Milk-alkali syndrome

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Milk-alkali syndrome
Other namesCalcium-alkali syndrome [1]
Glass of Milk (33657535532).jpg
Symptoms Vertigo, confusion, apathy, nausea and vomiting, anorexia, tremors, psychosis, myalgia, polyuria, renal calcifications, and pruitus.
Complications Renal failure, death.
CausesIntake of large amounts of calcium and absorbable alkali.
Risk factors Older age; acute and chronic renal failure; bulimia nervosa; use of certain drugs such as thiazide, NSAIDs, and ACE inhibitors.
Diagnostic method Based on physical symptoms, laboratory findings, ECG, and X-ray (to exclude other causes of hypercalcemia).
Differential diagnosis Other disorders that can cause hypercalcemia such as: hyperparathyroidism, malignancies, hyperthyroidism, sarcoidosis, and other malignancies.
PreventionDecrease calcium intake (1.2-1.5 g/daily for individuals with risk factors for MAS).
TreatmentWithdrawal of the offending agent, hydration, hemodialysis (in extreme cases).

Milk-alkali syndrome (MAS), also referred to as calcium-alkali syndrome, is the third most common cause of hypercalcemia. [2] [3] Milk-alkali syndrome is characterized by elevated blood calcium levels, metabolic alkalosis, and acute kidney injury. [4]

Contents

Milk-alkali syndrome can be caused by the excessive intake of calcium and absorbable alkali. Sources of calcium and alkali include dietary supplements taken for the prevention of osteoporosis or hyperparathyroidism and antacids taken for peptic ulcer disease. [5] Common acute symptoms of milk-alkali syndrome include nausea and vomiting, dry mouth, confusion, lethargy, and distaste for milk. [3] [4] [6] If left untreated, milk-alkali syndrome may lead to kidney failure or even death. [5] [7]

Signs and symptoms

The signs and symptoms of milk-alkali syndrome can develop after only a few days and up to several months following the initial ingestion of absorbable calcium and alkali. [3] However, the severity of signs and symptoms of milk-alkali syndrome is largely dependent upon the duration and quantity of calcium and alkali ingested. [4]

Acute milk-alkali syndrome is characterized by several biochemical alterations, mainly alkalosis, hypochloremia, hypokalemia, and hypercalcemia. [4] In the acute phase of milk-alkali syndrome (Cope syndrome), the first symptoms of toxicity are nausea, vomiting, anorexia, headache, dizziness, vertigo, apathy, weakness, confusion, irritability, dry mouth, and repulsion to milk. [3] [4] [6] In individuals with chronic milk-alkali syndrome (Burnett syndrome), symptoms may include muscle aches, psychosis, tremor, polyuria (producing large volumes of dilute urine), polydipsia (intense thirst), pruritus (itchy sensation on skin), band keratopathy and abnormal calcifications. These abnormal calcium deposits often collect metastatically in the body, including throughout the periarticular tissue, subcutaneous tissue, central nervous system, liver, kidneys, adrenal, bones, and lungs. [3] If ingestion of calcium and alkali is continued, neurologic symptoms such as memory loss, personality changes, lethargy, stupor, and coma will persistently develop over time, as a result of the extreme hypercalcemia and electrolyte imbalances. [4]

People with milk-alkali syndrome commonly show signs of renal dysfunction, a hallmark symptom of milk-alkali syndrome, at early stages of disease progression. [4] Several lab test results, such as elevated blood urea nitrogen (BUN) and elevated creatinine, are illustrative of azotemia and kidney impairment. [4] [6] Histologically, the kidneys of individuals with milk-alkali syndrome have been shown to have "complete glomerulus hyalinization, thickening of the Bowman's capsule, tubular atrophy, vascular changes, and diffuse lymphocytic infiltration." [3]

Other laboratory tests, such as measuring serum bicarbonate, pH, 1,25-OH vitamin D, and parathyroid hormone (PTH) can show signs of milk-alkali syndrome. Specifically, bicarbonate and pH would be elevated while 1,25-OH vitamin D and PTH would be suppressed. [3]

Causes

Milk-alkali syndrome is caused by ingesting excessive amounts of both calcium (usually in the form of dietary supplements such as calcium carbonate, which is commonly taken to prevent or treat osteoporosis) and absorbable alkali (as are found in antacid drugs). [3] [8]

