Shi Y, Zhang Y, Zhou AD, Zou HY, Wang MM, Xu F, Cai MY. Association between circulating sex hormone levels and diabetic kidney disease in men and postmenopausal women with type 2 diabetes mellitus. World J Diabetes 2025; 16(11): 111366 [DOI: 10.4239/wjd.v16.i11.111366]
Corresponding Author of This Article
Meng-Yin Cai, PhD, Chief Physician, Department of Endocrinology and Metabolism, The Third Affiliated Hospital, Sun Yat-sen University, No. 600 Tianhe Road, Tianhe District, Guangzhou 510630, Guangdong Province, China. caimengyin@mail.sysu.edu.cn
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Endocrinology & Metabolism
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Retrospective Study
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Nov 15, 2025 (publication date) through Nov 14, 2025
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World Journal of Diabetes
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Shi Y, Zhang Y, Zhou AD, Zou HY, Wang MM, Xu F, Cai MY. Association between circulating sex hormone levels and diabetic kidney disease in men and postmenopausal women with type 2 diabetes mellitus. World J Diabetes 2025; 16(11): 111366 [DOI: 10.4239/wjd.v16.i11.111366]
Yi Shi, An-Dong Zhou, Hui-Yu Zou, Man-Man Wang, Fen Xu, Meng-Yin Cai, Department of Endocrinology and Metabolism, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Yao Zhang, Department of Endocrinology and Metabolism, The Third Affiliated Hospital of Sun Yat-sen University, Zhaoqing Hospital, Zhaoqing 510630, Guangdong Province, China
Co-corresponding authors: Fen Xu and Meng-Yin Cai.
Author contributions: Shi Y and Zhang Y contributed to the data analysis and interpretation, and manuscript drafting; they contributed equally to this manuscript and are co-first authors. Shi Y, Zhang Y, Zhou AD, and Zou HY contributed to the data collection; Shi Y, Zhang Y, and Wang MM contributed to the conception and design of the study; Xu F and Cai MY participated in the manuscript revision and editing; they contributed equally to this manuscript and are co-corresponding authors. All authors reviewed and approved the final version of the manuscript. Shi Y and Zhang Y contributed equally to this manuscript and are co-first authors. Xu F and Cai MY contributed equally to this manuscript and are co-corresponding authors.
Supported by the National Natural Science Foundation of China, No. 82270942.
Institutional review board statement: This study was approved by the Ethics Committee of the Third Affiliated Hospital of Sun Yat-sen University, No. II2024-056-01 Guangzhou, China.
Informed consent statement: Written informed consent was obtained from all participants prior to their involvement in the study.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: The raw data supporting the conclusions of this article will be made available by the authors without undue reservation.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Meng-Yin Cai, PhD, Chief Physician, Department of Endocrinology and Metabolism, The Third Affiliated Hospital, Sun Yat-sen University, No. 600 Tianhe Road, Tianhe District, Guangzhou 510630, Guangdong Province, China. caimengyin@mail.sysu.edu.cn
Received: July 7, 2025 Revised: August 22, 2025 Accepted: October 22, 2025 Published online: November 15, 2025 Processing time: 132 Days and 11.8 Hours
Abstract
BACKGROUND
Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease. The disease characteristics, morbidity, and renal function progression rate of patients with DKD are all related to sex. This suggests that sex hormones may play an important role in changing renal function in patients with diabetes. There have been only a few studies on the correlation between sex hormones and DKD, which have contradictory conclusions.
AIM
To investigate the relationship between circulating sex hormone levels and DKD in men and postmenopausal women with type 2 diabetes mellitus (T2DM).
METHODS
This retrospective cross-sectional study included 356 patients with T2DM. Pearson or Spearman rank correlation analyses assessed the relationships between sex hormone levels and renal function indices. By adjusting for age, body mass index, systolic blood pressure, diastolic blood pressure, duration of diabetes, use of sodium-glucose cotrasporter-2 inhibitor, use of glucagon-like peptide-1 receptor agonist, hypertension, use of angiotensin-converting enzyme inhibitor/ angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor, diabetic retinopathy, diabetic peripheral vascular disease, triglyceride, uric acid, and hemoglobin A1c, multiple linear regression and logistic regression analyses were conducted to identify factors influencing the urinary albumin/creatinine ratio (UACR) and DKD.
