Prevalence and Drivers of Erectile Dysfunction in CKD

Introduction

Chronic kidney disease (CKD) is characterized by a sustained, progressive loss of renal function arising from diverse etiologies. Globally, its prevalence is estimated at approximately 13.4% (95% CI: 11.7-15.1%), with the number of individuals reaching ESKD ranging between 4.9 and 7.1 million worldwide.¹ In India, CKD affects an estimated 17.2% of the population, distributed across stages I through V at rates of 7.0%, 4.3%, 4.3%, 0.8%, and 0.8%, respectively.²

Sexual dysfunction is a common complication among males with CKD,³ encompassing a range of disorders including erectile dysfunction (ED), ejaculatory and orgasmic disturbances, and diminished sexual desire. ED, defined as the persistent inability to attain or maintain an erection sufficient for satisfactory sexual performance, may result from psychological, neurological, hormonal, vascular or cavernosal factors.⁴ Although often perceived as an age-related issue affecting about 20% of males over 40, it can occur at any age, particularly in the presence of comorbidities such as, diabetes, metabolic syndrome, or cardiovascular disease.

The impact of sexual dysfunction on quality of life is profound, undermining self-image, confidence, and overall well-being.⁵ Despite its prevalence, <1/5 affected individuals seek medical evaluation,⁶ and clinicians frequently prioritize other health concerns, compounded by limited experience in managing male sexual health. Thus, systematic recognition and appropriate management of these disorders are critical to enhancing patient-reported outcomes.

There are few studies on sexual dysfunction among Indian patients with CKD. In this study, we evaluated the prevalence of ED and identified its predictors in a cohort of Indian non-dialysis CKD patients.

Materials and Methods

This study is a cross-sectional, observational, real-world analysis conducted at the nephrology and Urology Department of AIIMS, Patna, from January to June 2025. The study was conducted in accordance with the Declaration of Helsinki and received approval from the Institutional Ethics Committee (AIIMS/Pat/IEC/1361). Consecutive patients with CKD were screened and enrolled as per the following inclusion and exclusion criteria. Inclusion criteria: Male patients aged between 25 and 50 years; confirmed CKD diagnosis as per KDIGO criteria; and willing to give signed informed consent. Exclusion criteria absence of sexual activity, urogenital cancer, severe conditions like heart failure, diagnosed psychiatric disorders, use of psychiatric medication, incomplete questionnaire data, and congenital urogenital disorders. Data on demographics (age, height, weight, body mass index (BMI), smoking and drinking status, marital status), clinical diagnosis, main symptoms, and treatments were collected via interviews and medical records. Blood investigations include serum creatinine (Scr), estimated glomerular filtration rate (eGFR), urea nitrogen (BUN), urinary albumin-to-creatinine ratio (ACR), and uric acid levels (UA). The eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. The recruitment flowchart has been shown in Figure 1.

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Figure 1:

Flowchart of patient recruitment. CKD: Chronic kidney disease, UTI: Urinary tract infection.

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The sexual dysfunction was evaluated by a questionnaire called the 5-item version of the International Index of Erectile Function (IIEF-5) in Hindi. A certified translator translated the version used and was independently assessed by four urologists and four hospital staff (non-medical) who were fluent in both Hindi and English. A consensus was then made, and the unanimously agreed version was used in the study. IIEF-5 consists of five items focusing on erectile function and the degree of satisfaction in sexual intercourse. Scores from 25-30 were considered normal (without ED), while scores between 1-24 indicated ED carriers. The ED was classified according to the score, from 19-24 (mild ED), 13-18 (mild to moderate), 7-12 (moderate), and 1-6 (severe).

Statistical analysis: Continuous variables (age, height, weight, BMI, serum creatinine, eGFR, BUN, ACR, uric acid, lipid levels, and IIEF-5 scores) were expressed as mean ± standard deviation (SD), while categorical variables (CKD stage, sex, marital status, smoking, alcohol use, hypertension, diabetes) were expressed as counts and percentages. Group comparisons across CKD stages (mild: stages I-II, moderate: stages IIIa-IIIb, severe: stages IV-V) were performed using one-way ANOVA or Kruskal-Wallis H test for continuous variables and Chi-square test for categorical variables.

Spearman correlation analysis assessed associations between IIEF-5 scores and continuous laboratory parameters and age, while categorical comorbidities were analyzed using point-biserial correlations. Variables showing p < 0.02 in univariate analysis were included in multivariable linear regression using a stepwise approach to identify independent predictors of IIEF-5 scores. Multicollinearity was assessed via the variance inflation factor (VIF ≤ 1.25) and tolerance (≥ 0.82). A two-sided p < 0.05 was considered statistically significant. All analyses were performed using SPSS version 26.0 (IBM Corp, Armonk, NY, USA).

