Uric Acid Nephropathy/Gout

Uric Acid Nephropathy/Gout

Shane M. Meehan, MBBCh

Gross photograph reveals a brown calculus with a rough surface in the renal pelvis. There is marked calyceal dilation, pyramidal effacement, and parenchymal thinning. (Courtesy V. Nickeleit, MD.)

Gross photograph reveals distinct yellow striae in the medulla image, with congestion at the corticomedullary junction, of a kidney with acute uric acid nephropathy. (Courtesy V. Nickeleit, MD.)



  • Uric acid nephropathy (UAN)


  • Urate nephropathy, gouty nephropathy with tophi, gout nephropathy


  • Intrarenal precipitation of uric acid associated with hyperuricemia or hyperuricosuria


Normal Metabolism

  • Uric acid is final degradation product of purine metabolism

  • Sources are endogenous from adenine or guanine nucleotides or exogenous from diet

  • Uric acid can be generated in all cells but most markedly by hepatocytes

  • Urate is filtered freely, reabsorbed, secreted, and undergoes post-secretory reabsorption, all in proximal tubules

  • 10% of filtered load is excreted in urine


  • Defined as plasma uric acid > 7 mg/dL

    • Due to

      • Decreased excretion (75-90%)

      • Overproduction (10-25%)

  • Decreased tubular secretion/increased reabsorption

    • Idiopathic

    • Drugs: Thiazide diuretics, cyclosporine A, low dose salicylates

    • Chronic heavy metal toxicity: Lead (saturnine gout), beryllium

    • Metabolic: Ketoacidosis, lactic acidosis, dehydration, Bartter syndrome, chronic renal failure

    • Endocrine: Hypothyroidism, hyperparathyroidism

    • Genetic: Familial juvenile hyperuricemic nephropathy (uromodulin storage disease)

    • Miscellaneous: Sickle cell anemia, Down syndrome, sarcoidosis, eclampsia

  • Overproduction/excessive release

    • Idiopathic (60%)

    • Massive tissue destruction

      • Hematologic diseases: Leukemia, lymphoma, myeloma, polycythemia

      • Tumor lysis syndrome: Treatment of leukemia, lymphoma, multiple myeloma, and solid tumors with cytotoxic agents or radiation

      • Crush injury, rhabdomyolysis, seizures (prolonged, severe)

    • Hereditary enzyme deficiencies

      • X-linked: Hypoxanthine guanine phosphoribosyl transferase deficiency; complete (Lesch-Nyhan syndrome) or partial

      • Autosomal recessive: Glucose-6-phosphatase deficiency in glycogen storage disease type 1

Hyperuricemia and Kidney Disease

Jul 7, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Uric Acid Nephropathy/Gout
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