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New NKF-K/DOQI guidelines

New NKF-K/DOQI guidelines. Shahrzad Ossareh-M.D. Kidney Disease Outcome Quality Initiative. Definition of Chronic Kidney Disease Criteria. Kidney damage ≥ 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by either:

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New NKF-K/DOQI guidelines

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  1. New NKF-K/DOQI guidelines Shahrzad Ossareh-M.D. Kidney Disease Outcome Quality Initiative

  2. Definition of Chronic Kidney DiseaseCriteria • Kidney damage ≥ 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by either: • Pathologic abnormalities; or • Markers of damage including abnormalities in blood or urine tests or imaging studies. • GFR< 60 ml/min/1.73 m2 for ≥ 3 months, with or without kidney damage

  3. Estimated GFR (mL/min/1.73 m2) • Cockraft-Gault Formula • MDRD study formula: 186 x [SCr(-1.154)] x [Age(-0.203)] x (0.742 if female) x (1.21 if African American)

  4. Stages of Chronic Kidney Disease

  5. Guidelines for Bone Metabolism in Chronic Kidney Disease

  6. GUIDELINE 1. Evaluation of Ca and P metabolism

  7. 1.1- Serum levels of calcium, phosphorus, and intact PTH should be measured in all patients with CKD and GFR <60 ml/min/1.73 m2. (EVIDENCE)

  8. Frequency of measurement of PTH and Ca/P by stage of CKD *More frequently in patients receiving therapy for the abnormalities in Ca, P or PTH and in transplant recipients.

  9. Target Range of plasma iPTH by CKD stage

  10. Relationship between serum I-PTH levels and CCR based on data extracted from Martinez et al (1997). Values on the y-axis are serum I-PTH levels (pg/ml). Values on the x-axis are CCR in ml/min. The lines fitted to the data set are based on 4 different mathematical functions (power, linear, exponential, and logarithmic), rather than on any assumptions about an underlying physiological mechanism. The horizontal line represents the upper limit of the normal range of serum I-PTH levels.

  11. Newer assays specific for 1-84 PTH. • The normal range for the new assay for 1-84 PTH is 7 to 36 pg/ml compared to 16 to 65 pg/ml for iPTH. • Thus the relationship between the 2 assays is about 1:2 (1-84 PTH to intact PTH). • The differences in the levels between the 2 types of assays are a reflection of the levels of circulating PTH fragments that are detected by the intact PTH assay but not by the new 1-84 PTH assay.

  12. GUIDELINE 2. ASSESSMENT OF BONE DISEASE ASSOCIATED WITH CKD

  13. 2.1- The most accurate diagnostic test for determining the type of bone disease in CKD is iliac crest bone biopsy with double tetracycline labeling and bone histomorphometric analysis. (EVIDENCE)

  14. 2.2- It is not necessary to perform bone biopsy for most situations in clinical practice. It should be considered in patients with kidney failure (Stage 5) who have:

  15. 2.2- It is not necessary to perform bone biopsy for most situations in clinical practice. It should be considered in patients with kidney failure (Stage 5) who have: 2.2a-Fractures with minimal or no trauma (pathological fractures); (OPINION)

  16. 2.2- It is not necessary to perform bone biopsy for most situations in clinical practice. It should be considered in patients with kidney failure (Stage 5) who have: 2.2a- Fractures with minimal or no trauma (pathological fractures); (OPINION) 2.2b-Intact PTH levels between 100 and 500 pg/ml (in CKD Stage 5) with coexisting conditions such as unexplained hypercalcemia, severe bone pain, or unexplained increases in bone alkaline phosphatase activity;(OPINION)

  17. 2.2- It is not necessary to perform bone biopsy for most situations in clinical practice. It should be considered in patients with kidney failure (Stage 5) who have: 2.2a- Fractures with minimal or no trauma (pathological fractures); (OPINION) 2.2b- Intact PTH levels between 100 and 500 pg/ml (in CKD Stage 5) with coexisting conditions such as unexplained hypercalcemia, severe bone pain, or unexplained increases in bone alkaline phosphatase activity;(OPINION) 2.2c- Suspected aluminum bone disease, based upon clinical symptoms or history of aluminum exposure (OPINION)

  18. 2.3-Bone radiographs are not indicated for the assessment of bone disease of CKD, (EVIDENCE) but they are useful in detecting severe peripheral vascular calcification (OPINION) and bone disease due to ß2-microglobulin amyloidosis. (EVIDENCE) 2.4- Bone mineral density (BMD) should be measured by dual energy X-ray absorptiometry (DEXA) in patients with fractures and in those with known risk factors for osteoporosis. (OPINION)

