Acute uric acid nephropathy is caused by deposition of uric acid crystals within the kidney interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter. This obstruction is usually bilateral, and patients follow the clinical course of acute renal failure.

Acute uric acid nephropathy (AUAN, also acute urate nephropathy) is a rapidly worsening (decreasing) kidney function (renal insufficiency) that is caused by high levels of uric acid in the urine (hyperuricosuria).

Phosphate nephropathy consists of damage to the kidneys caused by the formation of phosphate crystals within the kidney's tubules, damaging the nephron, and can cause acute kidney failure.

Phosphate nephropathy frequently occurs following the ingestion of oral sodium phosphate laxatives such as C.B. Fleet's Phospho soda and Salix's Visocol taken for bowel cleansing prior to a colonoscopy. The risk of this complication is increased with age, dehydration, or in the presence of hypertension or if the patient is taking an ACE inhibitor or angiotensin receptor blocker. Other agents used for bowel preparation (e.g. magnesium citrate or PEG-3350 & electrolyte-based purgatives such as Colyte or Golytely) do not carry this risk.

According to the U.S. Food and Drug Administration (FDA), "Acute phosphate nephropathy is a form of acute kidney injury that is associated with deposits of calcium-phosphate crystals in the renal tubules that may result in permanent renal function impairment. Acute phosphate nephropathy is a rare, serious adverse event that has been associated with the use of OSPs. The occurrence of these events was previously described in an Information for Healthcare Professionals sheet and an FDA Science Paper issued in May 2006. Additional cases of acute phosphate nephropathy have been reported to FDA and described in the literature since these were issued."

When a kidney damaged by phosphate nephropathy is biopsied, the pathological findings are typical of nephrocalcinosis: diffuse tubular injury with calcium phosphate crystal deposition.

Hyperuricosuria is a medical term referring to the presence of excessive amounts of uric acid in the urine. For men this is at a rate greater than 800 mg/day, and for women, 750 mg/day. Notable direct causes of hyperuricosuria are dissolution of uric acid crystals in the kidneys or urinary bladder, and hyperuricemia. Notable indirect causes include uricosuric drugs, rapid breakdown of bodily tissues containing large quantities of DNA and RNA, and a diet high in purine.

Drugs that may contribute to the cure or amelioration of hyperuricosuria include allopurinol which acts by inhibiting xanthine oxidase and reducing uric acid production.Hyperuricosuria "may" be a medical sign of:

- Gout (very common)

- Kidney stones of uric acid (uric acid nephrolithiasis)

- Acute uric acid nephropathy

- Acute renal failure

- Tumor lysis syndrome

- Fanconi syndrome

- Dent's disease (very rare)

Symptoms (and signs) consistent with renal papillary necrosis are:

Acute hyperuricosuria is a common complication of tumor lysis syndrome. This syndrome appears not to contribute to gout and to uric acid nephrolithiasis, which is evidence that these two conditions have chronic, not acute, causes.

Chronic hyperuricosuria is associated with gout and uric acid nephrolithiasis. However, both conditions can occur in the absence of hyperuricosuria. Treatment of gout with uricosuric drugs can lead to uric acid nephrolithiasis.

Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months or years. Early on there are typically no symptoms. Later, leg swelling, feeling tired, vomiting, loss of appetite, or confusion may develop. Complications may include heart disease, high blood pressure, bone disease, or anemia.

Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of the condition. Diagnosis is generally by blood tests to measure the glomerular filtration rate and urine tests to measure albumin. Further tests such as an ultrasound or kidney biopsy may be done to determine the underlying cause. A number of different classification systems exist.

Screening at-risk people is recommended. Initial treatments may include medications to manage blood pressure, blood sugar, and lower cholesterol. NSAIDs should be avoided. Other recommended measures include staying active and certain dietary changes. Severe disease may require hemodialysis, peritoneal dialysis, or a kidney transplant. Treatments for anemia and bone disease may also be required.

Chronic kidney disease affected about 323 million people globally in 2015. In 2015 it resulted in 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

CKD is initially without specific symptoms and is generally only detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

- Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin-angiotensin system, increasing one's risk of developing hypertension and/or suffering from congestive heart failure.

- Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic circulation, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost").

- Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 ml/min/1.73 m, at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.

- Erythropoietin synthesis is decreased causing anemia.

- Fluid volume overload symptoms may range from mild edema to life-threatening pulmonary edema.

- Hyperphosphatemia, due to reduced phosphate excretion, follows the decrease in glomerular filtration. Hyperphosphatemia is associated with increased cardiovascular risk, being a direct stimulus to vascular calcification. Moreover, circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the renal capacity for phosphate excretion declines, but this adaptative response may also contribute to left ventricular hypertrophy and increased mortality in CKD patients.

