BACKGROUND: Anti-angiotensin II type 1 receptor antibodies (AT1R-Abs) have been demonstrated to increase the risk of antibody-mediated rejection. We report a case of AT1R-Ab mediated rejection which caused early critical cortical infarction.
METHODS: A 52-year-old man with end-stage kidney disease underwent preemptive kidney transplantation (KT) from his wife. He had no immunologic risk except ABO incompatibility. Proper desensitization treatment were applied prior to KT. On postoperative day 1, he showed stable clinical course with adequate urine output, but there was no decrease in serum creatinine level and imaging studies showed hypoperfusion in the transplanted kidney.
METHODS: Allograft biopsy revealed total cortical infarction with severe necrotizing vasculitis, but the medullary area was preserved. Serum AT1R-Ab concentration was elevated from 10.9 U/mL before KT to 19.1 U/mL on 7 days after KT.
METHODS: He was treated with plasmapheresis, intravenous immunoglobulin, rituximab, high-dose methylprednisolone, and bortezomib.
RESULTS: The treatment showed a partial response, and he was discharged with 7.3 mg/dL creatinine level. At 4 months, his creatinine plateaued at 5.5 mg/dL and AT1R-Ab decreased to 3.6 U/mL.
CONCLUSIONS: This case highlights the risk of early active antibody-mediated rejection by preformed AT1R-Ab, suggesting its ability to exhibit atypical histopathologic findings, such as total cortical infarction.

BACKGROUND: Sickle cell disease (SCD) is a well-known multisystem illness characterized by vascular injury due to vasoocclusion and hemolysis, as well as infectious complications and iron overload, all of which contribute to high morbidity and mortality rates among children. In these patients, some authors have previously described iron cortical deposition in the kidney. We here report the first case in the literature of a girl affected by SCD showing an anomalous metal and rare element retention in the renal cortex.
METHODS: A 10-year-old white girl affected by SCD underwent a routine magnetic resonance imaging investigation that evidenced a reduced signal intensity in the renal cortex, compatible with hemosiderin precipitation. Histologic and elemental analyses of the hepatic and the renal biotic samples, performed with inductively coupled plasma mass spectrometry, revealed that concomitant with the high iron deposition, toxic and potentially carcinogenic elements such as nickel, magnesium, rubidium, and gadolinuim were anomalously retained particularly in the kidney.
CONCLUSIONS: The finding of rare and toxic elements in the kidney of SCD patients might be linked to the development of specific neoplastic transformations already described in this patient cohort. To be confirmed, our speculations need to be demonstrated in large sampling of patients.

A 32-year-old patient sustained a penetrating injury to the left flank and kidney after a fall backward onto a glass table. On computed tomography imaging, a 12×10×4 cm glass shard was identified penetrating the renal cortex. The patient was taken to the operating room to remove the foreign object. A rubber-shodded clamp was used to successfully remove the glass shard without complication. Although we commonly encounter stab wounds at our trauma center, the penetrating object is rarely present. The presence of the glass object resulted in a technically challenging and rare case.

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease characterized by fever, hemorrhage, and renal failure. Among the various hemorrhagic complications of HFRS, the spontaneous rupture of an arteriovenous malformation of the testicular vessels with a retroperitoneal hematoma is a rare finding. Here, we report a case of HFRS complicated by a massive retroperitoneal hematoma that was treated with transcatheter arterial embolization.

