Secondary Hyperparathyroidism Of Renal Origin
Disease Details
Family Health Simplified
- Description
- Secondary hyperparathyroidism of renal origin is a complication of chronic kidney disease where the parathyroid glands secrete excess parathyroid hormone due to imbalances in calcium, phosphate, and vitamin D.
- Type
- Secondary hyperparathyroidism of renal origin is not directly classified as a genetic disorder. It is a complication that arises due to chronic kidney disease (CKD), where impaired kidney function affects calcium, phosphate, and vitamin D metabolism, leading to overactivity of the parathyroid glands. While the condition itself is not genetically transmitted, genetic factors contributing to CKD can play a role indirectly.
- Signs And Symptoms
-
Secondary hyperparathyroidism of renal origin, commonly seen in chronic kidney disease (CKD) patients, has signs and symptoms including:
1. **Bone pain and skeletal deformities**: Due to renal osteodystrophy (a type of bone disease).
2. **Muscle weakness**.
3. **Itching (pruritus)**.
4. **Fatigue**.
5. **Joint pain**.
6. **Fractures**: Increased risk due to weakened bones.
7. **Calcium deposits**: Can occur in blood vessels, skin, heart, and lungs.
8. **Vascular calcification**: Leading to cardiovascular issues.
9. **Abnormal laboratory results**: Elevated parathyroid hormone (PTH) levels, altered calcium, phosphate, and vitamin D levels. - Prognosis
- Prognosis: The prognosis of secondary hyperparathyroidism of renal origin largely depends on the management of the underlying chronic kidney disease (CKD) and the effectiveness of treatments to control parathyroid hormone (PTH) levels. With appropriate interventions such as dietary modifications, phosphate binders, vitamin D analogs, and potentially calcimimetics, patients can experience improved outcomes. However, if left untreated or inadequately managed, this condition can lead to complications such as bone disease, cardiovascular issues, and an increased risk of mortality. Regular monitoring and medical follow-up are crucial for optimizing prognosis.
- Onset
- The onset of secondary hyperparathyroidism of renal origin is typically gradual and occurs as a consequence of chronic kidney disease (CKD). As kidney function declines, the kidneys are less able to maintain optimal levels of minerals and electrolytes, leading to imbalances that stimulate the parathyroid glands to overproduce parathyroid hormone (PTH). This condition often becomes apparent in the later stages of CKD.
- Prevalence
- Secondary hyperparathyroidism of renal origin is common in patients with chronic kidney disease (CKD). It has been reported to affect approximately 40% to 60% of patients with advanced stages of CKD (stage 3 to 5). The condition becomes more prevalent as kidney function declines.
- Epidemiology
-
Secondary hyperparathyroidism of renal origin (SHPT) is a common complication in individuals with chronic kidney disease (CKD). It occurs due to the kidneys' decreased ability to maintain calcium and phosphate balance, leading to overactivity of the parathyroid glands.
### Epidemiology:
- **Prevalence**: SHPT is highly prevalent among patients with CKD, particularly those in stages 3 to 5.
- **Dialysis Population**: Almost all patients undergoing dialysis (CKD stage 5) exhibit some degree of secondary hyperparathyroidism.
- **Risk Factors**: The likelihood of developing SHPT increases with the duration and severity of renal impairment. Other risk factors include older age, higher phosphate levels, vitamin D deficiency, and African-American ethnicity.
### Nan:
- No relevant information is available specifically related to nan (presumably referring to nanoparticles or nanotechnology) in the context of secondary hyperparathyroidism of renal origin. - Intractability
- Secondary hyperparathyroidism of renal origin can be intractable if not managed properly. This condition is often associated with chronic kidney disease, where the kidneys fail to maintain calcium and phosphorus balance, leading to overproduction of parathyroid hormone (PTH). Effective management typically involves addressing the underlying renal impairment, medication to control PTH levels, dietary modifications, and sometimes surgical intervention. However, if these measures fail or the underlying kidney disease is severe, the condition may become difficult to control.
- Disease Severity
- Unfortunately, the information provided is unclear. Could you please clarify your question?
- Healthcare Professionals
- Disease Ontology ID - DOID:12465
- Pathophysiology
-
Secondary hyperparathyroidism of renal origin refers to the overactivity of the parathyroid glands due to chronic kidney disease (CKD). The pathophysiology involves:
1. **Impaired Phosphate Excretion**: As kidney function declines, phosphate excretion is reduced, leading to hyperphosphatemia.
2. **Hypocalcemia**: Increased phosphate levels lead to decreased serum calcium levels, as phosphate binds to calcium, reducing its bioavailability.
3. **Reduced Calcitriol (1,25-dihydroxyvitamin D) Synthesis**: The kidneys fail to convert enough calcidiol to calcitriol, essential for calcium absorption from the gut, exacerbating hypocalcemia.
4. **Stimulation of Parathyroid Hormone (PTH) Secretion**: Low calcium and calcitriol levels stimulate the parathyroid glands to produce more PTH in an attempt to normalize blood calcium levels by increasing bone resorption, calcium reabsorption in the kidneys, and activating vitamin D.