Presently, consumption of extensively large amounts of calcium carbonate has replaced the over-ingestion of milk products, or milk and bicarbonate, as the most prominent cause of MAS. Excessive consumption of calcium generally means taking in more than 4 to 5 g of calcium carbonate every day. [3] This can be attributed to the greater availability of over-the-counter calcium carbonate supplements to treat osteoporosis and dyspepsia, as well as the growing awareness among consumers of the potential health benefits of calcium intake. [3] [5] Calcium carbonate is also often prescribed to people with chronic kidney disease for the prevention of secondary hyperparathyroidism and to people receiving prolonged corticosteroid therapy that may lead to bone loss, putting them at a higher risk of calcium over-consumption and developing MAS. [3] [5]

Other drugs reported to be associated with the development of MAS include thiazide diuretics, which cause increased reabsorption of calcium in the kidneys; resulting hypovolemia can lead to contraction alkalosis. [5] [9] Angiotensin-converting enzyme (ACE) inhibitors and non-steroidal anti-inflammatory drugs (NSAIDs) are also drugs associated with MAS because they decrease glomerular filtration rate (GFR) and thus reduce calcium excretion. [5] [9] Taking medications such as aluminum hydroxide and magnesium hydroxide, which are absorbable alkali, can also contribute to MAS in those who already consume a large amount of calcium. [9]

Pregnant individuals have an increased risk for developing MAS due to hyperemesis (which can cause hypovolemia) and enhanced gastrointestinal calcium absorption as a result of higher levels of prolactin or placental lactose signaling (resulting in hypercalcemia). [5] [9] Calcium carbonate is also commonly used in pregnant individuals to treat acid reflux, further putting them at risk for overconsumption of calcium and developing MAS. [5]

Mechanism

The mechanism of how milk-alkali syndrome develops from ingesting too much of calcium and absorbable alkali is still unclear. However, it is well known that MAS is usually associated with a triad of symptoms that include hypercalcemia, alkalosis, and acute kidney injury. [10] In general, milk-alkali syndrome starts with excess calcium levels in the body (hypercalcemia), which causes the body's pH to increase (become more alkaline) resulting in metabolic alkalosis and ultimately contributes to a decrease in renal function. [8]

Factors involved in the development of hypercalcemia include excess intestinal absorption of calcium, saturation of the bone's buffering capacity for calcium, decreased renal excretion, and abnormal vitamin D metabolism. [3] [10] [11] Underlying kidney disease is a risk factor for MAS, but even people with healthy kidneys can develop the syndrome. [3]

For a healthy individual, if calcium levels are high, the kidneys will decrease its production of calcitriol (active vitamin D) by reducing the hydroxylation of calcidiol (inactive vitamin D); lower calcitriol levels means a lower rate of calcium absorption in the small intestine, which eventually offsets the elevated calcium levels. [10] However, excessive ingestion of calcium of more than 10-15 g per day has been reported to cause calcium levels too high for renal calcitriol suppression to control, resulting in net calcium absorption that ultimately causes hypercalcemia. [3] [10]

Hypercalcemia affects the kidneys in multiple ways that altogether contributes to hypovolemia. [5] [10] Prolonged hypercalcemia can decrease glomerular filtration rate (GFR) via vasoconstriction, reduce creatinine clearance, and eventually cause renal insufficiency. [5] [10] Hypercalcemia also causes natriuresis by blocking the Na-K-Cl cotransporter (NKCC) in the medullary thick ascending limb of the loop of Henle, leading increased sodium excretion followed by water excretion that leads to hypovolemia. [5] Additionally, hypercalcemia can decrease the reabsorption of water in the kidney's collecting ducts by suppressing antidiuretic hormone (ADH) receptors, contributing to more hypovolemia. [5] Hypercalcemia also results in lower parathyroid hormone (PTH) levels via a negative feedback loop, in which calcium-sensing receptors in the PTH gland are activated by the elevated calcium levels to inhibit PTH production, thus decreasing renal reabsorption of calcium. [5] [10]

Hypovolemia then leads to metabolic alkalosis (increase in blood pH) by stimulating bicarbonate reabsorption in order to maintain extracellular volume. [5] [10] In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate. [5] Alkalosis, in turn, increases calcium-reabsorption from the distal tubules of the nephron, thus exacerbating the hypercalcemia and hypovolemia. [5] [10]

Altogether, these result in a cycle of hypercalcemia, alkalosis, and renal injury characteristic of MAS. [5] [10]

Diagnosis

Prior to an official diagnosis of milk-alkali syndrome, other causes of hypercalcemia must be ruled out. Other causes of hypercalcemia can include elevated vitamin D levels, hyperthyroidism, and hyperparathyroidism.

