IPLab:Lab 6:Glomerulonephritis

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Clinical Summary

This 27-year-old male had end-stage renal disease requiring hemodialysis for 10 years. For the previous four years he had hypertension which slowly increased to about 180/120 mm Hg. Laboratory findings included a markedly elevated BUN and creatinine. He underwent bilateral nephrectomy and was placed on the transplant list.

On examination the kidneys were similar in appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.

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Virtual Microscopy

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Study Questions

  • <spoiler text="What is the usual clinical course of poststreptococcal glomerulonephritis?">One to two weeks after infection (usually sore throat or skin infection) by certain types of group A beta-hemolytic streptococci, patients develop malaise, fever, nausea, oliguria, and hematuria. Most patients recover with conservative treatment aimed at maintaining sodium and water balance. The renal injury usually resolves with no loss of function.</spoiler>
  • <spoiler text="What is the pathogenetic mechanism of poststreptococcal glomerulonephritis?">Patients have elevated antibody titers to streptococcal antigens, decreased complement levels, and accumulations of immune complexes and complement in the glomeruli suggesting immune complex mediated glomerular injury. Some streptococcal antigens (endostreptosin and several cationic antigens) have been demonstrated on the glomerular basement membrane. Thus, it is not known for sure if the glomerular damage is caused by circulating antigen antibody complexes, antibodies attacking streptococcal antigens that are attached to the basement membrane, or a combination of both processes. In any event, antibodies bind to antigens, activate complement, and cause damage to the glomeruli.

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Additional Resources

Reference

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