Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Advertise | Login 
 
Search Article 
  
Advanced search 
  Users Online: 1608 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size  

 
Table of Contents
REVIEW ARTICLE
Year : 2012  |  Volume : 16  |  Issue : 2  |  Page : 214-219

Sexual and gonadal dysfunction in chronic kidney disease: Pathophysiology


Department of Nephrology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication13-Mar-2012

Correspondence Address:
Manish Rathi
Department of Nephrology, Post Graduate Institute of Medical Education and Research, Chandigarh - 160012
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2230-8210.93738

Rights and Permissions
   Abstract 

Sexual and gonadal dysfunction/infertility are quite common in patients with chronic kidney disease. Forty percent of male and 55% of female dialysis patients do not achieve orgasm. The pathophysiology of gonadal dysfunction is multifactorial. It is usually a combination of psychological, physiological, and other comorbid factors. Erectile dysfunction in males is mainly due to arterial factors, venous leakage, psychological factors, neurogenic factors, endocrine factors, and drugs. Sexual dysfunction in females is mainly due to hormonal factors and manifests mainly as menstrual irregularities, amenorrhea, lack of vaginal lubrication, and failure to conceive. Treatment of gonadal dysfunction in chronic kidney disease is multipronged and an exact understanding of underlying pathology is essential in proper management of these patients.

Keywords: Chronic kidney disease, gonadal dysfunction, infertility, menstrual abnormalities


How to cite this article:
Rathi M, Ramachandran R. Sexual and gonadal dysfunction in chronic kidney disease: Pathophysiology. Indian J Endocr Metab 2012;16:214-9

How to cite this URL:
Rathi M, Ramachandran R. Sexual and gonadal dysfunction in chronic kidney disease: Pathophysiology. Indian J Endocr Metab [serial online] 2012 [cited 2019 Dec 10];16:214-9. Available from: http://www.ijem.in/text.asp?2012/16/2/214/93738


   Introduction Top


Gonadal dysfunction is a common occurrence in patients with chronic kidney disease (CKD). Sexual dysfunction begins much before CKD-stage 5 and usually does not reverse with renal replacement therapy. [1],[2] There is limited literature on sexual problems (other than fertility related) in CKD patients. While male sexual dysfunction in CKD includes decreased libido, erectile dysfunction, premature or delayed ejaculation, and difficulty in achieving orgasm, female CKD patients have decreased libido, difficulty in achieving orgasm, lack of vaginal lubrication, pain during intercourse, and infertility. [1] The gonadal dysfunction worsens with progression of CKD. Up to 40% of male patients and 55% of female patients on hemodialysis have difficulty in achieving orgasm. [1] Thirty-three percent patients report no sexual activity and 44% report only one sexual activity per week. Menstrual irregularities in CKD patients include amenorrhea (most common) and premature menopause, oligomenorrhea, polymenorrhea, and menorrhagia. Pregnancy is extremely uncommon as one progress from CKD-3 to 5D. [3] Frequency of conception among females of childbearing age undergoing renal replacement therapy ranges from 0.3 to 1.5% per year. [4]

Pathophysiology of gonadal dysfunction differs in male and female CKD patients and includes psychological factors and organic factors. The important factors playing a role in gonadal dysfunction in patients with CKD are discussed below.


   Male Sexual Dysfunction Top


Erectile dysfunction

Erectile dysfunction can be seen in up to 40-80% of hemodialysis patients. Although psychological factor plays an important role, effective renal replacement therapy improves fitness, libido, and potency. Erectile dysfunction in CKD is multifactorial and includes decreased arterial blood flow, venous leakage due to shunts, altered penile smooth muscle function, hormonal disturbances, side effect of medications, and neurogenic dysfunction. The etiological factors are often classified into organic and psychological causes; however, the two factors are interwoven. An optimal therapy for erectile dysfunction should be able to manage all the above-mentioned factors. [5],[6]

Arterial factors

A prerequisite for penile erection includes adequate penile blood flow and intracavernosal arterial blood pressure (BP) >80 mmHg. During the initial stages of erection, the penile arterial BP is 20 mmHg less than the pelvic arterial BP. During the later stages, the penile blood flow increases above the systemic BP by contraction of penile muscles (bulbus spongiosus and ischiocavernosus). The pelvic arterial BP needs to be around 80-100 mmHg to maintain a penile BP of 80 mmHg. However, with arterial occlusive disease, the BP in pelvic vessels drops to around 70 mmHg, and hence erectile dysfunction occurs before other peripheral manifestations of arterio-occlusive disease.

