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%

Male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidemia, older age, familial disease and elevated creatinine concentrations are markers of a poor outcome. Frank hematuria has shown discordant results with most studies showing a better prognosis, perhaps related to the early diagnosis, except for one group which reported a poorer prognosis. Proteinuria and hypertension are the most powerful prognostic factors in this group.

There are certain other features on kidney biopsy such as interstitial scarring which are associated with a poor prognosis. ACE gene polymorphism has been recently shown to have an impact with the DD genotype associated more commonly with progression to kidney failure.

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.

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

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

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.

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.

The epidemiology of rapidly progressive glomerulonephritis according to Hedger, et al., is an incidence rate of 3.9 individuals per million (3.3–4.7) with a 95% confidence intervals.

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.

Men are affected three times as often as women. There is also marked geographic variation in the prevalence of IgA nephropathy throughout the world. It is the most common glomerular disease in the Far East and Southeast Asia, accounting for almost half of all the patients with glomerular disease. However, it accounts for only about 25% of the proportion in European and about 10% among North Americans, with African–Americans having a very low prevalence of about 2%. However, a confounding factor in this analysis is the existing policy of screening and use of kidney biopsy as an investigative tool. School children in Japan undergo routine urinalysis (as do army recruits in Singapore) and any suspicious abnormality is pursued with a kidney biopsy, which might partly explain the high observed incidence of IgA nephropathy in those countries.

There is no proven therapy for the CFHR5 nephropathy, although research is currently underway to develop ways of preventing kidney failure developing in those affected.

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.

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.

Over time, kidney failure can develop and most men with the disease will eventually require dialysis or kidney transplantation. For reasons which are not understood, women with the disease, although they often have blood in their urine, only rarely develop kidney failure. The disease has been shown to recur following kidney transplantation, however in most cases the kidney transplant has a normal lifespan.

Complications of analgesic nephropathy include pyelonephritis and end-stage kidney disease. Risk factors for poor prognosis include recurrent urinary tract infection and persistently elevated blood pressure. Analgesic nephropathy also appears to increase the risk of developing cancers of the urinary system.

About a third of untreated patients have spontaneous remission, another third progress to require dialysis and the last third continue to have proteinuria, without progression of renal failure.

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.

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

Diabetic nephropathy in type 2 diabetes can be more difficult to predict because the onset of diabetes is not usually well established. Without intervention, 20-40 percent of patients with type 2 diabetes/microalbuminuria, will evolve to macroalbuminuria.

Diabetic nephropathy is the most common cause of end-stage kidney disease, which may require hemodialysis or even kidney transplantation. It is associated with an increased risk of death in general, particularly from cardiovascular disease.

The scarring of the small blood vessels, called capillary sclerosis, is the initial lesion of analgesic nephropathy. Found in the renal pelvis, ureter, and capillaries supplying the nephrons, capillary sclerosis is thought to lead to renal papillary necrosis and, in turn, chronic interstitial nephritis.

How phenacetin and other analgesics lead to this damage is incompletely understood. It is currently thought that the kidney toxicities of NSAIDs and the antipyretics phenacetin and paracetamol may combine to give rise to analgesic nephropathy. A committee of investigators reported in 2000 that there was insufficient evidence to suggest that non-phenacetin analgesics by themselves are associated with analgesic nephropathy.

The molecular basis for thin basement membrane disease has yet to be elucidated fully; however, defects in type IV collagen have been reported in some families.

Some individuals with TBMD are thought to be carriers for genes that cause Alport syndrome.

Proteinuria may be a feature of the following conditions:

- Nephrotic syndromes (i.e. intrinsic renal failure)

- Pre-eclampsia

- Eclampsia

- Toxic lesions of kidneys

- Amyloidosis

- Collagen vascular diseases (e.g. systemic lupus erythematosus)

- Dehydration

- Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis)

- Strenuous exercise

- Stress

- Benign orthostatic (postural) proteinuria

- Focal segmental glomerulosclerosis (FSGS)

- IgA nephropathy (i.e. Berger's disease)

- IgM nephropathy

- Membranoproliferative glomerulonephritis

- Membranous nephropathy

- Minimal change disease

- Sarcoidosis

- Alport's syndrome

- Diabetes mellitus (diabetic nephropathy)

- Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin)

- Fabry's disease

- Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)

- Aminoaciduria

- Fanconi syndrome in association with Wilson disease

- Hypertensive nephrosclerosis

- Interstitial nephritis

- Sickle cell disease

- Hemoglobinuria

- Multiple myeloma

- Myoglobinuria

- Organ rejection:

- Ebola virus disease

- Nail patella syndrome

- Familial Mediterranean fever

- HELLP Syndrome

- Systemic lupus erythematosus

- Granulomatosis with polyangiitis

- Rheumatoid arthritis

- Glycogen storage disease type 1

- Goodpasture's syndrome

- Henoch–Schönlein purpura

- A urinary tract infection which has spread to the kidney(s)

- Sjögren's syndrome

- Post-infectious glomerulonephritis

85% of MGN cases are classified as "primary membranous glomerulonephritis"—that is to say, the cause of the disease is idiopathic (of unknown origin or cause). This can also be referred to as "idiopathic membranous nephropathy". One study has identified antibodies to an M-type phospholipase A receptor in 70% (26 of 37) cases evaluated. Other studies have implicated neutral endopeptidase and cationic bovine serum albumin as antigens.

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).

There are three main mechanisms to cause proteinuria:

- Due to disease in the glomerulus

- Because of increased quantity of proteins in serum (overflow proteinuria)

- Due to low reabsorption at proximal tubule (Fanconi syndrome)

Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. Excessive fluid intake (drinking in excess of 4 litres of water per day) is another cause.

Also leptin administration to normotensive Sprague Dawley rats during pregnancy significantly increases urinary protein excretion.

Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field.

With severe proteinuria, general hypoproteinemia can develop which results in

diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax.