It has been estimated that VUR is present in more than 10% of the population. Younger children are more prone to VUR because of the relative shortness of the submucosal ureters. This susceptibility decreases with age as the length of the ureters increases as the children grow. In children under the age of 1 year with a urinary tract infection, 70% will have VUR. This number decreases to 15% by the age of 12. Although VUR is more common in males antenatally, in later life there is a definite female preponderance with 85% of cases being female.

The American Urological Association recommends ongoing monitoring of children with VUR until the abnormality resolves or is no longer clinically significant. The recommendations are for annual evaluation of blood pressure, height, weight, analysis of the urine, and kidney ultrasound.

There is a genetic predisposition, first-degree relatives have a great increase in the chance of VUR. The gene frequency is estimated to be 1:600. The American Academy of Pediatrics recommends that children from 2 to 24 months presenting with a UTI should be investigated for VUR.

The causes of diseases of the body are common to the urinary tract. Structural and or traumatic change can lead to hemorrhage, functional blockage or inflammation. Colonisation by bacteria, protozoa or fungi can cause infection. Uncontrolled cell growth can cause neoplasia.

For example:

- Urinary tract infections (UTIs), interstitial cystitis

- incontinence (involuntary loss of urine), benign prostatic hyperplasia (where the prostate overgrows), prostatitis (inflammation of the prostate).

- Urinary retention, which is a common complication of benign prostatic hyperplasia (BPH), though it can also be caused by other types of urinary tract obstruction, nerve dysfunction, tethered spinal cord syndrome, constipation, infection and certain medications.

- Transitional cell carcinoma (bladder cancer), renal cell carcinoma (kidney cancer), and prostate cancer are examples of neoplasms affecting the urinary system.

- Urinary tract obstruction

The term "uropathy" refers to a disease of the urinary tract, while "nephropathy" refers to a disease of the kidney.

Occurring at a rate between 1 in 10,000 to 1 in 50,000 with a male-to-female ratio of 2.3-6:1, bladder exstrophy is relatively rare. For those individuals with bladder exstrophy who maintain their ability to reproduce, the risk of bladder exstrophy in their children is approximately 500-fold greater than the general population.

Duplicated ureter is the most common renal abnormality, occurring in approximately 1% of the population.

Race: Duplicated ureter is more common in Caucasians than in African-Americans.

Sex: Duplicated ureter is more common in females. However, this may be due to the higher frequency of urinary tract infections in females, leading to a higher rate of diagnosis of duplicated ureter.

Urologic disease can involve congenital or acquired dysfunction of the urinary system.

Kidney diseases are normally investigated and treated by nephrologists, while the specialty of urology deals with problems in the other organs. Gynecologists may deal with problems of incontinence in women.

Diseases of other bodily systems also have a direct effect on urogenital function. For instance, it has been shown that protein released by the kidneys in diabetes mellitus sensitises the kidney to the damaging effects of hypertension.

Diabetes also can have a direct effect on urination due to peripheral neuropathies which occur in some individuals with poorly controlled diabetics.

Gastroesophageal reflux disease (GERD) affects approximately 40% of adults. Strictures occur in 7 to 23% of patients with GERD who are untreated.

The female homolog to the male verumontanum from which the valves originate is the hymen.

Involutional stenosis is probably the most common cause of NLD obstruction in older persons. It affects women twice as frequently as men. Although the inciting event in this process is unknown, clinicopathologic study suggests that compression of the lumen of the NLD is caused by inflammatory infiltrates and edema. This may be the result of an unidentified infection or possibly an autoimmune disease.

The prognosis of hydronephrosis is extremely variable, and depends on the condition leading to hydronephrosis, whether one (unilateral) or both (bilateral) kidneys are affected, the pre-existing kidney function, the duration of hydronephrosis (acute or chronic), and whether hydronephrosis occurred in developing or mature kidneys.

For example, unilateral hydronephrosis caused by an obstructing stone will likely resolve when the stone passes, and the likelihood of recovery is excellent. Alternately, severe bilateral prenatal hydronephrosis (such as occurs with posterior urethral valves) will likely carry a poor long-term prognosis, because obstruction while the kidneys are developing causes permanent kidney damage even if the obstruction is relieved postnatally.