Physical Examination: [4]

Symptoms such as vertigo, confusion, apathy, nausea and vomiting, anorexia, tremors, psychosis, myalgia, polyuria, abnormal calcifications such as renal calcifications, and pruitus could be observed in people.

Lab work:

Lab work must be done to diagnose milk-alkali syndrome. Lab workup includes serum calcium levels, parathyroid hormone (PTH), phosphorus, creatinine, blood urea nitrogen (BUN), magnesium, and vitamin D levels. Primary hyperparathyroidism has to be excluded. [12] Diagnosis is made by looking at past medical history and laboratory studies.[ citation needed ]

  1. Serum calcium levels: high serum calcium levels.
  2. PTH: low serum PTH levels are indicative of MAS. Low serum PTH levels also exclude primary hyperthyroidism.
  3. Phosphorus: low serum phosphorus levels due to low PTH.
  4. Creatinine and BUN: high levels can indicate severity of renal damage.
  5. Magnesium: serum magnesium levels are low as hypercalcemia inhibits mg^2+ reabsorption in the renal tubules.
  6. Vitamin D levels: low vitamin D levels are found. Normal vitamin D levels eliminate primary hypercalcemia.
ECG intervals ECG Intervals.svg
ECG intervals

Electrocardiograms (ECG):

An ECG can also be used to diagnose MAS. The following findings related to hypercalcemia could appear on an ECG: [13]

  1. Short QT interval: most commonly seen as short OoT or OaT changes.
  2. Prolongation of PR and QRS intervals.
  3. Increased Amplitude of QRS complex.
  4. Osborn wave
  5. Short ST segment.

Radiology:

Chest x-rays can help exclude any malignancy or sarcoidosis when evaluating for hypercalcemia. [5]

Prevention

Increasing education in both people and clinicians surrounding milk-alkali syndrome can help prevent the disease. [3] Over recent years, people have become more aware of the benefits of calcium and how to access it, leading to a consequential rise in cases of milk-alkali syndrome. It is crucial that people are educated by their healthcare provider(s) about how hypercalcemia can develop and the hallmark symptoms to monitor for. Often unknown to the person, calcium can come from many different dietary sources in addition to self- or prescribed-supplementation. [5] Unfortunately, this can lead to the intake of amounts of calcium that exceed recommended doses, causing harmful effects. [3] [5] Particularly in persons with any degree of renal disease, supplementation of calcium can more easily result in deadly hypercalcemia and alkalosis. [5] Generally, the daily intake of less than 2 grams of calcium is considered to be safe. [3] Prior to starting any calcium supplementation, it is recommended to discuss the individualized calcium requirements of the person. If a person begins a calcium supplementation regimen, they should be educated on the common signs and symptoms of hypercalcemia and milk-alkali syndrome, as well as how to reverse the syndrome by discontinuing the offending agent and seeking medical attention. [5]

Treatment

For mild cases of MAS, the only intervention needed is to withdraw the offending agent. By having the person stop taking any calcium supplements and any other alkali agents they have been taking rapidly corrects hypercalcemia and alkalosis in MAS. [3] [14]

In severe cases, hospitalization may be required to manage this syndrome. Withholding calcium and initiating IV fluids such as saline to correct hypovolemia. [14] The initial rate of infusion is generally around 200-300 mL/h in people not experiencing edema then it is adjusted to maintain urine output of 100 - 150 mL/h. However, the rate is variable depending on the individual's age, renal status, comorbidities, and the severity of hypercalcemia. [5]

Furosemide can be used to treat hypercalcemia as it induces caliuresis (excreting calcium in the urine). Standard practice of adequate rehydration and electrolyte monitoring should be used to avoid alkalosis and renal insufficiency. [15]

If kidney failure is advanced then treatment for that is required, namely chronic dialysis. [14]

Calcimimetic agents may be necessary, e.g. Cinacalcet.[ citation needed ]

Outcomes

In mild cases of milk-alkali syndrome, full recovery is expected and reduction to renal function is reversible. However, in severe cases that are chronic, permanent kidney failure or death may result. [3] Long term consumption of large amounts of calcium supplementation associated with milk-alkali syndrome has also been linked to adverse cardiovascular outcomes. It was found that over supplementation of calcium can lead to an increased risk for myocardial infarction and vascular calcification. [16]

Epidemiology

In the early years after the discovery of milk-alkali syndrome, the prevalence of the disease among people treated with Sippy's treatment varied from 2% to 18%. The wide range was attributed to the differing amounts of alkali absorbed among people. In the 1900s, the mortality rate of people with milk-alkali syndrome was found to be 4.4%. [3]

