Male accessory gland infection (MAGI) is a condition with signs of inflammation involving one or more sites in the male genital tract. Diagnosis is made according to parameters defined by the World Health Organization, and it is particularly made in relation to infectious or inflammatory causes of male infertility. Although it is usually caused by infection spreading from the urethra, non-infectious causes also exist. Definition
Along with testicles (orchitis), MAGI includes infections (bacterial, viral, fungal etc.) involving one or more of the following male genital organs or tracts:
epididymis (epididymitis)
vas deferens
seminal vesicles (seminal vesiculitis)
prostate gland (prostatitis)
Cowpers glands
urethra (urethritis)

Diagnosis
As infection has a negative impact on the secretory function of the accessory glands, findings that could indicate the presence of MAGI include:
signs of inflammation in a semen analysis (leukocytes ≥ 1x106/mL and/or elastase ≥ 230 ng/mL)
low semen volume
elevated semen pH
low levels of alpha-glucosidase, fructose and zinc

WHO criteria
MAGI can be diagnosed when there are two or more factors present that meet criteria defined by the World Health Organization (WHO):

Biomarkers
One study has proposed that elevated levels of soluble urokinase-type plasminogen activator receptor (SuPAR) in seminal plasma might be useful as a marker for MAGI. Causes
The main infectious agents are Enterobacteriaceae (such as Escherichia coli and Klebsiella), Neisseria gonorrhoeae, and Chlamydia trachomatis.One study has shown that men with MAGI who have lower serum levels of total testosterone tend to have a more complicated form of MAGI, such as involving more than one site, than those with normal levels.
About 80% of lithium ingested appears to affect the proximal tubules by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to antidiuretic hormone in a mechanism that is not yet fully understood. High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the calcium-sensing receptor. Osmotic
Other causes of acquired nephrogenic diabetes insipidus include hypokalemia (low blood potassium), post-obstructive polyuria, sickle cell disease or trait, amyloidosis, Sjögren syndrome, renal cystic disease, Bartter syndrome, and various medications (amphotericin B, orlistat, ifosfamide, ofloxacin, cidofovir, vaptans).In addition to kidney and systemic disorders, nephrogenic diabetes insipidus can present itself as a side effect of some medications. The most common and well known of these medications is lithium, although there are many other medications that cause this effect with lesser frequency. Hereditary
This form of diabetes insipidus can also be hereditary due to defects in the following genes:

Diagnosis
Differential diagnosis includes nephrogenic diabetes insipidus, neurogenic/central diabetes insipidus and psychogenic polydipsia. They may be differentiated by using the water deprivation test. Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis. If able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range.