Diabetes Insipidus (DI)

Central Diabetes Insipidus (CDI)

• A deficiency in arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), which is synthesised in the hypothalamus and secreted by the posterior pituitary gland.

Nephrogenic Diabetes Insipidus (NDI)

• A condition where the kidneys are resistant to AVP, impairing urine concentration despite sufficient hormone levels.

Diabetes Insipidus (DI)

• Can be classified into two primary types based on the underlying mechanism:

Central DI (CDI)

• Results from an absolute or relative deficiency of arginine vasopressin (AVP) production or secretion.

Nephrogenic DI (NDI)

• Arises due to renal insensitivity or resistance to AVP's action within the collecting ducts.

Central DI

Idiopathic (30%)

• Often linked to autoimmune mechanisms with lymphocytic infiltration of the posterior pituitary or pituitary stalk.
• Antibodies directed against AVP-secreting cells have been identified but are not always diagnostic due to overlaps with other conditions like Langerhans cell histiocytosis and germinomas.
• Close monitoring with MRI is essential in idiopathic cases, especially those with pituitary stalk thickening.

Tumor-Associated (25%)

• Primary intracranial tumors such as craniopharyngiomas, germinomas, and pineal tumors can lead to central DI.
• Craniopharyngiomas are particularly common in pediatric cases and often present pre- or postoperatively with DI and other hypothalamic manifestations.

Postoperative (20%)

• Neurosurgery, particularly involving transsphenoidal approaches, frequently results in transient or permanent DI.
• Factors such as cerebrospinal fluid leaks during surgery significantly increase the risk of postoperative DI.

Head Trauma (16%)

• Central DI is a potential complication of moderate to severe head injuries.
• Often presents transiently but sometimes progresses to a permanent state.

Hereditary Central DI

• Constitutes approximately 10% of cases.
• Autosomal dominant inheritance is common, associated with mutations in the AVP-NP2 gene, causing toxic accumulation of mutant proteins in magnocellular neurons.
• Autosomal recessive forms include mutations in the WFS1 gene, leading to Wolfram syndrome (DIDMOAD).

Other Causes

• Includes hypoxic encephalopathy, granulomatous diseases (e.g., sarcoidosis, histiocytosis X), vascular lesions (e.g., arteriovenous malformations, Sheehan syndrome), and certain cancers (e.g., metastases from lung cancer).

Nephrogenic DI

Acquired Causes

• Medications:
  • Lithium therapy is the leading cause, affecting up to 40% of long-term users.
  • Other implicated drugs include demeclocycline, amphotericin B, cisplatin, and foscarnet.
• Electrolyte Imbalances:
  • Chronic hypercalcemia and hypokalemia impair AVP action.
• Chronic Renal Conditions:
  • Conditions like sickle cell disease, renal amyloidosis, or obstructive uropathy can disrupt the AVP response.

Hereditary Causes

• AVPR2 Gene Mutations:
  • X-linked recessive inheritance accounts for 90% of cases.
  • These mutations lead to defective vasopressin receptor function.
• AQP2 Gene Mutations:
  • Autosomal recessive and dominant forms arise from defects in aquaporin-2 water channels in the renal collecting ducts.

Other Specific Situations

Pregnancy

• Gestational DI occurs due to increased vasopressinase activity from the placenta, unmasking subclinical AVP deficiencies.

Drug-Induced DI

• Aside from lithium, various drugs induce NDI, usually reversible upon discontinuation.

Key Mechanisms Regulating Water Balance

AVP Synthesis and Release

• AVP is synthesised in magnocellular neurons of the hypothalamus, specifically in the supraoptic (SON) and paraventricular (PVN) nuclei.
• It undergoes post-translational processing, producing AVP, neurophysin II, and copeptin. These are transported along axons to the posterior pituitary for storage and secretion.
• Plasma osmolality, sensed by hypothalamic osmoreceptors, is the primary trigger for AVP release.
• Baroreceptors also regulate AVP secretion in response to blood volume or pressure changes.

Renal Action of AVP

• AVP binds to V2 receptors in renal collecting duct cells, increasing water permeability by promoting the insertion of aquaporin-2 (AQP2) water channels into the apical membrane.
• This mechanism enhances water reabsorption, concentrating the urine and maintaining plasma osmolality within a narrow range.

