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Complications of chronic kidney disease

Updated on February 7, 2013

Osteomalacia

Severe osteoporosis of the spine

Fracture of the neck of the femur due to osteoporosis

Chronic kidney disease can affect almost all the systems of the body. Therefore it has very high morbidity and mortality if not identified early and treated properly. Chronic kidney disease can cause:

  • Increased incidence of cardiovascular disease
  • Anemia
  • Renal osteodystrophy
  • Endocrine abnormalities
  • Neurological complications
  • Increased rate of infections
  • Dermatological abnormalities
  • Psychological manifestations
  • Malnutrition
  • Metabolic abnormalities
  • Gastrointestinal tract abnormalities


Anemia
Renal anemia, which is normochromic and normocytic, accounts for many of the symptoms that previously were attributed to uremia. These include lethargy, cold intolerance, and loss of stamina.

Factors contributing to renal anemia

  • Relative deficiency of erythropoietin.
  • Reduced RBC survival as a result of hemolysis or hypersplenism.
  • ‘Uremic inhibitors’ of erythropoiesis.
  • Hyperparathyroidism with marrow fibrosis.


Factors contributing to renal anemia

  • Aluminium toxicity.
  • Iron/folate deficiency.
  • Blood loss.
  • Bone marrow toxins.

Renal osteodystrophy
The term 'renal osteodystrophy' embraces the various forms of bone disease that may develop alone or in combination in chronic renal failure. This includes:

  • Hyperparathyroid bone disease
  • Osteomalacia
  • Osteoporosis
  • Osteosclerosis
  • Adynamic bone disease


Problems of renal osteodystrophy can develop early and patients with a glomerular filtration rate (GFR) of 60 ml/minute/1.73m2 or low are at risk and should be evaluated. Renal osteodystrophy manifest as bone pain, deformity, pathological fractures, soft tissue and especially vascular calcification, and proximal myopathy.

Pathogenesis of renal osteodystrophy

  • Reduced activation of vitamin D receptors in the parathyroid glands leads to increased release of parathyroid hormone(PTH).
  • 1, 25-Dihydroxycholecalciferol deficiency also results in gut calcium malabsorption.
  • Phosphate retention owing to reduced excretion by the kidneys, also indirectly by lowering ionized calcium (and probably directly via a putative but unrecognized phosphate receptor), results in an increase in PTH synthesis and release.
  • PTH promotes reabsorption of calcium from bone and increased proximal renal tubular reabsorption of calcium, and this opposes the tendency to develop hypocalcemia induced by 1, 25-(OH)2D3 deficiency and phosphate retention.
  • This 'secondary' hyperparathyroidism leads to increased osteoclastic activity, cyst formation and bone marrow fibrosis (osteitis fibrosa cystica).

Endocrine abnormalities

  • Hyperprolactinemia, which may present with galactorrhoea in men as well as women.
  • Increased luteinizing hormone (LH) levels in both sexes and abnormal pulsatility of LH release.
  • Decreased serum testosterone levels (only seldom below the normal level); sexual dysfunction and decreased spermatogenesis are common.
  • Absence of normal cyclical changes in female sex hormones, resulting in oligomenorrhoea or amenorrhoea.
  • Complex abnormalities of growth hormone secretion and action, resulting in impaired growth in uremic children (pharmacological treatment with recombinant growth hormone and insulin-like growth factor is used).
  • Abnormal thyroid hormone levels, partly because of altered protein binding.

Metabolic abnormalities

  • Urate retention is a common feature of chronic renal failure. This leads to gout.
  • Treatment of clinical gout is complicated by the nephrotoxic potential of NSAIDs.
  • Colchicine is useful in treatment of the acute attack, and allopurinol should be introduced later under colchicine cover to prevent further attacks.
  • The dose of allopurinol should be reduced in renal impairment.
  • Insulin is catabolized by and to some extent excreted via the kidneys.
  • For this reason, insulin requirements in diabetic patients decrease as renal failure progresses.


Lipid abnormalities are common in renal failure

  • Impaired clearance of triglyceride-rich particles.
  • Hypercholesterolemia (particularly in advanced renal failure).

Dermatological abnormalities

  • Retention of nitrogenous waste products.
  • Hypercalcemia .
  • Hyperphosphatemia.
  • Elevated calcium × phosphate product.
  • Hyperparathyroidism (even if calcium and phosphate levels are normal).
  • Iron deficiency.

Gastrointestinal complications

  • Decreased gastric emptying and increased risk of reflux esophagitis.
  • Increased risk of peptic ulceration.
  • Increased risk of acute pancreatitis.
  • Constipation - particularly in patients on continuous ambulatory peritoneal dialysis (CAPD).

Neurological abnormalities

  • Asterixis.
  • Tremor.
  • Myoclonus.
  • Convulsions.
  • Peripheral neuropathy.
  • Carpel tunnel syndrome.
  • Autonomic dysfunction.



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