Vascular problems accounts for 60% of non-uremic impotence. [7],[8] However, there is no sufficient data on obstructive vascular problems causing impotence in CKD. Patients with CKD have accelerated atherosclerosis and vascular calcification, and hence obstructive vascular problem could contribute to impotence in at least similar fraction in CKD patients. CKD patients have delayed erection at early stages, followed by decreased penile rigidity and nocturnal penile tumescence (NPT) and finally erectile impotence. The exact pathophysiology of CKD resulting in vascular impotence is not clear. However, increasing age, diabetes mellitus, dyslipidemia, hyperhomocysteinemia, and disturbed calcium/phosphorous metabolism could result in accelerated atherosclerosis and vascular calcification of pelvic arteries. Autonomic neuropathy of CKD could also alter penile blood circulation, which is discussed later. The arterial causes of erectile dysfunction can be diagnosed by Doppler ultrasound or angiography [Table 1].
Table 1: Diagnosis of arteriogenic impotence

Click here to view


Venous leakage

Venous occlusion with normal arterial flow is also an important cause of impotence in uremic patients. Inability to have persistent erection is suggestive of smooth muscle dysfunction and impaired veno-occlusion. [9] Impaired relaxation of penile smooth muscle results in efflux of blood from cavernous space, resulting in erectile dysfunction. Precocious aging and enhanced fibrosis results in decreased fibroelastic compliance of smooth muscle. Pentosidine concentrations are 22 times higher in CKD and 3-4 times in transplant recipients in comparison to healthy controls. Pentosidine concentration is also higher in the corpus cavernosum and thought to be involved in pathogenesis of erectile dysfunction. [10],[11],[12] Diagnosis of venous leakage is summarized in [Table 2].
Table 2: Diagnosis of venous insufficiency

Click here to view


Neurogenic and psychogenic factors

Neurogenic: Erection is a complex process and includes neural, hormonal, and local substances. Three neurogenic process of erection are:

  1. Psychogenic erection: Visual and auditory stimuli/impulse from brain reach via thoracolumbar nerve to cavernous nerve.
  2. Reflex erection: Occurs with sensory stimulation of receptors along the shaft of penis. Somatic nerve provides the afferent supply while the efferent supply is by the pelvic nerve (S2, 3, 4).
  3. Nocturnal erection: Occurs during rapid eye movement (REM) sleep due to increased sensitivity to low androgen levels. [14]
Sacral parasympathetic stimulation causes vasodilatation of penile arteries and increases the blood flow. Increase in blood flow results in increased oxygen concentration and hence increased ability to synthesize nitric oxide (NO). NO in turn leads to smooth muscle relaxation and progressive entrapment of blood in corpus cavernosum. [15],[16]

Autonomic neuropathy is a common complication seen in CKD patients. Parasympathetic dysfunction is seen in two-third of patients >65 years of age and one-third of younger patients. Autonomic neuropathy improves after several months of intensive renal replacement therapy. [17],[18]

Psychogenic: CKD patients have higher prevalence of depression. [19] There are also other psychogenic factors like stress, decreased appetite, fear of procedure or medications, etc. which can aggravate impotence in CKD patients. Male hemodialysis patients with psychogenic cause of impotence have a normal 3-5 NPT/night during REM sleep. Lack of nocturnal erection is a reliable test for organic erectile impotence in patients with psychogenic erectile dysfunction. [20],[21]

Drug-induced erectile dysfunction

Decreased libido and potency can also be due to adverse effect of many drugs used in CKD [Table 3]. These drugs interfere with neurovascular control of penile arteries and smooth muscle and neuro-endocrine regulation. Alcohol and tobacco are also important causes of reduced sexual function in CKD. [22] Antihypertensive drugs are one of the commonly used class of drugs, which can lead to erectile dysfunction in CKD patients. [23]
Table 3: Commonly used drugs causing erectile dysfunction in patients with CKD

Click here to view



   Female Sexual Dysfunction Top


Vaginal and menstrual abnormalities

Female patients on dialysis have low plasma estrogen levels (due to hyperprolactinemia) resulting in atrophic vaginitis, decreased pubic hair, and pruritus. Normal midcycle karyopyknosis (vaginal cytology) is absent. [24],[25] However, the prevalence and spectrum of vaginal infections remain the same as in general population. Menstrual irregularities are very common in uremia. Amenorrhea is seen in 50-100% of patients with CKD-5. Many patients start to have menstrual cycles on initiation of dialysis while others remain amenorrheic. Of the patients who menstruate, 50-80% have polymenorrhea, menorrhagia (probably due to anovualtory cycle which is seen in >90%) or oligomenorrhea. [26],[27],[28] Uremic coagulopathy and heparinization during hemodialysis intensify abnormal menstrual bleeding. Increase in ovarian cyst formation can occur in uremic patients and it needs to be distinguished from polycystic ovarian syndrome and other androgen producing tumors. [29]

No data is available regarding the prevalence of female sexual dysfunction, such as desire, orgasm, or pain disorders in chronic kidney disease.


