Uploaded on

1-я часть лекции "Осложнения терминальной стадии хронической почечной недостаточности"

1-я часть лекции "Осложнения терминальной стадии хронической почечной недостаточности"

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
570
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
2
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide
  • There is a complex homeostatic system that exists to maintain serum calcium levels within 2% of normal. The system comprises sensing tissues such as the parathyroid glands, calciotropic hormones (e.g. parathyroid hormone [PTH] and vitamin D [calcitriol]) and effector tissues upon which the hormones act (e.g. kidney, bone and intestine). PTH is the most important calciotropic hormone. Build 1 For example, suppression of serum calcium leads to the release of PTH from parathyroid glands. Build 2 PTH acts on the kidneys to increase reabsorption of calcium from urine and increase excretion of phosphorus. PTH induces the release of calcium and phosphorus from bone. Build 3 Renal retention of calcium and its release from bone stores result in the normalization of serum calcium levels. Build 4 PTH also induces production of active vitamin D (calcitriol; 1,25 dihydroxy vitamin D 3 ) in the kidney. Calcitriol facilitates absorption of calcium from the gastrointestinal tract, thus helping to normalize serum calcium levels. Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) pp. 167 – 82
  • There is a complex homeostatic system that exists to maintain serum calcium levels within 2% of normal. The system comprises sensing tissues such as the parathyroid glands, calciotropic hormones (e.g. parathyroid hormone [PTH] and vitamin D [calcitriol]) and effector tissues upon which the hormones act (e.g. kidney, bone and intestine). PTH is the most important calciotropic hormone. Build 1 For example, suppression of serum calcium leads to the release of PTH from parathyroid glands. Build 2 PTH acts on the kidneys to increase reabsorption of calcium from urine and increase excretion of phosphorus. PTH induces the release of calcium and phosphorus from bone. Build 3 Renal retention of calcium and its release from bone stores result in the normalization of serum calcium levels. Build 4 PTH also induces production of active vitamin D (calcitriol; 1,25 dihydroxy vitamin D 3 ) in the kidney. Calcitriol facilitates absorption of calcium from the gastrointestinal tract, thus helping to normalize serum calcium levels. Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) pp. 167 – 82
  • There is a complex homeostatic system that exists to maintain serum calcium levels within 2% of normal. The system comprises sensing tissues such as the parathyroid glands, calciotropic hormones (e.g. parathyroid hormone [PTH] and vitamin D [calcitriol]) and effector tissues upon which the hormones act (e.g. kidney, bone and intestine). PTH is the most important calciotropic hormone. Build 1 For example, suppression of serum calcium leads to the release of PTH from parathyroid glands. Build 2 PTH acts on the kidneys to increase reabsorption of calcium from urine and increase excretion of phosphorus. PTH induces the release of calcium and phosphorus from bone. Build 3 Renal retention of calcium and its release from bone stores result in the normalization of serum calcium levels. Build 4 PTH also induces production of active vitamin D (calcitriol; 1,25 dihydroxy vitamin D 3 ) in the kidney. Calcitriol facilitates absorption of calcium from the gastrointestinal tract, thus helping to normalize serum calcium levels. Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) pp. 167 – 82
  • There is a complex homeostatic system that exists to maintain serum calcium levels within 2% of normal. The system comprises sensing tissues such as the parathyroid glands, calciotropic hormones (e.g. parathyroid hormone [PTH] and vitamin D [calcitriol]) and effector tissues upon which the hormones act (e.g. kidney, bone and intestine). PTH is the most important calciotropic hormone. Build 1 For example, suppression of serum calcium leads to the release of PTH from parathyroid glands. Build 2 PTH acts on the kidneys to increase reabsorption of calcium from urine and increase excretion of phosphorus. PTH induces the release of calcium and phosphorus from bone. Build 3 Renal retention of calcium and its release from bone stores result in the normalization of serum calcium levels. Build 4 PTH also induces production of active vitamin D (calcitriol; 1,25 dihydroxy vitamin D 3 ) in the kidney. Calcitriol facilitates absorption of calcium from the gastrointestinal tract, thus helping to normalize serum calcium levels. Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) pp. 167 – 82
