This 17-year-old white male had end-stage renal disease requiring hemodialysis for 10 years. For the previous four years he had hypertension which slowly increased to about 180/120A normal alkaline phosphatase is 39 to 117 U/L. mm Hg. Laboratory findings included a greatly elevated BUN and creatinineThese tests are measures of kidney function. High levels mean low function.. He was admitted for bilateral nephrectomy and discharged in satisfactory condition on the 10th postoperative day. He was to be contacted in the future for transplantation.
The left (97 gramsA normal kidney weighs 157 grams (range: 115 to 220 grams).) and right (88 gramsA normal kidney weighs 157 grams (range: 115 to 220 grams).) kidneys were of similar 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.
This immunofluorescent photomicrograph of a glomerulus from a case of acute poststreptococcal glomerulonephritis shows a granular immunofluorescence pattern consistent with immune complex disease. The primary antibody used for this staining was specific for IgG; however antibodies for complement would show a similar pattern.
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, oliguriaOliguria is the occurrence of decreased urine output., and hematuriaHematuria is the presence of blood in the urine.. Most patients recover with conservative treatment aimed at maintaining sodium and water balance. The renal injury usually resolves with no loss of function.
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.
- eMedicine Medical Library: Assessment and Management of the Renal Transplant Patient
- eMedicine Medical Library: Poststreptococcal Glomerulonephritis
- Merck Manual: Nephritic Syndrome
- Merck Manual: Chronic Kidney Disease
- Merck Manual: Hemodialysis
- Merck Manual: Kidney Transplantation
- Lan HY, Yang N, Nikolic-Paterson DJ, Yu XQ, Mu W, Isbel NM, Metz CN, Bucala R, Atkins RC. Expression of macrophage migration inhibitory factor in human glomerulonephritis. Kidney Int 2000 Feb;57(2):499-509.