   Hormonal Abnormalities in Chronic Kidney Disease Top


Pulsatile secretion of gonadotrophin releasing hormone (GnRH) from hypothalamus regulates pituitary secretion of gonadotrophins [luteinizing hormone (LH) and follicular stimulating hormone (FSH)]. In addition to GnRH, adrenergenic, dopaminergic substances, endorphins, oxytocin, neuropeptide-Y, and leptin also regulate pituitary gonadotrophin secretion.

Uremic effect on gonadotrophins (LH and FSH)


Males

Uremia affects local amino acid neurotransmitter outflow in hypothalamus, significantly affecting the release of GnRH and hence affecting gonadotrophin synthesis and secretion in both males and females. [30],[31] In vast majority of patients, there is a normal LH secretion response to exogenous LH releasing hormone (LHRH) stimulation. The plasma LH level is elevated in hemodialysis patients compared to healthy controls. This increased level is due to prolonged half-life of immunoreactive and bioactive LH as well as increased secretion of immunoreactive LH. [32] Although the frequency of LH peaks remains normal, the maximal level and duration of LH peaks is reduced. In view of prolonged half-life of LH in uremia, there is significant decrease in pulsatile secretion of LH. [33] This leads to low levels of testosterone in uremic patients while the serum estradiol and total estrogens levels are usually elevated. [34],[35] The decreased testosterone level produces a diminished normal feedback suppression of LH, thus causing persistently high levels of LH. [36] In addition, endogenous opiates also negatively control pulsatile LH release. [37] Plasma β-endorphin and β-lipotropin levels are normal in uremic subjects. However, administration of naloxone increases LH pulses in uremic patients in both males and females. [38],[39] Tumor necrosis factor (TNF)-α increases LH, reduces testosterone, and has no effect on FSH. TNF-α levels are increased in CKD due to inflammatory state of the disease. [40] Similar to LH, FSH levels are normal toelevated in CKD. FSH stimulates spermatogenesis and has a negative feedback via inhibin (synthesized by  Sertoli cells More Details of the ovary). Inhibin levels increases in CKD but do not correlate with FSH/LH levels. FSH secretion is also inhibited by increased estrogen in CKD, resulting in only mildly elevated level of FSH in CKD despite decreased spermatogenesis. [41],[42],[43],[44]

Females

The pulsatile secretion of GnRH is disturbed in females as well, resulting in infertility. Gonadotrophin secretion is calcium dependent. Disturbed calcium and phosphorous metabolism in CKD results in altered gonadotrophin secretion. Serum LH level is significantly elevated and response to LHRH stimulation is delayed; however, the negative feedback of estrogen on hypothalamus is intact. The pulsatile secretion of LH is disturbed in females and some studies have even documented complete absence of pulsatile secretion. Exogenous estrogen does not induce LH surge in uremic patients, suggesting impaired positive feedback mechanism. FSH is within normal limits in follicular and luteal phases. LHRH causes only mild rise in FSH and decreased FSH/LH ratio is suggestive of hypothalamic - hypophyseal dysregulation. [45]

Uremic effect on prolactin

Serum prolactin level as well as its biological activity is increased in CKD. [46] Serum prolactin level rise correlates with decline in glomerular filtration rate. Increase in serum prolactin levels is primarily due to decreased dopaminergic inhibition of prolactin release from pituitary gland and secondarily due to decreased LHRH release. Prolactin is considered as a uremic toxin causing loss of libido, impaired erection, and infertility. It can also cause gynecomastia and galactorrhea in males and menstrual abnormalities (amenorrhea and oligomenorrhea) and galactorrhea in females (0-40% of CKD-5D patients). The prolactin increase is blunted with thyrotrophin-releasing hormone stimulation in both the sexes. [47]

Uremic effect on testicular/ovarian hormones

In addition to the effect on hypothalamus and pituitary, uremia also affects the adrenal, ovarian, and testicular hormones directly. Massachusetts Male Aging Study concluded that only dehydroepiandrosterone sulfate (adrenal androgen) and not testosterone correlated with impotence. [19] Androgen receptors are present in parasympathetic system and limbic system and thought to play an important role in erection. Uremic patients have low serum testosterone levels. Testosterone binding capacity remains normal; hence, free testosterone levels are also decreased. [48],[49] Low testosterone is due to decreased production, increased metabolic and dialytic clearance, alteration in testosterone binding capacity. The normal circadian rhythm is, however, maintained. High serum LH and normal testosterone level suggests resistance at the level of interstitial cells of Leydig. Low testosterone levels along with high FSH levels (described above) leads to impaired spermatogenesis. [50] Not only spermatogenesis, but sperm motility is also affected causing oligospermia and azoospermia and thus male infertility. These changes occur early in the disease course and worsen as kidney disease progresses. A successful kidney transplantation restores the hypothalamic-pituitary-testicular axis and recovery of spermatogenesis can occur. However, this recovery depends on the extent of injury to seminiferous tubules and males with higher levels of FSH tend to have poor recovery. [50]