  • Build 1 Declining kidney function leads to reduced production of active calcitriol in the kidney. Reduced renal excretion of phosphate results in increased serum phosphorus levels (hyperphosphataemia). 1 Build 2 The combination of low calcitriol levels and hyperphosphataemia means that patients with CKD have a tendency to develop hypocalcaemia. As a result of calcitriol deficiency, less calcium is absorbed from the gastrointestinal tract. Hyperphosphataemia prevents the release of calcium from bone (see later slides). 2 The failing kidney is also less able to reabsorb calcium from urine. Build 3 Phosphorus has a role in vitamin D homeostasis, with elevated levels suppressing calcitriol production and its inhibitory effect on parathyroid function. 3,4 Build 4 How does hypocalcaemic demand affect the CaR and PTH secretion? In normo- or hypercalcaemia, the CaR is agonized and PTH secretion/synthesis is restrained. 5 Build 5 Hypocalcaemic demand means that there is insufficient calcium to agonize the CaR and the receptor is relaxed. Parathyroid cells respond by increasing PTH secretion (serum PTH levels rise). The sustained hypocalcaemic demand seen in patients with CKD and SHPT eventually leads to increased PTH synthesis and parathyroid cell proliferation. 6 Hypocalcaemic demand is a potent driver of PTH production in patients with SHPT. Block GA et al. Am J Kidney Dis 2000;35:1226–37 Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Almaden Y et al. Kidney Int 2003;64:2311–7 Silver J et al. Am J Physiol Renal Physiol 2002;283:F367 – 76 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93
  • Build 1 Declining kidney function leads to reduced production of active calcitriol in the kidney. Reduced renal excretion of phosphate results in increased serum phosphorus levels (hyperphosphataemia). 1 Build 2 The combination of low calcitriol levels and hyperphosphataemia means that patients with CKD have a tendency to develop hypocalcaemia. As a result of calcitriol deficiency, less calcium is absorbed from the gastrointestinal tract. Hyperphosphataemia prevents the release of calcium from bone (see later slides). 2 The failing kidney is also less able to reabsorb calcium from urine. Build 3 Phosphorus has a role in vitamin D homeostasis, with elevated levels suppressing calcitriol production and its inhibitory effect on parathyroid function. 3,4 Build 4 How does hypocalcaemic demand affect the CaR and PTH secretion? In normo- or hypercalcaemia, the CaR is agonized and PTH secretion/synthesis is restrained. 5 Build 5 Hypocalcaemic demand means that there is insufficient calcium to agonize the CaR and the receptor is relaxed. Parathyroid cells respond by increasing PTH secretion (serum PTH levels rise). The sustained hypocalcaemic demand seen in patients with CKD and SHPT eventually leads to increased PTH synthesis and parathyroid cell proliferation. 6 Hypocalcaemic demand is a potent driver of PTH production in patients with SHPT. Block GA et al. Am J Kidney Dis 2000;35:1226–37 Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Almaden Y et al. Kidney Int 2003;64:2311–7 Silver J et al. Am J Physiol Renal Physiol 2002;283:F367 – 76 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93
  • Build 1 Declining kidney function leads to reduced production of active calcitriol in the kidney. Reduced renal excretion of phosphate results in increased serum phosphorus levels (hyperphosphataemia). 1 Build 2 The combination of low calcitriol levels and hyperphosphataemia means that patients with CKD have a tendency to develop hypocalcaemia. As a result of calcitriol deficiency, less calcium is absorbed from the gastrointestinal tract. Hyperphosphataemia prevents the release of calcium from bone (see later slides). 2 The failing kidney is also less able to reabsorb calcium from urine. Build 3 Phosphorus has a role in vitamin D homeostasis, with elevated levels suppressing calcitriol production and its inhibitory effect on parathyroid function. 