Hypercalcemia - Nephrology Lectures 2025

🚨 EMERGENCY HYPERCALCEMIA PROTOCOL (Ca++ ≥ 14 mg/dL)

⚡ IMMEDIATE (First Hour)

Normal saline 200-300 mL/hr
Calcitonin 4 IU/kg IM/SC q12h
Monitor cardiac rhythm
Neuro checks q2h

🏥 WITHIN 4-6 HOURS

Bisphosphonate (zoledronic acid)
Continue aggressive hydration
Furosemide if volume overloaded
Avoid thiazides and calcium

🔍 WORKUP PRIORITIES

PTH level (stat)
PTHrP if PTH suppressed
25-OH vitamin D, 1,25-OH vitamin D
CBC, CMP, phosphorus

⚠️ Calcium >14 mg/dL is life-threatening - Treat aggressively! ⚠️

🎯 CRITICAL: Calcium >13 mg/dL = High Suspicion for MALIGNANCY

📊 Statistical Reality

Ca++ >13 mg/dL: 80-90% malignancy
Ca++ >14 mg/dL: >95% malignancy
Inpatient hypercalcemia: Malignancy #1 cause
Outpatient hypercalcemia: Primary hyperparathyroidism #1

🔬 Immediate Workup

PTH level (should be suppressed)
PTHrP (parathyroid hormone-related protein)
Chest X-ray, CT chest/abdomen/pelvis
Protein electrophoresis, SPEP/UPEP
25-OH and 1,25-OH vitamin D

🚨 Don't delay cancer workup when Ca++ >13 - Time is critical! 🚨

🔍 Diagnostic Approach: PTH-Dependent vs PTH-Independent

⚡ PTH-Guided Diagnostic Algorithm

📈 PTH ELEVATED or INAPPROPRIATELY NORMAL

PTH-Dependent Hypercalcemia

Primary Hyperparathyroidism (85%):
- Adenoma (80-85%)
- Hyperplasia (10-15%)
- Carcinoma (<5%)
Tertiary Hyperparathyroidism: CKD, post-transplant
FHH (Familial Hypocalciuric Hypercalcemia):
- Check 24h urine calcium
- Ca/Cr clearance ratio <0.01
Lithium-induced: Chronic lithium therapy

Next Step: Neck ultrasound, Tc-99m sestamibi scan

📉 PTH SUPPRESSED (<20 pg/mL)

PTH-Independent Hypercalcemia

Malignancy (90% of cases):
- PTHrP-mediated (80%)
- Osteolytic metastases (20%)
- 1,25(OH)2D production (lymphoma)
Granulomatous Diseases:
- Sarcoidosis, histoplasmosis
- Extra-renal 1α-hydroxylase
Endocrine: Thyrotoxicosis, adrenal insufficiency
Medications: Vitamin D, thiazides, calcium

Next Step: PTHrP, imaging for malignancy

🩸 Lymphoma-Associated Hypercalcemia: Comprehensive Analysis

🎯 Lymphoma Subtypes & Hypercalcemia Risk

🧬 HODGKIN LYMPHOMA

Classical Subtypes: Nodular sclerosis (most common)
Hypercalcemia Incidence: 10-15% of cases
Reed-Sternberg Cells: Express CD30, CD15
Cytokines: IL-1, TNF-α, IL-6 production
Age Groups: Bimodal distribution (20s, >55y)
B-symptoms: Fever, night sweats, weight loss
Staging: Often localized at presentation

🧬 NON-HODGKIN LYMPHOMA

High-Risk Subtypes: DLBCL, Burkitt, PTCL
B-cell Lymphomas: 85% of NHL cases
Hypercalcemia Rate: 5-20% depending on subtype
Extra-nodal Disease: 40% have extra-nodal involvement
Aggressive Course: Rapidly progressive
CNS Involvement: Higher risk in aggressive subtypes
Bone Marrow: Frequent involvement

🩸 ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL)

HTLV-1 Associated: Retroviral oncogenesis
Hypercalcemia Rate: 50-70% of acute/lymphoma types
Geographic Distribution: Japan, Caribbean, South America
Clinical Subtypes: Acute, lymphoma, chronic, smoldering
PTHrP Production: Common mechanism
Skin Lesions: Characteristic feature (70%)
Prognosis: Poor (median survival 6-10 months)

