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This 39-year-old male had malignant hypertension with malignant nephrosclerosis, progressing to chronic renal failure. He underwent a bilateral nephrectomy for control of his hypertension and received a cadaveric renal transplant. He did well, although he developed diabetes mellitus and had persistent, but less severe controllable hypertension. Two years following transplantation he was admitted to the hospital for control of his hypertension and evaluation of his chronic rejection. Initial blood bllod pressure while in the hospital was in the range of 160/110 to 160/100 mm Hg. He was placed on a more intensive hypertension regimen, elevated and he gradually became normotensive. He received one hemodialysis treatment prior to discharge. At the time of discharge, his blood pressure was 100 to 110 over 60 to 70 and he was doing well on dialysis. His BUN was 113 mg/dL and creatinine 5were gradually rising despite aggressive treatment.2 mg/dL, and he had a hematocrit (PCV) of 27%. The patient was again admitted one month later for evaluation of azotemia and for control of his hypertension. It was felt that his chronic rejection was end-stage and that he would have to be dialyzed periodically. He was put on a renal failure diet, and over the period of his hospitalization, his BUN and creatinine finally stabilized at high levels. He tolerated dialysis well, and a A transplant nephrectomy was done at 2 1/2 performed 4 years post after his transplant. At the time of discharge, the patient's BUN was 78 mg/dL, creatinine 3.6 mg/dL, WBC 5000 cells/cmm, and the PCV was 26%he resumed hemodialysis.

== Autopsy Findings ==The kidney weighed 215 125 grams and was covered by a thick capsule, which was partially adherent to the cortex, but could be stripped from the kidney with slight difficulty. The cortex was thinned but calyces and pelvis of the kidney appeared normal. The vessels were not prominent. The renal arteries and vein appeared normal.

File:IPLab6ChronicRejection1IPLab6ChronicRejection1b.jpg|This is a low-power photomicrograph of the kidney from this case of chronic transplant rejection. Note the focal areas of hemorrhage and inflammatory cell infiltrate in this section. File:IPLab6ChronicRejection2.jpg|This is a higher-power photomicrograph of kidney containing a section of blood vessel that demonstrates a marked neointimal proliferative response (1). In this case the lumen of the artery is obliterated. Also note the cellular infiltrate in the interstitium of the kidney (2) and the paucity of tubules. File:IPLab6ChronicRejection3IPLab6ChronicRejection2b.jpg|This is a photomicrograph of kidney with a focal area of hemorrhage around a small blood vessel (left) congestion and congestion sclerosis of the glomeruli. Note that there is a marked loss of renal tubules throughout this section with replacement by fibrous connective tissue. Also note the cellularity of the glomeruli. File:IPLab6ChronicRejection4IPLab6ChronicRejection3b.jpg|This is another area of renal cortex similar to the previous image. Note the fibrosis (1) and loss of renal tubules throughout this section. Also note the focus of inflammatory cells (2) indicating that despite the chromic nature of this lesion, there is still ongoing active rejection and renal damage. File:IPLab6ChronicRejection5IPLab6ChronicRejection4b.jpg|This high-power photomicrograph of glomeruli from this kidney demonstrates congestion (1), demonstrating increased cellularity of glomeruli with mesangial expansion, (arrows). There is generalized loss of tubules and a glomerulus that is almost completely obliterated or sclerosed replacement by fibrosis in this section (21). File:IPLab6ChronicRejection6IPLab6ChronicRejection5b.jpg|This is a photomicrograph of rejected kidney with a focus of cellular infiltrate (left) infiltrates and a small artery with neointimal proliferation and stenosis (arrow).

File:IPLab6ChronicRejection9IPLab6ChronicRejection9b.jpg|This is a high-power photomicrograph demonstrates the characteristic manifestations of a damaged chronic antibody-mediated rejection. The glomerulus. Note shows inflammatory cells within the loss of normal capillary structureloops (glomeruliitis), the accumulation of mesangial expansion matrix, and duplication (or multilamination) of the infiltration of large mononuclear cellscapillary basement membrane (arrow).