3,4 Build 4 How does hypocalcaemic demand affect the CaR and PTH secretion? In normo- or hypercalcaemia, the CaR is agonized and PTH secretion/synthesis is restrained. 5 Build 5 Hypocalcaemic demand means that there is insufficient calcium to agonize the CaR and the receptor is relaxed. Parathyroid cells respond by increasing PTH secretion (serum PTH levels rise). The sustained hypocalcaemic demand seen in patients with CKD and SHPT eventually leads to increased PTH synthesis and parathyroid cell proliferation. 6 Hypocalcaemic demand is a potent driver of PTH production in patients with SHPT. Block GA et al. Am J Kidney Dis 2000;35:1226–37 Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Almaden Y et al. Kidney Int 2003;64:2311–7 Silver J et al. Am J Physiol Renal Physiol 2002;283:F367 – 76 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93
  • In addition to its effects on serum calcium, serum phosphorus directly affects parathyroid cell function. The actions of phosphorus may be mediated by a cell-surface receptor, but no such protein has been identified to date. Build 1 Excess phosphorus acts directly on parathyroid cells to increase: - PTH secretion 1,2 - PTH synthesis 3 - parathyroid cell proliferation. 3,4 1. Almaden Y et al . J Am Soc Nephrol 1998;9:1845–52 2. De Francisco A et al. Kidney Int 1998;54:2140–5 3. Naveh-Many T et al. J Clin Invest 1995;96:1786–93 4. Denda M et al . Am J Kidney Dis 1996;28:596–602
  • Calcitriol has a direct effect on parathyroid cells through its agonism of a specific nuclear receptor (VDR). Build 1 Activation of the VDR by vitamin D leads to: - a decrease in PTH synthesis (decreased expression of PTH mRNA) 1 - a decrease in PTH secretion (secondary to the decrease in PTH synthesis). Thus, in SHPT, low vitamin D levels result in insufficient activation of VDRs. The inhibitory effect on PTH synthesis is compromised and eventually serum PTH levels begin to rise. If vitamin D deficiency is prolonged, proliferation of parathyroid cells begins to increase. 2,3 Studies show that calcitriol prevents parathyroid cell proliferation. 4,5 The direct effect of vitamin D on PTH production is probably less important than its indirect effect through calcium. 1,6 Furthermore, its direct effect is relatively slow since it determines synthesis of PTH and not secretion. Navey-Many T et al . J Clin Invest 1990;86:1968–75 Hendy GN et al. Am J Physiol 1989;256:E765 – 72 Parfitt AM. Kidney Int 1997;52:3 – 9 Szabo A et al. Kidney Int 1989;35:1049 –56 Almaden Y et al. Kidney Int 2003;64:2311 –7 Li X et al. J Cell Biochem 2003;89:709 – 19
  • Parathyroid hyperplasia develops in tandem with the progressive decline in renal function. The constantly increasing functional demand on parathyroid glands (mainly as a result of hypocalcaemia) drives cell proliferation. Initially, the parathyroid glands respond by increasing the proportion of secretory (chief) cells within the gland and then by increasing the total number of cells, resulting in diffuse hyperplasia of the gland. 1 In diffuse hyperplasia, cell growth is polyclonal, but is accompanied by down-regulation of the CaR and VDR. 1 As CKD progresses to stage 5 (end-stage renal disease [ESRD]), parathyroid hyperplasia evolves even further; monoclonal abnormalities lead to nodular hyperplasia of the glands. 2,3 These grossly enlarged parathyroid glands are associated with significantly reduced expression of CaRs and VDRs. 4,5 Parathyroid glands with nodular hyperplasia therefore become less responsive to serum calcium levels 6,7 and resistant to the medical treatment of SHPT. 6,8   1. Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 2. Tominaga Y et al. World J Surg 1996;20:744–50 3. Tominaga Y et al. Clin Nephrol 1995;44(Suppl 1):S42–7 4. Gogusev J et al. Kidney Int 1997;51:328–36 5. Wang X et al. Chin Med J (Engl) 2001;114:410–4 6. Rodriguez M et al. Kidney Int 2002;80:S155–60 7. Almaden Y et al. J Am Soc Nephrol 1998;9:1845–52 8. Rodriguez M et al . Kidney Int 1999;56:306–17
