Renal Manifestations of Primary Hyperparathyroidism (PHPT)

Rodrigo Arrangoiz MS, MD, FACS, FSSO
  • The renal manifestations implicated with PHPT are:
    • Decreased glomerular filtration rate:
      • Up to 20% of patients with asymptomatic PHPT:
        • Have an estimated glomerular filtration rate (eGFR):
          • Below 60 mL/min/1.73 m2
      • The development of kidney insufficiency in PHPT is related to:
        • The degree and duration of hypercalcemia:
          • Mild hypercalcemia is rarely associated with kidney insufficiency
          • In randomized trials of two to three years duration, there is little evidence that kidney function deteriorates in patients with mild chronic hypercalcemia due to PHPT
    • Hypercalciuria:
      • Hypercalciuria is a contributing factor for stone formation in PHPT
      • Although PTH directly stimulates the distal tubular reabsorption of calcium:
        • This effect is overshadowed by the increase in filtered calcium due to hypercalcemia:
          • Leading to increased urinary calcium excretion in 35% to 40% of patients with PHPT
          • Nephrolithiasis
          • Nephrocalcinosis
          • Impaired urinary concentrating ability sometimes leading to polyuria, polydipsia, nocturia
          • Reduced fractional phosphate reabsorption leading to hypophosphatemia
          • Increased urinary exertion of magnesium
  • Nephrolithiasis:
    • Is the universally accepted:
      • Classical kidney manifestation of PHPT
      • It was previously reported in approximately 40% to 80% of patients with PHPT:
        • But now occur only in about 20% to 25% (5% to 55% in some series) of the cases:
          • This wide range likely reflects differences in the methods used for kidney imaging, as well as heterogeneity in PHPT severity
      • Conversely, approximately 5% of patients with nephrolithiasis have hyperparathyroidism
      • Among normocalcemic patients with nephrolithiasis:
        • PHPT should be suspected if the serum calcium concentration is in the high-normal range:
          • Because the hypercalcemia of PHPT may be intermittent and detected only by multiple measurements
      • In one series of 48 patients with nephrolithiasis and PHPT:
        • 30 patients (63%) had serum calcium concentrations between 10.2 and 11 mg/dL
      • The pathophysiology is thought to be related to the filtered load of calcium in the glomerulus:
        • That increases proportionately with the degree of hypercalcemia
      • Most renal stones in patients with PHPT are composed of:
        • Calcium oxalate although slightly alkaline urine may favor the precipitation of calcium phosphate stones
        • Contributing factors for calcium oxalate stone formation in PHPT include:
          • Hypercalciuria
          • Hyperoxaluria
          • Hypocitraturia
          • Hypomagnesuria
          • Dietary risk factors such as a low calcium intake, high oxalate intake, high animal protein intake, high sodium intake, low fluid intake
          • A high serum calcitriol concentration – The high serum calcitriol concentration, caused by PTH stimulation of renal hydroxylation of 25-hydroxyvitamin D (25[OH]D), may contribute to both hypercalciuria and stone formation. Genetic factors such as polymorphisms in calcium-sensing receptor (CaSR) gene have also been described
        • Stone formers are more likely to be hypercalciuric:
          • But less than one-third of the hypercalciuric patients with PHPT actually develop renal stones
        • Hypercalciuria is not a predictor of nephrolithiasis in patients with PHPT and is no longer considered as an indication for surgery:
          • At the present time, it is almost impossible to securely foresee which patients with PHPT will develop nephrolithiasis bases on biochemical analysis of urine
  • Nephrocalcinosis:
    • Which refers to renal parenchymal calcification:
      • Is found in less than five percent of patients and is more likely to lead to renal dysfunction
  • Subclinical nephrocalcinosis and nephrolithiasis:
    • Are more common in patients with than without hyperparathyroidism
    • In a retrospective review of 271 renal ultrasounds from patients with surgically proven, asymptomatic PHPT:
      • The prevalence of kidney stones on ultrasound performed within six months prior to surgery was significantly higher than in age-matched subjects who had renal ultrasounds for other reasons (7% versus 1.6%)
    • In a cross-sectional analyses of asymptomatic patients with PHPT:
      • Occult urolithiasis or kidney calcifications (nephrolithiasis and / or nephrocalcinosis) were identified in approximately 20% of patients
  • Hypertension:
    • The incidence of hypertension is variable:
      • Anywhere between 30% to 50% of patients with PHPT
    • Hypertension appears to be more common in:
      • Older patients and correlates with the magnitude of renal dysfunction
    • In contrast to other symptoms:
      • Is least likely to improve after parathyroidectomy
    • Another plausible explanation of the origin of hypertension in patients with PHPT:
      • Is the synthesis of parathyroid hypertensive factor that triggers an increase in blood pressure
    • The elevated levels of PTH is also linked with the disruption in the renin-angiotensin- aldosterone system
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Published by Rodrigo Arrangoiz MS, MD, FACS, FSSO

My name is Rodrigo Arrangoiz I am a breast surgeon/ thyroid surgeon / parathyroid surgeon / head and neck surgeon / surgical oncologist that works at Center for Advanced Surgical Oncology in Miami, Florida. I was trained as a surgeon at Michigan State University from (2005 to 2010) where I was a chief resident in 2010. My surgical oncology and head and neck training was performed at the Fox Chase Cancer Center in Philadelphia from 2010 to 2012. At the same time I underwent a masters in science (Clinical research for health professionals) at the University of Drexel. Through the International Federation of Head and Neck Societies / Memorial Sloan Kettering Cancer Center I performed a two year head and neck surgery and oncology / endocrine fellowship that ended in 2016. Mi nombre es Rodrigo Arrangoiz, soy cirujano oncólogo / cirujano de tumores de cabeza y cuello / cirujano endocrino que trabaja Center for Advanced Surgical Oncology en Miami, Florida. Fui entrenado como cirujano en Michigan State University (2005 a 2010 ) donde fui jefe de residentes en 2010. Mi formación en oncología quirúrgica y e n tumores de cabeza y cuello se realizó en el Fox Chase Cancer Center en Filadelfia de 2010 a 2012. Al mismo tiempo, me sometí a una maestría en ciencias (investigación clínica para profesionales de la salud) en la Universidad de Drexel. A través de la Federación Internacional de Sociedades de Cabeza y Cuello / Memorial Sloan Kettering Cancer Center realicé una sub especialidad en cirugía de cabeza y cuello / cirugia endocrina de dos años que terminó en 2016.

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