Milk-Alkali Syndrome or MAS is a relatively rare chronic disorder characterized by hypercalcemia, metabolic alkalosis, and renal insufficiency. Most commonly it arises from too high levels of calcium together with absorbable alkali; these are mostly found in diets either through supplements or medications. Hypercalcemia, metabolic alkalosis, and renal insufficiency are caused by an excessive intake of calcium and absorbable alkali, which most often comes from dietary supplements or medications.
Epidemiology
A study done earlier indicated that, of all hypercalcemia cases, only 1 % were attributable to milk-alkali syndrome. However, current literature suggests that the condition may be more common. Milk-alkali syndrome was found to be responsible for hypercalcaemia in 6 out of 49 patients (12%) admitted for severe hypercalcaemia over a period of four years. It was identified to be one of the third major causes of hypercalcemia that requires admission in hospitals following hyperparathyroidism and solid malignancy and, in most cases, was established to be more prevalent than multiple myelomas.
Anatomy
Pathophysiology
Calcium Overload:
Over-intake of calcium increases serum calcium levels (hypercalcemia).
Hypercalcemia decreases parathyroid hormone (PTH) secretion, which further reduces calcium excretion by the kidneys and leads to further retention of calcium. Absorbable Alkali:
Consumption of absorbable alkali, such as bicarbonate in antacids, results in metabolic alkalosis.
Metabolic alkalosis increases calcium reabsorption in the kidneys, thereby increasing calcium overload. Renal Dysfunction: Hypercalcemia-induced nephropathy: Elevated calcium causes vasoconstriction of renal afferent arterioles, thus lowering GFR.
Tubular damage results from calcium precipitation in renal tubules, which also impairs renal function further. Alkalosis Effect:
Alkalosis reduces excretion of calcium by kidneys because alkali enhances reabsorption of tubular calcium.
Alkalosis increases protein binding of calcium with a resultant decrease in the ionized calcium levels although maintaining high total calcium.
Etiology
Excessive calcium intake:
Taking excessive amounts of calcium supplements, often to prevent osteoporosis.
Consuming too much dairy or other calcium-containing foods. Excessive Absorbable Alkali:
Taking antacids that contain calcium carbonate (e.g., Tums, Rolaids).
Eating sodium bicarbonate (baking soda) or other alkali substances. Excessive Vitamin D or A:
Oversupplementation with vitamin D, which increases the absorption of calcium.
High levels of vitamin A worsen hypercalcemia. Predisposing Conditions:
CKD (chronic kidney disease) diminishes the kidneys’ capacity to excrete calcium.
Primary hyperparathyroidism may worsen the condition.
Thiazide diuretics, which lower calcium excretion.
Genetics
Prognostic Factors
Severity of Hypercalcemia: The higher the calcium levels, the greater the risk of complications such as renal failure, arrhythmias, and neurologic disturbances. Severe hypercalcemia is associated with a poorer prognosis if not corrected quickly.
Age: Older adults may have a more difficult time recovering from the effects of MAS, especially if there are additional age-related renal or metabolic changes.
Degree of Metabolic Alkalosis: Severe alkalosis can affect cardiac and neurologic function, increasing the risk of adverse outcomes. The extent of alkalosis and its management plays a role in determining recovery.
Timeliness of Treatment: Early recognition and treatment, which typically involves discontinuation of calcium and alkali intake, aggressive hydration, and medications like loop diuretics or bisphosphonates, improve the prognosis. Delayed treatment can lead to irreversible kidney damage and other complications.
Clinical History
Clinical history
Age Group:
MAS is typically an adult condition, with most cases occurring in people who are between 40 to 70 years of age.
Physical Examination
Signs of Hypercalcemia
Hypertension
Tachycardia
Other Findings
Age group
Associated comorbidity
Chronic Kidney Disease (CKD)
Hypercalcemia
Metabolic Alkalosis
Osteoporosis
Hypertension
Associated activity
Acuity of presentation
Milk-Alkali Syndrome (MAS) typically presents acutely with symptoms related to hypercalcemia and metabolic alkalosis. These may include:
Nausea and vomiting
Confusion or altered mental status
Abdominal pain
Weakness or fatigue
Polyuria (increased urination)
Polydipsia (increased thirst)
It can result from excessive intake of calcium and absorbable alkali (like in antacids or milk), leading to high serum calcium levels. If untreated, MAS can progress to renal failure and more severe complications. Prompt recognition and management, including fluid resuscitation, electrolyte correction, and discontinuation of the offending agents, are crucial.
