Andrology · KIMS Secunderabad
Male Infertility — Causes, Diagnosis, and Treatment Options at KIMS Secunderabad
Infertility affects approximately 15% of couples attempting to conceive, and in 40 to 50% of these couples, a male factor is involved — either as the sole cause or as a contributing factor alongside female causes. Despite this, male infertility receives disproportionately little attention in India. Fertility investigations frequently begin and end with the woman, sometimes for years, before the man is assessed. The reality is straightforward: a semen analysis is the simplest, cheapest, and most informative test in the fertility workup — and it should be done at the very start of any fertility investigation, not as an afterthought.
At KIMS Secunderabad, male infertility is evaluated and managed by the andrology team with the full range of diagnostic and surgical tools — semen analysis and morphology assessment, hormonal profiling, scrotal ultrasound, diagnostic and surgical sperm retrieval (PESA, TESA, microTESE), and surgical correction of varicocele by laparoscopic ligation. Many couples who have spent years pursuing IVF with poor outcomes do so with an undiagnosed or under-treated male factor that, if corrected, would significantly improve the chances of natural conception or reduce the IVF stimulation required.
What male infertility means — the basics
Fertility in the male requires the production of normal sperm in sufficient numbers (sperm count), the ability of those sperm to move effectively toward the egg (motility), and sperm with the correct shape to penetrate the egg (morphology). It also requires the effective transport of sperm through the reproductive tract — from the testes through the epididymis, vas deferens, and urethra — and normal ejaculatory function. A problem at any point in this sequence can cause infertility.
The semen analysis — performed on a sample collected after 2 to 5 days of abstinence — is the primary diagnostic test. The World Health Organisation (WHO 2021) reference values define the lower reference limits for normal semen: sperm concentration above 16 million per millilitre, total motility (progressive + non-progressive) above 42%, progressive motility above 30%, and normal morphology (Kruger strict criteria) above 4%. Results below any of these thresholds indicate a potential male factor requiring further evaluation.
Causes of male infertility
Male infertility is grouped into clinical categories based on the underlying mechanism — from correctable structural problems like varicocele, through obstructive and non-obstructive azoospermia, to hormonal and genetic causes. Identifying the correct category is the foundation of a successful treatment plan.
Varicocele — the most common correctable cause
A varicocele is an abnormal dilation of the pampiniform venous plexus — the network of veins that drains the testicle. It is found in approximately 15% of all men and in 35 to 40% of men presenting with primary infertility. Varicoceles impair sperm production and function through multiple mechanisms: the dilated veins increase scrotal temperature (sperm production requires a temperature 2 to 3°C below body temperature), cause venous reflux delivering adrenal metabolites to the testes, and reduce testicular blood flow and oxygenation. The left varicocele is more common (90%) because the left testicular vein drains into the left renal vein at a right angle — increasing the resistance to venous drainage. Varicocele repair by laparoscopic ligation at KIMS interrupts the dilated venous channels while preserving the testicular artery and lymphatics. Multiple meta-analyses demonstrate that varicocele repair in men with clinical varicocele and abnormal semen analysis results in significant improvement in sperm concentration and motility, and is associated with spontaneous pregnancy rates of 30 to 40% within 12 months. For men undergoing IVF or ICSI, varicocele repair before assisted reproduction improves outcomes by improving sperm quality.
Azoospermia — no sperm in the ejaculate
Azoospermia — complete absence of sperm in the ejaculate — affects 1% of all men and 10 to 15% of infertile men. It is categorised as obstructive or non-obstructive: Obstructive azoospermia (OA). Sperm are produced normally in the testes but cannot reach the ejaculate due to a blockage — in the epididymis (post-infectious, post-vasectomy, congenital absence of the vas deferens in CFTR carriers), the vas deferens, or the ejaculatory ducts. The testes are normal size and FSH is normal. Sperm can be retrieved surgically (PESA or TESE) and used for ICSI. Surgical reconstruction of the obstruction (vasoepididymostomy, vasovasostomy for vasectomy reversal) may restore natural fertility. Non-obstructive azoospermia (NOA). Sperm production is severely impaired — due to Klinefelter syndrome (47,XXY), Y chromosome microdeletions, cryptorchidism, prior chemotherapy or radiation, or idiopathic testicular failure. FSH is elevated, testes may be small. Sperm are not present in the epididymis or vas deferens. microTESE (microsurgical testicular sperm extraction) — performed under the operating microscope to identify and extract the rare sperm-producing tubules within the testis — achieves sperm retrieval in 40 to 60% of selected cases. Retrieved sperm are used for ICSI.