Pathogenesis in Central and Nephrogenic DI

Central DI (CDI)

• Results from damage to the neurohypophysis, which includes the hypothalamus, pituitary stalk, and posterior pituitary.
• Causes include trauma, neurosurgery, tumors, autoimmune diseases, or genetic mutations affecting AVP synthesis or secretion.
• A deficiency in AVP leads to impaired renal water reabsorption, excessive urine output, and stimulation of thirst.

Nephrogenic DI (NDI)

• Arises from the kidney’s inability to respond to AVP despite normal hormone levels.
• Can be caused by genetic mutations (e.g., AVPR2 or AQP2) or acquired factors like chronic lithium use, hypercalcemia, or chronic kidney disease.
• The absence of AVP-mediated AQP2 insertion results in dilute urine and polyuria.

Additional Pathophysiological Insights

Adipsic DI

• Occurs due to damage to hypothalamic osmoreceptors, leading to deficient AVP secretion and impaired thirst response.
• This condition is often associated with hypernatremia because thirst-dependent water intake does not compensate for urinary water losses.

Pregnancy-Associated Changes

• Pregnancy alters osmoregulation, with a lower osmotic threshold for AVP release.
• Increased placental vasopressinase activity accelerates AVP clearance, occasionally unmasking subclinical central DI.

Global Prevalence

• The estimated global prevalence of DI is approximately 1 in 25,000 individuals (0.004%).
• Central DI (CDI) is more common than nephrogenic DI (NDI), but precise data on the relative proportions are limited.

Prevalence in the United States

• DI occurs at a rate of about 3 cases per 100,000 population in the United States.
• Both CDI and NDI demonstrate similar prevalence rates between males and females, with no significant differences observed across ethnic groups.

Genetic vs. Acquired Causes

• Most cases of DI are acquired rather than hereditary.
• Hereditary forms of DI, including those caused by mutations in the AVPR2 or AQP2 genes, account for only 1–2% of all cases.
• NDI due to AQP2 gene mutations is particularly rare, with an incidence of about 1 in 20 million births.

Age of Onset

• DI may develop at any age.
• Hereditary forms often present earlier in life, while acquired forms are commonly seen in adults, often secondary to trauma, surgery, or disease.

Variations in Sex and Genetic Influences

• While both CDI and NDI show equal prevalence among sexes, NDI is more common in males when it results from X-linked recessive AVPR2 gene mutations.
• In contrast, autosomal forms of NDI due to AQP2 mutations affect males and females equally.

Clinical Relevance

• Despite its rarity, DI can significantly affect patient quality of life if left undiagnosed or mismanaged.
• Misdiagnosis or delayed diagnosis, particularly in inherited or atypical cases, can lead to poor clinical outcomes.

Common Symptoms

 Polyuria

• Excessive urination, with volumes ranging from 3–20 liters per day.
• Consistent daily urine output is a hallmark feature, distinguishing it from urinary frequency seen in other conditions.

Polydipsia

• Increased fluid intake, often due to extreme thirst.
• Patients often prefer cold liquids, particularly water, to compensate for fluid losses.

Nocturia

• Frequent urination during nighttime, commonly disrupting sleep patterns.

Patterns of DI

Triphasic Response (associated with CDI following trauma or surgery)

 Polyuric Phase (4–5 days)

• Characterised by abrupt increases in urine output and reduced urinary osmolality due to suppression of AVP release.

Antidiuretic Phase (5–6 days)

• Urinary osmolality improves temporarily as stored AVP is released.

Permanent DI Phase

• Occurs if AVP-secreting cells are permanently damaged.

Age-Related Presentation

 Infants

• Manifestations include irritability, crying, growth retardation, hyperthermia, and weight loss.
• May present with dehydration if fluid intake does not match urinary losses.

Children

• Enuresis (bedwetting), fatigue, anorexia, and growth defects are common.

Adults

• Symptoms vary widely based on the aetiology, with possible additional signs related to the underlying cause (e.g., neurological deficits).

Specific Scenarios

 Pregnancy

• DI can be unmasked due to increased AVP clearance by placental vasopressinase.
• Typically resolves postpartum but may aggravate pre-existing subclinical DI.

Adipsic DI

• Caused by hypothalamic lesions impairing both AVP release and thirst mechanisms.
• Results in severe dehydration and hypernatremia due to lack of compensatory fluid intake.