Differential Diagnoses
Hypercalcemia of Malignancy
Primary Hyperparathyroidism
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Discontinuation of the causative agents
Stop the intake of milk, calcium, and alkali-containing substances immediately. This is the first and most crucial step in managing MAS.
Hydration
IV fluids (normal saline or lactated Ringer’s) are given to correct dehydration and dilute the calcium levels. It also helps promote renal excretion of excess calcium.
Fluids help lower serum calcium and restore kidney function.
Correction of Hypercalcemia
Intravenous hydration to correct the fluid balance which promotes renal elimination of calcium.
Once the patient is adequately hydrated then loop diuretics, for example furosemide may be used to increase renal calcium clearance.
In severe cases of high renal osteodystrophy, bisphosphonates (e.g., pamidronate, zoledronic acid) or calcitonin can be used to reduce bone resorption.
Occasionally, corticosteroid therapies such as prednisone should be used if renal calcium suppression is severe.
Metabolic Alkalosis treatment
The treatment of Metabolic alkalosis depends on the cause of the specific form of the disease; however, the general therapeutic approach will be aimed at correcting the compensatory response of the body.
Acetazolamide may be prescribed to treat metabolic alkalosis due to its ability to increase renal clearance of bicarbonate.
Careful attention should be made to electrolyte levels (calcium, potassium, bicarbonate), as well as renal function. Dialysis is, however, used where renal failure is severe or where other forms of treatments do not work well in controlling hypercalcemia.
Addressing Renal Function:
Since renal failure may be a complication, attention should be paid to manifestation of AKI, and in this case electrolytes monitoring is essential. In extreme cases, the patient might require dialysis therapy.
Long-Term Management
Once the acute episode resolves, a review of the patient’s calcium and vitamin D intake is necessary to prevent recurrence. This includes counselling on appropriate use of calcium supplements.
Limit calcium and alkali intake: Reducing the consumption of calcium-rich foods and antacid products containing calcium and bicarbonate can prevent MAS. This might involve adjusting the intake of dairy products (milk, cheese, etc.) and supplements.
Monitor calcium supplements: People using calcium supplements should be advised to follow the recommended daily intake and avoid taking them in excess.
Hydration and Fluid Balance:
Adequate hydration is essential to prevent renal complications from MAS. Sufficient water intake helps the kidneys process excess calcium and alkali, reducing the risk of kidney damage and hypercalcemia.
If someone is experiencing MAS, intravenous fluids may be administered to help balance electrolytes and correct dehydration or renal insufficiency.
Regular Monitoring of Blood Chemistry:
Regularly check serum calcium levels, metabolic pH, and renal function, especially for individuals prone to MAS (those on high-dose calcium supplements or antacids).
Monitoring kidney function is crucial, as MAS can lead to renal failure if left unaddressed.
Effectiveness of Loop diuretics in treating Milk-alkali syndrome
Furosemide
Loop diuretics can help with calcium excretion via the kidneys. However, they should only be used once adequate hydration is restored to prevent renal injury.
Use of Calcium metabolism modifiers in treating Milk-alkali syndrome
Zoledronic acid
These are used to inhibit osteoclast-mediated bone resorption, thus lowering calcium levels. Bisphosphonates are often used in cases of severe hypercalcemia when other measures are insufficient.
Discontinue offending agents (calcium and alkali sources).
Hydration: IV fluids to correct dehydration and promote renal function.
Monitor serum calcium levels: Correct hypercalcemia with hydration, and if severe, use medications like bisphosphonates (e.g., pamidronate) or calcitonin.
Monitor renal function: Renal failure is a concern, so renal support may be necessary.
Correction of Hypercalcemia:
IV fluids (saline) to dilute calcium and increase renal calcium excretion.
Diuretics: After rehydration, loop diuretics (e.g., furosemide) may be used to help eliminate calcium.
Bisphosphonates or calcitonin may be administered to lower calcium levels if needed.
Management of Renal Impairment:
Monitor kidney function (creatinine, electrolytes) and address any kidney damage.
Dialysis may be required in severe cases of renal failure.
