Error message

Deprecated function: The each() function is deprecated. This message will be suppressed on further calls in book_prev() (line 775 of /home/pathwa23/public_html/modules/book/book.module).

Uremia

Overview
  • Uremia is a syndrome which arises as a direct consequence of complete loss of renal function and is the clinical end-point of progressive acute or chronic renal failure. Renal failure, acute or chronic, occurs due to a decline in Glomerular Filtration Rate (GFR). Uremia arises when GFR is extremely low, resulting in an inability of the kidneys to properly regulate electrolyte and water levels along with an inability to secrete sufficient amounts of metabolic waste products. Additional components of uremia arise because the highly dysfunctional kidneys can no longer secrete sufficient levels of hormones.
Clinical Consequences
  • Azotemia
    • A generic term referring to build up of metabolites such as creatinine and BUN due to reduced GFR.
  • Generalized Edema
    • Recall that ECF volume regulation is performed by the kidney through regulation of sodium excretion. When uremia arises, the rate of sodium excretion declines below that of daily sodium intake, resulting in build up of total body sodium. Maintenance of ECF osmolarity requires dilution of the retained sodium with water, ultimately resulting in expansion of the ECF volume. Over time and when renal dysfunction is extreme this will manifest as generalized edema.
  • Secondary Hypertension
    • Hypertension manifests very early even in chronic renal failure and is present at the clinical endpoint of uremia. Hypertension is a direct result of expanded ECF volume, mediated by the same processes that lead to sodium and water retention described under the "ECF Volume and Arterial Pressure" section under Systemic Arterial Pressure - Long-term Regulation).
  • Hyperkalemia
    • Recall that the kidneys normally secrete large amounts of potassium as part of their role in external potassium balance. As GFR declines, potassium intake rises above the capacity of renal potassium secretion, resulting in hyperkalemia.
  • Metabolic Acidosis
    • Recall from renal acid-base control that the kidneys are responsible for excreting large amounts of acids derived from metabolic processes in the urine. With declining GFR, the kidneys capacity to excrete acids falls below their metabolic production, resulting in metabolic acidosis.
  • Secondary Hyperparathyroidism
    • See the secondary hyperparathyroidism page for pathogenesis and clinical consequences. Briefly, renal failure induces mild hypocalcemia which results increased PTH levels that ultimately cause bone pathology and increased risk of bone fractures.
  • Normocytic Anemia
    • As renal function declines, the kidney's capacity to synthesize erythropoietin does as well. This manifests as a normocytic anemia.
  • Acute Pericarditis