🧬 BURKITT LYMPHOMA

MYC Translocation: t(8;14), t(2;8), t(8;22)
Hypercalcemia Rate: 10-25% of cases
Variants: Endemic (Africa), sporadic, immunodeficiency
Rapid Growth: Doubling time 24-48 hours
EBV Association: Strong in endemic variant
Tumor Lysis Risk: Very high with treatment
CNS Involvement: 15-20% at presentation

🔬 Mechanism: Extra-Renal 1α-Hydroxylase in Lymphomas

Cellular Source

Tumor-Associated Macrophages: M2 phenotype activation
Lymphoma Cells: Direct 1α-hydroxylase expression
Cytokine Milieu: IFN-γ, TNF-α, IL-2 upregulation
CYP27B1 Gene: Upregulated in tumor microenvironment

Biochemical Pattern

25(OH)D: Normal or low (substrate consumption)
1,25(OH)2D: Markedly elevated (>100 pg/mL)
PTH: Appropriately suppressed (<10 pg/mL)
FGF23: May be elevated as compensatory response

📊 Clinical Presentation & Diagnostic Workup

🎯 Clinical Features

Constitutional Symptoms: B-symptoms in 30-50%
Lymphadenopathy: Mediastinal, abdominal, peripheral
Organomegaly: Splenomegaly (40%), hepatomegaly (30%)
Hypercalcemia Symptoms: Often early presentation
Performance Status: Often decreased at presentation
Age Distribution: Variable by subtype

🔬 Laboratory Workup

Complete Metabolic Panel: Calcium, phosphorus, renal function
PTH: Suppressed (<20 pg/mL)
25(OH)D & 1,25(OH)2D: Elevated 1,25 diagnostic
Lactate Dehydrogenase: Often markedly elevated
Uric Acid: May be elevated (tumor burden)
Flow Cytometry: Blood and bone marrow

📷 Imaging Studies

CT Chest/Abdomen/Pelvis: Staging assessment
PET-CT: Gold standard for staging lymphoma
Brain MRI: If CNS symptoms or high-risk histology
Bone Marrow Biopsy: Staging for most subtypes
Tissue Biopsy: Core needle or excisional
Lumbar Puncture: High-risk cases (Burkitt, DLBCL)

⚗️ Molecular/Genetic Testing

Immunohistochemistry: CD20, CD30, CD15, etc.
Flow Cytometry: Surface markers, clonality
Cytogenetics: Chromosomal translocations
FISH Studies: MYC, BCL2, BCL6 rearrangements
NGS Panels: Mutation analysis for prognosis
HTLV-1 Testing: If T-cell lymphoma suspected

📊 Treatment Approach: Lymphoma-Associated Hypercalcemia

🚑 EMERGENCY MANAGEMENT

Hydration: NS 200-300 mL/hr immediately
Glucocorticoids: Prednisone 40-60 mg daily (first-line)
Calcitonin: 4 IU/kg q12h (rapid effect)
Bisphosphonates: Zoledronic acid 4mg IV
Monitor Closely: Tumor lysis syndrome risk
Dialysis: If severe hypercalcemia + renal failure

💊 STEROID THERAPY (PREFERRED)

Mechanism: Suppresses extra-renal 1α-hydroxylase
Dosing: Prednisone 40-60 mg daily
Response Time: 24-72 hours typically
Dual Benefit: Treats lymphoma AND hypercalcemia
Monitoring: Blood glucose, infections
Duration: Continue until chemotherapy initiated

🧬 LYMPHOMA-SPECIFIC THERAPY

Hodgkin: ABVD, BEACOPP regimens
DLBCL: R-CHOP or R-EPOCH
Burkitt: Intensive regimens (R-CODOX-M/IVAC)
ATLL: Combination therapy, often poor response
Timing: Start within 48-72 hours if possible
TLS Prophylaxis: Allopurinol, hydration, rasburicase

🚨 COMPLICATIONS & MONITORING

Tumor Lysis Syndrome: High risk with treatment
Renal Failure: From hypercalcemia or TLS
CNS Involvement: Requires intrathecal therapy
Hypercalcemic Crisis: Neurologic emergency
Response Monitoring: Daily calcium, phosphorus
Long-term: May need vitamin D supplementation

⚠️ CRITICAL PEARLS: Lymphoma Hypercalcemia

🔴 Glucocorticoids are FIRST-LINE therapy (unlike other hypercalcemia)
🔴 Dual mechanism: Treats both lymphoma and hypercalcemia
🔴 1,25(OH)2D elevation is diagnostic hallmark

🔴 High TLS risk: Prevent with allopurinol/rasburicase
🔴 Rapid progression: Don't delay systemic therapy
🔴 Poor prognosis: Especially with hypercalcemia at presentation