Follow-up and Long-term Management:
Prevent recurrence: Avoid excessive calcium and alkali intake in the future.
Monitor for complications such as renal damage or bone mineralization abnormalities.
Milk-Alkali Syndrome or MAS is a relatively rare chronic disorder characterized by hypercalcemia, metabolic alkalosis, and renal insufficiency. Most commonly it arises from too high levels of calcium together with absorbable alkali; these are mostly found in diets either through supplements or medications. Hypercalcemia, metabolic alkalosis, and renal insufficiency are caused by an excessive intake of calcium and absorbable alkali, which most often comes from dietary supplements or medications.
A study done earlier indicated that, of all hypercalcemia cases, only 1 % were attributable to milk-alkali syndrome. However, current literature suggests that the condition may be more common. Milk-alkali syndrome was found to be responsible for hypercalcaemia in 6 out of 49 patients (12%) admitted for severe hypercalcaemia over a period of four years. It was identified to be one of the third major causes of hypercalcemia that requires admission in hospitals following hyperparathyroidism and solid malignancy and, in most cases, was established to be more prevalent than multiple myelomas.
Calcium Overload:
Over-intake of calcium increases serum calcium levels (hypercalcemia).
Hypercalcemia decreases parathyroid hormone (PTH) secretion, which further reduces calcium excretion by the kidneys and leads to further retention of calcium. Absorbable Alkali:
Consumption of absorbable alkali, such as bicarbonate in antacids, results in metabolic alkalosis.
Metabolic alkalosis increases calcium reabsorption in the kidneys, thereby increasing calcium overload. Renal Dysfunction: Hypercalcemia-induced nephropathy: Elevated calcium causes vasoconstriction of renal afferent arterioles, thus lowering GFR.
Tubular damage results from calcium precipitation in renal tubules, which also impairs renal function further. Alkalosis Effect:
Alkalosis reduces excretion of calcium by kidneys because alkali enhances reabsorption of tubular calcium.
Alkalosis increases protein binding of calcium with a resultant decrease in the ionized calcium levels although maintaining high total calcium.
Excessive calcium intake:
Taking excessive amounts of calcium supplements, often to prevent osteoporosis.
Consuming too much dairy or other calcium-containing foods. Excessive Absorbable Alkali:
Taking antacids that contain calcium carbonate (e.g., Tums, Rolaids).
Eating sodium bicarbonate (baking soda) or other alkali substances. Excessive Vitamin D or A:
Oversupplementation with vitamin D, which increases the absorption of calcium.
High levels of vitamin A worsen hypercalcemia. Predisposing Conditions:
CKD (chronic kidney disease) diminishes the kidneys’ capacity to excrete calcium.
Primary hyperparathyroidism may worsen the condition.
Thiazide diuretics, which lower calcium excretion.
Severity of Hypercalcemia: The higher the calcium levels, the greater the risk of complications such as renal failure, arrhythmias, and neurologic disturbances. Severe hypercalcemia is associated with a poorer prognosis if not corrected quickly.
Age: Older adults may have a more difficult time recovering from the effects of MAS, especially if there are additional age-related renal or metabolic changes.
Degree of Metabolic Alkalosis: Severe alkalosis can affect cardiac and neurologic function, increasing the risk of adverse outcomes. The extent of alkalosis and its management plays a role in determining recovery.
Timeliness of Treatment: Early recognition and treatment, which typically involves discontinuation of calcium and alkali intake, aggressive hydration, and medications like loop diuretics or bisphosphonates, improve the prognosis. Delayed treatment can lead to irreversible kidney damage and other complications.
Clinical history
Age Group:
MAS is typically an adult condition, with most cases occurring in people who are between 40 to 70 years of age.
Signs of Hypercalcemia
Hypertension
Tachycardia
Other Findings
Chronic Kidney Disease (CKD)
Hypercalcemia
Metabolic Alkalosis
Osteoporosis
Hypertension
Milk-Alkali Syndrome (MAS) typically presents acutely with symptoms related to hypercalcemia and metabolic alkalosis. These may include:
Nausea and vomiting
Confusion or altered mental status
Abdominal pain
Weakness or fatigue
Polyuria (increased urination)
Polydipsia (increased thirst)
It can result from excessive intake of calcium and absorbable alkali (like in antacids or milk), leading to high serum calcium levels. If untreated, MAS can progress to renal failure and more severe complications. Prompt recognition and management, including fluid resuscitation, electrolyte correction, and discontinuation of the offending agents, are crucial.