Primary Sjögren\'s syndrome (SS) is a rare autoimmune disease, especially in children. Juvenile primary SS with interstitial nephritis is rare in Japan. We report on a 12-year-old girl in whom salivary gland swelling had recurred from the age of 5 years, SS was diagnosed at the age of 10 years, and interstitial nephritis developed at the age of 12 years. The patient presented with a chief complaint of swelling of both parotid glands. The patient had a history of recurrent parotitis from 5 years of age, with episodes recurring 5 to 6 times a year and resolving within 3 days each time. However, at the age of 11 years, the patient had continuous mild swelling of the parotid glands. Examination on admission showed bilateral nontender parotid gland swelling; mild swelling of the lower extremities, xerostomia, and xerophthalmia but no exanthem. Laboratory findings were as follows: serum protein, 10.1 g/dL; immunoglobulin (Ig) G, 3,828 mg/dL; antinuclear antibodies, 1,280-fold; anti-Ro/SS-A antibody, 512-fold; anti-Ro/SS-B antibody, 4-fold; creatinine, 0.45 mg/dL; blood β2-microglobulin, 2.2 mg/L (slightly elevated); and cystatin C, 0.86 mg/L. Urinalysis showed proteinuria and a β2-microglobulin concentration of 11,265 mg/L. Thus, this patient had low molecular weight proteinuria. Schirmer\'s test showed decreased tear secretion (5 mm), and fluorescein staining showed marked bilateral superficial punctate keratitis. A lip biopsy showed infiltration by small round cells (mild to moderate), interstitial fibrosis, loss of salivary gland parenchyma, and atrophy, with no obvious epimyoepithelial islands, leading to a diagnosis of SS. Light microscopic examination of the renal biopsy specimens showed expansion of mononuclear cell infiltration in the renal interstitium, inflammatory cell infiltration of interstitial areas with edema and mild fibrosis, and tubulitis and mononuclear cell infiltration that included many lymphocytes and plasma cells. There were no pathological findings of glomerulonephritis. Small arteries showed no obvious abnormalities. Immunofluorescent staining showed slight, nonspecific deposition of IgM, but no deposition of IgG, complement 1q, 3, or 4. On the basis of the renal biopsy showing nonspecific chronic interstitial nephritis, renal tubular atrophy, and interstitial enlargement, tubulointerstitial nephritis associated with SS was diagnosed.

BACKGROUND: Adrenal oncocytoma is a very rare lesion, non functioning and benignin most cases. Only 46 cases have been reported in the medical literature.
OBJECTIVE: This study aimed to report a new case of adrenal oncocytic tumor with uncertain malignant potential.
METHODS: A 72 year-old- man, consulted for renal fossa pain. Ultrasonography and omputed tomography scan revealed a large mass in the right adrenal gland with extension to the right kidney. A right adrenalectomy and nephrectomy was performed. The diagnosis of adrenal oncocytoma with malignant potential was confirmed by pathology. Patient had a well recovery and left hospital on the fifth day post operatively. He was followed up for 8 months, no tumor recurrence detected.
CONCLUSIONS: Adreno cortical oncocytoma is a rare tumor. The majority of reported cases had good prognosis.

We report a case of 58-year-old woman referred to our service for an (18)FFDG PET/CT study of initial staging after being diagnosed of a pelvic kidney mass consistent with malignancy. The FDG-PET showed an abnormal mass in the right kidney, a suspicious metastasis versus a second primary tumor in the cortex of the kidney and lymph node infiltration in the paracaval nodes. The histological analysis verification after exeresis of the lesions confirmed the diagnosis of renal metastases. In this article, we present a brief review of the literature published on the role of PET in the characterization and initial staging of kidney and urinary tract tumors. We also stress the clinical importance of carefully evaluating any low attenuation lesion or focal glucose uptake detected in these structures in a PET/CT study with (18)FFDG.

Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O(2) delivery, and O(2) consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O(2) delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O(2). Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen (P(t(O(2)))) of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O(2) consumption decreased proportionally to O(2) delivery during the graded stenosis (19 +/- 10.8, 48.2 +/- 9.1, 58.9 +/- 4.7 vs. 15.1 +/- 5, 35.4 +/- 3.5, 57 +/- 2.3%, respectively) while arterial venous O(2) differences were unchanged. Acute RAS produced a sharp reduction in O(2) efficiency for sodium reabsorption (P < 0.01). Cortical (P(t(O(2)))) decreases are exceeded by medullary decreases during stenosis (34.8 +/- 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O(2) delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.

Angiography depicted the arteriovenous fistula at the peripheral cortex of the kidney, which was treated superselective transcatheter arterial embolization (TAE). Bleeding was controlled and did not recur. The contrast-enhanced computed tomographic (CT) scan performed on the 27th day after the procedure revealed a parenchymal perfusion deficit of 3% and the return of serum creatinine concentration to pre-injury levels. We considered the selective coil embolization as the best treatment for the aneurysmal arteriovenous fistula located in the renal cortex to keep ischemic damage at a minimum and preserve renal function. To our knowledge, this is the 4th report of a spontaneous rupture in the retroperitoneum of an aneurysmal arteriovenous fistula.

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