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.

Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies suggest people who take calcium or vitamin D as a dietary supplement have a higher risk of developing kidney stones. In the United States, kidney stone formation was used as an indicator of excess calcium intake by the Reference Daily Intake committee for calcium in adults.

In the early 1990s, a study conducted for the Women's Health Initiative in the US found that postmenopausal women who consumed 1000 mg of supplemental calcium and 400 international units of vitamin D per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a placebo. The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.

Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development. This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation—about 15 times stronger than calcium.

A 2004 study found that diets low in calcium are associated with a higher overall risk for kidney stone formation. For most individuals, other risk factors for kidney stones, such as high intakes of dietary oxalates and low fluid intake, play a greater role than calcium intake.

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.

Renal tuberculosis

And other causes of hypercalcemia (and thus hypercalciuria)

- Immobilization (leading to hypercalcemia and hypercalciuria)

- Milk-alkali syndrome

- Hypervitaminosis D

- Multiple myeloma

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

Nephrocalcinosis Is connected with conditions that cause hypercalcemia, hyperphosphatemia, and the increased excretion of calcium, phosphate, and/or oxalate in the urine. A high urine pH can lead to Nephrocalcinosis. In conjustion with Nephrocalcinosis, hypercalcemia and hypercalciuria the following can occur:

- Primary hyperparathyroidism: Nephrocalcinosis is one of the most common symptoms of primary hyperparathyroidism.

- Sarcoidosis: Nephrocalcinosis is one of the most common symptoms.

- Vitamin D therapy: This can cause nephrocalcinosis because of Vitamin D therapy becauseit increase the absorption of ingested calcium and bone resorption, resulting in hypercalcemia and hypercalciuria.

The "APOL1" gene has been proposed as a major genetic risk locus for a spectrum of nondiabetic renal failure in individuals of African origin, these include HIV-associated nephropathy (HIVAN), primary nonmonogenic forms of focal segmental glomerulosclerosis, and hypertension affiliated chronic kidney disease not attributed to other etiologies. Two western African variants in APOL1 have been shown to be associated with end stage kidney disease in African Americans and Hispanic Americans.

The long-term use of lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, is known to cause nephropathy.

In kidney stones, calcium oxalate is the most common mineral type (see Nephrolithiasis). Uric acid is the second most common mineral type, but an "in vitro" study showed uric acid stones and crystals can promote the formation of calcium oxalate stones.

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.

Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.

Chronic kidney disease (CKD) has numerous causes. The most common causes of CKD are diabetes mellitus and long-term, uncontrolled hypertension. Polycystic kidney disease is another well-known cause of CKD. The majority of people afflicted with polycystic kidney disease have a family history of the disease. Other genetic illnesses affect kidney function, as well.

Overuse of common drugs such as ibuprofen, and acetaminophen (paracetamol) can also cause chronic kidney disease.

Some infectious disease agents, such as hantavirus, can attack the kidneys, causing kidney failure.

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.

Stones can cause disease by several mechanisms:

- Irritation of nearby tissues, causing pain, swelling, and inflammation

- Obstruction of an opening or duct, interfering with normal flow and disrupting the function of the organ in question

- Predisposition to infection (often due to disruption of normal flow)

A number of important medical conditions are caused by stones:

- Nephrolithiasis (kidney stones)

- Can cause hydronephrosis (swollen kidneys) and renal failure

- Can predispose to pyelonephritis (kidney infections)

- Can progress to urolithiasis

- Urolithiasis (urinary bladder stones)

- Can progress to bladder outlet obstruction

- Cholelithiasis (gallstones)

- Can predispose to cholecystitis (gall bladder infections) and ascending cholangitis (biliary tree infection)

- Can progress to choledocholithiasis (gallstones in the bile duct) and gallstone pancreatitis (inflammation of the pancreas)

- Gastric calculi can cause colic, obstruction, torsion, and necrosis.

There are three main types of primary hyperoxaluria, each associated with specific metabolic defects. Type 1 is the most common and rapidly progressing form, accounting for about 80% of all cases. Type 2 and 3 account for about approximately 10% each of the population.

Mutations in these genes cause a decreased production or activity of the proteins they make, which stops the normal breakdown of glyoxylate.

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.

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

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

Cystinuria is an inherited autosomal recessive disease that is characterized by high concentrations of the amino acid cystine in the urine, leading to the formation of cystine stones in the kidneys, ureter, and bladder. It is a type of aminoaciduria.