Results

A total of 135 consecutive male non-dialysis CKD patients were screened, and 100 were enrolled as per the eligibility criteria [Figure 1]. The mean age of the participants was 38.5 ± 7.2 years. The clinical and laboratory characteristics of the study participants are shown in Table 1. Across the cohort, the leading causes of CKD were diabetic kidney disease (16%), obstructive uropathy (17%), hypertensive nephrosclerosis (9%), and chronic glomerulonephritis (7%), while the etiology was unknown in 51% of patients. Etiologic distribution remained consistent across CKD stages: stages I-II (n=45), stage III (n=30), and stages IV-V (n=25) showed a predominance of unknown causes (∼50%) followed by diabetic kidney disease and obstructive uropathy (∼15-20% each).

Prevalence of ED in various CKD groups [Figure 2], the severity of ED increased as the CKD stages advanced. In mild and moderate CKD groups, i.e., stages I, II, and III, mild ED was the commonest category of ED. In mild CKD, none of the patients has severe ED. In the severe CKD group, i.e., stage IV and V, the commonest category of ED was severe ED.

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Figure 2:

Distribution of ED score by IIEF-5 tool across CKD stages in the Indian population. IIEF: International index of erectile function.

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Spearman correlation analysis showed the strongest positive correlation of albumin with IIEF-5 scores (r = 0.51, p< 0.001), followed by eGFR (r= 0.32, p= 0.022). In contrast, Scr (r= –0.28, p= 0.006), ACR (r= –0.31, p= 0.004), and BuN (r= –0.26, p= 0.019) exhibited negative correlations. Age (r= –0.24, p= 0.011), hypertension (r= –0.18, p = 0.048), and diabetes (r= –0.25, p= 0.007) also correlated inversely with erectile function. Uric acid (UA), lipid profiles, and marital status showed no significant correlations.

Simple linear regression was performed to assess the association between IIEF-5 scores and various demographic, clinical, and biochemical variables [Table 2]. Among renal parameters, higher serum creatinine (p = 0.006), lower eGFR (p = 0.022), elevated urine albumin-to-creatinine ratio (ACR; p = 0.004), and increased blood urea nitrogen (BUN; p = 0.019) were significantly associated with lower IIEF-5 scores, indicating more severe ED. Serum albumin emerged as the most potent associated factor (p < 0.001), followed by age (p = 0.011) and comorbidities such as hypertension (p = 0.048) and diabetes (p = 0.007). No significant associations were observed for BMI, smoking, lipid levels, or marital status (p > 0.05).

Multivariate linear regression identified predictors of IIEF-5 scores [Table 3]. Model 3 showed the best fit (R² = 0.51). Serum albumin was the strongest predictor, with a 1 g/dL rise increasing IIEF-5 by ∼3.2 points and accounting for ∼40% of the variation. Adding ACR, a marker of proteinuria, improved predictive power to ∼49%, showing independent contributions of nutritional status and kidney damage. Age also remained significant, though less impactful after adjusting for albumin and ACR. The final model explained ∼51% of score variability. Statistical checks (tolerance ≥ 0.82, VIF ≤ 1.25) confirmed minimal multicollinearity and stable coefficients.

Discussion

In our study of non-dialysis Indian male CKD patients, we found a high prevalence of ED of 55%, with increasing severity as CKD stage advances. Mild ED was most common in early CKD (stages I-III), whereas severe ED predominated in advanced CKD (stages IV-V). Among the factors analyzed, serum albumin emerged as the strongest predictor of ED, followed by age and proteinuria (ACR), highlighting the importance of nutritional-inflammation status in erectile function.

Global estimated prevalence of ED in CKD patients is variable with ranging from 20 to 80%.⁷ Our study found an ED prevalence of 55% among non-dialysis Indian CKD males. A systematic review reported a prevalence of ED to be about 76% but acknowledged enormous heterogeneity in published literature. Most of the studies report that sexual dysfunction, including ED, worsens with worsening stages of CKD, but there are a few studies that have reported conflicting results.^8,9 Reported ED prevalence in CKD varies mainly because studies differ in the mix of disease stages included, the instruments and cut-offs used to define ED, like IIEF-15, IIEF-5, self-reporting by patients, or non-validated scoring systems, sample size, enrollment criteria, and differences in patient characteristics such as age, comorbidity profiles, and cultural factors affecting symptom reporting.