- Hypocalcemia, due to 1,25 dihydroxyvitamin D deficiency (caused by stimulation of FGF-23 and reduction of renal mass), and resistance to the calcemic action of parathyroid hormone. Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D). Later, this progresses to secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis.

- The concept of chronic kidney disease-mineral bone disorder (CKD-MBD) currently describes a broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism due to CKD manifested by either "one or a combination" of: 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and 3) vascular or other soft-tissue calcification. CKD-MBD has been associated to poor hard outcomes.

- Metabolic acidosis (due to accumulation of sulfates, phosphates, uric acid etc.) may cause altered enzyme activity by excess acid acting on enzymes; and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia). Acidosis is also due to decreased capacity to generate enough ammonia from the cells of the proximal tubule.

- Iron deficiency anemia, which increases in prevalence as kidney function decreases, is especially prevalent in those requiring haemodialysis. It is multifactoral in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone marrow suppression.

People with CKD suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with CKD and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.

Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.

Causes of kidney disease include deposition of the IgA antibodies in the glomerulus, administration of analgesics, xanthine oxidase deficiency, toxicity of chemotherapy agents, and long-term exposure to lead or its salts. Chronic conditions that can produce nephropathy include systemic lupus erythematosus, diabetes mellitus and high blood pressure (hypertension), which lead to diabetic nephropathy and hypertensive nephropathy, respectively.

Kidney disease is a non-communicable disease, having serious consequences if it cannot be controlled effectively. Generally, the process of kidney disease development is from light to serious. Some kidney diseases can cause renal failure.

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.

Nephrosis is any of various forms of kidney disease (nephropathy). In an old and broad sense of the term, it is any nephropathy, but in current usage the term is usually restricted to a narrower sense of nephropathy without inflammation or neoplasia, in which sense it is distinguished from nephritis, which involves inflammation. It is also defined as any purely degenerative disease of the renal tubules. Nephrosis is characterized by a set of signs called the nephrotic syndrome. Nephrosis can be a primary disorder or can be secondary to another disorder. Nephrotic complications of another disorder can coexist with nephritic complications. In other words, nephrosis and nephritis can be pathophysiologically contradistinguished, but that does not mean that they cannot occur simultaneously.

Types of nephrosis include amyloid nephrosis and osmotic nephrosis.

Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on renal function. There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.

Nephrotoxicity should not be confused with the fact that some medications have a predominantly renal excretion and need their dose adjusted for the decreased renal function (e.g., heparin).

The nephrotoxic effect of most drugs is more profound in patients already suffering from kidney failure.

Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula, or drugs such as pyridium.

Myeloma cast nephropathy, also cast nephropathy, is the formation of plugs (urinary casts) in the renal tubules from free immunoglobulin light chains leading to renal failure in the context of multiple myeloma.

CFHR5 nephropathy usually presents with microscopic amounts of blood in the urine, detectable on a routine urine dipstick test. Sometimes the disease is associated with visible blood in the urine, usually at the time of respiratory or other infections and this is thought to result from stimulation of the immune system leading to damage in the kidneys.

The underlying calyces lose their normal concave shape and show clubbing.

Most patients with thin basement membrane disease are incidentally discovered to have microscopic hematuria on urinalysis. The blood pressure, kidney function, and the urinary protein excretion are usually normal. Mild proteinuria (less than 1.5 g/day) and hypertension are seen in a small minority of patients. Frank hematuria and loin pain should prompt a search for another cause, such as kidney stones or loin pain-hematuria syndrome. Also, there are no systemic manifestations, so presence of hearing impairment or visual impairment should prompt a search for hereditary nephritis such as Alport syndrome.

The histopathology is characterized by interstitial fibrosis, tubular atrophy,

fibrotic intimal thickening of arteries and glomerulosclerosis.

The symptoms of reflux nephropathy are comparable to nephrotic syndrome and infection of the urinary tract, though some individuals may not exhibit any evidence (symptom) of reflux nephropathy.

Albuminuria is a pathological condition wherein the protein albumin is abnormally present in the urine. It is a type of proteinuria. Albumin is a major plasma protein (normally circulating in the blood); in healthy people, only trace amounts of it are present in urine, whereas larger amounts occur in the urine of patients with kidney disease. For a number of reasons, clinical terminology is changing to focus on albuminuria more than proteinuria.

It is usually asymptomatic but whitish foam may appear in urine. Swelling of the ankles, hands, belly or the face may occur if losses of albumin are significant and produce low serum protein levels (nephrotic syndrome).

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.

The onset of symptoms is 5 to 10 years after the disease begins. A usual first symptom is frequent urination at night: nocturia. Other symptoms include tiredness, headaches, a general feeling of illness, nausea, vomiting, frequent daytime urination, lack of appetite, itchy skin, and leg swelling.

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.