Historical Risk Factors

 Surgical History

• Pituitary or hypothalamic surgeries (e.g., transsphenoidal procedures) often precipitate CDI.

Trauma

• Traumatic brain injuries can lead to transient or permanent CDI.

Autoimmune Disorders

• Hashimoto’s thyroiditis and type 1 diabetes mellitus are associated with CDI.

Medications

• Long-term lithium use and other drugs (demeclocycline, cisplatin, amphotericin B) can induce NDI.

Family History

• X-linked mutations (AVPR2) and autosomal mutations (AQP2, AVP-neurophysin) are implicated in hereditary DI.

General Findings

 Hydration Status

• Most patients with access to fluids maintain normal hydration.
• Dehydration is uncommon unless the thirst mechanism is impaired or access to water is restricted, which can lead to:
  • Dry mucous membranes
  • Poor skin turgor
  • Tachycardia
  • Postural hypotension
  • Severe cases: Shock

Bladder and Renal Signs

• Bladder enlargement may occur due to chronic polyuria.
• Hydronephrosis may be present, causing:
  • Pelvic fullness
  • Flank pain or tenderness
  • Pain radiating to the genital area

Neurological and Visual Findings

 Visual Field Defects

• May suggest a mass or lesion affecting the optic chiasm, such as a pituitary tumor.

Focal Neurological Deficits

• Can indicate prior or coexisting intracranial pathology, such as trauma, meningitis, or tumor invasion.

Specific Findings Based on Underlying Aetiology

 Adipsic DI

• Characterised by signs of severe dehydration and hypernatremia without compensatory polydipsia due to an impaired thirst mechanism.

Endocrine and Dermatological Associations

 Wolfram Syndrome

• Sensorineural deafness
• Visual failure with optic atrophy

Autoimmune Diseases

• Skin manifestations like erythema nodosum or rashes in conditions like sarcoidosis or Langerhans cell histiocytosis

Examination in Paediatric Patients

 Infants and Children

• May present with symptoms indicative of chronic dehydration, including:
  • Irritability
  • Failure to thrive
  • Weight loss
  • Poor feeding

Initial Laboratory Investigations

 Urine Osmolality

• Findings: Low (<300 mOsm/kg) in the context of high serum osmolality or elevated sodium.
• Significance: Indicates impaired urinary concentration, a hallmark of DI.

Serum Osmolality

• Findings: Typically elevated (>290 mOsm/kg) in DI.
• Significance: Elevated levels with low urine osmolality confirm a water diuresis.

Serum Sodium

• Findings: May be normal in compensated DI but elevated in cases with impaired thirst or restricted access to fluids.
• Significance: Hypernatremia strengthens the suspicion of DI in appropriate clinical settings.

Serum Glucose

• Findings: Normal in DI.
• Significance: Rules out diabetes mellitus as the cause of polyuria.

Serum Potassium and Calcium

• Findings: Hypokalemia or hypercalcemia may be present.
• Significance: These abnormalities can contribute to nephrogenic DI.

Urine Dipstick

• Findings: Negative for glycosuria; may show proteinuria if renal disease is present.
• Significance: Excludes diabetes mellitus and highlights potential renal contributions.

24-Hour Urine Collection

• Findings: Polyuria, defined as urine output >3 litres/day.
• Significance: Quantifies the degree of water loss.

Dynamic and Specialised Tests

 Water Deprivation Test

• Method:
  • Fluid restriction for up to 8 hours or until 3% of body weight is lost.
  • Hourly monitoring of serum osmolality, urine osmolality, and urine volume.
• Findings:
  • Failure to concentrate urine (<300 mOsm/kg) despite elevated serum osmolality (>290 mOsm/kg) confirms DI.
• Significance: Differentiates DI from primary polydipsia.

Desmopressin (DDAVP) Stimulation Test

• Method: Administration of desmopressin followed by hourly measurements of serum and urine osmolality.
• Findings:
  • Central DI: Urine osmolality increases significantly (>750 mOsm/kg).
  • Nephrogenic DI: Minimal or no response.
• Significance: Helps distinguish central from nephrogenic DI.

