Improvement in Tubulointerstitial Nephritis With Glucocorticoid Therapy in an Anorexia Nervosa Patient.

Anorexia nervosa is a psychiatric disorder that is often diagnosed in adolescents and young adults. Renal-related complications of anorexia nervosa include abnormal water metabolism, electrolyte abnormalities, and nephrocalcinosis, which may lead to irreversible renal damage. Furthermore, tubulointerstitial nephritis has been reported as a renal pathological feature of anorexia nervosa. Immunosuppressive therapy, such as with glucocorticoids, has been recommended for idiopathic interstitial nephritis treatment; however, the effectiveness of immunosuppressive therapy for interstitial nephritis in patients with anorexia nervosa remains unestablished. Here, we report a case of interstitial nephritis in a patient with anorexia nervosa whose renal function was successfully improved with glucocorticoid therapy. The patient was a 38-year-old woman who was referred for renal dysfunction (estimated glomerular filtration rate: 7.6 mL/min/1.73 m2). She had anorexia nervosa and repeated episodes of vomiting. Hypokalemia (K: 2.1 mEq/L) and metabolic alkalosis (HCO3-: 54.2 mEq/L) were observed. Fluid therapy and potassium supplementation did not improve renal function; therefore, a percutaneous renal biopsy was performed. The renal pathology results revealed interstitial fibrosis, inflammatory cell infiltration in the interstitium, and tubulitis, suggesting a diagnosis of tubulointerstitial nephritis. Glucocorticoid therapy improved the patient's renal function to an estimated glomerular filtration rate of 19.91 mL/min/1.73 m2, and the renal function remained stable thereafter. This case suggests that glucocorticoid therapy may be considered for the treatment of interstitial nephritis in patients with anorexia.

Acute Kidney Injury Caused by Renin-Angiotensin System Inhibitors During Minimal Change Disease Treatment.

A 76-year-old Japanese man with nephrotic syndrome was admitted to our department for treatment. After his admission, he was administered prednisolone (PSL) at 40 mg/day, and a percutaneous renal biopsy was performed. However, on the first day of admission, his urinary protein decreased from 5.05 g/gCr to 1.85 g/gCr. On the fourth day of admission, his urinary protein further decreased to 0.38 g/gCr and the patient developed acute kidney injury (AKI). Renin-angiotensin system (RAS) inhibitors were suspected to be the cause of AKI; therefore, they were discontinued. After the renal function improved, the urinary protein worsened again to 5.49 g/gCr. Renal pathology suggested minimal change disease (MCD); therefore, PSL was continued. The patient's urinary protein subsequently improved and he had no renal function impairment. Minimal change disease can be complicated by AKI through intravascular volume depletion caused by high urinary protein and hypoalbuminemia. However, when MCD is complicated by RAS inhibitor-associated AKI, the urinary protein may notably decrease, and the patient may present with an atypical course of MCD-associated AKI.

A Comparative Study of the Hemoglobin-Maintaining Effects Between Epoetin-ß Pegol and Darbepoetin-α in Patients with Chronic Kidney Disease During 3 Months Before Dialysis Initiation.

BACKGROUND AND OBJECTIVE: We compared the hemoglobin-maintaining effects between continuous erythropoietin receptor activator (CERA) and darbepoetin-α (DA) in patients with chronic kidney disease (CKD) during the 3 months before dialysis initiation. METHODS: This study was conducted with 37 CERA-administered patients and 26 DA-administered patients who had initiated dialysis at a participating facility between January 2012 and December 2014. We investigated clinical laboratory data 3 months before and at dialysis initiation, and compared these data between the CERA and DA groups. RESULTS: No significant differences in hemoglobin level or reticulocyte count were found between the two groups 3 months before dialysis initiation. However, at dialysis initiation, the hemoglobin level (CERA 9.82 ± 1.52 vs. DA 8.79 ± 1.07 g/dL; P = 0.003) and the reticulocyte count (CERA 5.21 ± 2.95 vs. DA 3.15 ± 1.62 × 104/µL; P = 0.004) were significantly higher in the CERA group than in the DA group. Moreover, the extent of changes in the erythropoietin resistance index during the 3 months before dialysis initiation was significantly increased in the DA group compared with the CERA group. CONCLUSIONS: Our results suggest that CERA may be more effective than DA in maintaining hemoglobin levels in patients with CKD during 3 months before dialysis initiation.