In females, estradiol concentration is normal in premenopausal uremic patients; however, in patients with hyperprolactinemia, estradiol levels are lower. Cyclical variation in estradiol concentration is absent in uremic females. Luteinization of follicles is very rare in uremic patients, and hence the progesterone rise during second half of menstrual cycle is absent (non-luteal progesterone is normal to low). [45] The various changes in androgen levels are summarized in [Table 4].
Table 4: Androgen concentration in chronic kidney disease

Click here to view


Other hormonal abnormalities

Role of hyperparathyroidism in sexual problems is not clear. Interleukin-2 and TNF-α reduce plasma testosterone concentration with and without LH stimulation. [51],[52] Use of 1,25 dihydroxy vitamin D3 reduces prolactin secretion and lowers prolactin in uremic patients.


   Principle of Management of Sexual Dysfunction in Chronic Kidney Disease Top


As the sexual dysfunction in CKD is multifactorial, a careful assessment of the degree and nature of sexual dysfunction needs to be done. A detailed psychological evaluation should be carried out which includes assessment of marital and family discord, depression, stress, and life stage. Medication remains an important cause of sexual dysfunction and details of the drugs need to be noted and changed appropriately if permissible. Treatment of anemia to target range (11-12g%) and intensification of renal replacement therapy improves sexual dysfunction and quality of life in CKD patients. [25] Appropriate management of vascular insufficiency, zinc deficiency, secondary hyperparathyroidism, and autonomic dysfunction improves sexual performances in CKD patients. Endocrine assessment of serum estrogen, progesterone, and prolactin needs to be carried out. Female CKD patient with increased prolactin levels needs treatment with bromocriptine and improvement with bromocriptine is seen in patients with cyclic GnRH secretion. Sildenafil therapy improves erectile dysfunction caused by both psychogenic and organic factors. [14] For male CKD patients who do not respond to Sildenafil, treatment options include intracavernous injection of alprostadil and the use of vacuum or constriction devices. [53]


   Conclusion Top


Gonadal dysfunction is very common in male and female CKD patients. The frequency of sexual dysfunction increases as renal function deteriorates. Decreased libido, difficulty in becoming aroused and achieving orgasm, erectile and ejaculatory dysfunction, lack of vaginal lubrication, menstrual irregularities, and amenorrhea are the common problems in patients with CKD. The pathophysiology of gonadal dysfunction in CKD is multifactorial, hence it is important to identify the primary etiology and treat it.

 
   References Top

1.Finkelstein SH, Finkelstein FO. Evaluation of sexual dysfunction in dialysis patients. In: Nissenson AR, Fine RN, editors. Dialysis Therapy. 3 rd ed. Philadelphia: Hanley and Belfus; 2002. p. 368-73.  Back to cited text no. 1
    
2.Palmer BF. Sexual dysfunction in uremia. J Am Soc Nephrol 1999;10:1381-8.  Back to cited text no. 2
    
3.Zingraff J, Jungers P, Pélissier C, Nahoul K, Feinstein MC, Scholler R. Pituitary and ovarian dysfunctions in women on haemodialysis. Nephron 1982;30:149-53.  Back to cited text no. 3
    
4.Holley JL, Schmidt RJ, Bender FH, Dumler F, Schiff M. Gynecologic and reproductive issues in women on dialysis. Am J Kidney Dis 1997;29:685-90.  Back to cited text no. 4
    
5.Abram HS, Hester LR, Sheridan WF, Epstein GM. Sexual functioning in patients with chronic renal failure. J Nerv Ment Dis 1975;160:220-6.  Back to cited text no. 5
    
6.Bommer J, Tschöpe W, Ritz E, Andrassy K. Sexual behaviour of haemodialyzed patients. Clin Nephrol 1976;6:315-8.  Back to cited text no. 6
    
7.May AG, DeWeese JA, Rob CG. Changes in sexual function following operation on the abdominal aorta. Surgery 1969;65:41-7.  Back to cited text no. 7
    
8.Virag R. Impotence: A new field in angiology. Int Angiol 1984;13:217-20.  Back to cited text no. 8
    
9.Bellinghieri G, Lo Forti B, Savica V. The penile color wave doppler test in the study of uraemic impotence. Med Sci Res 1992;20:95-7.  Back to cited text no. 9
    
10.Sell DR, Monnier VM. End-stage renal disease and diabetes catalyze the formation of pentose derived cross-link from aging human collagen. J Clin Invest 1990;85:380-4.  Back to cited text no. 10
    
