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.

Patients with ESKD are at increased overall risk for cancer. This risk is particularly high in younger patients and gradually diminishes with age. Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in patients with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved patient outcomes.

To minimize the risk for contrast-induced nephropathy, various actions can be taken if the patient has predisposing conditions. These have been reviewed in a meta-analysis. A separate meta-analysis addresses interventions for emergency patients with baseline insufficient kidney function.

Individuals with chronic kidney disease, diabetes mellitus, high blood pressure, reduced intravascular volume, or who are elderly are at increased risk of developing CIN after exposure to iodinated contrast.

A clinical prediction rule is available to estimate probability of nephropathy (increase ≥25% and/or ≥0.5 mg/dl in serum creatinine at 48 h):

Risk Factors:

- Systolic blood pressure <80 mm Hg - 5 points

- Intraarterial balloon pump - 5 points

- Congestive heart failure (Class III-IV or history of pulmonary edema) - 5 points

- Age >75 y - 4 points

- Hematocrit level <39% for men and <35% for women - 3 points

- Diabetes mellitus- 3 points

- Contrast media volume - 1 point for each 100 mL

- Decreased kidney function:

- Serum creatinine level >1.5 g/dL - 4 points

- Estimated Glomerular filtration rate (online calculator)

Scoring:

5 or less points

- Risk of CIN - 7.5

- Risk of Dialysis - 0.04%

6–10 points

- Risk of CIN - 14.0

- Risk of Dialysis - 0.12%

11–16 points

- Risk of CIN - 26.1*

- Risk of Dialysis - 1.09%

>16 points

- Risk of CIN - 57.3

- Risk of Dialysis - 12.8%

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.

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.

CKD increases the risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure.

Chronic kidney disease results in worse all-cause mortality (the overall death rate) which increases as kidney function decreases. The leading cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.

While renal replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected. Kidney transplantation increases the survival of people with stage 5 CKD when compared to other options; however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis.

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.

In ADPKD patients, gradual cyst development and expansion result in kidney enlargement, and during the course of the disease, glomerular filtration rate (GFR) remains normal for decades before kidney function starts to progressively deteriorate, making early prediction of renal outcome difficult. The CRISP study, mentioned in the treatment section above, contributed to build a strong rationale supporting the prognostic value of total kidney volume (TKV) in ADPKD; TKV (evaluated by MRI) increases steadily and a higher rate of kidney enlargement correlated with accelerated decline of GFR, while patient height-adjusted TKV (HtTKV) ≥600 ml/m predicts the development of stage 3 chronic kidney disease within 8 years.

Besides TKV and HtTKV, the estimated glomerular filtration rate (eGFR) has also been tentatively used to predict the progression of ADPKD. After the analysis of CT or MRI scans of 590 patients with ADPKD treated at the Mayo Translational Polycystic Kidney Disease Center, Irazabal and colleagues developed an imaging-based classification system to predict the rate of eGFR decline in patients with ADPKD. In this prognostic method, patients are divided into five subclasses of estimated kidney growth rates according to age-specific HtTKV ranges (1A, 6.0%) as delineated in the CRISP study. The decline in eGFR over the years following initial TKV measurement is significantly different between all five patient subclasses, with those in subclass 1E having the most rapid decline.

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.

According to the United States Renal Data System (USRDS), hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%.

Haemodialysis is recommended for patients who progress to end-stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes.

Patient prognosis is dependent on numerous factors including age, ethnicity, blood pressure and glomerular filtration rate. Changes in lifestyle factors, such as reduced salt intake and increased physical activity have been shown to improve outcomes but are insufficient without pharmacological treatment.

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

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

Depending on the cause, a proportion of patients (5–10%) will never regain full kidney function, thus entering end-stage kidney failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after being discharged from hospital, even if their kidney function has recovered.

The risk of developing chronic kidney disease is increased (8.8-fold).

The osmolality of the contrast agent was previously believed to be an important factor in contrast-induced nephropathy. Today it has become increasingly clear that other physicochemical properties play a greater role, such as viscosity. Attention should be paid to using contrast agents of low viscosity. Moreover, sufficient fluids should be supplied to limit fluid viscosity of urine. Modern iodinated contrast agents are non-ionic, the older ionic types caused more adverse effects, and their use has diminished.

It is accepted that kidney transplantation is the preferred treatment for ADPKD patients with end-stage renal disease (ESRD). Among American patients on the kidney transplant waiting list (as of December 2011), 7256 (8.4%) were listed due to cystic kidney disease and of the 16,055 renal transplants performed in 2011, 2057 (12.8%) were done for patients with cystic kidney disease, with 1,189 from deceased donors and 868 from living donors.

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.

Mortality after AKI remains high. Overall it is 20%, 30% if the patient is referred to nephrology, 50% if dialyzed, and 70% if on ICU.

If AKI develops after major surgery (13.4% of all people who have undergone major surgery) the risk of death is markedly increased (over 12-fold).

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).

Cortical necrosis is a severe and life-threatening condition, with mortality rates over 50%. Those mortality rates are even higher in neonates with the condition due to the overall difficult nature of neonatal care and an increased frequency of comorbid conditions. The extent of the necrosis is a major determinant of the prognosis, which in turn is dependent on the duration of ischemia, duration of oliguria, and the severity of the precipitating conditions. Of those that survive the initial event, there are varying degrees of recovery possible, depending on the extent of the damage.

Overall, most people with thin basement membrane disease have an excellent prognosis. Some reports, however, suggest that a minority might develop hypertension.

Thin basement membrane disease may co-exist with other kidney diseases, which may in part be explained by the high prevalence of thin basement membrane disease.

Management of sickle nephropathy is not separate from that of overall patient management. In addition, however, the use of ACE inhibitors has been associated with improvement of the hyperfiltration glomerulopathy. Three-year graft and patient survival in kidney transplant recipients with sickle nephropathy is lower when compared to those with other causes of end-stage kidney disease.

Many forms of cystic kidney disease can be detected in children prior to birth. Abnormalities which only affect one kidney are unlikely to cause a problem with the healthy arrival of a baby. Abnormalities which affect both kidneys can have an effect on the baby's amniotic fluid volume which can in turn lead to problems with lung development. Some forms of obstruction can be very hard to differentiate from cystic renal disease on early scans.

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 incidence of hypertensive nephropathy varies around the world. For instance, it accounts for as many as 25% and 17% of patients starting dialysis for end-stage kidney disease in Italy and France respectively. Contrastingly, Japan and China report only 6 and 7% respectively. Since the year 2000, nephropathy caused by hypertension has increased in incidence by 8.7% In reality, these figures may be even higher, as hypertension is not always reported as the specific cause of kidney disease.

It has been recognized that the incidence of hypertensive nephropathy varies with ethnicity. Compared to Caucasians, African Americans in the USA are much more likely to develop hypertensive nephropathy. Of those who do, the proportion who then go on to develop end-stage renal failure is 3.5 times higher than in the Caucasian population. In addition to this, African Americans tend to develop hypertensive nephropathy at a younger age than Caucasians (45 to 65, compared to >65).