The use of milk and alkali to treat gastric ulcers greatly contributed to the development of milk-alkali syndrome in people but the incidence of milk-alkali syndrome greatly diminished when the true cause of most gastric ulcers was identified and drugs other than antacids were developed to treat heartburn, such as acid-reducing drugs like H2-receptor antagonists or proton pump inhibitors. [3] These new drugs replaced Sippy's diet treatment for peptic ulcers. However, the incidence of milk-alkali syndrome has increased again since the 1990s due to increased osteoporosis awareness and the preventative routine use of calcium supplements. [16] The consumption of calcium supplementation in today's society, mostly to prevent osteoporosis, has aided in the resurgence of milk-alkali syndrome [17] and has sparked conversation about changing the name of milk-alkali syndrome to calcium alkali syndrome as it more accurately reflects the cause of this syndrome. [18] Currently, milk-alkali syndrome is the third most common cause of people hospitalized with high blood calcium, after hyperparathyroidism and cancer. [3] [19]

In regards to populations at risk, there has been a shift in the condition's demographic over time. Previously, milk-alkali syndrome was predominantly seen amongst males with ulcers. As new treatments for peptic ulcers arose, there was change in the causation of hypercalcemia. Presently, individuals who are at a higher risk of developing milk-alkali syndrome are pregnant or postmenopausal individuals and the elderly. [9]

History

Milk-alkali syndrome is an illness that is characterized by hypercalcaemia, kidney damage, and metabolic alkalosis. [17] This syndrome was discovered in the early 1900s when people began experiencing adverse effects from Bertrand Sippy's gastric ulcer treatment consisting of milk and alkali. Sippy prescribed patients with ulcers milk and alkali, on the theory that ulcers were caused by excessive gastric acid. [3] Further research by Cuthbert Cope and Charles H. Burnett revealed varying degrees of milk-alkali syndrome. Cope identified an acute phase which was named Cope's Syndrome while Burnett described a more severe chronic form which was named Burnett's Syndrome. [4] However, both the acute and chronic form of this illness involve renal impairment which is a key contributor to the hypercalcemia seen in people with MAS. Cope and Burnett believe that the kidney damage caused by ingesting high amounts of calcium and alkali occurs first which subsequently makes removal of calcium from the body difficult. [3] [16]

Related Research Articles

<span class="mw-page-title-main">Parathyroid hormone</span> Mammalian protein found in Homo sapiens

Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.

<span class="mw-page-title-main">Hypocalcemia</span> Low calcium levels in ones blood serum

Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. The normal range of blood calcium is typically between 2.1–2.6 mmol/L while levels less than 2.1 mmol/L are defined as hypocalcemic. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or cardiac arrest.

Hypercalcemia, also spelled hypercalcaemia, is a high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. In those with greater levels or rapid onset, symptoms may include abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.

Disorders of calcium metabolism occur when the body has too little or too much calcium. The serum level of calcium is closely regulated within a fairly limited range in the human body. In a healthy physiology, extracellular calcium levels are maintained within a tight range through the actions of parathyroid hormone, vitamin D and the calcium sensing receptor. Disorders in calcium metabolism can lead to hypocalcemia, decreased plasma levels of calcium or hypercalcemia, elevated plasma calcium levels.

Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone (PTH). This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany, and several other symptoms. It is a very rare disease. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage as well as a number of rarer causes. The diagnosis is made with blood tests, and other investigations such as genetic testing depending on the results. The primary treatment of hypoparathyroidism is calcium and vitamin D supplementation. Calcium replacement or vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and chronic kidney disease. Additionally, medications such as recombinant human parathyroid hormone or teriparatide may be given by injection to replace the missing hormone.

<span class="mw-page-title-main">Hyperparathyroidism</span> Increase in parathyroid hormone levels in the blood

Hyperparathyroidism is an increase in parathyroid hormone (PTH) levels in the blood. This occurs from a disorder either within the parathyroid glands or as response to external stimuli. Symptoms of hyperparathyroidism are caused by inappropriately normal or elevated blood calcium excreted from the bones and flowing into the blood stream in response to increased production of parathyroid hormone. In healthy people, when blood calcium levels are high, parathyroid hormone levels should be low. With long-standing hyperparathyroidism, the most common symptom is kidney stones. Other symptoms may include bone pain, weakness, depression, confusion, and increased urination. Both primary and secondary may result in osteoporosis.

