The evidence linking vitamin C supplements with an increased rate of kidney stones is inconclusive. The excess dietary intake of vitamin C might increase the risk of calcium oxalate stone formation, in practice this is rarely encountered. The link between vitamin D intake and kidney stones is also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium; correction of a deficiency does not.

There are no conclusive data demonstrating a cause-and-effect relationship between alcoholic beverage consumption and kidney stones. However, some have theorized that certain behaviors associated with frequent and binge drinking can lead to dehydration, which can, in turn, lead to the development of kidney stones.

The American Urological Association has projected that global warming will lead to an increased incidence of kidney stones in the United States by expanding the "kidney stone belt" of the southern United States.

People with lymphoproliferative/myeloproliferative disorders who were treated with chemotherapy developed symptomatic kidney stones 1.8% of the time in one study.

In the general population, the frequency of medullary sponge kidney disease is reported to be 0.02–0.005%; that is, 1 in 5000 to 1 in 20,000. The frequency of medullary sponge kidney has been reported by various authors to be 1221% in patients with kidney stones. The disease is bilateral in 70% of cases.

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.

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.

Complications associated with medullary sponge kidney include the following:

- Kidney stones

- Urinary tract infection (UTI)

- Blood in the urine

- Distal renal tubular acidosis (Type 1 RTA)

- Chronic kidney disease (rarely)

- Marked chronic pain

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.

In regard to the epidemiology of multicystic dysplasia kidney, the incidence of MCDK is estimated to be 1 in every 4,000 live births, making it rare in terms of the general population.

Renal failure is defined by functional impairment of the kidney. Renal failure can be acute or chronic, and can be further broken down into categories of pre-renal, intrinsic renal and post-renal.

Pre-renal failure refers to impairment of supply of blood to the functional nephrons including renal artery stenosis. Intrinsic renal diseases are the classic diseases of the kidney including drug toxicity and nephritis. Post-renal failure is outlet obstruction after the kidney, such as a kidney stone or prostatic bladder outlet obstruction.

Renal failure may require medication, dietary and lifestyle modification and dialysis.

Primary renal cell carcinomas as well as metastatic cancers can affect the kidney.

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.

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.

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.

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.

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.

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.

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.

Inflammation of or injury to the glomeruli can cause leakage of red blood cells, resulting in misshapen cells and red blood cell casts in the urine. Glomerular bleeding is frequently accompanied by proteinuria, or leakage of protein into the urine.

Common causes include

- IgA nephropathy

- Hereditary nephritis (Alport's disease)

- Benign familiar hematuria

- Glomerulonephritis–a group of inflammatory diseases of the glomeruli, leading to hematuria, hypertension, and peripheral edema

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.

Greater than 50% of cases of visible hematuria in children have an identifiable cause. Common causes of visible hematuria in pediatric populations are:

- urinary tract infection

- perineal or urethral irritation

- congenital abnormalities–

- Non-vascular—ureteropelvic junction obstruction, posterior urethral valves, urethral prolapse, urethral diverticula, multicystic dysplastic kidney

- Vascular—arteriovenous malformations, hereditary hemorrhagic telangiectasias, renal vascular thromboses

- trauma

- acute nephritis—characterized by visible hematuria, white blood cells in the urine, and a transient decline in renal function, commonly caused by medications

- coagulopathy

- kidney stones

- IgA nephropathy–suspected in a child with dark urine and recent upper respiratory infection

- Post-streptococcal glomerulonephritis–suspected in a child with dark brown urine following recent streptoccocal pharyngitis or impetigo

It can be caused by a lesion at any point in the urinary tract.

Causes include urolithiasis, posterior urethral valves and ureteral herniation.

LPHS is listed as a rare disease in the US National Institute of Health Rare Diseases database. While exact numbers worldwide are not available, the primary LPHS research clinic located in Ohio has over 200 patients. In addition, several hundred other patients have been reported in one study as of 2006. The prevalence of LPHS is estimated at about 0.012 percent, which qualifies LPHS as a rare disease (prevalence less than 0.07 percent) according to the Rare Diseases Act of 2002. Those affected are usually young, with an average age of 31 years, and 70% to 80% are women.

