In terms of cause, almost any condition that involves ischemia can lead to renal papillary necrosis. A mnemonic for the causes of renal papillary necrosis is POSTCARDS: pyelonephritis, obstruction of the urogenital tract, sickle cell disease, tuberculosis, cirrhosis of the liver, analgesia/alcohol abuse, renal vein thrombosis, diabetes mellitus, and systemic vasculitis. Often, a patient with renal papillary necrosis will have numerous conditions acting synergistically to bring about the disease.

Analgesic nephropathy is a common cause of renal papillary necrosis. The damage is cumulative and most patients of renal papillary necrosis would have ingested at least 2 kg of analgesics in the past. The risk is higher for phenacetin (which was withdrawn from market in the United States) and paracetamol (acetaminophen) compared to aspirin and other NSAIDs.

The pathophysiology of this condition can be due to analgesic nephropathy, which in turn is a result of long-term use of aspirin. It is a sequence of vascular occlusion, vasospasm, then infection and finally obstruction which leads to RPN.

The prognosis of nephrocalcinosis is determined by the underlying cause. Most cases of nephrocalcinosis do not progress to end stage renal disease, however if not reated it can lead to renal dysfunction this includes primary hyperoxaluria, hypomagnesemic hypercalciuric nephrocalcinosis and Dent's disease. Once nephrocalcinosis is found, it is unlikely to be reversed, however, partial reversal has been reported in patients who have had successful treatment of hypercalciuria and hyperoxaluria following corrective intestinal surgery.

Renal tuberculosis

And other causes of hypercalcemia (and thus hypercalciuria)

- Immobilization (leading to hypercalcemia and hypercalciuria)

- Milk-alkali syndrome

- Hypervitaminosis D

- Multiple myeloma

Small angiomyolipomas and those without dilated blood vessels (aneurysms) cause few problems, but angiomyolipomas have been known to grow as rapidly as 4 cm in one year. An angiomyolipoma larger than 5 cm and those containing an aneurysm pose a significant risk of rupture, which is a medical emergency as it is potentially life-threatening. One population study found the cumulative risk of haemorrhage to be 10% in males and 20% in females.

A second problem occurs when the renal angiomyolipomas take over so much kidney that the function is impaired leading to chronic kidney disease. This may be severe enough to require dialysis. A population survey of patients with TSC and normal intelligence found 1% were on dialysis.

Treatment varies according to severity, ranging from monitoring of the hematoma (in haemodynamic stability) to emergency surgery (when patients develop hypovolemic shock requiring seminephrectomy or nephrectomy). Vascular causes lead to surgery due to severity of hemorrhage. Robotic-assisted partial nephrectomy has been proposed as a surgical treatment of a ruptured angiomyolipoma causing retroperitoneal hemorrhage, combining the advantages of a kidney preservation procedure and the benefits of a minimally invasive procedure without compromising the safety of the patient.

PKD is caused by abnormal genes which produce a specific abnormal protein which has an adverse affect on tubule development. PKD is a general term for two types, each having their own pathology and genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD).

Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Given their importance in massive nutrient and electrolyte reabsorption, the proximal tubule and medullary thick ascending limb require significant ATP and are most susceptible to ischemic damage. Thus, ischemic ATN specifically causes "skip lesions" through the tubules.

IIAs are uncommon, accounting for 2.6% to 6% of all intracranial aneurysms in autopsy studies.

Mortality of IIA is high, unruptured IIA are associated with a mortality reaching 30%, while ruptured IIA has a mortality of up to 80%. IIAs caused by fungal infections have a worse prognosis than those caused by bacterial infection.

Toxic ATN can be caused by free hemoglobin or myoglobin, by medication including antibiotics such as aminoglycoside, statins such as atorvastatin, and cytotoxic drugs such as cisplatin, or by intoxication (ethylene glycol, "anti-freeze").

Histopathology: Toxic ATN is characterized by proximal tubular epithelium necrosis (no nuclei, intense eosinophilic homogeneous cytoplasm, but preserved shape) due to a toxic substance (poisons, organic solvents, drugs, heavy metals). Necrotic cells fall into the tubule lumen, obturating it, and determining acute kidney failure. Basement membrane is intact, so the tubular epithelium regeneration is possible. Glomeruli are not affected.

Angiomyolipomas are the most common benign tumour of the kidney and are found either in patients with tuberous sclerosis or sporadically. About 80–90% of cases are sporadic and these are most commonly found in middle-aged women.

In patients with TSC, a longitudinal study found 80% will have some form of renal lesion by around 10 years of age. Of these, 75% are angiomyolipomas and 17% cysts. The angiomyolipomas increased in size in around 60% of these children. An autopsy study and TSC clinic survey found a prevalence of 67% and 85% respectively for patients with TSC. Both genders are affected equally.

Wunderlich syndrome is spontaneous, nontraumatic renal hemorrhage confined to the subcapsular and perirenal space. It may be the first manifestation of a renal angiomyolipoma (AML), or rupture of renal artery or intraparechymal aneurysm.

PKD is one of the most common hereditary diseases in the United States, affecting more than 600,000 people. It is the cause of nearly 10% of all end-stage renal disease. It equally affects men, women, and all races. PKD occurs in some animals as well as humans.

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.

The cause of LPHS is not known. One theory proposes that it is caused by a thin glomerular basement membrane and red blood cell (RBC) renal tubular congestion that leads to swelling of the kidney and distension of the renal fascia resulting in pain.