RESULTS
In men, dehydroepiandrosterone sulfate levels were inversely associated with log-transformed UACR after adjustment for covariate factors [regression coefficient (β) = -0.691, 95% confidence interval (CI): -1.241 to -0.141 for quartile 4 vs quartile 1; P = 0.006 for trend]. Elevated levels of estradiol were positively associated with DKD [odds ratio (OR) = 3.097, 95%CI: 1.083-8.856 for quartile 4 vs quartile 1; P = 0.041 for trend], and higher luteinizing hormone (LH) levels were similarly associated with DKD (OR = 4.164, 95%CI: 1.30-13.330 for quartile 4 vs quartile 1; P = 0.048 for trend). In postmenopausal women, LH levels were positively correlated with log-transformed UACR and DKD (β = 1.039, 95%CI: 0.284-1.794 for quartile 4 vs quartile 1; P = 0.006 for trend and OR = 15.117, 95%CI: 2.191-104.326 for quartile 4 vs quartile 1; P = 0.004 for trend). Follicle-stimulating hormone (FSH) levels were also positively associated with DKD (OR = 9.588, 95%CI: 1.680-54.709 for quartile 4 vs quartile 1; P = 0.014 for trend).
CONCLUSION
In men with T2DM, elevated levels of estradiol and LH levels were positively associated with increased risk of DKD. In postmenopausal women with T2DM, high FSH and LH levels were positively associated with increased risk of DKD.
Core Tip: This was a retrospective study that comprehensively analyzed the relationship between sex hormones and diabetic kidney disease (DKD) in men and postmenopausal women with type 2 diabetes mellitus. Few studies have focused on the association between gonadal hormones and DKD. In this study, we identified the relationship between gonadotropins and the risk of DKD for the first time and between overall sex hormone levels and DKD, providing a new perspective for the diagnosis and treatment of DKD.
Citation: Shi Y, Zhang Y, Zhou AD, Zou HY, Wang MM, Xu F, Cai MY. Association between circulating sex hormone levels and diabetic kidney disease in men and postmenopausal women with type 2 diabetes mellitus. World J Diabetes 2025; 16(11): 111366
Diabetic kidney disease (DKD) refers to chronic kidney disorders caused by diabetes mellitus (DM), defined by a reduction in glomerular filtration rate and increasing proteinuria[1]. DKD is a microvascular complication of type 2 DM (T2DM) and a primary contributor to chronic kidney disease (CKD). Reports indicate that 20%-40% of patients with T2DM are affected by DKD[2]. As the leading cause of end-stage renal disease, DKD imposes considerable suffering and financial burden on patients. In the United States, > 25% of healthcare expenditure is attributed to T2DM, with the majority directed toward managing diabetes-related complications, particularly DKD[3-5]. DKD heightens the risk of cardiovascular disease and mortality in individuals with T2DM, serving as an independent predictor of cardiovascular mortality[6,7].
Population-based surveys have shown that the prevalence of CKD is higher among women than men in most regions, with exceptions noted in Japan and Singapore[8,9]. By contrast, other studies have revealed that men with CKD experience a more rapid decline in kidney function than women[10]. Women generally have a longer life expectancy than men, and age and postmenopausal status appear to influence the relationship between sex and the progression of nondiabetic kidney disease. Neugarten et al[10] reported that kidney function deteriorated more rapidly in older postmenopausal women than in age-matched men. These contrasting findings suggest that sex hormones play a critical role in renal function progression.
Sex hormones, including testosterone, dehydroepiandrosterone sulfate (DHEAS), and estrogen, have been linked to insulin resistance and blood glucose regulation[11-14]. A cross-sectional study conducted in Poland found an inverse association between androgen levels and estimated renal function in apparently healthy young men[15]. However, one study reported a negative correlation between DHEAS and urinary albumin levels in men with T2DM[16]. In a study by Inada et al[17], the implantation of 17β-estradiol (E2) particles in transgenic diabetic male mice demonstrated that E2 therapy was effective in both the early and late stages of DKD. Estrogen can improve oxidative stress in the kidneys. Estrogen may inhibit renal cell apoptosis, inflammatory response, and fibrosis by promoting the expression of sirtuin 1[18]. However, contrasting conclusions have been observed in studies involving Cohen mice[19]. As an androgen, androstenedione is second only to testosterone in biological activity, although research on the association between androstenedione and renal function remains limited. With age, androgen and estrogen levels decline while gonadotropin levels increase; however, few studies have explored the relationship between gonadotropins and DKD in individuals with T2DM. One cross-sectional study found that elevated luteinizing hormone (LH) levels were associated with an increased risk of DKD in men and postmenopausal women with T2DM[20], yet the association between follicle-stimulating hormone (FSH) and DKD in men and postmenopausal women has not been investigated.
