Renal tuberculosis

And other causes of hypercalcemia (and thus hypercalciuria)

- Immobilization (leading to hypercalcemia and hypercalciuria)

- Milk-alkali syndrome

- Hypervitaminosis D

- Multiple myeloma

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.

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).

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).

ADPKD individuals might have a normal life; conversely, ARPKD can cause kidney dysfunction and can lead to kidney failure by the age of 40-60. ADPKD1 and ADPKD2 are very different, in that ADPKD2 is much milder.

Currently, there are no therapies proven effective to prevent the progression of polycystic kidney disease (autosomal dominant).

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).

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

Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. Common causes of ATN include low blood pressure and use of nephrotoxic drugs. The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN. Management relies on aggressive treatment of the factors that precipitated ATN (e.g. hydration and cessation of the offending drug). Because the tubular cells continually replace themselves, the overall prognosis for ATN is quite good if the cause is corrected, and recovery is likely within 7 to 21 days.

Dent's disease (or Dent disease) is a rare X-linked recessive inherited condition that affects the proximal renal tubules of the kidney. It is one cause of Fanconi syndrome, and is characterized by tubular proteinuria, excess calcium in the urine, formation of calcium kidney stones, nephrocalcinosis, and chronic kidney failure.

"Dent's disease" is often used to describe an entire group of familial disorders, including X-linked recessive nephrolithiasis with kidney failure, X-linked recessive hypophosphatemic rickets, and both Japanese and idiopathic low-molecular-weight proteinuria. About 60% of patients have mutations in the "CLCN5" gene (Dent 1), which encodes a kidney-specific chloride/proton antiporter, and 15% of patients have mutations in the "OCRL1" gene (Dent 2).

ATN may be classified as either "toxic" or "ischemic". Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and susceptible to, due to their very high metabolism.

Dent disease 2 (nephrolithiasis type 2) is associated with the "OCRL" gene. Both Lowe syndrome (oculocerebrorenal syndrome) and Dent disease can be caused by truncating or missense mutations in "OCRL".

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.

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.

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.

In one study, hypouricemia was found in 4.8% of hospitalized women and 6.5% of hospitalized men. (The definition was less than 0.14 mmol l-1 for women and less than 0.20 mmol l-1 in men.)

Osmotic nephrosis refers to structural changes that occur at the cellular level in the human kidney. Cells, primarily of the straight proximal tubule, swell due to the formation of large vacuoles in the cytoplasm. These vacuoles occur in the presence of large amounts of certain solutes circulating in the tubules. However, despite the condition's name, the solutes do not cause change through osmotic forces but through pinocytosis. Once inside the cytoplasm, pinocytic vacuoles combine with each other and with lysosomes to form large vacuoles that appear transparent under microscopic examination.

There may be no symptomatic presentation with this condition, or it may confused with other nephrotic conditions such as Tubular calcineurin-inhibitor toxicity. Affected cells of the proximal tubule may be passed in the urine, but a kidney biopsy is the only sure way to make a diagnosis.

Responsible exogenous solutes include sucrose-containing IVIg, mannitol, dextran, contrast dye, and hydroxyethyl starch. Prevention includes standard preventions for iatrogenic kidney damage. Osmotic nephrosis is usually reversible but can lead to chronic renal failure.

Medical conditions that can cause hypouricemia include:

- Fanconi syndrome

- Hyperthyroidism

- Multiple sclerosis

- Myeloma

- Nephritis

- Wilson's disease

Familial disorders

- Cystinosis

- Galactosemia

- Glycogen storage disease (type I)

- Hereditary fructose intolerance

- Lowe syndrome

- Tyrosinemia

- Wilson's disease

Acquired disorders

- Amyloidosis

- Multiple myeloma

- Paroxysmal nocturnal hemoglobinuria

- Toxins, such as HAART, ifosfamide, lead, and cadmium

Prompt treatment of some causes of azotemia can result in restoration of kidney function; delayed treatment may result in permanent loss of renal function. Treatment may include hemodialysis or peritoneal dialysis, medications to increase cardiac output and increase blood pressure, and the treatment of the condition that caused the azotemia.

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).

Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately the urine. In renal physiology, when blood is filtered by the kidney, the passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other before it drains into the bladder as urine. The metabolic acidosis that results from RTA may be caused either by failure to reabsorb sufficient bicarbonate ions (which are alkaline) from the filtrate in the early portion of the nephron (the proximal tubule) or by insufficient secretion of hydrogen ions (which are acidic) into the latter portions of the nephron (the distal tubule). Although a metabolic acidosis also occurs in those with renal insufficiency, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes.

The word "acidosis" refers to the tendency for RTA to cause an excess of acid, which lowers the blood's pH. When the blood pH is below normal (7.35), this is called "acidemia". The metabolic acidosis caused by RTA is a normal anion gap acidosis.

It is possible to acquire this disease later in life.

Causes include ingesting expired tetracyclines (where tetracycline changes to form epitetracycline and anhydrotetracycline which damage proximal tubule), and as a side effect of tenofovir in cases of pre-existing renal impairment. In the HIV population, Fanconi syndrome can develop secondary to the use of an antiretroviral regimen containing tenofovir and didanosine.

Lead poisoning also leads to Fanconi syndrome.

Multiple myeloma or monoclonal gammopathy of undetermined significance can also cause the condition.

Additionally, Fanconi Syndrome can develop as a secondary or tertiary effect of certain autoimmune disorders.

Inborn errors of renal tubular transport are metabolic disorders which lead to impairment in the ability of solutes, such as salts or amino acids, to be transported across the brush border of the renal tubule. This results in disruptions of renal reabsorption.

Examples of these disorders include Iminoglycinuria, renal tubular acidosis and Gitelman syndrome.

Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.

The BUN:Cr in postrenal azotemia is initially >15. The increased nephron tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine. Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.