  • Refractory SHPT is characterized by severe nodular hyperplasia of the parathyroid glands. 1 Here, the mass of cells generating PTH is very large and monoclonal growth patterns ensure that CaRs and VDRs are significantly under-expressed. 2–4 Thus, control of PTH secretion/synthesis by calcium and vitamin D is marginalized. Build 1 The enlarged, resistant parathyroid glands produce excessive quantities of PTH (e.g. serum iPTH > 800 pg/mL). 1 Severely elevated PTH causes large amounts of calcium and phosphorus to be released from skeletal stores (despite skeletal resistance). Severe SHPT can therefore be associated with both hyperphosphataemia and hypercalcaemia. Build 2 Increased serum phosphorus leads to further stimulation of the parathyroid glands. 5 Normally, elevated serum calcium would inhibit PTH production, but reduced expression of the CaR blunts this control mechanism. Thus, a vicious cycle of increasing PTH secretion is established and elevated mineral levels put patients at further risk of calcification.   Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 2. Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 3. Gogusev J et al. Kidney Int 1997;51:328–36 4. Tokumoto M et al. Kidney Int 2002;62:1196–207 5. Almaden Y et al . J Am Soc Nephrol 1998;9:1845–52
  • Refractory SHPT is characterized by severe nodular hyperplasia of the parathyroid glands. 1 Here, the mass of cells generating PTH is very large and monoclonal growth patterns ensure that CaRs and VDRs are significantly under-expressed. 2–4 Thus, control of PTH secretion/synthesis by calcium and vitamin D is marginalized. Build 1 The enlarged, resistant parathyroid glands produce excessive quantities of PTH (e.g. serum iPTH > 800 pg/mL). 1 Severely elevated PTH causes large amounts of calcium and phosphorus to be released from skeletal stores (despite skeletal resistance). Severe SHPT can therefore be associated with both hyperphosphataemia and hypercalcaemia. Build 2 Increased serum phosphorus leads to further stimulation of the parathyroid glands. 5 Normally, elevated serum calcium would inhibit PTH production, but reduced expression of the CaR blunts this control mechanism. Thus, a vicious cycle of increasing PTH secretion is established and elevated mineral levels put patients at further risk of calcification.   Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 2. Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 3. Gogusev J et al. Kidney Int 1997;51:328–36 4. Tokumoto M et al. Kidney Int 2002;62:1196–207 5. Almaden Y et al . J Am Soc Nephrol 1998;9:1845–52
  • Refractory SHPT is characterized by severe nodular hyperplasia of the parathyroid glands. 1 Here, the mass of cells generating PTH is very large and monoclonal growth patterns ensure that CaRs and VDRs are significantly under-expressed. 2–4 Thus, control of PTH secretion/synthesis by calcium and vitamin D is marginalized. Build 1 The enlarged, resistant parathyroid glands produce excessive quantities of PTH (e.g. serum iPTH > 800 pg/mL). 1 Severely elevated PTH causes large amounts of calcium and phosphorus to be released from skeletal stores (despite skeletal resistance). Severe SHPT can therefore be associated with both hyperphosphataemia and hypercalcaemia. Build 2 Increased serum phosphorus leads to further stimulation of the parathyroid glands. 5 Normally, elevated serum calcium would inhibit PTH production, but reduced expression of the CaR blunts this control mechanism. Thus, a vicious cycle of increasing PTH secretion is established and elevated mineral levels put patients at further risk of calcification.   Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 2. Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 3. Gogusev J et al. Kidney Int 1997;51:328–36 4. Tokumoto M et al. Kidney Int 2002;62:1196–207 5. Almaden Y et al . J Am Soc Nephrol 1998;9:1845–52

Transcript

  • 1. Осложнения терминальной стадии хронической почечной недостаточности Пушкина А.В. Москва 23 октября 2011 Осенние встречи “ НЕФРО-ЛИГИ ” 2011 Часть I
  • 2. Распространенность заболеваний почек
    • Превышает 100 новых пациентов на млн. жителей
    • Количество больных терминальной стадией ХПН (тХПН) в странах Европы и США увеличивается на 4-7% в год
    • Количество больных тХПН в России увеличивается на 12% в год
  • 3. Стадии хронической почечной недостаточности
    • 1 стадия СКФ ≥90 мл/мин
    • 2 стадия СКФ 60-89 мл/мин
    • 3 стадия СКФ 30-59 мл/мин
    • 4 стадия СКФ 15-29 мл/мин
    • 5 стадия СКФ < 15 мл/мин
    • СКФ- скорость клубочковой фильтрации
  • 4. По данным крупных регистров
    • Распространенность стойкого снижения СКФ (15-59 мл/мин) составляет не менее 3,8% в общей популяции
    • При этом только ¼ лиц информирована о наличии у них ХБП
  • 5.  