Given these findings, the relationship between sex hormones and renal function remains inconclusive, and limited research has addressed the association between gonadotropins and DKD. In postmenopausal women, the levels of sex hormones and gonadotropins no longer fluctuate with the menstrual cycle. Therefore, this retrospective cross-sectional study was conducted in Chinese men and postmenopausal women with T2DM to investigate the association between a comprehensive spectrum of sex hormones and renal function. This study focused on the roles of sex hormones and gonadotropins in patients with DKD, with the objective of identifying both risk and protective factors associated with DKD.
MATERIALS AND METHODS
Ethical approval
This study received approval from the Ethics Committee of the Third Affiliated Hospital of Sun Yat-sen University (Guangzhou, China). All participants provided written informed consent prior to enrollment.
Inclusion and exclusion criteria
This cross-sectional study was conducted in the Department of Endocrinology and Metabolism at the Third Affiliated Hospital of Sun Yat-sen University. A total of 356 hospitalized men and postmenopausal women with T2DM were enrolled between February 2023 and October 2023. The sample size of this study was calculated using PASS software. Eligible participants were required to be aged ≥ 18 years. Female participants needed to be postmenopausal, defined as either having a confirmed menopause status or aged ≥ 60 years, or aged ≥ 55 years with FSH ≥ 25 mIU/mL[21]. Exclusion criteria were: Acute diabetes complications, severe heart failure, severe liver disease, urinary tract infection, nondiabetic kidney disease, polycystic ovarian syndrome, pituitary or adrenal tumors, malignancies, or a history of sex hormone replacement therapy within the past 3 months. T2DM was defined according to World Health Organization criteria (1999)[22]. DKD was diagnosed based on a urinary albumin/creatinine ratio (UACR) > 30 mg/g or an estimated glomerular filtration rate (eGFR) < 60 mL/minute/1.73 m2, demonstrated by two measurements with at least a 3-month difference in the timing. At the same time, other causes of CKD should be excluded[1]. Figure 1 presents the flowchart of the study population selection.
Figure 1 Flowchart of the inclusion and exclusion of participants.
DKA: Diabetic ketoacidosis; DKD: Diabetic kidney disease; HHS: Hyperosmolar hyperglycemic syndrome.
Measurements
Data were extracted from electronic medical records, including information on age, sex, height, weight, body mass index (BMI), smoking and drinking status, blood pressure, diabetes duration, hypertension duration, medical history (antidiabetic and antihypertensive medications), triglyceride (TG), total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, uric acid (UA), fasting blood glucose, glycated hemoglobin, fasting C-peptide, and renal function parameters blood urea nitrogen (BUN), creatinine, eGFR, serum cystatin C (CysC), UACR, and 24-hour urinary albumin excretion rate (24hUAER). Additional chronic complications of T2DM were also documented.
Blood samples were collected between 06:00 and 09:00 hours after a minimum fasting period of 8 hours. Sex hormones, including total testosterone, DHEAS, androstenedione, E2, FSH, and LH, were measured via electrochemiluminescence immunoassay. Renal function parameters, including BUN, creatinine, serum CysC, UACR, and 24hUAER, were analyzed using an automated biochemical analyzer. BMI was calculated as weight divided by height squared (kg/m2), and eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration formula. UACR was calculated by dividing the urine microalbumin concentration (mg/L) by the urine creatinine concentration (mmol/L).