Hypertonic Saline-Stimulated Copeptin Test

• Method: Baseline and post-hypertonic saline copeptin levels measured.
• Findings:
  • Copeptin >21.4 pmol/L: Nephrogenic DI.
  • Copeptin >4.9 pmol/L post-stimulation: Central DI.
• Significance: High accuracy in differentiating DI subtypes.

Imaging Studies

 Cranial MRI

• Findings:
  • Absence of the posterior pituitary "bright spot."
  • Pituitary stalk thickening, sellar or para-sellar mass.
• Significance: Identifies structural abnormalities causing central DI.

Advanced and Aetiology-Specific Tests

 Genetic Testing

• Indications: Family history of DI or early onset.
• Findings:
  • AVPR2 mutations: X-linked nephrogenic DI.
  • AQP2 mutations: Autosomal nephrogenic DI.
• Significance: Confirms hereditary DI and guides familial risk assessment.

Tumor Markers

• Findings: Elevated alpha-fetoprotein and beta-hCG in germinomas.
• Significance: Evaluates for malignancies in young patients with pituitary stalk lesions.

Autoantibody Testing

• Findings: Positive antithyroid peroxidase antibodies in Hashimoto's thyroiditis.
• Significance: Supports autoimmune causes of DI.

Pituitary Hormone Evaluation

• Tests:
  • Morning cortisol and ACTH
  • TSH, T3/T4
  • IGF-1 and growth hormone
• Significance: Identifies associated hypopituitarism in central DI.

Psychogenic Polydipsia

• Signs and symptoms:
  • Associated with psychiatric conditions such as schizophrenia or anxiety disorders.
  • Daytime symptoms or waking with a need to drink rather than urinate are more common.
• Investigations:
  • Water Deprivation Test: A rise in urine osmolality >700 mOsm/kg during dehydration indicates normal AVP axis function, but long-standing psychogenic polydipsia may impair renal concentrating ability.
  • Hypertonic Saline-Stimulated Copeptin Test: Copeptin level ≤4.9 pmol/L suggests psychogenic polydipsia.

Diabetes Mellitus

• Signs and symptoms:
  • Polyuria and polydipsia may mimic DI.
  • Often accompanied by weight loss, fatigue, and hyperglycemia.
• Investigations:
  • Plasma Glucose: Elevated glucose levels confirm diabetes mellitus.
  • Urine Dipstick: Presence of glycosuria supports the diagnosis.

Diuretic Use

• Signs and symptoms:
  • Symptoms similar to DI but associated with a history of diuretic use.
• Investigations:
  • Clinical diagnosis based on patient history.
  • Urinary electrolyte excretion patterns may help confirm.

Hypercalcemia

• Signs and symptoms:
  • Often asymptomatic but may include abdominal pain, constipation, fatigue, renal stones, and anorexia.
• Investigations:
  • Serum Calcium: Elevated levels confirm hypercalcemia.
  • Further Tests: Assess parathyroid hormone (PTH) levels if hypercalcemia is confirmed.

Hypokalemia

• Signs and symptoms:
  • May cause nephrogenic DI-like symptoms due to impaired urinary concentrating ability.
• Investigations:
  • Serum Potassium: Low levels support the diagnosis.
  • Evaluate for underlying causes, such as gastrointestinal losses or diuretic use.

Histiocytosis (e.g., Langerhans Cell Histiocytosis)

• Signs and symptoms:
  • Associated with central DI, systemic symptoms, and lytic bone lesions.
• Investigations:
  • MRI: Pituitary stalk thickening.
  • Biopsy: Confirms histiocytosis.

Sickle Cell Disease

• Signs and symptoms:
  • Polyuria related to renal tubular dysfunction.
• Investigations:
  • Haemoglobin Electrophoresis: Confirms sickle cell trait or disease.
  • Urine osmolality shows impaired concentrating ability.

Medullary Cystic Disease

• Signs and symptoms:
  • Chronic polyuria with signs of progressive renal failure.
• Investigations:
  • Renal Ultrasound: Shows medullary cysts.
  • Genetic Testing: May identify causative mutations.

Paediatric Head Trauma

• Signs and symptoms:
  • Polyuria may follow traumatic brain injury due to central DI.
• Investigations:
  • MRI: Evaluates hypothalamic-pituitary damage.
  • Water Deprivation Test: Confirms DI if indicated.

