Renal artery stenosis presenting with nephrotic-range proteinuria: a case report.

Renal artery stenosis (RAS) is commonly presented with hypertension and chronic kidney disease. We report a rare case of RAS occurring in a 78-year-old man who presented with nephrotic-range proteinuria. Renal biopsy on the left side was performed, and results showed mesangiopathic glomerulonephritis, which was not compatible with the cause of nephrotic-range proteinuria. Proteinuria was decreased by angiotensin receptor blocker, but azotemia was aggravated. Therefore, angiotensin receptor blocker was discontinued inevitably and thorough evaluation for the possibility of RAS was performed. Computed tomography angiography revealed significant RAS on the left side and a renal artery stent was inserted. After stenting, aortic dissection developed and progressed despite tight control of blood pressure. After inserting another stent graft through the true lumen of the left renal artery, the patient's renal function and proteinuria improved markedly.

The impact of slow graft function on graft outcome is comparable to delayed graft function in deceased donor kidney transplantation.

PURPOSE: Slow graft function (SGF) can influence overall prognosis in patients receiving deceased donor kidney transplantation (DKT). However, the impact of SGF on renal function remains uncertain. We investigated retrospectively renal function in cases with SGF compared with early graft function (EGF) and delayed graft function (DGF). METHODS: Renal function after transplantation was analyzed in 199 patients who underwent DKT. Patients were classified into 130 (65.3 %) cases with EGF, 27 (13.6 %) cases with SGF, 6 (3.0 %) cases with DGF and one dialysis (DGF1), and 36 (18.1 %) cases with DGF and two or more dialyses (DGF2). RESULTS: The 1-year estimated glomerular filtration rate (eGFR) in the SGF group was lower than that in the EGF group (P = 0.027), but the rate of eGFR decline did not differ between the groups. The risk factors for renal function were evaluated using the area under the eGFR curve over 3 years (AUCeGFR). Donor age was negatively, and recipient age and the number of HLA matches were positively correlated with the AUCeGFR (all P < 0.05). A multivariate analysis revealed that the AUCeGFR was lower in cases of younger recipient age, older donor age, and acute rejection (all P < 0.05). The AUCeGFR was significantly lower in the SGF and DGF2 groups compared with the EGF group (P = 0.031 and 0.006, respectively). CONCLUSIONS: SGF may be an independent risk factor for poor renal function after DKT. Moreover, it was comparable to DGF. Efforts should be dedicated to minimizing the development of SGF and DGF.

Increased risk of everolimus-associated acute kidney injury in cancer patients with impaired kidney function.

BACKGROUND: Everolimus was recently introduced as a second-line treatment for renal cell carcinoma (RCC) and many other cancers. Several prospective studies have shown that serum creatinine levels are increased in a significant proportion of patients receiving everolimus. However, data on the occurrence of acute kidney injury (AKI) during everolimus treatment in clinical practice are sparse. Here, we report the incidence, risk factors, and clinical significance of AKI associated with everolimus treatment in patients with cancer. METHODS: We analyzed patients who received everolimus for more than 4 weeks as an anticancer therapy. AKI was defined as increase in creatinine levels from baseline levels greater than 1.5-fold. RESULTS: The majority of the 110 patients enrolled in this analysis had RCC (N=93, 84.5%). AKI developed in 21 (23%) RCC patients; none of the patients (N=17) with other cancers had AKI. Fourteen of 21 cases were considered to be everolimus-associated AKI, in which there were no other nephrotoxic insults other than everolimus at the onset of AKI. The incidence of AKI increased progressively as baseline estimated glomerular filtration rate (eGFR) decreased (10% in subjects with eGFR >90 mL/min/1.73 m2, 17% in subjects with eGFR 60-90 mL/min/1.73 m2, 28% in subjects with eGFR 30-60 mL/min/1.73 m2, and 100% in subjects with eGFR 15-30 mL/min/1.73 m2; P=0.029 for trend). Baseline eGFR was an independent risk factor for the development of everolimus-associated AKI (hazard ratio per 10 mL/min/1.73 m2 increase, 0.70; 95% confidential interval, 049-1.00; P=0.047). Nine of 14 patients with everolimus-associated AKI continued receiving the drug at a reduced dose or after a short-term off period. Administration of the drug was discontinued in four of 14 patients because of progression of an underlying malignancy. Only one patient stopped taking the drug because of AKI. CONCLUSIONS: This paper suggests that AKI is a common adverse effect of everolimus treatment, especially in subjects with impaired renal function. However, the occurrence of AKI did not require the discontinuation of the drug, and the treatment decision should be made via a multidisciplinary approach, including the assessment of the oncological benefits of everolimus and other therapeutic options.