Statistical analyses
All statistical analyses were conducted using SPSS version 26.0 (IBM SPSS Software, Armonk, NY, United States). The K-S normality test was conducted on the continuous variables. Normally distributed continuous variables are presented as the mean ± SD, whereas non-normally distributed continuous variables are expressed as median (interquartile range), and categorical variables as frequency (%). Differences between groups for normally distributed variables were assessed using the t-test, whereas the Mann-Whitney U test was applied to non-normally distributed variables. Categorical variables were compared between groups using the χ2 test. Associations between sex hormone levels and renal function variables were examined using Pearson or Spearman correlation tests. Sex hormone levels were divided into four quartiles, with the first quartile indicating the lowest levels and the fourth quartile indicating the highest. Multiple linear regression analysis was used to calculate regression coefficients (β) and 95% confidence intervals (CIs) for log-transformed UACR across sex hormone quartiles. Multiple logistic regression analysis was conducted to calculate odds ratios (ORs) and 95%CIs for DKD across sex hormone quartiles. All statistical tests were two-sided, with P < 0.05 considered statistically significant.
RESULTS
Clinical characteristics of participants by sex and DKD
The clinical characteristics of the study population are presented in Table 1. The 359 participants were stratified by sex and the presence of DKD. Among men with DKD, levels of TG, UA, and fasting C-peptide, prevalence of hypertension and diabetic retinopathy, and use of angiotensin-converting enzyme inhibitor/angiotensin receptor blocker/ angiotensin receptor-neprilysin inhibitor were higher compared to men without DKD. Men with DKD were also shorter in height. Additionally, elevated levels of E2 and LH were observed in men with DKD. As expected, men with DKD exhibited higher levels of urea nitrogen, creatinine, CysC, UACR, and 24hUAER, along with reduced eGFR. In women with DKD, the mean age, diabetes duration, and prevalence of hypertension, diabetic retinopathy, and peripheral vascular disease were greater than in women without DKD. Women with DKD also exhibited elevated levels of LH and FSH. These participants displayed increased BUN, creatinine, CysC, UACR, and 24hUAER, and lower eGFR values.
Table 1 Clinical characteristics of patients classified by renal function and sex, n (%).
Association of sex hormone levels with renal function indices
Tables 2 and 3 present the correlations between sex hormone levels and renal function indices. Spearman analysis was applied. In men, DHEAS was negatively correlated with BUN and CysC and positively correlated with eGFR. E2 was positively correlated with CysC, UACR, and 24hUAER. FSH was positively correlated with BUN, creatinine, CysC, UACR, and 24hUAER, while demonstrating a negative correlation with eGFR. LH showed positive correlations with BUN and CysC and a negative correlation with eGFR. In women, E2 exhibited a negative correlation with eGFR and positive correlations with creatinine and CysC. FSH demonstrated positive correlations with BUN, creatinine, CysC, UACR, and 24hUAER, and negative correlations with eGFR. The correlation pattern of LH with renal function indices was similar to that of FSH.
Table 2 Correlation between sex hormones and renal function indexes in men with type 2 diabetes mellitus.
The results of regression analyses are shown in Tables 4 and 5. UACR shows a significantly skewed distribution; therefore, converting UACR to log-transformed UACR (lnUACR) tends to a normal distribution, making the results of regression analysis more reliable. In the regression model, the selection of covariate factors was based on the factors that may be related to renal function as defined by previous studies and clinical experience. The variables significantly related to renal function that were preliminarily screened through univariate analysis were included in the model for adjustment. In men, after adjusting for age, BMI, systolic and diastolic blood pressure, diabetes duration, TG, UA, glycated hemoglobin, use of sodium-glucose cotrasporter-2 inhibitor, glucagon-like peptide-1 receptor agonist, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor, diabetic peripheral vascular disease, diabetic retinopathy, and risk of DKD increased with higher E2 levels. The fully adjusted OR (95%CI) for DKD in the highest quartile (quartile 4) vs the lowest quartile (quartile 1) of E2 was 3.097 (1.083-8.856; P = 0.041 for trend). Additionally, each SD increment in E2 was associated with a 52.7% increased risk of DKD (OR = 1.527, 95%CI: 1.077-2.165). Elevated LH levels were also significantly associated with an increased risk of DKD (OR = 4.164, 95%CI: 1.30-13.330 for quartile 4 vs quartile 1; P = 0.048 for trend). However, when analyzed as a continuous variable, the association between LH and DKD was not significant (OR = 1.175, 95%CI: 0.819-1.687). DHEAS levels were inversely associated with lnUACR after adjustment for covariate factors (regression coefficient [β], -0.691, 95%CI: -1.241 to -0.141 for quartile 4 vs quartile 1; P = 0.006 for trend).