Oligospermia and asthenospermia
Oligospermia (low sperm count — below 16 million/ml), asthenospermia (poor motility), and teratospermia (abnormal morphology) are the most common semen analysis findings in infertile men. These may occur individually or in combination (oligoasthenoteratospermia — OAT syndrome). Causes include: varicocele (the most important correctable cause), hormonal imbalance (low testosterone, elevated FSH/LH, hyperprolactinaemia), lifestyle factors (obesity, smoking, alcohol, excessive heat exposure, anabolic steroid use — which suppresses the HPG axis and stops sperm production), and idiopathic causes where no specific aetiology is identified despite full investigation.
Hormonal causes
The hypothalamic-pituitary-gonadal (HPG) axis regulates sperm production. FSH stimulates Sertoli cells to support sperm development; LH stimulates Leydig cells to produce testosterone, which is essential within the testis for spermatogenesis. Hypogonadotropic hypogonadism — low FSH and LH with low testosterone, from pituitary tumour, hyperprolactinaemia, or Kallmann syndrome — causes azoospermia or severe oligospermia that is highly responsive to hormonal treatment (gonadotropin injections — FSH + hCG). This is one of the most treatable causes of male infertility and is identified by a simple blood test.
Genetic causes
Y chromosome microdeletions in the AZF (azoospermia factor) region are found in 5 to 15% of men with severe oligospermia or azoospermia. AZFc deletions retain some residual sperm production (sperm may be retrieved by TESE). AZFa and AZFb deletions are associated with complete Sertoli-cell-only syndrome — no sperm are produced and microTESE will not find any. Klinefelter syndrome (47,XXY) — affecting 1 in 660 male births — causes hypergonadotropic hypogonadism and azoospermia, but sperm can be retrieved by microTESE in approximately 50% of cases. Genetic testing (Y microdeletion panel, karyotype) is part of the KIMS male infertility workup for severe oligospermia and azoospermia.
The investigation pathway at KIMS
The KIMS andrology workup for male infertility is structured to identify both correctable causes and conditions requiring assisted reproduction — in the right order, without sending the patient through unnecessary or repeated investigations.
Semen analysis
Two samples on separate occasions (2 to 5 days abstinence each). WHO 2021 reference values. Strict Kruger morphology. Performed at KIMS NABL-accredited laboratory.
Hormonal profile
Fasting morning FSH, LH, testosterone, prolactin, oestradiol. Identifies hypogonadotropic and hypergonadotropic hypogonadism. Distinguishes pre-testicular (hormonal) from testicular and post-testicular causes.
Scrotal Doppler ultrasound
Identifies varicocele (grade 1–3), testicular volume, epididymal pathology, and any testicular masses. Performed at KIMS.
Genetic testing
Y chromosome microdeletion analysis and karyotype (47,XXY) for severe oligospermia (below 5 million/ml) or azoospermia.
Sperm DNA fragmentation
DFI (DNA fragmentation index) above 25% is associated with reduced fertilisation rates and early pregnancy loss, even with IVF/ICSI. Available at KIMS.
Testicular biopsy / sperm retrieval (PESA, TESA, microTESE)
For azoospermia, to determine whether sperm production is occurring and to retrieve sperm for ICSI.
Treatment options at KIMS
Each cause of male infertility has a specific intervention at KIMS. The cards below pair each underlying cause with its standard treatment — from day-care procedures and hormonal therapy to microsurgical sperm retrieval for azoospermia.
Varicocele
Laparoscopic varicocelectomy — interrupts dilated veins, preserves testicular artery and lymphatics. Day-care procedure. Sperm improvement expected at 3 months.
Hypogonadotropic hypogonadism
Gonadotropin injections (hCG + FSH) — stimulates testosterone production and spermatogenesis. Monthly injections. Response assessed at 6 months.
Elevated prolactin
Dopamine agonist (cabergoline or bromocriptine) — reduces prolactin, restores FSH/LH and testosterone.
Obstructive azoospermia
Surgical sperm retrieval (PESA — percutaneous epididymal sperm aspiration) or TESE. Sperm frozen for ICSI. Reconstruction (vasoepididymostomy) where feasible.
Non-obstructive azoospermia
microTESE (microsurgical testicular sperm extraction) — operating microscope identification of sperm-producing tubules. 40–60% sperm retrieval success. Sperm frozen for ICSI.
Lifestyle-related poor sperm quality
Weight loss, smoking cessation, alcohol reduction, heat avoidance, stopping anabolic steroids. Re-assess semen analysis at 3 months (one full spermatogenesis cycle).
Antisperm antibodies
Corticosteroid therapy or IUI/ICSI depending on titre.
