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  • Image not available. Chronic kidney disease (CKD) is classified based on the cause of kidney disease, assessment of glomerular filtration rate, and extent of proteinuria.
  • Image not available. Frequent complications of advanced CKD include altered sodium and water balance, hyperkalemia, metabolic acidosis, anemia, CKD-related mineral and bone disorder (CKD-MBD), and cardiovascular disease.
  • Image not available. Reduction of kidney mass, development of glomerular hypertension, and intratubular proteinuria are key mechanisms responsible for the progression of CKD.
  • Image not available. Anemia of CKD is primarily caused by a deficiency in the production of endogenous erythropoietin by the kidney with iron deficiency as a contributing factor.
  • Image not available. CKD-MBD includes abnormalities in parathyroid hormone (PTH), calcium, phosphorus, the calcium–phosphorus product, vitamin D, bone turnover, and soft-tissue calcifications and contributes to extravascular calcifications.
  • Image not available. Guidelines by the National Kidney Foundation Kidney Disease/Dialysis Outcomes Quality Initiative (NKF-KDOQI) and Kidney Disease: Improving Global Outcomes (KDIGO) provide information to assist healthcare providers in clinical decisions and the design of appropriate therapy to manage CKD progression and the associated complications.
  • Image not available. Patient education plays a critical role in the appropriate management of patients with CKD and related complications. A multidisciplinary team structure is a rational approach to provide this education and effectively design and implement the extensive nonpharmacologic and pharmacologic interventions required.
  • Image not available. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are key pharmacologic treatments of CKD because of their effects on renal hemodynamics and reduction of blood pressure, which help to limit kidney disease progression.
  • Image not available. Management of anemia includes administration of erythropoietic-stimulating agents (ESAs) (epoetin alfa, darbepoetin alfa) and regular iron supplementation (oral or IV administration) to maintain hemoglobin and prevent the need for blood transfusions. There is evidence indicating a higher risk of cardiovascular events when hemoglobin is targeted to greater than 11 g/dL (110 g/L; 6.83 mmol/L).
  • Image not available. Management of CKD-MBD includes dietary phosphorus restriction, phosphate-binding agents, vitamin D supplementation, and calcimimetic therapy.

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On completion of the chapter, the reader will be able to:

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  1. Identify the most common causes of chronic kidney disease (CKD) in the United States.

  2. Discuss the current screening recommendations for diabetic kidney disease.

  3. Describe the typical clinical presentation of a patient with advanced CKD including subjective and objective findings.

  4. Apply nonpharmacologic and pharmacologic treatments to address risk factors for progression of CKD.

  5. Describe the association between decreased kidney function (decreased glomerular filtration rate) and development of secondary complications.

  6. Select appropriate therapy for CKD progression and secondary complications that is individualized for the patient based on patient-specific data and factors that affect response to pharmacologic therapy.

  7. Recommend an appropriate regimen for management of anemia of CKD incorporating iron supplementation and the available erythropoietic-stimulating agents (ESAs) in individuals with CKD.

  8. Explain the pathophysiology of CKD-related mineral and bone disorder (CKD-MBD), and design an appropriate treatment regimen including phosphate-binding agents, vitamin D supplementation, and cinacalcet as appropriate based on the stage of CKD and goals of therapy.

  9. Describe the risks of cardiovascular events and mortality associated with ESA therapy in the CKD population.

  10. Discuss the importance of regular patient education to ...

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