5. **Parathyroid Hyperplasia**: Chronic stimulation of the parathyroid glands can lead to their enlargement (hyperplasia), which perpetuates elevated levels of PTH despite attempts to manage underlying causes.
Overall, this results in a cycle of mineral imbalance that contributes to bone demineralization and vascular calcification, common complications in CKD patients. - Carrier Status
- Secondary hyperparathyroidism of renal origin is not a genetic disorder, so the concept of "carrier status" does not apply. It is a condition that arises due to chronic kidney disease, which leads to imbalances in calcium, phosphate, and vitamin D. These imbalances stimulate the parathyroid glands to produce more parathyroid hormone (PTH).
- Mechanism
-
Secondary hyperparathyroidism of renal origin primarily develops due to chronic kidney disease (CKD). The mechanism involves reduced kidney function leading to several biochemical disturbances:
1. **Phosphate Retention**: Impaired renal excretion of phosphate results in hyperphosphatemia.
2. **Hypocalcemia**: Elevated phosphate levels and decreased renal production of calcitriol (the active form of vitamin D) lead to lower calcium absorption in the gut, contributing to hypocalcemia.
3. **Vitamin D Deficiency**: CKD impairs the conversion of 25-hydroxyvitamin D to calcitriol, reducing calcium absorption and further contributing to hypocalcemia.
4. **Parathyroid Hormone (PTH) Secretion**: In response to hypocalcemia, hyperphosphatemia, and low calcitriol levels, the parathyroid glands hyperactivate and secrete excessive amounts of PTH to compensate.
### Molecular Mechanisms:
1. **Calcium-Sensing Receptor (CaSR)**: Reduced calcium levels are sensed by the CaSR on parathyroid cells, leading to increased PTH synthesis and secretion.
2. **Phosphate Regulatory Factors**: Elevated phosphate levels directly stimulate PTH secretion and modify the expression of genes associated with PTH synthesis.
3. **Vitamin D Receptor (VDR) and Calcium Handling**: Reduced levels of calcitriol decrease VDR activation, thereby impairing feedback inhibition of PTH synthesis and promoting parathyroid hyperplasia.
4. **Fibroblast Growth Factor 23 (FGF23)**: Elevated phosphate levels increase FGF23 secretion from osteocytes, which further suppresses calcitriol production and thus exacerbates hypocalcemia and PTH production.
These mechanisms collectively drive the parathyroid glands to become hyperplastic and secrete elevated levels of PTH, characterizing secondary hyperparathyroidism in the context of kidney disease. - Treatment
-
Treatment for secondary hyperparathyroidism of renal origin typically focuses on managing the underlying chronic kidney disease and controlling levels of calcium, phosphate, and parathyroid hormone (PTH). Common treatment strategies include:
1. **Phosphate Binders**: These medications help reduce phosphate levels in the blood by preventing its absorption from food.
2. **Vitamin D Supplements**: Activated forms of vitamin D, such as calcitriol or analogs, are often used to help control PTH levels and maintain appropriate calcium levels.
3. **Calcimimetics**: Medications like cinacalcet can decrease PTH secretion by increasing the sensitivity of the parathyroid glands to calcium.
4. **Dietary Modifications**: Restricting dietary phosphate intake can help manage phosphate levels.
5. **Dialysis**: For patients with advanced chronic kidney disease, dialysis helps regulate phosphate and calcium balance.
6. **Parathyroidectomy**: In cases where medical therapy is ineffective, surgical removal of the parathyroid glands may be necessary. - Compassionate Use Treatment
-
Secondary hyperparathyroidism of renal origin, often associated with chronic kidney disease (CKD), primarily revolves around managing mineral imbalances, particularly calcium, phosphorus, and vitamin D. The following lists compassionate use, off-label, or experimental treatments that may be considered:
1. **Calcimimetics (e.g., Etelcalcetide and Cinacalcet)**: While these are often FDA-approved for SHPT, they may be used off-label in specific patient populations or stages of disease not specified in labeling.
2. **Vitamin D Receptor Activators**: Different types of vitamin D analogs (e.g., Paricalcitol) might be used off-label in cases where standard treatments fail to manage parathyroid hormone (PTH) levels effectively.
3. **Non-Calcium-Based Phosphate Binders**: Experimental use of novel phosphate binders that do not increase calcium levels, such as Ferric Citrate, may be considered for better phosphate control.
4. **Monoclonal Antibodies**: Research is ongoing into monoclonal antibodies targeting PTH or involved pathways, and these may be available under compassionate use programs.
5. **Newer Therapies Under Clinical Trials**: Patients might have access to new treatment options being tested in clinical trials, which could encompass innovative approaches to managing SHPT.