Hydronephrosis can be a cause of pyonephrosis - which is a urological emergency.

Sinus disease often occurs in conjunction with, and in other instances may contribute to the development of NLD obstruction. Patients should be asked about previous sinus surgery, as the NLD is sometimes damaged when the maxillary sinus ostium is being enlarged anteriorly.

Without diagnostic evaluation, the cause of UAB is unclear, as there are multiple possible causes. UAB symptoms can accurately reflect impaired bladder emptying due either to DU or obstruction (normal or large storage volumes, elevated post-void residual volume), or can result from a sense of incomplete emptying of a hypersensitive bladder (small storage volumes, normal or elevated postvoid residual volume). UAB potentially might also result from inaccurate perceptions of bladder function, such as in neurologic or psychiatric disease. DU itself is often linked to a weak detrusor muscle (impaired contractility), however this association is weak. Both UAB and DU have been associated with diminished sensitivity to bladder volumes rather than objective detrusor weakness, suggesting both symptoms (UAB) and function (DU) have a significant component of sensory dysfunction, leading to impaired bladder sensations and control (Smith et al., 2015).

The underlying contributors to UAB include neurologic disease, metabolic disease (e.g. diabetes), chronic bladder outlet obstruction (e.g. obstructive BPH or complications of anterior vaginal surgery), cognitive decline (such as with aging), psychiatric disorders, and adverse effects of medications. Additionally, structural abnormalities expanding the urinary reservoir beyond the bladder, such as massive vesicoureteral reflux or large bladder diverticulae, can result in UAB. While aging itself is often associated with UAB (and DU), there is scant evidence to support this claim.

The most important criterion for improving long-term prognosis is success of the initial closure. If a patient requires more than one closure their chance of continence drops off precipitously with each additional closure - at just two closures the chance of voiding continence is just 17%.

Even with successful surgery, people may have long-term complications. Some of the most common include:

- Vesicoureteral reflux

- Bladder spasm

- Bladder calculus

- Urinary tract infections

Hydronephrosis is the result of any of several abnormal pathophysiological occurrences. Structural abnormalities of the junctions between the kidney, ureter, and bladder that lead to hydronephrosis can occur during fetal development. Some of these congenital defects have been identified as inherited conditions, however the benefits of linking genetic testing to early diagnosis have not been determined. Other structural abnormalities could be caused by injury, surgery, or radiation therapy.

Compression of one or both ureters can also be caused by other developmental defects not completely occurring during the fetal stage such as an abnormally placed vein, artery, or tumor. Bilateral compression of the ureters can occur during pregnancy due to enlargement of the uterus. Changes in hormone levels during this time may also affect the muscle contractions of the bladder, further complicating this condition.

Sources of obstruction that can arise from other various causes include kidney stones, blood clots, or retroperitoneal fibrosis.

The obstruction may be either partial or complete and can occur anywhere from the urethral meatus to the calyces of the renal pelvis. Hydronephrosis can also result from the reverse flow of urine from the bladder back into the kidneys. This reflux can be caused by some of the factors listed above as well as compression of the bladder outlet into the urethra by prostatic enlargement or impaction of feces in the colon, as well as abnormal contractions of bladder muscles resulting from neurological dysfunction or other muscular disorders.

While most cases of horseshoe kidneys are asymptomatic and discovered upon autopsy, the condition may increase the risk for:

- Kidney obstruction – abnormal placement of ureter may lead to obstruction and dilation of the kidney.

- Kidney infections – associated with vesicoureteral reflux.

- Kidney stones – deviant orientation of kidneys combined with slow urine flow and kidney obstruction may lead to kidney stones.

- Kidney cancer – increased risk of renal cancer, especially Wilms' tumor, transitional cell carcinoma, and an occasional case report of carcinoid tumor. Despite increased risk, the overall risk is still relatively low.

The prevalence of horseshoe kidneys in females with Turner Syndrome is about 15%.

It can be associated with trisomy 18.

It can be associated with venous anomalies like left sided IVC 9.

Ask-Upmark kidneys are a cause of secondary hypertension that can be curable.