  19. 2.3- Bone radiographs are not indicated for the assessment of bone disease of CKD, (EVIDENCE) but they are useful in detecting severe peripheral vascular calcification (OPINION) and bone disease due to ß2-microglobulin amyloidosis. (EVIDENCE) 2.4- Bone mineral density (BMD) should be measured by dual energy X-ray absorptiometry (DEXA) in patients with fractures and in those with known risk factors for osteoporosis. (OPINION)

  20. Beginning at Stage 3, patients with CKD almost always have secondary hyperparathyroidism and elevated PTH. • In these patients, the classical lesion seen in bone biopsy is osteitis fibrosa cystica althoug increasing prevalence of other bone lesions such as low-turnover bone disease has recently been shown.

  21. Factors Prevalent in CKD patients Which May Influence the Type of Osteodystrophy Lesion • Prolonged Al exposure • G.C. therapy in patients with parenchymatous kidney disease & renal Tx recipients • Previous PTX • Vitamin D Rx • Diabetes Mellitus* • 2 microglobulin amyloidosis • Hypophosphatemia secondary to aggressive dietary phosphate restriction or excessive use of P binders *Responsible for 30-40% of ESRD cases

  22. GUIDELINE 3. EVALUATION OF SERUM P

  23. 3.1- In CKD patients (Stages 3 and 4), the serum P should be maintained between 2.7 mg/dl (EVIDENCE) and 4.6 mg/dl. (OPINION) • 3.2- In CKD patients with kidney failure (Stage 5) and those treated with HD or PD, the serum P should be maintained between 3.5 and 5.5 mg/dl. (EVIDENCE)

  24. Prolonged hyperphosphatemia causes soft-tissue and vascular calcification due at least in part to an increase in Ca-P product and is associated with increased morbidity and mortality.

  25. Prolonged hyperphosphatemia causes soft-tissue and vascular calcification due at least in part to an increase in Ca-P product and is associated with increased morbidity and mortality. • Hyperphosphatemia exerts a direct calcifying effect on vascular smooth muscle cells.

  26. Prolonged hyperphosphatemia causes soft-tissue and vascular calcification due at least in part to an increase in Ca-P product and is associated with increased morbidity and mortality. • Hyperphosphatemia exerts a direct calcifying effect on vascular smooth muscle cells. • Calcification of coronary arteries, cardiac valves, and pulmonary tissues produces cardiac disease, the leading cause of death in patients with CKD.

  27. Prolonged hyperphosphatemia causes soft-tissue and vascular calcification due at least in part to an increase in Ca-P product and is associated with increased morbidity and mortality. • Hyperphosphatemia exerts a direct calcifying effect on vascular smooth muscle cells. • Calcification of coronary arteries, cardiac valves, and pulmonary tissues produces cardiac disease, the leading cause of death in patients with CKD. • It is therefore imperative to prevent hyperphosphatemia and maintain serum P levels within the normal range.

  28. Most data indicate that < 30% of dialysis patients are able to maintain P in the suggested target range. • The goal should be to increase the percentage of patients in this target range. • This needs: • An increased dietitian-to-patient ratio, • Educational tools to increase patient compliance, • Studies for dialytic techniques that are better able to control serum P (such as nocturnal or daily HD), • The widespread availability and affordability of different phosphate binders, regardless of patient insurance.

  29. GUIDELINE 4. RESTRICTION OF DIETARY PHOSPHORUS IN PATIENTS WITH CKD

  30. 4.1- Dietary phosphorus should be restricted to 800 to 1,000mg/day (adjusted for dietary protein needs): • When the serum P>4.6 mg/dl at Stages 3 and 4 of CKD, (OPINION) and >5.5 mg/dl at stage 5 kidney failure (EVIDENCE). • When the plasma iPTH are elevated. (EVIDENCE) • The serum P should be monitored every month following the initiation of dietary phosphorus restriction. (OPINION)

  31. GUIDELINE 5. USE OF PHOSPHATE BINDERS

  32. 5.1- If P or intact PTH levels cannot be controlled despite dietary P restriction, phosphate binders should be prescribed. (OPINION) • Either calcium-based phosphate binders and other noncalcium-, nonaluminum-, nonmagnesium- phosphate binders (such as sevelamer HCl) may be used as the primary therapy.