<span class="mw-page-title-main">Hypophosphatemia</span> Lack of phosphate in the blood

Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.

<span class="mw-page-title-main">Parathyroidectomy</span> Surgical removal of one or more of the parathyroid glands

Parathyroidectomy is the surgical removal of one or more of the (usually) four parathyroid glands. This procedure is used to remove an adenoma or hyperplasia of these glands when they are producing excessive parathyroid hormone (PTH): hyperparathyroidism. The glands are usually four in number and located adjacent to the posterior surface of the thyroid gland, but their exact location is variable. When an elevated PTH level is found, a sestamibi scan or an ultrasound may be performed in order to confirm the presence and location of abnormal parathyroid tissue.

<span class="mw-page-title-main">Gitelman syndrome</span> Medical condition

Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. It is the most frequent hereditary salt-losing tubulopathy. Gitelman syndrome is caused by disease-causing variants on both alleles of the SLC12A3 gene. The SLC12A3 gene encodes the thiazide-sensitive sodium-chloride cotransporter, which can be found in the distal convoluted tubule of the kidney.

<span class="mw-page-title-main">Calcitriol</span> Active form of vitamin D

Calcitriol is the active form of vitamin D, normally made in the kidney. It is also known as 1,25-dihydroxycholecalciferol. It is a hormone which binds to and activates the vitamin D receptor in the nucleus of the cell, which then increases the expression of many genes. Calcitriol increases blood calcium (Ca2+) mainly by increasing the uptake of calcium from the intestines.

<span class="mw-page-title-main">Primary hyperparathyroidism</span> Medical condition

Primary hyperparathyroidism is a medical condition where the parathyroid gland produce excess amounts of parathyroid hormone (PTH). The symptoms of the condition relate to the resulting elevated serum calcium (hypercalcemia), which can cause digestive symptoms, kidney stones, psychiatric abnormalities, and bone disease.

<span class="mw-page-title-main">Osteitis fibrosa cystica</span> Medical condition

Osteitis fibrosa cystica is a skeletal disorder resulting in a loss of bone mass, a weakening of the bones as their calcified supporting structures are replaced with fibrous tissue, and the formation of cyst-like brown tumors in and around the bone. Osteitis fibrosis cystica (OFC), also known as osteitis fibrosa, osteodystrophia fibrosa, and von Recklinghausen's disease of bone, is caused by hyperparathyroidism, which is a surplus of parathyroid hormone from over-active parathyroid glands. This surplus stimulates the activity of osteoclasts, cells that break down bone, in a process known as osteoclastic bone resorption. The hyperparathyroidism can be triggered by a parathyroid adenoma, hereditary factors, parathyroid carcinoma, or renal osteodystrophy. Osteoclastic bone resorption releases minerals, including calcium, from the bone into the bloodstream, causing both elevated blood calcium levels, and the structural changes which weaken the bone. The symptoms of the disease are the consequences of both the general softening of the bones and the excess calcium in the blood, and include bone fractures, kidney stones, nausea, moth-eaten appearance in the bones, appetite loss, and weight loss.

<span class="mw-page-title-main">Secondary hyperparathyroidism</span> Medical condition

Secondary hyperparathyroidism is the medical condition of excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia, with resultant hyperplasia of these glands. This disorder is primarily seen in patients with chronic kidney failure. It is sometimes abbreviated "SHPT" in medical literature.

<span class="mw-page-title-main">Bartter syndrome</span> Medical condition

Bartter syndrome (BS) is a rare inherited disease characterised by a defect in the thick ascending limb of the loop of Henle, which results in low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic. A closely associated disorder, Gitelman syndrome, is milder than both subtypes of Bartter syndrome.

<span class="mw-page-title-main">Tertiary hyperparathyroidism</span> Medical condition

Tertiary hyperparathyroidism is a condition involving the overproduction of the hormone, parathyroid hormone, produced by the parathyroid glands. The parathyroid glands are involved in monitoring and regulating blood calcium levels and respond by either producing or ceasing to produce parathyroid hormone. Anatomically, these glands are located in the neck, para-lateral to the thyroid gland, which does not have any influence in the production of parathyroid hormone. Parathyroid hormone is released by the parathyroid glands in response to low blood calcium circulation. Persistent low levels of circulating calcium are thought to be the catalyst in the progressive development of adenoma, in the parathyroid glands resulting in primary hyperparathyroidism. While primary hyperparathyroidism is the most common form of this condition, secondary and tertiary are thought to result due to chronic kidney disease (CKD). Estimates of CKD prevalence in the global community range from 11 to 13% which translate to a large portion of the global population at risk of developing tertiary hyperparathyroidism. Tertiary hyperparathyroidism was first described in the late 1960s and had been misdiagnosed as primary prior to this. Unlike primary hyperparathyroidism, the tertiary form presents as a progressive stage of resolved secondary hyperparathyroidism with biochemical hallmarks that include elevated calcium ion levels in the blood, hypercalcemia, along with autonomous production of parathyroid hormone and adenoma in all four parathyroid glands. Upon diagnosis treatment of tertiary hyperparathyroidism usually leads to a surgical intervention.