Hypercalcemia of Malignancy
Primary Hyperparathyroidism
Discontinuation of the causative agents
Stop the intake of milk, calcium, and alkali-containing substances immediately. This is the first and most crucial step in managing MAS.
Hydration
IV fluids (normal saline or lactated Ringer’s) are given to correct dehydration and dilute the calcium levels. It also helps promote renal excretion of excess calcium.
Fluids help lower serum calcium and restore kidney function.
Correction of Hypercalcemia
Intravenous hydration to correct the fluid balance which promotes renal elimination of calcium.
Once the patient is adequately hydrated then loop diuretics, for example furosemide may be used to increase renal calcium clearance.
In severe cases of high renal osteodystrophy, bisphosphonates (e.g., pamidronate, zoledronic acid) or calcitonin can be used to reduce bone resorption.
Occasionally, corticosteroid therapies such as prednisone should be used if renal calcium suppression is severe.
Metabolic Alkalosis treatment
The treatment of Metabolic alkalosis depends on the cause of the specific form of the disease; however, the general therapeutic approach will be aimed at correcting the compensatory response of the body.
Acetazolamide may be prescribed to treat metabolic alkalosis due to its ability to increase renal clearance of bicarbonate.
Careful attention should be made to electrolyte levels (calcium, potassium, bicarbonate), as well as renal function. Dialysis is, however, used where renal failure is severe or where other forms of treatments do not work well in controlling hypercalcemia.
Addressing Renal Function:
Since renal failure may be a complication, attention should be paid to manifestation of AKI, and in this case electrolytes monitoring is essential. In extreme cases, the patient might require dialysis therapy.
Long-Term Management
Once the acute episode resolves, a review of the patient’s calcium and vitamin D intake is necessary to prevent recurrence. This includes counselling on appropriate use of calcium supplements.
Endocrinology, Metabolism
Dietary Modifications:
Limit calcium and alkali intake: Reducing the consumption of calcium-rich foods and antacid products containing calcium and bicarbonate can prevent MAS. This might involve adjusting the intake of dairy products (milk, cheese, etc.) and supplements.
Monitor calcium supplements: People using calcium supplements should be advised to follow the recommended daily intake and avoid taking them in excess.
Hydration and Fluid Balance:
Adequate hydration is essential to prevent renal complications from MAS. Sufficient water intake helps the kidneys process excess calcium and alkali, reducing the risk of kidney damage and hypercalcemia.
If someone is experiencing MAS, intravenous fluids may be administered to help balance electrolytes and correct dehydration or renal insufficiency.
Regular Monitoring of Blood Chemistry:
Regularly check serum calcium levels, metabolic pH, and renal function, especially for individuals prone to MAS (those on high-dose calcium supplements or antacids).
Monitoring kidney function is crucial, as MAS can lead to renal failure if left unaddressed.
Endocrinology, Metabolism
Furosemide
Loop diuretics can help with calcium excretion via the kidneys. However, they should only be used once adequate hydration is restored to prevent renal injury.
Endocrinology, Metabolism
Zoledronic acid
These are used to inhibit osteoclast-mediated bone resorption, thus lowering calcium levels. Bisphosphonates are often used in cases of severe hypercalcemia when other measures are insufficient.
Endocrinology, Metabolism
Initial Phase (Acute Management):
Discontinue offending agents (calcium and alkali sources).
Hydration: IV fluids to correct dehydration and promote renal function.
Monitor serum calcium levels: Correct hypercalcemia with hydration, and if severe, use medications like bisphosphonates (e.g., pamidronate) or calcitonin.
Monitor renal function: Renal failure is a concern, so renal support may be necessary.
Correction of Hypercalcemia:
IV fluids (saline) to dilute calcium and increase renal calcium excretion.
Diuretics: After rehydration, loop diuretics (e.g., furosemide) may be used to help eliminate calcium.
Bisphosphonates or calcitonin may be administered to lower calcium levels if needed.
Management of Renal Impairment:
Monitor kidney function (creatinine, electrolytes) and address any kidney damage.
Dialysis may be required in severe cases of renal failure.
Follow-up and Long-term Management:
Prevent recurrence: Avoid excessive calcium and alkali intake in the future.