11.Tarcan T, Azadzoi KM, Siroky MB, Goldstein I, Krane RJ. Age-related erectile and voiding dysfunction: The role of arterial insufficiency. Br J Urol 1998;82 Suppl 1:26-33.  Back to cited text no. 11
    
12.Hricik DE, Schulak JA, Sell DR, Fogarty J, Monnier M. Effects of kidney-pancreas transplantation on plasma pentosidine. Kidney Int 1993;43:398-403.  Back to cited text no. 12
    
13.Truss MC, Djamilian MH, Tan HK, Hinrichs H, Feistner H, Stief CG, et al. Single potential analysis of cavernous electrical activity. Eur Urol 1993;24:358-65.  Back to cited text no. 13
    
14.Levy A, Crowley T, Gingell C. Non-surgical management of erectile dysfunction. Clin Endocrinol (Oxf) 2000;52:253-60.  Back to cited text no. 14
    
15.Kim N, Vardi Y, Padma Nathan H, Daley J, Goldstein I, Saenz de Tejada I. Oxygen tension regulates the nitric oxide pathway: Physiological role in penile erection. J Clin Invest 1993;91:437-42.  Back to cited text no. 15
    
16.Rajfer J, Aronson WJ, Bush PA, Dorey FJ, Ignarro LJ. Nitric oxide as a mediator of relaxation of the corpus cavernosum in response to nonadrenergic, noncholinergic neurotransmission. N Engl J Med 1992;326:90-4.  Back to cited text no. 16
    
17.Campese VM, Procci WR, Levitan D, Romoff MS, Goldstein DA, Massry SG. Autonomic nervous system dysfunction and impotence in uraemia. Am J Nephrol 1982;2:140-3.  Back to cited text no. 17
    
18.Zucchelli P, Turani A, Zuccala A, Santoro A, Degli Esposti E, Chiarini C. Dysfunction of the autonomic nervous system in patients with end-stage renal failure. Contrib Nephrol 1985;45:69-81.  Back to cited text no. 18
    
19.Feldman HA, Goldstein I, Hatzchristou DG, Krane RL. Impotence and its medical and psychosocial correlates: Results of the Massachusetts male aging study. J Urol 1994;151:54-61.  Back to cited text no. 19
    
20.Massry SG, Goldstein DA, Procci WR, Kletsky OA. Impotence in patients with uraemia. A possible role for parathyroid hormone. Nephron 1997;19:305-10.  Back to cited text no. 20
    
21.Muir JW. Bromocriptine improves reduced libido and potency in men receiving maintenance hemodialysis. Clin Nephrol 1983;20:8-14.  Back to cited text no. 21
    
22.Mannino DH, Klevens RM, Flanders WD. Cigarette-smoking: An independent risk factor for impotence. Am J Epidemiol 1994;140:1003-8.  Back to cited text no. 22
    
23.Grimm RH Jr, Grandits GA, Prineas RJ, McDonald RH, Lewis CE, Flack JM, et al. Long term effects on sexual function of 5 antihypertensive drugs and nutritional hygienic treatment in hypertensive men and women. Treatment of Mild Hypertension Study (TOMHS). Hypertension 1997;29:8-14.  Back to cited text no. 23
    
24.Michaelides N, Humke W. Erfahrungen bei der gynäkologischen Betrteuung von Patientinnen mit chronischer Niereninsuffizienz. Nieren-und Hochdruckkrankheiten 1993;22:187-92.  Back to cited text no. 24
    
25.Schaefer RM, Kokot F, Wernze H, Geiger H, Heideland A. Improved sexual function in hemodialysis patients on recombinant erythropoietin: A possible role for prolactin. Clin Nephrol 1989;31:1-5.  Back to cited text no. 25
    
26.Goodwin NJ, Valenti C, Hall JE, Friedman EA. Effects of uraemia and chronic hemodialysis on the reproductive cycle. Am J Obstet Gynaecol 1968;100:528-35.  Back to cited text no. 26
    
27.Larsen NA. Sexual problems of patients on RDT and after renal transplantation. In: Cameron JS, editors. Proceedings of the European Dialysis and Transplantation Association. Baltimore, MD; 1972. p. 271.  Back to cited text no. 27
    
28.Morley JE, Distiller LA, Epstein S, Katz M, Gold C, Sagel J, et al. Menstrual disturbances in chronic renal failure. Horm Metab Res 1979;11:68-72.  Back to cited text no. 28
    
29.Thaysen JH, Olgaard K, Jensen HG. Ovarian cysts in women on chronic intermittent haemodialysis. Acta Med Scand 1975;197:433-7.  Back to cited text no. 29
    
30.Schaefer F, Vogel M, Kerkhoff G, Woitzik J, Daschner M, Mehls O. Experimental uraemia affects hypothalamic amino acid neurotransmitter milieu. J Am Soc Nephrol 2001;12:1218-27.  Back to cited text no. 30
    