Phosphate nephropathy or nephrocalcinosis is an adverse renal condition that arises with a formation of phosphate crystals within the kidney's tubules. This renal insufficiency is associated with the use of oral sodium phosphate (OSP) such as C.B. Fleet's Phospho soda and Salix's Visocol, for bowel cleansing prior to a colonoscopy.   

<span class="mw-page-title-main">Nephrocalcinosis</span> Medical condition caused by the deposition of calcium salts in the kidneys

Nephrocalcinosis, once known as Albright's calcinosis after Fuller Albright, is a term originally used to describe the deposition of poorly soluble calcium salts in the renal parenchyma due to hyperparathyroidism. The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. It is caused by multiple different conditions and is determined by progressive kidney dysfunction. These outlines eventually come together to form a dense mass. During its early stages, nephrocalcinosis is visible on x-ray, and appears as a fine granular mottling over the renal outlines. It is most commonly seen as an incidental finding with medullary sponge kidney on an abdominal x-ray. It may be severe enough to cause renal tubular acidosis or even end stage kidney disease, due to disruption of the kidney tissue by the deposited calcium salts.

<span class="mw-page-title-main">Parathyroid disease</span> Medical condition

Many conditions are associated with disorders of the function of the parathyroid gland. Some disorders may be purely anatomical resulting in an enlarged gland which will raise concern. Such benign disorders, such as parathyroid cyst, are not discussed here. Parathyroid diseases can be divided into those causing hyperparathyroidism, and those causing hypoparathyroidism.

Familial hypocalciuric hypercalcemia (FHH) is an inherited condition that can cause hypercalcemia, a serum calcium level typically above 10.2 mg/dL; although uncommon. It is also known as familial benign hypocalciuric hypercalcemia (FBHH) where there is usually a family history of hypercalcemia which is mild, a urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day.

Chronic kidney disease–mineral and bone disorder (CKD-MBD) is one of the many complications associated with chronic kidney disease. It represents a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following:

References

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  2. ↑ Picolos, Michalis K.; Lavis, Victor R.; Orlander, Philip R. (2005). "Milk–alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients". Clinical Endocrinology. 63 (5): 566–576. doi:10.1111/j.1365-2265.2005.02383.x. ISSN   1365-2265. PMID   16268810. S2CID   26770851.
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  12. ↑ "Milk-Alkali Syndrome". Cancer Therapy Advisor. 2019-01-17. Retrieved 2021-07-27.
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  16. 1 2 3 Patel, Ami M.; Adeseun, Gbemisola A.; Goldfarb, Stanley (2013). "Calcium-Alkali Syndrome in the Modern Era". Nutrients. 5 (12): 4880–4893. doi: 10.3390/nu5124880 . ISSN   2072-6643. PMC   3875933 . PMID   24288027.
  17. 1 2 Medarov, MD, Boris I. (March 2009). "Milk-Alkali Syndrome". Mayo Clinic Proceedings. 84 (3): 261–267. doi:10.4065/84.3.261. PMC   2664604 . PMID   19252114.
  18. ↑ Rehan, Mehboob A.; Rashid, Asma; Krell, Kenneth; Gabutti, Cristina; Singh, Reema (2020). "Calcium Alkali Thiazide Syndrome: What We Need to Know". Cureus. 12 (10): e10856. doi: 10.7759/cureus.10856 . ISSN   2168-8184. PMC   7652029 . PMID   33178509.
  19. ↑ Beall, Douglas P.; Henslee, Heidi B.; Webb, Heather R.; Scofield, R. Hal (May 2006). "Milk-alkali syndrome: a historical review and description of the modern version of the syndrome". The American Journal of the Medical Sciences. 331 (5): 233–242. doi:10.1097/00000441-200605000-00001. ISSN   0002-9629. PMID   16702792. S2CID   45802184.
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