  • 6. Осложнения тХПН
    • АНЕМИЯ
    • АРТЕРИАЛЬНАЯ ГИПЕРТЕНЗИЯ
    • ВТОРИЧНЫЙ ГИПЕРПАРАТИРЕОЗ
  • 7. АНЕМИЯ
    • Целевой уровень Hb 100-120 г/л (не более 130 г/л)
    • Целевой уровень Ht 33-36%
  • 8. Проявления анемии
    • Слабость
    • Одышка
    • Плохое самочувствие
    • Рассеянность
    • Расстройства сна
    • Повышение АД
    • Тахикардия
    • Снижение иммунитета
    • И др.
  • 9. Причины анемии
    • Снижение выработки эритропоэтина в почках
    • Дефицит железа (ферритин 200-500 нг/мл, КНТ- 30%)
    • Дефицит фолиевой кислоты
    • Дефицит вит.В12
    • Хронические кровопотери
    • Кровотечения
    • Инфекции
    • Неадекватный гемодиализ
  • 10. Лечение анемии
    • Препараты эритропоэтина (Эпрекс, Рекормон, Эральфон, Эпокрин, Эритростим, Аранесп, Мирцера)
    • Препараты железа (Венофер, Космофер)
    • Минимизация кровопотерь
    • Адекватный гемодиализ
    • Лечение сопутствующих осложнений
  • 11. Артериальная гипертензия
    • Целевое АД < 140/90 мм рт.ст.
    • Контроль гипертензии
    • оказывает благоприятное
    • воздействие на состояние
    • сердечно-сосудистой
    • системы, предотвращает
    • повреждение
    • органов-мишеней
  • 12.  
  • 13. Причины артериальной гипертензии у пациентов с тХПН
    • Избыток в организме натрия и жидкости
    • Избыток сосудосуживающих факторов
    • Недостаток вазодилатирующих факторов
  • 14. Лечение артериальной гипертензии
    • Подбор «сухого веса»
    • Ограничение в рационе жидкости и отказ от поваренной соли
    • Контроль натрия в диализате
    • Медикаментозная коррекция
  • 15. Вторичный гиперпаратиреоз- многофакторное прогрессирующее заболевание Кальциноз Вторичный Гиперпаратиреоз Заболевание костей Отклонения лабораторных показателей
  • 16. Целевые показатели фосфорно-кальциевого обмена у пациентов на гемодиализе
    • Р 1,1-1,78 ммоль/л
    • Са 2,1-2,37 ммоль/л
    • ПТГ 150-300 пг/мл (16,5-33 пмоль/л)
  • 17. Нормальный обмен минеральных веществ Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) ПТГ , паратиреоидный гормон паратиреоидный гормон Паращитовидные железы
  • 18. Нормальный обмен минеральных веществ PTH Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) ПТГ , паратиреоидный гормон паратиреоидный гормон Ca 2+ Паращитовидные железы
  • 19. Нормальный обмен минеральных веществ Нормальный Ca 2+ Ca 2+ PO 4 3– Высвобождение Кость Почки Ca 2+ реабсорбция PO 4 3– экскреция PTH Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) ПТГ , паратиреоидный гормон паратиреоидный гормон Ca 2+ Паращитовидные железы