31.Schaefer F, van Kaick B, Veldhuis JD, Stein G, Schärer K, Robertson WR, et al. Changes in the kinetics and biopotency of luteinizing hormone in hemodialyzed men during treatment with recombinant human erythropoietin. J Am Soc Nephrol 1994;5:1208-15.  Back to cited text no. 31
    
32.Schaefer F, Veldhuis JD, Robertson WR, Dunger D, Schärer K. The Cooperative Study Group on Pubertal Development in Chronic Renal Failure. Immunoreactive and bioactive luteinizing hormone in pubertal patients with chronic renal failure. Kidney Int 1994;45:1465-76.  Back to cited text no. 32
    
33.Veldhuis JD, Wilkowski MJ, Zwart AD, Urban RJ, Lizarralde G, Iranmanesh A, et al. Evidence for attention of hypothalamine gonadotropin-releasing hormone (GnRH) impulse strength with preservation of GnRH pulse frequency in men with chronic renal failure. J Clin Endocrinol Metab 1993;76:648-54.  Back to cited text no. 33
    
34.Bommer J, Kugel M, Schwöbel B, Ritz E, Barth HP, Seelig R. Improved sexual function during recombinant human erythropoeitin therapy. Nephrol Dial Transplant 1990;5:204-7.  Back to cited text no. 34
    
35.Sawin CT, Longcope C, Schmitt GW, Ryan RJ. Blood levels of gonadotropins and gonadal hormones in gynecomastia associated with chronic haemodialysis. J Clin Endocrinol Metab 1973;36:988-90.  Back to cited text no. 35
    
36.Rodger RS, Morrison L, Dewar JH, Wilkinson R, Ward MK, Kerr DN. Loss of pulsatile luteinising hormone secretion in men with chronic renal failure. Br Med J (Clin Res Ed) 1985;291:1598-600.  Back to cited text no. 36
    
37.Swamy AP, Woolf PD, Cestero RV. Hypothalmic pituitary-ovarian axis in uraemic women. J Lab Clin Med 1979;93:1066-72.  Back to cited text no. 37
    
38.Grzeszcak W, Kokot F, Dulawa J. Effects of naloxone administration on endocrine abnormalities in chronic renal failure. Am J Nephrol 1987;7:93-100.  Back to cited text no. 38
    
39.Tay CC, Glasier AF, Illingworth PJ, Baird DT. Abnormal twenty-four hour pattern of pulsatile luteinizing hormone secretion and the response to naloxone in women with hyperprolactinaemic amenorrhoea. Clin Endocrinol (Oxf) 1993;39:599-606.  Back to cited text no. 39
    
40.Van der Poll T, Romijn JA, Endert E, Sauerwein HP. Effects of tumor on the hypothalamic-pituitary-testicular axis in healthy men. Metabolism 1993;42:303-7.  Back to cited text no. 40
    
41.Sasagawa I, Tateno T, Suzuki Y, Yazawa H, Ichiyanagi O, Nakada T, et al. Circulating levels of inbibin in hemodialysis males. Arch Androl 1998;41:167-71.  Back to cited text no. 41
    
42.Rudolf K, Kunkel S, Rudolf H, Falkenhagen D, Rüting M. [Basal and gonadotropin releasing hormone-stimulated gonadotropin secretion in patients with chronic uraemia]. Zentralbl Gynakol 1988;110:683-8.  Back to cited text no. 42
    
43.Lim VS, Fang VS. Restoration of plasma testosterone levels in uraemic men with clomiphene citrate. J Clin Endocrinol Metab 1976;43:1370-7.  Back to cited text no. 43
    
44.Barton CH, Mirahamadi MK, Vairi ND. Effects of long-term testosterone administration on pituitary-testicular axis in end-stage renal failure. Nephron 1982;31:61-4.  Back to cited text no. 44
    
45.Lim VS, Henriquez C, Sievertsen G, Frohman LA. Ovarian function in chronic renal failure: Evidence suggesting hypothalamic anovulation. Ann Intern Med 1980;93:21-7.  Back to cited text no. 45
    
46.Biasioli S, Mazzali A, Foroni R, D'Andrea G, Feriani M, Chiaramonte S, et al. Chronobiological variations of prolactin (PRL) in chronic renal failure (CRF). Clin Nephrol 1988;30:86-92.  Back to cited text no. 46
    
47.Bommer J, Ritz E, del Pozo E, Bommer G. Improved sexual function in male haemodialysis patients on bromocriptine. Lancet 1979;2:496-7.  Back to cited text no. 47
    
48.Ramirez G, Butcher D, Brüggemeyer CD, Ganguly A. Testicular defect: The primary abnormality in gonadal dysfunction of uraemia. South Med J 1987;80:698-701.  Back to cited text no. 48
    
