Complications

• Pulmonary edema

• Hyperkalemia

• Infection [25]

  • Bacteremia secondary to UTI or pneumonia

  • IV catheter-related infection

  • Hemodialysis catheter-related infection

  • Peritoneal dialysis-associated peritonitis

• Drug toxicity [26]

• Pathophysiology: ↓ synthesis of erythropoietin → ↓ stimulation of RBC production → normocytic, normochromic anemia

• Laboratory findings

  • ↓ Hemoglobin (Hb)

  • MCV is usually normal.

Management

• Manage correctable causes of anemia.

  • Obtain diagnostic studies for iron deficiency.

  • Check for and potentially treat vitamin B12 deficiency and folate deficiency.

• Consider erythropoietin-stimulating agents (ESAs): for patients with Hb < 10.0 g/dL [29]

  • Treatment target: usually Hb concentration between 11 and 12 g/dL

  • Measure TSAT and ferritin at least every 3 months to determine if adjunctive iron replacement therapy is needed.

  • Adverse effects include increased risk of thrombosis, an increase in blood pressure, and headache.

• Avoid blood transfusions: particularly in patients eligible for renal transplantation (risk of alloimmunization)

• Definitions:

  • CKD-MBD refers to abnormalities in mineral and/or bone metabolism in CKD.

  • Renal osteodystrophy refers specifically to issues with bone metabolism due to CKD.

• Pathophysiology

  • CKD results in hypocalcemia via different mechanisms.

    • ↓ Renal excretion of phosphate → hyperphosphatemia → calcium phosphate precipitation in tissues → ↓ Ca2+

    • ↓ Renal hydroxylation of vitamin D → ↓ 1,25-dihydroxyvitamin D → ↓ intestinal Ca2+ absorption → ↓ Ca2+

  • Chronically decreased calcium levels can cause secondary hyperparathyroidism, which can progress to tertiary hyperparathyroidism.

• Histological classification

  • Secondary hyperparathyroidism: high turnover bone disease or osteitis fibrosa cystica (metabolic bone disease)

  • Osteomalacia: defective bone mineralization

  • Mixed uremic bone disease: secondary hyperparathyroidism with osteomalacia

  • Adynamic bone disease: decreased bone formation without osteomalacia

• Clinical features (may be asymptomatic initially)

  • Musculoskeletal

    • Fractures

    • Bone and periarticular pain

    • Muscular weakness and pain

  • Extraskeletal

    • Focal vascular calcification (atherosclerotic plaques)

    • Diffuse vascular calcification (medial calcific sclerosis and calcific uremic arteriolopathy)

• Diagnostics [31]

  • Laboratory studies: frequent monitoring with a mineral and bone disorder panel

  • Imaging (not routinely indicated)

    • X-ray may show sclerotic changes (rugger jersey spine), brown tumors, and/or subperiosteal bone thinning.

    • Consider bone mineral density testing for patients with CKD category G3–G5.

• Treatment (under specialist guidance): The goal is to normalize phosphate, calcium, and PTH levels. [30][31]

  • Treatment of hyperphosphatemia, e.g.:

    • Dietary phosphate restriction

    • Phosphate binders (e.g., sevelamer)

  • Treatment of hyperparathyroidism, e.g.:

    • Cholecalciferol or ergocalciferol supplementation for vitamin D deficiency or insufficiency

    • Calcitriol (not routinely recommended)

    • Calcimimetics (e.g., cinacalcet)

    • Parathyroidectomy (last-line therapy)