Researchers have hypothesized that the syndrome may be due to blood vessel diseases of the kidney, spasms of the kidney vessels, or other bleeding disorders (coagulopathy).

The hematuria in LPHS may be due to an abnormal (thick or thin) glomerular basement membrane. The glomerular basement membrane is a tissue in the kidney that filters the blood. An abnormal glomerular basement membrane may allow red blood cells into the urinary space. Because kidney stones are so common in people with LPHS, crystals in the kidney tubules may also play a part in bleeding and pain.

Other speculations on cause include

- IgA nephropathy. This is a condition in which small amount of a type of normal antibody (called IgA) get stuck in the kidney as it passes through in the bloodstream. This is a chronic condition, which sometimes goes away on its own but occasionally can cause damage to the kidneys. A related condition called IgM nephropathy can sometimes cause pain.

- Thin membrane disease. In this condition the membrane that filters the blood to make urine is too thin, and blood can pass across it in very small amounts. In a few cases of this condition, there is pain in the kidneys, usually occurring in attacks every so often. Although this condition can be painful, kidney failure does not seem to occur in the long term, so that the only real problem is the symptoms.

- Infection. In some cases, loin pain-haematuria syndrome occurs after a bladder infection with involvement of the kidney. Even when the infection has been treated and bugs can no longer be found in the urine, pain may persist for 6 months, or even longer in some cases.

- "Classic loin pain-haematuria syndrome". Some patients have none of the above diagnoses. In these cases there may be minor abnormalities on a kidney biopsy. Angiogram tests to look at the blood vessels in the kidney may show abnormal blood flow, perhaps causing a cramp like pain. The cause is not fully understood. It certainly is [more common] in women than in men, and there may be hormonal influences. Some women find the pain is worse at different times of their menstrual cycle, or comes on during pregnancy, or if they are taking [oral contraceptives].

It has also been reported to be caused by microscopic granules of calcium oxylate into the glomerulus itself, causing blood vessels to rupture and increase the distention of the renal capsule.

This condition may persist for some years, and can be lifelong. Damage to the kidneys leading to kidney failure does not occur. However, because LPHS is unusual in patients older than 60 years, some clinicians believe that LPHS eventually resolves.

At this time no cure has been found for this disease. LPHS is a debilitating disease due to chronic pain and the inability to know how to control the glomerular aspect. The pain of LPHS can be worsened by acts as simple as riding in the car and undertaking daily activities. Many people with this disease are unable to maintain employment due to the debilitating pain.

Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules.

Nephritis is often caused by infections, and toxins, but is most commonly caused by autoimmune disorders that affect the major organs like kidneys.

- Pyelonephritis is inflammation that results from a urinary tract infection that reaches the renal pelvis of the kidney.

- Lupus nephritis is inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system.

- "Athletic nephritis" is nephritis resulting from strenuous exercise. Bloody urine after strenuous exercise may also result from march hemoglobinuria, which is caused by trauma to red blood cells, causing their rupture, which leads to the release of hemoglobin into the urine.

Death occurs immediately after traumatic rupture of the thoracic aorta 75%–90% of the time since bleeding is so severe, and 80–85% of patients die before arriving at a hospital. Of those who live to reach a hospital, 23% die at the time of or shortly after arrival. In the US, an estimated 7,500–8,000 cases occur yearly, of which 1,000–1,500 make it to a hospital alive; these low numbers make it difficult to estimate the efficacy of surgical options. However, if surgery is performed in time, it can offer a chance of survival.

Though there is a concern that a small, stable tear in the aorta could enlarge and cause complete rupture of the aorta and heavy bleeding, this may be less common than previously believed as long as the patient's blood pressure does not get too high.

The vascular subtype of Ehlers-Danlos Syndrome (type IV) has been associated with multi-focal FMD. This syndrome should be suspected in patients with multiple aneurysms and/or tears (dissections) in arteries in addition to the typical angiographic findings of FMD. There have been isolated reports of FMD associated with other disorders, including Alport syndrome, pheochromocytoma, Marfan syndrome, Moyamoya disease, and Takayasu's arteritis.

The incidence of myocardial rupture has decreased in the era of urgent revascularization and aggressive pharmacological therapy for the treatment of an acute myocardial infarction. However, the decrease in the incidence of myocardial rupture is not uniform; there is a slight increase in the incidence of rupture if thrombolytic agents are used to abort a myocardial infarction. On the other hand, if primary percutaneous coronary intervention is performed to abort the infarction, the incidence of rupture is significantly lowered. The incidence of myocardial rupture if PCI is performed in the setting of an acute myocardial infarction is about 1 percent.

Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.

Bladder tamponade is obstruction of the bladder outlet due to heavy blood clot formation within it. It generally requires surgery. Such heavy bleeding is usually due to bladder cancer.

Prognosis and outcome research is scant. In some cases if not managed properly FMD-related aneurysms can occur causing bleeding into the brain, resulting in stroke, permanent nerve damage, or death. Shedding light in the importance of detection and seeking appropriate care in reference to outcomes. What we do know is patients with multi-focal fibroplasia generally have a favorable prognosis. However, those who present with FMD in multiple vascular beds, or focal disease involving multiple branches of the renal arteries may develop renal artery dissection or progressive renal impairment. Therefore, having a more difficult and complex prognostic course. There are presently no specific studies or reports on the long-term prognosis and outcome of FMD in children.

Urinary bladder disease includes urinary bladder inflammation such as cystitis, bladder rupture and bladder obstruction (tamponade).