49.Johansen KL. Testosterone metabolism and replacement therapy in patients with end-stage renal disease. Semin Dialysis 2004;17:202-208.  Back to cited text no. 49
    
50.Anantharaman P, Schmidt RJ. Sexual function in chronic kidney disease. Adv Chr Kidney Dis 2007;14:119-25.  Back to cited text no. 50
    
51.Wark JD. Regulation by 1,25-dihydroxyvitamin D3 (1,25(OH) 2 D3) of specific gene expression in GH pituitary cells. In: Norman AW, Schaefer K, Grigolet HG, Herrath DV, editors. Vitamin D: A Chemical, Biochemical and Clinical Update. Berlin: Walter de Gruyter; 1985. p. 901-2.  Back to cited text no. 51
    
52.Mauduit C, Jaspar JM, Poncelet E, Charlet C, Revol A, Franchimont P, et al. Tumor necrosis factor-alpha antagonizes follicle-stimulating hormone action in cultured sertoli cells. Endocrinology 1993;133:69-76.  Back to cited text no. 52
    
53.Finkelstein FO, Shirani S, Wuerth D, Finkelstein SH. Therapy Insight: Sexual dysfunction in patients with chronic kidney disease. Nat Clin Pract Nephrol 2007;3:200-7.  Back to cited text no. 53
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]


