30
.
25.
Zouboulis
CC
,
Desai
N
,
Emtestam
L
,
Hunger
RE
,
Ioannides
D
,
Juhász
I
.
European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa
.
J Eur Acad Dermatol Venereol
.
2015
;
29
(
4
):
619
44
.
26.
Vossen
ARJV
,
van der Zee
HH
,
Prens
EP
.
Hidradenitis suppurativa: a systematic review integrating inflammatory pathways into a cohesive pathogenic model
.
Front Immunol
.
2018
;
9
:
2965
.
27.
Ring
HC
,
Bay
L
,
Nilsson
M
,
Kallenbach
K
,
Miller
IM
,
Saunte
DM
.
Bacterial biofilm in chronic lesions of hidradenitis suppurativa
.
Br J Dermatol
.
2017
;
176
(
4
):
993
1000
.
28.
Ring
HC
,
Thorsen
J
,
Saunte
DM
,
Lilje
B
,
Bay
L
,
Riis
PT
.
The follicular skin microbiome in patients with hidradenitis suppurativa and healthy controls
.
JAMA Dermatol
.
2017
;
153
(
9
):
897
905
.
29.
Chiu
HY
,
Huang
HL
,
Li
CH
,
Yin
YJ
,
Chen
HA
,
Hsu
ST
.
Increased risk of glomerulonephritis and chronic kidney disease in relation to the severity of psoriasis, concomitant medication, and comorbidity: a nationwide population-based cohort study
.
Br J Dermatol
.
2015
;
173
(
1
):
146
54
.
30.
Titze
J
,
Schneider
M
,
Krause
H
,
Jacobi
J
,
Stolte
M
,
Linke
RP
.
Diarrhea, nephrotic syndrome and hidradenitis suppurativa: an unusual case
.
Nephrol Dial Transpl
.
2003
;
18
(
1
):
192
4
.
31.
Girouard
SD
,
Falk
RH
,
Rennke
HG
,
Merola
JF
.
Hidradenitis suppurativa resulting in systemic amyloid A amyloidosis: a case report and review of the literature
.
Dermatol Online J
.
2012
;
18
:
2
.
32.
Utrera-Busquets
M
,
Romero-Maté
A
,
Castaño
Á
,
Alegre
L
,
García-Donoso
C
,
Borbujo
J
.
Severe hidradenitis suppurativa complicated by renal AA amyloidosis
.
Clin Exp Dermatol
.
2016
;
41
(
3
):
287
9
.
33.
Gertz
MA
,
Kyle
RA
.
Secondary systemic amyloidosis: response and survival in 64 patients
.
Medicine
.
1991
;
70
(
4
):
246
56
.
34.
Minsker
OB
,
Moskovskaia
MA
.
Surgical treatment of a disseminated form of chronic suppurative hidradenitis
.
Vestn Khir Im I I Grek
.
1980
;
124
(
1
):
78
82
.
35.
Schonmann
Y
,
Mansfield
KE
,
Mulick
A
,
Roberts
A
,
Smeeth
L
,
Langan
SM
.
Inflammatory skin diseases and the risk of chronic kidney disease: population-based case-control and cohort analyses
.
Br J Dermatol
.
2021
;
185
(
4
):
772
80
.
36.
Kimball
AB
,
Sundaram
M
,
Gauthier
G
,
Guérin
A
,
Pivneva
I
,
Singh
R
.
The comorbidity burden of hidradenitis suppurativa in the United States: a claims data analysis
.
Dermatol Ther
.
2018
;
8
(
4
):
557
69
.
37.
Kjærsgaard Andersen
R
,
Jørgensen
IF
,
Reguant
R
,
Jemec
GBE
,
Brunak
S
.
Disease trajectories for hidradenitis suppurativa in the Danish population
.
JAMA Dermatol
.
2020 July 1
156
7
780
6
.
38.
Xia
J
,
Wang
L
,
Ma
Z
,
Zhong
L
,
Wang
Y
,
Gao
Y
.
Cigarette smoking and chronic kidney disease in the general population: a systematic review and meta-analysis of prospective cohort studies
.
Nephrol Dial Transpl
.
2017
;
32
(
3
):
475
87
.
39.
Mahé
E
,
Morelon
E
,
Lechaton
S
,
Sang
KHLQ
,
Mansouri
R
,
Ducasse
MF
.
Cutaneous adverse events in renal transplant recipients receiving sirolimus-based therapy
.
Transplantation
.
2005
;
79
(
4
):
476
82
.
40.
Arnadottir
M
,
Jonsson
E
,
Jonsson
J
.
Inactivity of hidradenitis suppurativa after renal transplantation
.
Transplantation
.
2006
;
82
(
6
):
849
.
41.
Dauden
E
,
Lazaro
P
,
Aguilar
MD
,
Blasco
AJ
,
Suarez
C
,
Marin
I
.
Recommendations for the management of comorbidity in hidradenitis suppurativa
.
J Eur Acad Dermatol Venereol
.
2018
;
32
(
1
):
129
44
.