🔤 VITAMINS TRAP: Complete Hypercalcemia Differential

📚 VITAMINS TRAP: Comprehensive Hypercalcemia Mnemonic

🆅 - VITAMIN D INTOXICATION

Excessive Supplementation: >50,000 IU daily
25(OH)D Level: >100 ng/mL (toxicity)
1,25(OH)2D: Elevated (conversion overload)
Mechanism: ↑ intestinal Ca absorption
Treatment: Stop vitamin D, glucocorticoids

🅸 - IMMOBILIZATION

Paget's Disease: Especially with immobilization
Young Patients: Spinal cord injury, fractures
Bone Turnover: ↑ resorption vs formation
Time Course: Weeks to months of bedrest
Treatment: Early mobilization, bisphosphonates

🅣 - THIAZIDE DIURETICS

Prevalence: 8-10% of patients
Mechanism: ↑ distal Ca reabsorption
Unmasking: May reveal hyperparathyroidism
Reversible: Usually within days of stopping
Testing: Stop drug, recheck in 2-4 weeks

🅰 - VITAMIN A INTOXICATION

Chronic Toxicity: >25,000 IU daily for months
Acute Toxicity: >300,000 IU single dose
Symptoms: Hepatotoxicity, bone pain
Mechanism: ↑ bone resorption
Diagnosis: Elevated retinol levels

🅼 - MALIGNANCY

PTHrP (80%): Squamous cell, lung, H&N, RCC
Osteolytic (20%): Breast, multiple myeloma
Lymphomas: Extra-renal 1α-hydroxylase
Ca++ >13 mg/dL: 80-90% malignancy
Prognosis: Median survival 2-3 months

🅸 - INTOXICATIONS

Milk-Alkali Syndrome: Ca + absorbable alkali
Aluminum Hydroxide: With Ca supplements
Theophylline: Overdose (rare)
Calcium Supplements: Excessive intake
Lithium: Affects CaSR, ↑ PTH

🅽 - NEOPLASM (LYMPHOMAS)

Hodgkin Lymphoma: Classical subtype
Non-Hodgkin: B-cell lymphomas
ATLL: HTLV-1 associated T-cell
Mechanism: Macrophage 1α-hydroxylase
1,25(OH)2D: Markedly elevated

🆂 - SARCOIDOSIS & GRANULOMAS

Sarcoidosis: 10-20% develop hypercalcemia
Histoplasmosis: Ohio/Mississippi valleys
Tuberculosis: Miliary TB especially
Coccidioidomycosis: Southwest US
Treatment: Glucocorticoids first-line

🅣 - THYROTOXICOSIS

Prevalence: 20% of hyperthyroid patients
Mechanism: ↑ bone resorption via osteoclasts
T3/T4 Effects: Direct bone effects
Reversible: With treatment of hyperthyroidism
Mild: Usually Ca <12 mg/dL

🆁 - RENAL FAILURE

Tertiary HPT: Autonomous parathyroid glands
Post-Transplant: 30-50% develop hypercalcemia
Aluminum Toxicity: In dialysis patients
Recovery Phase: AKI with bone remineralization
Treatment: Cinacalcet, parathyroidectomy

🅰 - ADRENAL INSUFFICIENCY

Addison's Disease: Primary adrenal failure
Mechanism: Volume depletion, ↓ renal excretion
Associated: Hyperkalemia, hyponatremia
Diagnosis: Cortisol stimulation test
Treatment: Glucocorticoid replacement

🅿 - PRIMARY HYPERPARATHYROIDISM

Adenoma (85%): Single gland disease
Hyperplasia (15%): Multiple glands
Carcinoma (<1%): Very rare
PTH: Elevated or inappropriately normal
Treatment: Parathyroidectomy (cure >95%)

🎯 VITAMINS TRAP Clinical Application

PTH-Independent Causes (PTH <20)

Vitamin D, Vitamin A
Malignancy (most common)
Intoxications
Neoplasm (lymphomas)
Sarcoidosis & granulomas
Thyrotoxicosis
Adrenal insufficiency

PTH-Dependent Causes (PTH ≥20)

Primary hyperparathyroidism
Renal failure (tertiary HPT)
Thiazide diuretics (unmasking)
Immobilization (with hyperparathyroidism)
FHH (Familial Hypocalciuric Hypercalcemia)
Lithium-induced hyperparathyroidism