Monitor for complications such as renal damage or bone mineralization abnormalities.
Milk-Alkali Syndrome or MAS is a relatively rare chronic disorder characterized by hypercalcemia, metabolic alkalosis, and renal insufficiency. Most commonly it arises from too high levels of calcium together with absorbable alkali; these are mostly found in diets either through supplements or medications. Hypercalcemia, metabolic alkalosis, and renal insufficiency are caused by an excessive intake of calcium and absorbable alkali, which most often comes from dietary supplements or medications.
A study done earlier indicated that, of all hypercalcemia cases, only 1 % were attributable to milk-alkali syndrome. However, current literature suggests that the condition may be more common. Milk-alkali syndrome was found to be responsible for hypercalcaemia in 6 out of 49 patients (12%) admitted for severe hypercalcaemia over a period of four years. It was identified to be one of the third major causes of hypercalcemia that requires admission in hospitals following hyperparathyroidism and solid malignancy and, in most cases, was established to be more prevalent than multiple myelomas.
Calcium Overload:
Over-intake of calcium increases serum calcium levels (hypercalcemia).
Hypercalcemia decreases parathyroid hormone (PTH) secretion, which further reduces calcium excretion by the kidneys and leads to further retention of calcium. Absorbable Alkali:
Consumption of absorbable alkali, such as bicarbonate in antacids, results in metabolic alkalosis.
Metabolic alkalosis increases calcium reabsorption in the kidneys, thereby increasing calcium overload. Renal Dysfunction: Hypercalcemia-induced nephropathy: Elevated calcium causes vasoconstriction of renal afferent arterioles, thus lowering GFR.
Tubular damage results from calcium precipitation in renal tubules, which also impairs renal function further. Alkalosis Effect:
Alkalosis reduces excretion of calcium by kidneys because alkali enhances reabsorption of tubular calcium.
Alkalosis increases protein binding of calcium with a resultant decrease in the ionized calcium levels although maintaining high total calcium.
Excessive calcium intake:
Taking excessive amounts of calcium supplements, often to prevent osteoporosis.
Consuming too much dairy or other calcium-containing foods. Excessive Absorbable Alkali:
Taking antacids that contain calcium carbonate (e.g., Tums, Rolaids).
Eating sodium bicarbonate (baking soda) or other alkali substances. Excessive Vitamin D or A:
Oversupplementation with vitamin D, which increases the absorption of calcium.
High levels of vitamin A worsen hypercalcemia. Predisposing Conditions:
CKD (chronic kidney disease) diminishes the kidneys’ capacity to excrete calcium.
Primary hyperparathyroidism may worsen the condition.
Thiazide diuretics, which lower calcium excretion.
Severity of Hypercalcemia: The higher the calcium levels, the greater the risk of complications such as renal failure, arrhythmias, and neurologic disturbances. Severe hypercalcemia is associated with a poorer prognosis if not corrected quickly.
Age: Older adults may have a more difficult time recovering from the effects of MAS, especially if there are additional age-related renal or metabolic changes.
Degree of Metabolic Alkalosis: Severe alkalosis can affect cardiac and neurologic function, increasing the risk of adverse outcomes. The extent of alkalosis and its management plays a role in determining recovery.
Timeliness of Treatment: Early recognition and treatment, which typically involves discontinuation of calcium and alkali intake, aggressive hydration, and medications like loop diuretics or bisphosphonates, improve the prognosis. Delayed treatment can lead to irreversible kidney damage and other complications.
Clinical history
Age Group:
MAS is typically an adult condition, with most cases occurring in people who are between 40 to 70 years of age.
Signs of Hypercalcemia
Hypertension
Tachycardia
Other Findings
Chronic Kidney Disease (CKD)
Hypercalcemia
Metabolic Alkalosis
Osteoporosis
Hypertension
Milk-Alkali Syndrome (MAS) typically presents acutely with symptoms related to hypercalcemia and metabolic alkalosis. These may include:
Nausea and vomiting
Confusion or altered mental status
Abdominal pain
Weakness or fatigue
Polyuria (increased urination)
Polydipsia (increased thirst)
It can result from excessive intake of calcium and absorbable alkali (like in antacids or milk), leading to high serum calcium levels. If untreated, MAS can progress to renal failure and more severe complications. Prompt recognition and management, including fluid resuscitation, electrolyte correction, and discontinuation of the offending agents, are crucial.