  33. 5.4- In dialysis patients who remain hyperphosphatemic (P>5.5 mg/dl)despite the use of either of phosphate binders, a combination of both should be used. (OPINION)

  34. 5.5- The total dose of elemental calcium provided by the calcium-based phosphate binders should not exceed 1,500 mg/day (OPINION), and the total intake of elemental calcium (including dietary calcium) should not exceed2,000 mg/day. (OPINION)

  35. 5.5- The total dose of elemental calcium provided by the calcium-based phosphate binders should not exceed 1,500 mg/day (OPINION), and the total intake of elemental calcium (including dietary calcium) should not exceed2,000mg/day. (OPINION) • 5.6- Calcium-based phosphate binders should not be used in dialysis patients who are hypercalcemic (corrected serum Ca >10.2 mg/dl, or have plasma PTH <150 pg/ml on 2 consecutive measurements. (EVIDENCE)

  36. 5.7-Noncalcium-containing phosphate binders are preferred in dialysis patients with severe vascular and/or other soft tissue calcifications. (OPINION)

  37. 5.7- Noncalcium-containing phosphate binders are preferred in dialysis patients with severe vascular and/or other soft tissue calcifications. (OPINION) • 5.8-In patients with serum P>7.0 mg/dl, aluminum-based phosphate binders may be used as a short-term therapy (4 weeks), and for one course only, to be replaced thereafter by other phosphate binders. (OPINION) In such patients, more frequent dialysis should also be considered. (EVIDENCE)

  38. GUIDELINE 6. SERUM Ca & Ca-P PRODUCT

  39. In CKD Patients (Stages 3 and 4): 6.1- The serum levels of corrected total calcium should be maintained within the "normal" range for the laboratory used. (EVIDENCE) • In CKD Patients With Kidney Failure (Stage 5): 6.2- Serum levels of corrected total calcium should be maintained within the normal range for the laboratory used, preferably toward the lower end (8.4 to 9.5 mg/dl). (OPINION)

  40. 6.3- In the event corrected total serum Ca >10.2 mg/dl, therapies that cause serum Ca to rise should be adjusted as follows:

  41. 6.3- In the event corrected total serum Ca >10.2 mg/dl, therapies that cause serum Ca to rise should be adjusted as follows: 6.3a- In patients taking calcium-based phosphate binders, the dose should be reduced or therapy switched to a noncalcium-, nonaluminum-, nonmagnesium-containing phosphate binder. (OPINION)

  42. 6.3b- In patients taking active vitamin D sterols, the dose should be reduced or therapy discontinued until the serum levels of corrected total calcium return to the target range (8.4 to 9.5 mg/d). (OPINION)

  43. 6.3b- In patients taking active vitamin D sterols, the dose should be reduced or therapy discontinued until the serum levels of corrected total calcium return to the target range (8.4 to 9.5 mg/d). (OPINION) 6.3c- If hypercalcemia persists despite modification of therapy, dialysis using low dialysate calcium (1.5 to 2.0 mEq/L) may be used for 3 to 4 weeks. (OPINION)

  44. In CKD Patients (Stages 3 to 5): 6.4-Total elemental calcium intake (dietary calcium+ calcium-based phosphate binders) should not exceed 2,000 mg/day. (OPINION) 6.5-The serum Ca-P product should be maintained at <55 mg2/dl2. (EVIDENCE) This is best achieved by controlling serum levels of P within the target range. (OPINION)

  45. 6.6- Patients whose serum Ca level are below the lower limit (<8.4 mg/dl) should receive therapy to increase serum Ca if:

  46. 6.6- Patients whose serum Ca level are below the lower limit (<8.4 mg/dl) should receive therapy to increase serum Ca if: 6.6a-There are clinical symptoms of hypocalcemia such as paresthesia, Chvostek’s and Trousseau’s signs, bronchospasm, laryngospasm, tetany, and/or seizures (OPINION); or

  47. 6.6- Patients whose serum Ca level are below the lower limit (<8.4 mg/dl) should receive therapy to increase serum Ca if: 6.6a-There are clinical symptoms of hypocalcemia such as paresthesia, Chvostek’s and Trousseau’s signs, bronchospasm, laryngospasm, tetany, and/or seizures (OPINION); or 6.6b-The plasma iPTH level is above the target. (OPINION)

  48. 6.7-Therapy for hypocalcemia should include calcium salts such as calcium carbonate (EVIDENCE) and/or oral vitamin D sterols. (EVIDENCE)

  49. GUIDELINE 7. PREVENTION AND TREATMENT OF VITAMIN D INSUFFICIENCY AND DEFICIENCY IN CKD PATIENTS

  50. In CKD Patients (Stages 3 and 4): • 7.1- If plasma intact PTH is above the target range serum 25-(OH)D should be measured at first encounter. If it is normal, repeat annually. (EVIDENCE) • 7.2- If the serum level of 25-(OH)D is <30 ng/ml, supplementation with vitamin D2 should be initiated.(OPINION)

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