🔬 Comprehensive Laboratory Differential Diagnosis

📊 Hypercalcemia Laboratory Patterns by Etiology

Complete diagnostic framework for identifying the underlying cause of hypercalcemia

ETIOLOGY	PTH	PTHrP	1,25(OH)₂D	25(OH)D	Phosphate	Other Key Labs
PRIMARY HYPERPARATHYROIDISM	↑↑	Normal	↑ or normal	Normal	↓	ALP ↑, 24h UCa ↑
MALIGNANCY - PTHrP-mediated	↓	↑↑	↓ or normal	Normal	↓	ALP ↑, SPEP abnormal
MALIGNANCY - Local osteolytic	↓	Normal	↓ or normal	Normal	Normal/↑	ALP ↑, imaging shows lesions
MALIGNANCY - Lymphoma	↓	Normal	↑↑	Normal/↑	Normal/↑	LDH ↑, lymphadenopathy
VITAMIN D INTOXICATION	↓	Normal	↑	↑↑	Normal/↑	History of supplements
VITAMIN A INTOXICATION	↓	Normal	Normal	Normal	Normal	Vitamin A level ↑↑
IMMOBILIZATION	↓	Normal	↓ or normal	Normal	Normal/↑	↑ bone resorption markers
THIAZIDES	↑ or normal	Normal	Normal	Normal	Normal	Recent thiazide use
THYROTOXICOSIS	↓	Normal	Normal	Normal	Normal/↑	TSH ↓, T4 ↑, T3 ↑
ADDISON'S DISEASE	Normal/↑	Normal	Normal	Normal	Normal	Cortisol ↓, ACTH ↑
MILK-ALKALI SYNDROME	↓	Normal	Normal	Normal	Normal/↑	Metabolic alkalosis, ↑ Ca intake
SARCOIDOSIS	↓	Normal	↑↑	Normal/↓	Normal/↑	ACE ↑, chest imaging
GRANULOMATOUS DISEASES	↓	Normal	↑↑	Normal	Normal/↑	1α-hydroxylase activity
WILLIAMS SYNDROME	↓	Normal	↑	Normal	Normal	Characteristic facies
RENAL FAILURE (Tertiary HPT)	↑↑	Normal	Low/normal	Normal	↑↑	CrCl <30, long-standing CKD
ADRENAL INSUFFICIENCY	Normal/↑	Normal	Normal	Normal	Normal	Morning cortisol <3 μg/dL

🔑 Key Interpretation Guidelines

PTH Patterns

↑↑ Elevated: Primary hyperparathyroidism, tertiary HPT
↑ or N (inappropriately normal): May unmask mild primary HPT
↓ Suppressed (<20 pg/mL): PTH-independent causes

Vitamin D Patterns

↑↑ 1,25(OH)₂D: Granulomas, lymphoma (extra-renal production)
↑↑ 25(OH)D: Vitamin D intoxication (>100 ng/mL)
Both normal: Most other causes of hypercalcemia

Phosphate Patterns

↓ Low: PTH or PTHrP effect (phosphaturia)
↑↑ High: Renal failure, tumor lysis
Normal/variable: Most other etiologies

🧬 PTHrP-Mediated Malignancy: Specific Cancer Types

🎯 Malignancies That Cause PTHrP Elevation

PTHrP (Parathyroid Hormone-Related Protein): Mimics PTH action, causing calcium reabsorption and phosphate wasting

🫁 Lung Cancers (40% of PTHrP)

Squamous Cell: Most common overall
Large Cell: High PTHrP production
Adenocarcinoma: Less common but possible
Small Cell: Rarely causes PTHrP

🦴 Head & Neck Cancers (20%)

Squamous Cell: Oral, laryngeal, pharyngeal
Salivary Gland: Adenoid cystic carcinoma
Thyroid: Anaplastic, medullary (rare)

🏥 Genitourinary Cancers (15%)

Renal Cell Carcinoma: Clear cell type
Bladder Cancer: Squamous and transitional
Ovarian: Clear cell, squamous
Cervical: Squamous cell carcinoma

🔬 Other Malignancies (25%)

Breast Cancer: Especially with bone mets
Esophageal: Squamous cell type
Skin: Squamous cell carcinoma
Neuroendocrine: Pancreatic islet cell

🧪 PTHrP vs PTH Laboratory Differentiation

PTHrP-Mediated (Malignancy)

PTH: Suppressed (<20 pg/mL)
PTHrP: Elevated (>4.2 pmol/L)
Phosphorus: Low (PTHrP mimics PTH)
1,25(OH)2D: Low or normal
Alkaline phosphatase: Often elevated