Idiopathic oligospermia
Empirical antioxidant therapy (Co-Q10, vitamin E, selenium, carnitine) — evidence moderate. Referral for IUI or ICSI after 12 months without improvement.
All consultations at KIMS are confidential. The andrology team approaches male infertility in a clinical, non-judgmental manner — it is a medical condition with specific causes and specific treatments. Call 040-4488-5000 to book a confidential consultation.
Book a Male Infertility Consultation at KIMS
Frequently Asked Questions — Male Infertility
The World Health Organisation (WHO 2021) lower reference limit for sperm concentration is 16 million sperm per millilitre, with a total sperm count of 39 million per ejaculate. Total motility should be above 42% and progressive motility above 30%. Normal morphology (Kruger strict criteria) should be above 4%. These are lower reference limits, not optimal values — many men with counts above these thresholds still have fertility problems from other factors, and some men with counts below these thresholds father children naturally. The semen analysis must be interpreted in the clinical context and repeated before concluding that a problem exists.
Yes — in many cases. Obstructive azoospermia (where sperm are produced but blocked) is managed by surgical sperm retrieval (PESA or TESE) and ICSI. Non-obstructive azoospermia (where sperm production is impaired) is managed by microTESE — microsurgical extraction of sperm from the testes — which finds usable sperm in 40 to 60% of selected cases. Even men with Klinefelter syndrome (47,XXY) — a chromosomal cause of azoospermia — can father biological children through microTESE and ICSI in approximately 50% of cases. Azoospermia is not the same as permanent sterility. The evaluation and management should be completed before concluding that biological fatherhood is impossible.
No — most men with a varicocele (approximately 85%) are fertile. A varicocele is associated with male infertility, not synonymous with it. Varicocele repair is indicated when: a clinical varicocele is present (palpable or detectable on Doppler ultrasound), semen analysis shows abnormal results (low count, poor motility, or abnormal morphology), and there is no female factor that would prevent natural conception regardless of male semen quality. In the absence of abnormal semen analysis, varicocele repair does not improve fertility outcomes and is not recommended for fertility purposes.
Spermatogenesis — the full cycle of sperm production from stem cell to mature sperm — takes approximately 72 to 74 days. After varicocele repair, sperm parameters typically begin improving at 3 months and continue to improve for up to 12 months. The maximum benefit from varicocele repair on semen analysis is usually seen at 6 to 9 months. Pregnancy rates after varicocele repair continue to rise for 12 to 24 months. If semen analysis has not improved significantly by 12 months post-repair, assisted reproduction is considered.
Yes — for some causes of poor sperm quality, lifestyle changes make a clinically significant difference. Stopping anabolic steroids (which suppress the HPG axis and shut down spermatogenesis) allows sperm production to recover over 3 to 12 months. Smoking cessation improves sperm motility and morphology. Weight loss in obese men normalises testosterone and FSH. Reducing scrotal heat exposure (tight underwear, hot baths, laptop on lap) may help marginally. Antioxidant supplements (Co-Q10, carnitine, vitamin E) have moderate evidence for improving sperm parameters in idiopathic oligospermia. However, lifestyle changes alone are insufficient for genetic causes, hormonal disorders, or obstruction — specific treatment is required for these.
A couple trying to conceive should seek fertility evaluation after 12 months of regular unprotected intercourse (6 months if the female partner is above 35). However, male fertility evaluation — specifically semen analysis — should not wait for 12 months if there is a known risk factor: prior testicular surgery, undescended testis, chemotherapy or radiation, sexually transmitted infection, or known varicocele. Semen analysis is simple and non-invasive — there is no reason to delay it. At KIMS, semen analysis is available with a same-day result in most cases.
Psychological stress is associated with modest reductions in sperm quality — cortisol and other stress hormones can impair testosterone production and spermatogenesis. However, stress alone is rarely the primary cause of clinically significant infertility, and 'it is stress' should not be accepted as a final explanation for abnormal semen analysis without excluding the structural, hormonal, and genetic causes that require specific treatment. If semen analysis is abnormal, a full andrology workup should proceed regardless of stress levels.
KIMS Secunderabad — Dr. Neil Narendra Trivedi (MCh Urology KEM Hospital Mumbai, Member SIU), full andrology workup including WHO 2021 semen analysis, strict Kruger morphology, sperm DNA fragmentation, hormonal profile, genetic testing, scrotal Doppler, laparoscopic varicocelectomy, PESA/TESA/microTESE for azoospermia, gonadotropin therapy for hypogonadotropic hypogonadism. NABH and NABL accredited.