[A ten-year follow-up of a case with gastric adenoma accompanied with gastritis cystica profunda treated by endoscopic submucosal dissection].

Gastritis cystica profunda (GCP) is an uncommon hyperplastic benign lesion, and histologically characterized by hyperplasia and cystic dilatation of the gastric glands extending into the submucosal layer. GCP usually occurs at a gastroenterostomy site, although it can occasionally be found in an unoperated stomach. GCP is thought to be a possible precancerous lesion, since a few early gastric cancers associated with it were reported. Herein, we report a case of gastric adenoma associated with GCP in an unoperated patient. The sizes of both the GCP and adenoma overlying it have increased during a 10 year follow-up period. Adenoma on the latest biopsy showed low grade dysplasia, and it was successfully treated by endoscopic submucosal dissection.

[A case of idiopathic recurrent duodenojejunitis].

There are various etiologies of duodenojejunitis such as Henoch-Schönlei purpura (H-S purpura), vasculitis, Crohn's disease, celiac sprue, ischemia, lymphoma, Zollinger-Ellison syndrome, bacteria or parasite infection, radiation, drug induced jejunitis, eosinophilic jejunitis, and toxins. A 31-year-old man presented with left upper quadrant pain. He did not have febrile sense, hematochezia, melena, diarrhea, arthralgia and hematuria. He had neither drug history nor traveling history. Esophagogastroduodenoscopy showed diffuse mucosal erythema and segmental hemorrhagic erosions on the distal area to the descending portion of the duodenum and proximal jejunum, which were commonly observed in the gastrointestinal involvement of H-S purpura. However, he showed no skin lesions, joint and urologic problems until the discharge. Autoimmune markers such as antinuclear antibody and antineutrophil cytoplasmic antibody were negative. Celiac and mesenteric angiogram showed no vascular abnormality. After the administration of oral prednisolone 40 mg daily for therapeutic trial, abdominal pain and endoscopic lesions were improved. He experienced relapses of same episode without skin lesions 16 times during follow-up of 8 years, which were also treated with prednisolone. The abdominal computed tomography during the follow-up also showed no significant finding. We report a case of primary recurrent duodenojejunitis similar to the gastrointestinal involvement of H-S purpura without purpura.

A case of Castleman's disease mimicking a hepatocellular carcinoma: a case report and review of literature.

Castleman's disease is a rare disease characterized by lymph node hyperplasia. Although Castleman's disease can occur wherever lymphoid tissue is found, it rarely appears in the abdominal cavity, and is especially rare adjacent to the liver. Here, we report a rare case of Castleman's disease in the portal area that mimicked a hepatocellular carcinoma (HCC) in a chronic hepatitis B patient. A 40 year-old woman with chronic hepatitis B presented with right upper quadrant discomfort. Computed tomography and magnetic resonance imaging results showed a 2.2 cm-sized, exophytic hypervascular mass in the portal area. HCC was suspected. However, histologic examination revealed Castleman's disease. We suggest that Castleman's disease should be included as a rare differential diagnosis of a hypervascular mass in the portal area, even in patients with chronic hepatitis B.

De Novo Superinfection of Hepatitis B Virus in an Anti-HBs Positive Patient with Recurrent Hepatitis C Following Liver Transplantation.

A 60-year-old woman with end stage liver cirrhosis caused by genotype 2 hepatitis C virus (HCV) infection received an orthotopic liver transplantation (OLT). The patient was negative for the hepatitis B surface antigen (HBsAg) and positive for the anti-hepatitis B surface antibody (anti-HBs) prior to and one and a half months following the OLT. Due to reactivation of hepatitis C, treatment with interferon-alpha and Ribavirin started two months following the OLT and resulted in a sustained virological response. We performed a liver biopsy because a biochemical response was not achieved. Surprisingly, liver pathology showed HBsAg-positive hepatocytes with a lobular hepatitis feature, which had been negative in the liver biopsy specimen obtained one and a half months post-OLT. High titers of both HBsAg and HBeAg were detected, while anti-HBs antibodies were not found. Tests for IgM anti-hepatitis B core antibody and anti-delta virus antibodies were negative. The serum HBV DNA titer was over 1×10(7) copies/mL. A sequencing analysis showed no mutation in the "a" determinant region, but revealed a mixture of wild and mutant strains at an overlapping region of the S and P genes (S codon 213 (Leu/Ile); P codons 221 (Phe/Tyr) and 222 (Ala/Thr)). These findings suggest that de novo hepatitis B can develop in patients with HCV infection during the post-OLT period despite the presence of protective anti-HBs.