Type 1 Diabetes Mellitus

• Signs and symptoms:
  • Polyuria and polydipsia may mimic DI but are accompanied by hyperglycemia and weight loss.
• Investigations:
  • Serum Glucose and HbA1c: Elevated.
  • Urine Dipstick: Glycosuria.

General Principles

 Treatment Goals

• Restore and maintain fluid balance.
• Correct hypernatremia if present.
• Alleviate polyuria, polydipsia, and nocturia.
• Prevent long-term complications and improve quality of life.

Fluid Replacement

• Oral or Enteral Fluids: Preferred for correcting mild to moderate dehydration.
• Intravenous Fluids: Required for severe cases or when oral intake is inadequate.
• Hypotonic solutions such as 5% dextrose or 0.45% sodium chloride are recommended.
• Adjust infusion rates to avoid rapid shifts in serum sodium levels, especially in chronic hypernatremia.

Monitoring

• Regular assessment of serum electrolytes and osmolality to guide therapy.
• Frequent monitoring is crucial during fluid replacement and initiation of pharmacologic therapy to avoid hyponatremia or overcorrection.

Central Diabetes Insipidus (CDI)

 Desmopressin (DDAVP)

• A synthetic analog of arginine vasopressin (AVP), it is the treatment of choice for CDI.

Routes of Administration

• Intranasal, oral, subcutaneous, or intravenous.
• Parenteral forms are preferred for acute presentations due to rapid onset of action.

Dosage

• Start with the lowest effective dose to prevent water retention and hyponatremia.
• Nocturnal dosing may suffice for mild cases.

Acute Management

• Administer parenteral or oral DDAVP at the lowest dose.
• Monitor urine output, serum sodium, and osmolality closely.
• Ensure adequate fluid intake to match urine output.

Chronic Management

• Individualised dosing, often with a single nocturnal dose for mild cases.
• Patients should periodically skip doses (e.g., one day per week) to allow excess water excretion and reduce hyponatremia risk.

Nephrogenic Diabetes Insipidus (NDI)

 Fluid Management

• Encourage adequate oral fluid intake to compensate for urinary losses.
• Monitor for signs of dehydration, especially during intercurrent illness.

Address Underlying Causes

• Discontinue offending medications (e.g., lithium, demeclocycline).
• Correct electrolyte disturbances such as hypercalcemia or hypokalemia.

Dietary Modifications

• Implement a low-sodium diet (<500 mg/day) to reduce renal solute load.
• A low-protein diet may also help decrease urine output.

Pharmacologic Therapy

• Thiazide Diuretics:
  • Induce mild hypovolemia, enhancing proximal tubular water reabsorption and reducing urine output.
• Nonsteroidal Anti-Inflammatory Drugs (NSAIDs):
  • Reduce prostaglandin-mediated antagonism of AVP.
• Combination Therapy:
  • Thiazides and NSAIDs are often synergistic in reducing polyuria.
• High-Dose DDAVP:
  • May partially improve symptoms in cases of variable renal insensitivity to AVP.

Management of Hypernatremia

 Acute Hypernatremia

• Correct serum sodium rapidly but cautiously (≤1 mmol/L per hour) to prevent cerebral edema.

Chronic Hypernatremia

• Correct serum sodium at a slower rate (≤0.5 mmol/L per hour) to reduce the risk of cerebral edema.

Free Water Deficit Calculation

• Free water deficit = TBW × [(serum Na/140) - 1]
• TBW is estimated as:
  • 0.6 × body weight for men and children
  • 0.5 × body weight for women
  • 0.45 × body weight for elderly women

Paediatric Management

 Infants and Small Children

• Intranasal DDAVP or subcutaneous administration may be preferred due to challenges in oral dosing.
• Monitor serum sodium frequently, especially in the early stages of treatment.

Older Children

• Oral or intranasal DDAVP at doses tailored to age and weight.
• Encourage appropriate fluid intake, and educate caregivers about symptoms of hyponatremia and hypernatremia.

General Prognosis

 Central DI (CDI)

• CDI is often well-controlled with desmopressin (DDAVP), a synthetic analog of AVP.
• Postoperative or trauma-induced CDI may be transient, particularly after pituitary surgery or head trauma.
• Lifelong monitoring is needed for associated conditions, such as anterior pituitary deficiencies, and any underlying intracranial pathology.