It is thought to be congenital or the consequence of vesicoureteral reflux.

Duplicated ureter or Duplex Collecting System is a congenital condition in which the ureteric bud, the embryological origin of the ureter, splits (or arises twice), resulting in two ureters draining a single kidney. It is the most common renal abnormality, occurring in approximately 1% of the population. The additional ureter may result in a ureterocele, or an ectopic ureter.

Reflux nephropathy is kidney damage (nephropathy) due to urine flowing backward (reflux) from the bladder toward the kidneys; the latter is called vesicoureteral reflux (VUR). Longstanding VUR can result in small and scarred kidneys during the first five years of life in affected children. The end results of reflux nephropathy can include high blood pressure, excessive protein loss in the urine, and eventually kidney failure.

When reflux nephropathy is suspected as a cause of kidney disease, other conditions to consider include chronic pyelonephritis, obstructive uropathy, and analgesic overuse.

The term "reflux nephropathy" was introduced in 1973.

Horseshoe kidney, also known as "ren arcuatus" (in Latin), renal fusion or super kidney, is a congenital disorder affecting about 1 in 600 people, more common in men.

In this disorder, the patient's kidneys fuse together to form a horseshoe-shape during development in the womb. The fused part is the isthmus of the horseshoe kidney.

Fusion abnormalities of the kidney can be categorized into two groups: horseshoe kidney and crossed fused ectopia. The 'horseshoe kidney' is the most common renal fusion anomaly.

Posterior urethral valve (PUV) disorder is an obstructive developmental anomaly in the urethra and genitourinary system of male newborns. A posterior urethral valve is an obstructing membrane in the posterior male urethra as a result of abnormal "in utero" development. It is the most common cause of bladder outlet obstruction in male newborns. The disorder varies in degree, with mild cases presenting late due to milder symptoms. More severe cases can have renal and respiratory failure from lung underdevelopment as result of low amniotic fluid volumes, requiring intensive care and close monitoring. It occurs in about one in 8000 babies.

The cause of multicystic dysplastic kidney can be attributed to genetics. Renal dysplasia can be a consequence of a genetic syndrome, which in turn may affect the digestive tract, nervous system, or other areas of the urinary tract. If the mother had been taking certain prescription drugs such as those for hypertension, this may be a precipitating factor as well.

Smoking is the number one cause of Reinke's edema. Other factors include gastroesophageal reflux, hypothyroidism and chronic overuse of the voice. Smoking is the only risk factor that may lead to cancer. Additionally, the combination of several risk factors increase the likelihood of an individual developing Reinke's edema. For example, an individual who smokes and also has gastric reflux would have an increased susceptibility for developing Reinke's edema over time.

Reinke's edema is commonly diagnosed in middle-aged females with a history of smoking (aged 50 years or older). Because males have lower pitched voices than females, males are less likely to observe a significant changes in the voice, and are therefore less likely to seek treatment. Females also report more physical discomfort due to Reinke's edema. The risk of Reinke's edema increases with age and also with prolonged exposure to smoking. Additionally, individuals in professions that require constant use of the voice, such as singers, teachers, and radio hosts, may be at an increased risk for developing the disease.

Because the disease is heavily linked to smoking, there is no established way to screen for Reinke's edema. Similarly, the only way to prevent Reinke's edema is to avoid smoking. By adopting a non-smoking lifestyle after being diagnosed with Reinke's edema, it is possible to stop the disease's progression, although it is not possible to reverse it. Therefore, it is critical to maintain a non-smoking lifestyle even after surgery, because the fluid can re-emerge. In fact, in many cases surgeons will not perform surgery without the guarantee that the individual will stop smoking.

Hand-foot-genital syndrome is inherited in an autosomal dominant manner. The proportion of cases caused by de novo mutations is unknown because of the small number of individuals described. If a parent of the proband is affected, the risk to the siblings is 50%. When the parents are clinically unaffected, the risk to the sibs of a proband appears to be low. Each child of an individual with HFGS has a 50% chance of inheriting the mutation. Prenatal testing may be available through laboratories offering custom prenatal testing for families in which the disease-causing mutation has been identified in an affected family member.