These treatments are generally considered when conventional therapies do not adequately control the disease or cause significant side effects. Always consult with a healthcare provider to discuss the suitability and potential risks of pursuing these options. - Lifestyle Recommendations
-
For secondary hyperparathyroidism of renal origin, the following lifestyle recommendations can be beneficial:
1. **Dietary Modifications**:
- **Limit Phosphorus**: Reduce intake of high-phosphorus foods like dairy products, nuts, seeds, and sodas.
- **Adequate Calcium**: Ensure adequate calcium intake through diet or supplements as prescribed.
- **Limit Sodium**: Reduce salt intake to help manage blood pressure and fluid balance.
- **Monitor Protein**: Balance protein intake as per your healthcare provider's recommendations.
2. **Hydration**:
- Ensure adequate fluid intake unless restricted by your healthcare provider to help kidney function.
3. **Exercise**:
- Engage in regular physical activity to maintain overall health, but avoid excessive stress on bones.
4. **Medication Adherence**:
- Follow prescribed treatments, including phosphate binders, vitamin D analogs, and calcimimetics.
5. **Regular Monitoring**:
- Attend regular check-ups with your healthcare provider to monitor calcium, phosphorus, and parathyroid hormone (PTH) levels.
6. **Avoid Smoking and Limit Alcohol**:
- Avoid smoking and limit alcohol consumption as they can negatively affect bone health and overall well-being.
Always consult with a healthcare provider for personalized recommendations tailored to your specific condition. - Medication
-
Secondary hyperparathyroidism of renal origin is often treated with the following medications:
1. **Phosphate Binders**: Help reduce phosphate levels in the blood. Examples include calcium acetate, calcium carbonate, sevelamer, and lanthanum carbonate.
2. **Vitamin D Analogues**: Help manage calcium, phosphate, and parathyroid hormone levels. Examples include calcitriol, paricalcitol, and doxercalciferol.
3. **Calcimimetics**: Help reduce parathyroid hormone production by increasing the sensitivity of the parathyroid glands to calcium. The most commonly used medication is cinacalcet.
Always consult a healthcare provider for specific medical advice tailored to individual conditions. - Repurposable Drugs
-
In the context of secondary hyperparathyroidism of renal origin (often associated with chronic kidney disease), potential repurposable drugs include:
1. **Calcimimetics (e.g., Cinacalcet)**: These drugs mimic calcium and bind to the calcium-sensing receptors on parathyroid glands, thereby reducing parathyroid hormone (PTH) levels.
2. **Vitamin D analogs (e.g., Calcitriol, Paricalcitol)**: These drugs help manage calcium and phosphate balance, thereby reducing PTH secretion.
3. **Phosphate binders (e.g., Sevelamer)**: These drugs reduce phosphate absorption from the gut, addressing hyperphosphatemia and consequently reducing PTH levels.
4. **Bisphosphonates (e.g., Alendronate)**: Although primarily used for osteoporosis, these drugs can help manage bone disorders associated with renal failure.
Always consult with a healthcare provider for a treatment plan tailored to the specific medical condition and patient needs. - Metabolites
-
Secondary hyperparathyroidism of renal origin, often associated with chronic kidney disease (CKD), results in altered metabolism of calcium, phosphate, and vitamin D. The key metabolites involved include:
1. **Calcium**: Calcium levels often decrease due to impaired renal function leading to reduced conversion of vitamin D to its active form, resulting in decreased intestinal absorption of calcium.
2. **Phosphate**: Elevated phosphate levels (hyperphosphatemia) occur because the kidneys are less able to excrete phosphate.
3. **Vitamin D**: The kidneys are responsible for converting vitamin D to its active form, calcitriol (1,25-dihydroxyvitamin D). In CKD, this conversion is impaired, leading to decreased calcitriol levels which further contributes to hypocalcemia.
These imbalances stimulate the parathyroid glands to produce more parathyroid hormone (PTH) in an attempt to maintain normal calcium and phosphate levels, leading to secondary hyperparathyroidism. - Nutraceuticals
- For secondary hyperparathyroidism of renal origin, nutraceuticals such as active forms of vitamin D (e.g., calcitriol, paricalcitol), and phosphate binders (e.g., calcium acetate, sevelamer) can be beneficial. These help manage calcium and phosphate levels, and consequently parathyroid hormone (PTH) levels, in patients with chronic kidney disease. Always consult a healthcare provider for personalized medical advice.
- Peptides
-
Secondary hyperparathyroidism of renal origin, often associated with chronic kidney disease, involves the excessive secretion of parathyroid hormone (PTH) due to the kidneys' inability to maintain adequate calcium and phosphate balance. Specific peptides relevant in this condition include:
1. **Parathyroid Hormone (PTH)**: This peptide hormone regulates calcium levels in the blood.
2. **Fibroblast Growth Factor 23 (FGF23)**: This peptide helps regulate phosphate metabolism and is often elevated in renal disease.
The term "nan" typically refers to nanotechnology, which is not directly related to these peptides in the context of secondary hyperparathyroidism of renal origin. However, emerging research may explore nanotechnology for drug delivery systems aimed at improving treatment for this condition.