Nephrogenic DI (NDI)

• Prognosis depends on the underlying cause:
  • Medication-Induced NDI: Discontinuing the offending agent (e.g., lithium) may lead to resolution, though long-term lithium use can cause irreversible damage.
  • Electrolyte Imbalances: NDI secondary to hypercalcemia or hypokalemia often resolves with correction of the electrolyte disturbance.
  • Congenital NDI: Inherited forms, such as those caused by AVPR2 or AQP2 mutations, are lifelong conditions that require ongoing management to prevent complications.

Gestational DI

• Typically resolves postpartum, as placental vasopressinase activity ceases after delivery.

Long-Term Complications

 Hypernatremia and Dehydration

• Severe hypernatremia can lead to neurological complications, cardiovascular collapse, and, in rare cases, death.
• At-risk populations include children, elderly patients, and individuals with restricted access to water.

Bladder and Renal Issues

• Chronic polyuria can lead to bladder dysfunction, hydronephrosis, or chronic kidney disease (CKD).
• Regular imaging of the renal tract is recommended for patients with large-volume polyuria to detect and manage such complications early.

Growth and Development in Pediatric Patients

• A retrospective study reported that 61% of pediatric patients with congenital NDI required hospitalisation for hypernatremia and failure to thrive.
• Long-term follow-up showed a reduction in growth delays with optimal management.

Mortality

• DI-related mortality is rare if water intake is adequate.
• Life-threatening complications are more likely in neglected cases, such as those with undiagnosed DI or inability to access fluids.

Monitoring and Follow-Up

 Regular Monitoring

• Lifelong follow-up for patients with central DI to assess for evolving intracranial pathologies and anterior pituitary hormone deficiencies.
• Routine serum sodium and osmolality measurements to prevent complications from over- or under-treatment.

Imaging

• Periodic renal and bladder imaging is advised in patients with chronic polyuria to monitor for hydronephrosis or bladder dysfunction.

Management of Associated Conditions

• Address and monitor other comorbidities, such as electrolyte disturbances or anterior pituitary hormone deficiencies, as needed.

Short-Term Complications

Hypernatremia

• Develops when water intake is insufficient to compensate for excessive urinary losses, especially in patients with impaired thirst or restricted access to fluids.
  • Symptoms include irritability, restlessness, lethargy, muscle twitching, spasticity, and hyper-reflexia.
  • Severe cases may lead to delirium, seizures, or coma.
• Managed with oral or intravenous fluids to correct the free water deficit.
  • Serial serum sodium and osmolality must be monitored to guide therapy and avoid rapid correction.

Thrombosis

• Caused by dehydration and hypernatremia, which increase the risk of thrombotic events such as deep vein thrombosis.
  • Presents with swelling, pain, or redness in the affected limb.
• Management includes prompt correction of dehydration and consideration of anticoagulation in high-risk patients.

Therapy-Related Complications

Iatrogenic hyponatremia

• Occurs due to excessive desmopressin (DDAVP) dosing or overhydration during treatment of central DI.
  • Often asymptomatic but can cause nausea, headache, lethargy, seizures, or coma in severe cases.
• Management includes adjusting the DDAVP dose and monitoring serum sodium levels regularly.

Long-Term Complications

Bladder dysfunction

• Chronic high urinary output in nephrogenic DI can lead to bladder overdistension and dysfunction.
  • May present as urinary retention or incontinence.
• Requires regular bladder ultrasound to assess and monitor function.

Renal dysfunction

• Prolonged nephrogenic DI may cause renal impairment, including chronic kidney disease.
  • Clinical features include increased serum creatinine and reduced glomerular filtration rate.
• Management includes periodic renal function monitoring and correction of underlying causes (e.g. hypercalcaemia, nephrotoxic medications).

Other Possible Complications

Chronic dehydration

• Symptoms include tachycardia, hypotension, fatigue, weight loss, and headaches.
• May predispose patients to kidney damage and brain dysfunction if untreated.

Neurological damage

• Severe or prolonged hypernatremia may result in irreversible brain injury.

Monitoring Recommendations

Serum electrolytes and osmolality

• Frequent monitoring during acute treatment or DDAVP adjustment.
• Periodic checks during long-term management.

Renal and bladder imaging

• Regular ultrasound in patients with chronic polyuria to detect hydronephrosis or bladder dysfunction.

Thrombosis screening

• Consider in dehydrated or high-risk patients.

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