This article has been cited by
1 Body Changes and Decreased Sexual Drive after Dialysis: A Qualitative Study on the Experiences of Women at an Ambulatory Dialysis Unit in Spain
Miriam Álvarez-Villarreal,Juan Francisco Velarde-García,Lourdes Chocarro-Gonzalez,Jorge Pérez-Corrales,Javier Gueita-Rodriguez,Domingo Palacios-Ceña
International Journal of Environmental Research and Public Health. 2019; 16(17): 3086
[Pubmed] | [DOI]
2 HIV and amenorrhea
Elizabeth M. King,Arianne Y. Albert,Melanie C.M. Murray
AIDS. 2019; 33(3): 483
[Pubmed] | [DOI]
3 Ovarian reserve in an Egyptian cohort with end-stage kidney disease on hemodialysis and after successful kidney transplantation: a prospective study
Ahmed Fayed,Ahmed Soliman,Mervat Naguib,Mahmoud Soliman,M. Salaheldin
International Urology and Nephrology. 2019;
[Pubmed] | [DOI]
4 Male sexual dysfunction: A review of literature on its pathological mechanisms, potential risk factors, and herbal drug intervention
Lei Chen,Guang-rui Shi,Dan-dan Huang,Yang Li,Chen-chao Ma,Min Shi,Bin-xiao Su,Guang-jiang Shi
Biomedicine & Pharmacotherapy. 2019; 112: 108585
[Pubmed] | [DOI]
5 Effect of ovariectomy on the progression of chronic kidney disease-mineral bone disorder (CKD-MBD) in female Cy/+ rats
Colby J. Vorland,Pamela J. Lachcik,Elizabeth A. Swallow,Corinne E. Metzger,Matthew R. Allen,Neal X. Chen,Sharon M. Moe,Kathleen M. Hill Gallant
Scientific Reports. 2019; 9(1)
[Pubmed] | [DOI]
6 Sexual dysfunctions and related variables with sexual function in patients who undergo dialysis for chronic renal failure
Gülseren Keskin,Aysun Babacan Gümüs,Gülay Tasdemir Yigitoglu
Journal of Clinical Nursing. 2018;
[Pubmed] | [DOI]
7 Unravelling current sexual care in chronic kidney disease: perspective of social workers
Gaby F. van Ek,Dirry Keurhorst,Esmée M. Krouwel,Melianthe P.J. Nicolai,Marjolein E.M. Den Ouden,Henk W. Elzevier,Hein Putter,Rob C.M. Pelger,Brenda L. Den Oudsten
Journal of Renal Care. 2018; 44(1): 30
[Pubmed] | [DOI]
8 Never say never in medicine: successful pregnancy in a hemodialysis patient despite tubal ligation
Roohan Khan,A. Ahsan Ejaz,Abhilash Koratala
CEN Case Reports. 2018;
[Pubmed] | [DOI]
9 Assessment of ovarian reserve as an indicator of fertility and health consequences in patients with chronic kidney disease stages 3–4
Iwona Szydlowska,Aleksandra Marciniak,Agnieszka Brodowska,Marcin Lisak,Sylwia Przysiecka,Jacek Rózanski
Gynecological Endocrinology. 2018; : 1
[Pubmed] | [DOI]
10 Toxicological and nutritional status of trace elements in hair of women with in vitro fertilization (IVF) pregnancy and their 9-month-old children
Anatoly V. Skalny,Alexey A. Tinkov,Tatiana G. Bohan,Marina B. Shabalovskaya,Olga Terekhina,Svetlana B. Leshchinskaia,Lyubov A. Agarkova,Svetlana V. Notova,Margarita G. Skalnaya,Yulia Kovas
Reproductive Toxicology. 2018;
[Pubmed] | [DOI]
11 Reproductive Issues in Males with SLE
Omid Zahedi Niaki,Sasha Bernatsky,Evelyne Vinet
Current Treatment Options in Rheumatology. 2017;
[Pubmed] | [DOI]
12 The Discussion of Sexual Dysfunction Before and After Kidney Transplantation From the Perspective of the Renal Transplant Surgeon
Gaby F. van Ek,Esmée M. Krouwel,Els van der Veen,Melianthe P. J. Nicolai,Jan Ringers,Brenda L. Den Oudsten,Hein Putter,Rob C. M. Pelger,Henk W. Elzevier
Progress in Transplantation. 2017; 27(4): 354
[Pubmed] | [DOI]
13 Restoration of immune and renal function in aged females by re-establishment of active ovarian function
Rhett L. Peterson,Kate C. Parkinson,Jeffrey B. Mason
Reproduction, Fertility and Development. 2017; 29(10): 2052
[Pubmed] | [DOI]
14 Toward implementation of sexual healthcare, Response to: ‘The opinion and practices of providers toward the sexual issues of cervical cancer patients undergoing treatment’
L.F. Albers,G.F. van Ek,E.M. Krouwel,H.W. Elzevier
Gynecologic Oncology Reports. 2017;
[Pubmed] | [DOI]
15 Prevalence and factors associated with erectile dysfunction in patients with chronic kidney disease on conservative treatment
M R Costa,V C Ponciano,T R Costa,A M de Oliveira,C P Gomes,E C de Oliveira
International Journal of Impotence Research. 2017;
[Pubmed] | [DOI]
16 Sexual care for patients receiving dialysis: A cross-sectional study identifying the role of nurses working in the dialysis department
Gaby F. van Ek,Adina Gawi,Melianthe P. J. Nicolai,Esmée M. Krouwel,Brenda L. Den Oudsten,Marjolein E. M. Den Ouden,Alexander F. Schaapherder,Hein Putter,Rob C. M. Pelger,Henk W. Elzevier
Journal of Advanced Nursing. 2017;
[Pubmed] | [DOI]
17 An Overview on Fertility Outcome in Renal Transplant Recipients
Vineet V. Mishra,Sakshi S. Nanda,Kavita Mistry,Sumesh Choudhary,Rohina Aggarwal,Bhumika M. Vyas
The Journal of Obstetrics and Gynecology of India. 2016;
[Pubmed] | [DOI]
18 Hormone therapy and clinical and surrogate cardiovascular endpoints in women with chronic kidney disease
Sharanya Ramesh,Michelle C. Mann,Jayna M. Holroyd-Leduc,Stephen B. Wilton,Matthew T. James,Ellen W. Seely,Sofia B. Ahmed
Menopause. 2016; 23(9): 1028
[Pubmed] | [DOI]
19 Menopausal symptoms in women with chronic kidney disease
Katharine L. Cheung,Marcia L. Stefanick,Matthew A. Allison,Erin S. LeBlanc,Mara Z. Vitolins,Nawar Shara,Glenn M. Chertow,Wolfgang C. Winkelmayer,Manjula Kurella Tamura
Menopause. 2015; 22(9): 1006
[Pubmed] | [DOI]
20 Pediatric priority in kidney allocation: challenging its acceptability
Laura Capitaine,Kristof Van Assche,Guido Pennings,Sigrid Sterckx
Transplant International. 2014; : n/a
[Pubmed] | [DOI]
21 Sexual Partner Satisfaction of the Patients with Chronic Renal Failure
M. Ahmet Tunçkiran,M. Burak Hoscan
Renal Failure. 2013; 35(1): 101
[Pubmed] | [DOI]
22 Sexuality in Young Adult Men Aged 18–24 with Epilepsy
Erman Bagcioglu,Abdullah Acar,Kerem Senol Coskun,Abdullah Akpinar,Vedat Ali Yurekli,Serdar Oruc,Hasan Mayda,Bulent Bahceci
Sexuality and Disability. 2013; 31(3): 229
[Pubmed] | [DOI]
23 Women and ESRD: Modalities, Survival, Unique Considerations
Kelly E. Guglielmi
Advances in Chronic Kidney Disease. 2013; 20(5): 411
[Pubmed] | [DOI]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Male Sexual Dysf...
    Female Sexual Dy...
    Hormonal Abnorma...
    Principle of Man...
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed5341    
    Printed69    
    Emailed3    
    PDF Downloaded812    
    Comments [Add]    
    Cited by others 23    

Recommend this journal