Primary Hyperparathyroidism

PTH: Elevated or inappropriately normal
PTHrP: Normal (<4.2 pmol/L)
Phosphorus: Low
1,25(OH)2D: High or high-normal
24h urine calcium: Elevated

🌿 Granulomatous Diseases & Lymphoma: Vitamin D Pathway

🔬 Extra-Renal 1α-Hydroxylase Activity

Mechanism: Activated macrophages and granuloma cells produce 1α-hydroxylase, converting 25(OH)D to active 1,25(OH)2D

🫁 Sarcoidosis (Most Common)

10-20% develop hypercalcemia
50% have hypercalciuria
More common in summer (sun exposure)
Bilateral hilar lymphadenopathy on CXR
ACE level often elevated

🦠 Infectious Granulomas

Histoplasmosis: Ohio/Mississippi valleys
Coccidioidomycosis: Southwest US
Tuberculosis: Especially miliary TB
Blastomycosis: Great Lakes region

🩸 Lymphomas & Hematologic Malignancies

Hodgkin Lymphoma: Classical nodular sclerosis subtype
Aggressive B-cell NHL: DLBCL, Burkitt lymphoma
Adult T-cell Leukemia/Lymphoma: HTLV-1 associated
Plasmacytoma: Extra-medullary plasma cell tumor
Prevalence: 10-25% of lymphoma patients
Extra-nodal sites: GI, CNS, bone marrow

🧪 Laboratory Pattern

PTH: Suppressed
25(OH)D: Normal or low
1,25(OH)2D: ELEVATED (key finding)
Hypercalciuria prominent
Nephrolithiasis common

💊 Treatment of Granulomatous Hypercalcemia

First-Line Therapy

Corticosteroids: Prednisone 20-40 mg daily
Mechanism: Suppresses 1α-hydroxylase
Response: Usually within 7-10 days
Duration: Taper slowly over weeks

Adjunct Measures

Avoid sun exposure and vitamin D
Low calcium diet (800-1000 mg/day)
Treat underlying infection if present
Monitor for steroid side effects

🦴 Clinical Manifestations: "Stones, Bones, Groans, and Psychiatric Moans"

🎯 Classic Symptom Complex by Calcium Level

🗿 STONES (Nephrolithiasis)

Kidney Stones (20-30%): Calcium oxalate/phosphate
Nephrocalcinosis: Calcium deposition in tubules
Polyuria/Polydipsia: Nephrogenic diabetes insipidus
Progressive CKD: From chronic hypercalciuria
Mechanism: ↑ calcium excretion, ↓ concentrating ability

Occurs at Ca++ >11.5 mg/dL

🦴 BONES (Skeletal Effects)

Osteoporosis: Especially in hyperparathyroidism
Osteitis Fibrosa Cystica: "Brown tumors"
Pathologic Fractures: Vertebral, hip, wrist
Bone Pain: Generalized aching
Joint Stiffness: Morning stiffness

Long-term consequence of chronic elevation

😫 GROANS (Gastrointestinal)

Nausea and Vomiting: Common early symptom
Constipation: Decreased bowel motility
Abdominal Pain: Cramping, peptic ulcer disease
Anorexia: Loss of appetite, weight loss
Ileus: Severe hypercalcemia (>14 mg/dL)

Occurs at Ca++ >12 mg/dL

🧠 PSYCHIATRIC MOANS (Neuropsychiatric)

Depression: Most common psychiatric symptom
Cognitive Impairment: Memory loss, confusion
Psychosis: Paranoia, hallucinations
Personality Changes: Irritability, apathy
Coma: Severe hypercalcemia (>15 mg/dL)

Can occur with mild elevation

⚠️ SEVERE HYPERCALCEMIA MANIFESTATIONS (Ca++ ≥14 mg/dL)

💓 Cardiac

QT shortening
Arrhythmias
AV blocks
Cardiac arrest

🧠 Neurologic

Stupor/coma
Seizures
Muscle weakness
Hyporeflexia

🏥 Other

Acute kidney injury
Severe dehydration
Hypercalcemic crisis
Death (untreated)

💧 Hypercalcemia-Induced Nephrogenic Diabetes Insipidus

🎯 Mechanism: How Hypercalcemia Causes Nephrogenic DI

🔬 Cellular Mechanisms

Aquaporin-2 (AQP2) Downregulation:
- Hypercalcemia reduces AQP2 expression
- Decreased water channel insertion
- Impaired water reabsorption
ADH Receptor Dysfunction:
- Calcium interferes with V2 receptor
- Disrupted cAMP signaling
- Reduced ADH responsiveness
Medullary Damage:
- Calcium deposition (nephrocalcinosis)
- Chronic tubulointerstitial nephritis
- Loss of concentrating gradient