If the estimated prevalence of 0.012% is correct, a world population of 7 billion would imply approximately 840,000 cases worldwide.

In 2008 researchers found autosomal dominant mutations in the RET and GDNF genes to be linked to renal agenesis in unrelated stillborn fetuses through PCR and direct sequence analysis . In the study, DNA from 33 stillborn fetuses were sequenced for mutations in RET, GDNF and GFRA1. Nineteen of the fetuses had BRA, ten had URA and 4 had congenital renal dysplasia. Seven of the 19 BRA fetuses were found to have a mutation in the RET gene (37%), while two of the ten URA fetuses did (20%). One of the URA fetuses had two RET mutations and one GDNF mutation. There were no GFRA1 mutations found.

However, the results of Skinner et al. study were questioned by a more recent study with a larger number of cases . In this study 105 fetuses were analyzed. Sixty-five fetuses had BRA while 24 had URA with an abnormal contralateral kidney. Mutations in the RET gene were only found in seven of the fetuses (6.6%).

In 2014 researchers found autosomal recessive mutations in ITGA8 in three members of two unrelated families utilizing Exome Sequencing . One of the families was consanguineous.

In 2017 researchers identified heritable autosomal dominant mutations in the gene GREB1L in two unrelated families as being the cause of both BRA and URA utilizing Exome Sequencing and direct sequencing analysis . This is the first reported genetic lesion implicated in the activation of Retinoic Acid Receptor (RAR) Targets that has been associated with renal agenesis in humans. The researchers found two different GREB1L mutations, each being unique to their respective pedigrees. In total, there were 23 individuals analyzed between the two families, four of which had BRA and five of which had URA. GREB1L mutations were identified in all of the affected individuals as well as in three unaffected family members, demonstrating incomplete penetrance and variable expressivity.

There are several hundred to perhaps several thousand genes that, if they had the right kind of mutation, could lead to renal agenesis in humans. It is possible that each individual or family experiencing renal agenesis has a unique gene or genetic mutation causing the condition due to the fact that there are so many genes that are critical to proper renal development. See Rosenblum S et al. for an excellent review of Congenital abnormalities of the Kidney and Urinary Tract

Chromosomal anomalies have been associated with BRA in certain cases (chromosomes 1, 2, 5 and 21), but these anomalies were not inherited and have not been observed in subsequent cases. Additionally, neither extreme substance abuse or environmental factors (high power line, mercury, ground water issues, etc.) have been reported to be linked to an increased incidence of BRA or other cause of Potter sequence. However, renal agenesis and other causes of oligohydramnios sequence have been linked to a number of other conditions and syndromes to include Down syndrome, Kallmann syndrome, branchio-oto-renal syndrome and others.

This is much more common, but is not usually of any major health consequence, as long as the other kidney is healthy.

It may be associated with an increased incidence of Müllerian duct abnormalities, which are abnormalities of the development of the female reproductive tract and can be a cause of infertility, blocked menstrual flow (hematocolpos), increased need for Caesarean sections, or other problems. Herlyn-Werner-Wunderlich syndrome is one such syndrome in which unilaterial renal agenesis is combined with a blind hemivagina and uterus didelphys. Up to 40% of women with a urogenital tract anomaly also have an associated renal tract anomaly.

Adults with unilateral renal agenesis have considerably higher chances of hypertension (high blood pressure). People with this condition are advised to approach contact sports with caution.

The odds of a person being born with unilateral renal agenesis are approximately 1 in 750.

Urinary tract obstruction as a congenital disorder results in oligohydramnios which in turn can lead to the Potter sequence of atypical physical appearance. Pulmonary hypoplasia is by far the main cause of death in the early neonatal period for children with congenital lower urinary tract obstruction.

Fetal surgery of congenital lower urinary tract obstruction seems to improve survival, according to a randomized yet small study.

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.