ED in CKD is common, and several mechanisms have been proposed in the literature. CKD is associated with several hormonal imbalances and vascular abnormalities^10,11 which predispose patients to many reproductive problems, including ED. Uremic toxins such as indoxyl sulfate and asymmetric dimethylarginine elevate oxidative stress, inhibit endothelial nitric oxide synthase, and impair penile vasodilation.¹² Persistent systemic inflammation and protein-energy malnutrition further damage the vascular endothelium and cavernosal smooth muscle, reducing corpora cavernosa compliance.¹³ Endocrine dysregulation with hypogonadism and hyperprolactinemia disrupts hormonal support essential for libido and erectile physiology.¹⁴ Drugs (α-adrenergics, β-blockers), micronutrient deficiencies, and comorbidities, such as depression and diabetes, may also contribute. CKD-associated autonomic neuropathy impairs neurogenic reflexes required for erection, compounding vascular and hormonal deficits. The predominant cause varies among individuals. Indian CKD patients present younger (mean age ∼50 ± 14 years) than those in high-income countries (60-65 years).¹⁵ Our cohort had more early CKD and fewer diabetics (16%), likely influencing ED prevalence and severity. Smaller penile arteries (1-2 mm) develop atherosclerosis earlier than coronary arteries, making ED an early marker of systemic vascular disease. ED independently predicts cardiovascular events and mortality more accurately than traditional risk factors, nearly doubling future cardiovascular risk even after adjustment.^16,17 Thus, understanding ED in CKD is crucial for quality of life and cardiovascular outcomes. ED remains an important yet neglected issue in Indian CKD patients due to social inhibitions, and ours is the first study documenting its magnitude using a validated questionnaire.^18,19

In our study, serum albumin was found to be the strongest predictor of ED, underscoring its critical role as a marker of the malnutrition-inflammation complex (MICS) in CKD. Low albumin reflects both poor nutritional status and chronic systemic inflammation, which synergistically impair vascular endothelial function. In CKD, inflammation promotes oxidative stress, increases pro-inflammatory cytokines such as IL-6, and triggers endothelial damage, reducing nitric oxide bioavailability and impairing penile arterial dilation. Simultaneously, protein-energy malnutrition weakens smooth muscle function in the corpora cavernosa, further compromising erectile physiology. Together, these mechanisms explain why hypoalbuminemia is closely linked to more severe ED, making it not only a valuable risk marker but also a potentially modifiable target for intervention through nutritional optimization and anti-inflammatory strategies. Prior studies have reported serum albumin as an important association of ED both in otherwise healthy adults²⁰ and CKD.^21,22 This underscores albumin’s role as a proxy for nutritional-inflammation status, impairing vascular endothelial function, increasing inflammation, e.g., elevation in interleukin 6 levels that promote oxidative stress, thus damaging cavernosal arteries. ACR and age also amplify ED risk, but are less actionable. Proteinuria induces endothelial dysfunction via angiotensin II overexpression, reducing penile blood flow. With many newer drugs such as ‘flozins’ and non-steroidal mineralocorticoid receptor antagonists like empaglifozin and finerenone, respectively, that reduce proteinuria in CKD, it may be worth examining their effects on ED in CKD. Targeted interventions like albumin optimization by early and prompt diagnosis of malnutrition, protein supplementation, and anti-inflammatory agents or immune-modulatory agents (e.g., Sodium-Glucose Cotransporter 2 [SGLT2] inhibitors) are likely to make a significant impact in lowering the burden of ED in CKD.²³ Randomized trials in CKD have shown sildenafil to improve IIEF-5 scores by 4–6 points versus placebo, with good tolerability across stages G3–G5. The KDIGO 2024 heatmap visualizes CKD progression risk by eGFR and albuminuria, and could be adapted to flag patients at high risk for ED who might benefit from early PDE5-inhibitor referral.²⁴

Our study has a few limitations, such as a relatively smaller sample size, unequal distribution of all CKD stages, exclusion of patients with diagnosed heart disease, a lack of validation of the questionnaire in the local language, one-time assessment data, and a lack of data regarding subclinical or undiagnosed depression. Despite these limitations, our study represents the first step towards addressing sexual health-related problems in Indian CKD patients.

To conclude, this study documents the magnitude of the problem of ED in Indian CKD patients and confirms hypoalbuminemia as the strongest modifiable predictor of ED in CKD. An integrated care model for ED in CKD should combine early screening with validated tools, nutritional support to correct hypoalbuminemia, and proteinuria management using Angiotensin II Receptor Blockers (ARBs) and Angiotensin-Converting Enzyme (ACE) inhibitors, or SGLT2 inhibitors. Future research should validate albumin as a marker of early ED and explore SGLT2 inhibitors and nsMRAs for dual kidney/sexual function protection.