  • 20. Нормальный обмен минеральных веществ Нормальный Ca 2+ Ca 2+ PO 4 3– Высвобождение Кость Почки Ca 2+ реабсорбция PO 4 3– экскреция PTH Brown EM. In: The Parathyroids – Basic and Clinical Concepts 2 nd ed. 2001. Bilezikian JP et al. (eds) ПТГ , паратиреоидный гормон паратиреоидный гормон Ca 2+ Паращитовидные железы Кальцитриол
  • 21. Причины ВГПТ: гипокальциемия стимулирует синтез ПТГ Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93 Ca 2+
  • 22. Причины ВГПТ: гипокальциемия стимулирует синтез ПТГ Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93 Кальцитриол Фосфор Ca 2+ Ca 2+ Ca 2+
  • 23. Причины ВГПТ: гипокальциемия стимулирует синтез ПТГ Rodriguez M et al . Kidney Int 1991;40:1055–62 Tallon S et al. Kidney Int 1996;49:1441–6 Naveh-Many T et al. J Clin Invest 1995;96:1786 – 93 VDR Секреция ПТГ С интез ПТГ Пролиферация клеток Кальцитриол Фосфор Ca 2+ ПТГ
  • 24. Причины ВГПТ : гиперфосфатемия стимулирует синтез ПТГ Almaden Y et al . J Am Soc Nephrol 1998;9:1845–52 Naveh-Many T et al. J Clin Invest 1995;96:1786–93 Denda M et al . Am J Kidney Dis 1996;28:596–602 VDR CaR Кальцитриол Фосфор Ca 2+ Секреция ПТГ синтез ПТГ Пролиферация клеток ПТГ Секреция ПТГ С интез ПТГ Пролиферация клеток
  • 25. Причины ВГПТ : дефицит кальцитриола Navey-Many T et al . J Clin Invest 1990;86:1968–75 Parfitt AM. Kidney Int 1997;52:3 – 9 Almaden Y et al. Kidney Int 2003;64:2311–7 VDR CaR Кальцитриол Фосфор Ca 2+ Секреция ПТГ синтез ПТГ Пролиферация клеток ПТГ С интез ПТГ Пролиферация клеток
  • 26. Прогрессирование ВГПТ : паратиреоидная гиперплазия Норма Диффузная Начальная стадия узловатости Нодулярная Единичный узел Непрерывная функциональная потребность Объем железы Секреторные клетки Adapted, with permission, from Tominaga Y et al . Curr Opin Nephrol Hypertens 1996;5:336–41 Нормальный Очень высокий ПТГ VDR CaR VDR CaR
  • 27. Резистентный ВГПТ Нодулярная гиперплазия VDR CaR Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 Tominaga Y et al. Semin Surg Oncol 1997;13:78–86
  • 28. Резистентный ВГПТ Нодулярная гиперплазия VDR CaR Ca 2+ Фосфор Гиперкальциемия Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 ПТГ > 800 пг/мл + –
  • 29. Резистентный ВГПТ Нодулярная гиперплазия VDR CaR Ca 2+ Фосфор Гиперкальциемия Rodriguez M et al. Kidney Int Suppl 2002;80:155–60 Tominaga Y et al. Semin Surg Oncol 1997;13:78–86 ПТГ > 800 пг/мл + –
  • 30. Проявления ВГПТ
    • Боль в костях
    • Нарушения ремоделирования костей , минерализации , массы линейного роста или прочности кости
    • Переломы
    • Кардиотоксический эффект
    • Артериальная гипертензия
    • Кальциноз сосудов и мягких тканей
    • Анемия
    • Нейропатия
  • 31. Кальциноз сосудов и мягких тканей
  • 32. Кальциноз сосудов и мягких тканей