Table 4 Association of sex hormone level quartiles with diabetic kidney disease in men.
In women with T2DM, elevated FSH levels were associated with a heightened risk of DKD (OR = 9.588, 95%CI: 1.680-54.709 for quartile 4 vs quartile 1; P = 0.014 for trend). This association remained significant when FSH was analyzed as a continuous variable (OR = 2.590, 95%CI: 1.320-5.083). Likewise, increased LH levels were correlated with a higher risk of DKD (OR = 15.117, 95%CI: 2.191-104.326 for quartile 4 vs quartile 1; P = 0.004 for trend), and this association persisted when LH was examined as a continuous variable (OR = 4.213, 95%CI: 1.808-9.816). Additionally, LH levels were positively correlated with lnUACR (β = 1.039, 95%CI: 0.284-1.794 for quartile 4 vs quartile 1; P = 0.006 for trend and OR 15.117, 95%CI: 2.191-104.326 for quartile 4 vs quartile 1; P = 0.004 for trend).
DISCUSSION
Research on the association between gonadal hormones and DKD is limited. This study analyzed, for the first time, the relationship between gonadotropins and DKD risk, as well as the broader associations between sex hormone profiles and DKD. Elevated serum E2 and LH levels were independently associated with increased DKD risk after adjusting for traditional risk factors in men with T2DM. Similarly, elevated serum FSH and LH levels were independently associated with an increased DKD risk in postmenopausal women with T2DM. This study also identified a negative association between DHEAS and UACR in men with T2DM, suggesting that DHEAS has protective effects on renal function in T2DM. Consistent with this finding, Fukui et al[16] reported that DHEAS concentration was inversely correlated with urinary albumin excretion (UAE) in 357 men with T2DM. In their follow-up study of 207 men with T2DM, low serum DHEAS concentration predicted a worsening of UAE over 1 year[23]. Prior studies on the role of DHEAS in CKD have shown that low DHEAS levels may increase mortality in patients undergoing hemodialysis[24,25]. Additionally, low-dose DHEA supplementation has been reported to improve insulin sensitivity, lower blood glucose levels, and reduce abdominal obesity[11]. A cross-sectional study in 2022 also reported a negative association between serum DHEA and DKD in men with T2DM[26]. Animal studies have supported the beneficial effects of DHEA on metabolism and kidney health, as DHEA treatment in elderly female rats was shown to alter fatty acid composition in serum and adipose tissue, reduce body weight and obesity, and improve insulin sensitivity[27]. In hyperglycemic rats, DHEA treatment was found to prevent oxidative kidney damage[28].
Diabetes is known to disrupt sex hormone balance, typically resulting in decreased testosterone and elevated E2 levels, thereby accelerating the progression of kidney disease[29]. Studies have shown that low testosterone levels are linked to an increased risk of DKD[30] and that kidney injury in men correlates with elevated E2 levels. Yi et al[31] reported that higher E2 levels were associated with lower eGFR in patients with CKD. Maric et al[32] found that elevated E2 levels were significant predictors of progression from proteinuria to end-stage renal disease in men with type 1 diabetes. We observed that the level of testosterone decreased and the level of E2 increased in men with DKD. Elevated E2 levels occurred in patients with DKD, which makes it difficult to define the causal relationship between the two in cross-sectional studies. The early pathological change of diabetic nephropathy is the mesangial dilation and thickening of the glomerular basement membrane. Some studies have suggested protective effects of E2 on the kidneys, as E2 has been shown to safeguard mesangial cells and podocytes, reduce oxidative stress in renal tissue, and enhance renal perfusion[33,34]. However, Rosenmann et al[19] reported that E2 had no effect on proteinuria in OLEFT rats, whereas Tomiyoshi et al[35] found that E2 worsened kidney disease in diabetic rats fed a sucrose-rich diet. These contradictory findings suggest that the effects of E2 on renal health depend on the disease model, timing, and dose of E2 intervention. E2 replacement therapy can increase the secretion of growth hormone (GH)[36]. Studies have shown that GH may cause glomerular sclerosis[37]. E2 may affect renal function by influencing the levels of GH. In some cases, the impact of E2 on glomerular sclerosis may be greater than its protective effect on the kidneys. The condition for this balance may require more research.