Hypercalcemia of Malignancy
Primary Hyperparathyroidism
Discontinuation of the causative agents
Stop the intake of milk, calcium, and alkali-containing substances immediately. This is the first and most crucial step in managing MAS.
Hydration
IV fluids (normal saline or lactated Ringer’s) are given to correct dehydration and dilute the calcium levels. It also helps promote renal excretion of excess calcium.
Fluids help lower serum calcium and restore kidney function.
Correction of Hypercalcemia
Intravenous hydration to correct the fluid balance which promotes renal elimination of calcium.
Once the patient is adequately hydrated then loop diuretics, for example furosemide may be used to increase renal calcium clearance.
In severe cases of high renal osteodystrophy, bisphosphonates (e.g., pamidronate, zoledronic acid) or calcitonin can be used to reduce bone resorption.
Occasionally, corticosteroid therapies such as prednisone should be used if renal calcium suppression is severe.
Metabolic Alkalosis treatment
The treatment of Metabolic alkalosis depends on the cause of the specific form of the disease; however, the general therapeutic approach will be aimed at correcting the compensatory response of the body.
Acetazolamide may be prescribed to treat metabolic alkalosis due to its ability to increase renal clearance of bicarbonate.
Careful attention should be made to electrolyte levels (calcium, potassium, bicarbonate), as well as renal function. Dialysis is, however, used where renal failure is severe or where other forms of treatments do not work well in controlling hypercalcemia.
Addressing Renal Function:
Since renal failure may be a complication, attention should be paid to manifestation of AKI, and in this case electrolytes monitoring is essential. In extreme cases, the patient might require dialysis therapy.
Long-Term Management
Once the acute episode resolves, a review of the patient’s calcium and vitamin D intake is necessary to prevent recurrence. This includes counselling on appropriate use of calcium supplements.
Endocrinology, Metabolism
Dietary Modifications:
Limit calcium and alkali intake: Reducing the consumption of calcium-rich foods and antacid products containing calcium and bicarbonate can prevent MAS. This might involve adjusting the intake of dairy products (milk, cheese, etc.) and supplements.
Monitor calcium supplements: People using calcium supplements should be advised to follow the recommended daily intake and avoid taking them in excess.
Hydration and Fluid Balance:
Adequate hydration is essential to prevent renal complications from MAS. Sufficient water intake helps the kidneys process excess calcium and alkali, reducing the risk of kidney damage and hypercalcemia.
If someone is experiencing MAS, intravenous fluids may be administered to help balance electrolytes and correct dehydration or renal insufficiency.
Regular Monitoring of Blood Chemistry:
Regularly check serum calcium levels, metabolic pH, and renal function, especially for individuals prone to MAS (those on high-dose calcium supplements or antacids).
Monitoring kidney function is crucial, as MAS can lead to renal failure if left unaddressed.
Endocrinology, Metabolism
Furosemide
Loop diuretics can help with calcium excretion via the kidneys. However, they should only be used once adequate hydration is restored to prevent renal injury.
Endocrinology, Metabolism
Zoledronic acid
These are used to inhibit osteoclast-mediated bone resorption, thus lowering calcium levels. Bisphosphonates are often used in cases of severe hypercalcemia when other measures are insufficient.
Endocrinology, Metabolism
Initial Phase (Acute Management):
Discontinue offending agents (calcium and alkali sources).
Hydration: IV fluids to correct dehydration and promote renal function.
Monitor serum calcium levels: Correct hypercalcemia with hydration, and if severe, use medications like bisphosphonates (e.g., pamidronate) or calcitonin.
Monitor renal function: Renal failure is a concern, so renal support may be necessary.
Correction of Hypercalcemia:
IV fluids (saline) to dilute calcium and increase renal calcium excretion.
Diuretics: After rehydration, loop diuretics (e.g., furosemide) may be used to help eliminate calcium.
Bisphosphonates or calcitonin may be administered to lower calcium levels if needed.
Management of Renal Impairment:
Monitor kidney function (creatinine, electrolytes) and address any kidney damage.
Dialysis may be required in severe cases of renal failure.
Follow-up and Long-term Management:
Prevent recurrence: Avoid excessive calcium and alkali intake in the future.
Monitor for complications such as renal damage or bone mineralization abnormalities.
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