📊 Clinical Threshold & Presentation

Threshold: Ca++ >11.5 mg/dL consistently
Polyuria: >3L/day urine output
Polydipsia: Compensatory increased thirst
Urine Osmolality: <300 mOsm/kg (inappropriately dilute)
Dehydration Risk: If water access limited
Hypernatremia: Common complication

⚠️ Key Clinical Point

Reversibility: NDI usually reverses within days to weeks after calcium normalization, but chronic cases may have permanent damage

💊 Treatment Strategy for Hypercalcemic NDI

🎯 Primary Goal

Normalize Calcium: Treat underlying cause
Aggressive Hydration: NS 200-300 mL/hr
Bisphosphonates: Zoledronic acid 4mg IV
Calcitonin: 4 IU/kg q12h (rapid onset)

💧 NDI-Specific Measures

Free Water Access: Ensure adequate intake
Thiazide Diuretics: May help concentration
Amiloride: If lithium co-factor
Monitor Closely: Na+, urine output, volume status

💊 Comprehensive Treatment Protocol

1 IMMEDIATE HYDRATION (First-Line): Normal Saline 200-300 mL/hr
• Goal: Restore intravascular volume, increase calcium excretion • Monitor for volume overload • Continue until volume replete

2 FORCED DIURESIS (After Volume Restoration): Furosemide 20-40 mg IV q6-8h
• ONLY after adequate hydration • Increases calcium excretion • Replace losses with 0.45% saline • Monitor electrolytes closely

3 CALCITONIN (Rapid Onset): 4 IU/kg IM/SC every 12 hours
• Onset: 2-4 hours • Peak effect: 4-6 hours • Duration: 6-8 hours • TEMPORARY effect (tachyphylaxis in 48-72h)

💀 BISPHOSPHONATES: Definitive Long-Term Therapy

🥇 First-Line: Zoledronic Acid

Dose: 4 mg IV over 15-30 minutes
Onset: 24-48 hours
Peak: 4-7 days
Duration: 2-4 weeks
Efficacy: Most potent available

🥈 Alternative: Pamidronate

Dose: 60-90 mg IV over 2-4 hours
Onset: 24-72 hours
Peak: 5-7 days
Duration: 1-3 weeks
Use: If zoledronic acid unavailable

⚠️ BISPHOSPHONATE CONTRAINDICATIONS & WARNINGS

Absolute Contraindications

Severe renal impairment (CrCl <30)
Hypocalcemia
Pregnancy/breastfeeding
Known hypersensitivity

Monitoring & Precautions

Pre-infusion: CBC, CMP, Ca, Phos, Mg
Dental exam before long-term use
Monitor for osteonecrosis of jaw
Atypical fracture risk (rare)

4 ADDITIONAL THERAPIES (Refractory Cases): Based on underlying etiology
• Corticosteroids for granulomatous disease (prednisone 20-40 mg daily) • Dialysis for severe cases with renal failure • Cinacalcet for hyperparathyroidism • Gallium nitrate (rare use)

🧮 Interactive Hypercalcemia Calculator

Comprehensive Diagnostic & Treatment Calculator

Serum Calcium (mg/dL): 12.5

Albumin (g/dL): 4.0

PTH (pg/mL): 25

Age (years): 65

Clinical Setting:

Symptoms Present:

Urine Output:

Cancer History:

Calculating comprehensive diagnostic and treatment plan...

📋 Key Learning Points Summary

🎯 Essential Clinical Pearls

🔍 Diagnostic Priorities

Ca++ >13 mg/dL = 80-90% malignancy
PTH guides workup: elevated vs suppressed
PTHrP elevated in 80% of malignancy cases
1,25(OH)2D elevated in granulomatous disease

💊 Treatment Essentials

Hydration first: NS 200-300 mL/hr
Calcitonin rapid but temporary (tachyphylaxis)
Bisphosphonates definitive therapy
Furosemide only AFTER volume restoration

⚠️ Critical Complications

Nephrogenic DI at Ca++ >11.5 mg/dL
Cardiac arrhythmias, QT shortening
Nephrocalcinosis and chronic kidney disease
Hypercalcemic crisis at Ca++ ≥14 mg/dL

🔺 Hypercalcemia