The prevalence of CKD rises significantly, and renal function deteriorates more rapidly in postmenopausal than in premenopausal women[38,39]. This phenomenon cannot be attributed solely to a decline in E2 levels, as the decrease in E2 during menopause is accompanied by increased levels of FSH and LH. These elevated FSH and LH levels may contribute to impaired kidney function when postmenopausal women lose the protective effect of estrogen on the kidneys. Zhang et al[40] identified functional FSH receptors in renal tubular epithelial cells and found that FSH may promote renal tubulointerstitial fibrosis. Additionally, a 2021 observational cross-sectional study suggested that elevated circulating FSH levels could be a potential risk factor for renal dysfunction in postmenopausal women[41]. In our study, we observed, for the first time, that high FSH levels were associated with DKD in postmenopausal women with T2DM.
LH, another gonadotropin, was also associated with an increased risk of DKD in both men and postmenopausal women with T2DM. A cross-sectional study by Zhou et al[20] similarly found that elevated circulating LH levels were associated with diabetic macroalbuminuria in Chinese men and postmenopausal women. This study identified that elevated LH levels, by upregulating vascular endothelial growth factor expression in the kidneys[42], lead to progressive proteinuria, abnormal renal hemodynamics, glomerular hypertrophy, and even fibrosis. Recently, Muthusamy et al[43] demonstrated a linear relationship between LH levels and vascular endothelial growth factor expression in the kidneys of cattle and pigs, and sex hormones may regulate renal function through transforming growth factor-β[44], further supporting these findings. Many studies have proved that LH is associated with insulin resistance in patients with polycystic ovarian syndrome[45,46]. A study from Sweden indicated that diabetic patients with the most obvious insulin resistance have a significantly higher risk of developing diabetic nephropathy than other diabetic patients[13]. LH may increase the risk of diabetic nephropathy in patients with diabetes by enhancing insulin resistance, which requires more research to confirm. This study included more comprehensive indicators of renal function and sex hormones compared with previous studies. Moreover, previous studies have rarely explored the relationship between gonadotropins and DKD in patients with T2DM. The results of this study provide more evidence to support this.
This study had some limitations. First, while our findings suggest an association between sex hormone levels and DKD, they do not establish causation; further research is needed to clarify the underlying mechanisms. Prospective studies and clinical trials are needed to further reveal the causal relationship. For instance, the probability of diabetic patients with different gonadal functions developing DKD in the future can be further explored. The changes in renal function of diabetic patients after sex hormone replacement therapy can also be explored. Second, the sample size was small and geographically confined, which may limit the generalization of the results to other regions in China. Third, this study included multiple sex hormones and renal function indicators, and these sex hormones are associated in the process of synthesis, effect, and metabolism; therefore, these associations between the sex hormones may have an impact on the results. It may be necessary to further explore the impact of the ratio between hormones on the renal function of diabetic patients in the future. Severe renal insufficiency may affect the level of sex hormones. In this study, the prevalence of DKD in men and postmenopausal women with T2DM was 29.1% and 31.8%, respectively. The number of postmenopausal women with DKD was small. Therefore, more samples may need to be included in the future to conduct a sensitivity analysis of the relationship between sex hormones and DKD to eliminate the influence of severe renal insufficiency on the results.
CONCLUSION
In men with T2DM, elevated E2 and LH levels were associated with an increased risk of DKD. In postmenopausal women with T2DM, elevated FSH and LH levels were similarly associated with an increased risk of DKD. Our discovery may provide a new perspective for the diagnosis and treatment of DKD.
ACKNOWLEDGEMENTS
We extend our gratitude to all participants from the Department of Endocrinology and Metabolism, Third Affiliated Hospital of Sun Yat-sen University.
Footnotes
Provenance and peer review: Unsolicited article; Externally peer reviewed.
Peer-review model: Single blind
Specialty type: Endocrinology and metabolism
Country of origin: China
Peer-review report’s classification
Scientific Quality: Grade B, Grade C, Grade C
Novelty: Grade A, Grade B
Creativity or Innovation: Grade B, Grade B
Scientific Significance: Grade B, Grade B
P-Reviewer: Horowitz M, MD, PhD, Professor, Australia; Moreno-Gómez-Toledano R, PhD, Assistant Professor, Spain; Yu MK, PhD, China S-Editor: Bai SR L-Editor: Filipodia P-Editor: Zhao YQ
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