Cystinuria is a cause of persistent kidney stones. It is a disease involving the defective transepithelial transport of cystine and dibasic amino acids in the kidney and intestine, and is one of many causes of kidney stones. If not treated properly, the disease could cause serious damage to the kidneys and surrounding organs, and in some rare cases death. The stones may be identified by a positive nitroprusside cyanide test. The crystals are usually hexagonal, translucent, white. Upon removal, the stones may be pink or yellow in color, but later they turn to greenish due to exposure to air. Cystinuria is usually asymptomatic when no stone is formed. However, once a stone is formed, or if stone production is severe or frequent, symptoms may be present:

- Nausea/vomiting

- Dull ache or "colicky" pain

- Chronic pain

- Hematuria

- Obstructive syndromes like hydronephrosis

- Infective syndromes like pyelonephritis

Cystinurics can also experience chronic pain in one, or both, kidneys due to the scars that the jagged edges of the stones can leave or damage from multiple stone removal surgeries. This can leave a cystinuric in constant pain which often requires medical intervention, such as long-term use of analgesics or surgical procedures, including T11, T12 or T13 nerve blocks (although, these procedures are often not successful, they can provide some relief). Aside from the chronic pain, a cystinuric will often have severe breakthrough pain from passing stones. People with cystinuria pass stones monthly, weekly, or daily, and need ongoing care. Cystinurics have an increased risk for chronic kidney disease and since kidney damage or poor function is often present in cystinurics, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or over the counter (OTC) medications should be used with caution.

Cystine stones are often not visible on most x-rays, CT's, and ultrasounds. This does not mean the cystinuric doesn't have a stone. It takes a trained eye and experience to spot a cystine stone. It is not unusual for a cystinuric to pass a stone, or stones, after being released from the hospital with a CT or x-ray result of no stones in the kidneys.

Urine odor in cystinuria has a smell of rotten eggs due to the increase in cystine.

Urinary stones may be composed of the following substances:

- Calcium oxalate monohydrate (whewellite)

- Calcium oxalate dihydrate (weddellite)

- Calcium phosphate

- Magnesium phosphate

- Ammonium phosphate

- Ammonium magnesium phosphate (struvite)

- Calcium hydroxyphosphate (apatite)

- Uric acid and its salts (urates)

- Cystine

- Xanthine

- Indigotin (rare)

- Urostealith (rare)

- Sulfonamide (rare)

Increase the water intake to prevent oxalates to precipitate .

Minimize dietary intake of oxalates by restricting the intake of leafy vegetables , sesame seeds , tea , cocoa , beet root , spinach , rhubarb , etc.

Bladder stones may occur whenever the kidneys, bladder, or ureters become inflamed, which may occur when the urine becomes too concentrated or when the body becomes dehydrated. Minerals such as calcium and magnesium crystallize into the stones, which then can cause such symptoms as lower back or abdominal pain or difficulty with urination. The use of urinary catheters may cause a bladder stone. Individuals who are paralyzed or are unable to adequately pass urine may require the use of small plastic tubes (catheters) placed into the bladder. The use of these tubes may lead to an infection, which irritates the bladder, resulting in stone formation. Finally, a kidney stone may travel down the ureter into the bladder and become a bladder stone. There is some evidence indicating that chronic irritation of the bladder by retained stones may increase the chance of bladder cancer. Urinary schistosomiasis, a disease caused by the digenean trematode "Schistosoma haematobium", has been implicated in the development of vesical calculi. However, evidence accumulated thus far has not supported this hypothesis.

Failure of kidney function, which can have multiple causes including medications or toxins (e.g., antifreeze, cephalosporins, ACEIs); diabetes; high blood pressure. Stones or tumours in the urinary tract can also cause it by creating an obstruction to urinary flow. High blood calcium, oxalate, or uric acid, can contribute to the risk of stone formation. In males, an enlarged prostate gland is a common cause of obstructive anuria.

Acute anuria, where the decline in urine production occurs quickly, is usually a sign of obstruction or acute renal failure. Acute renal failure can be caused by factors not related to the kidney, such as heart failure, mercury poisoning, infection, and other conditions that cause the kidney to be deprived of blood flow.

Anuria, sometimes called anuresis, is nonpassage of urine, in practice is defined as passage of less than 100 milliliters of urine in a day. Anuria is often caused by failure in the function of kidneys. It may also occur because of some severe obstruction like kidney stones or tumours. It may occur with end stage renal disease. It is a more extreme reduction than oliguria (hypouresis), with 400 mL/day being the conventional (albeit slightly arbitrary) cutoff point between the two.