Improvements in Pneumatosis Cystoides Intestinalis and Hepatic Portal Venous Gas with Conservative Therapy in a Patient on Maintenance Dialysis.

A 77-year-old man on maintenance dialysis developed hypotension, nausea and abdominal pain one hour after beginning to undergo hemodialysis. Abdominal computed tomography (CT) showed gas shadows in the intrahepatic portal vein and the small intestinal wall, but no signs indicating intestinal necrosis. Three days later, the gas shadows on abdominal CT disappeared by conservative therapy. In cases with both pneumatosis cystoides intestinalis and hepatic portal venous gas, intestinal necrosis should therefore be suspected and surgical therapy should also be considered, particularly in hemodialysis patients with a risk of intestinal ischemia. However, conservative therapy may be an option in cases with no intestinal necrosis.

A case of membranoproliferative glomerulonephritis and AA amyloidosis complicated with pulmonary nontuberculous mycobacterial infection.

A 75-year-old man was diagnosed with pulmonary nontuberculous mycobacterial (NTM) infection in February 2005 and was treated with rifampicin, ethambutol, and clarithromycin. However, the infection was resistant to treatment, and his chest radiograph showed an abnormality that gradually seemed to aggravate. The patient's sputum was positive for Mycobacteria. Moreover, the patient had dyspnea and an underlying chronic inflammation in the lungs. He visited our hospital because of dyspnea and leg edema in June 2011. Laboratory evaluation on admission revealed proteinuria (6 g/day) and decreased serum total protein (5.8 g/dL) and albumin (1.6 g/dL) levels, indicating nephrotic syndrome. Percutaneous renal biopsy revealed membranoproliferative glomerulonephritis (MPGN) in the acute stage and AA amyloidosis of mild degree. AA amyloidosis was also diagnosed histologically on gastric and colonic biopsy, in addition to renal biopsy. His renal function decreased gradually, and therefore, he underwent hemodialysis therapy in January 2012. However, his gastrointestinal-related symptoms persisted, and his appetite diminished, because of which he had become severely malnourished; he died 8 months later. This is a rare case of a patient with two different renal lesions (MPGN and AA amyloidosis) complicated with NTM. Our case suggests that MPGN and amyloidosis should be considered in elderly patients with nephrotic syndrome onset and chronic inflammation.

Continuous inflammation and ascites 10 months after the initiation of peritoneal dialysis.

A 38-year-old man underwent peritoneal dialysis (PD) in May 2011 due to chronic renal failure with chronic glomerulonephritis. In early February 2012, he underwent laparoscopy to salvage and correct a malpositioned PD catheter. The laparoscopic intra-abdominal findings revealed turbid ascites and multiple fibrin lumps, despite the patient's lack of history of peritonitis. Based on these findings, in addition to the presence of continuous inflammation and ascites, a diagnosis of pre-encapsulating peritoneal sclerosis was suspected, and the treatment was switched from PD to hemodialysis. The administration of prednisolone at a dose of 20 mg/day and peritoneal lavage resulted in a decrease in the ascites and fibrin lumps.

An elderly patient with diabetic nephropathy complicated by ANCA-associated nephritis.

A 67-year-old man, on oral therapy for type 2 diabetes mellitus since 1990, had sustained proteinuria since 2005. When hematuria was first discovered in 2008, renal dysfunction [creatinine (Cr), 1.2 mg/dL], inflammation [C-reactive protein (CRP), 12 mg/dL] and high myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA) levels [546 ELISA units (EU)] were observed. Renal biopsy showed the diagnosis of ANCA-associated nephritis combined with diabetic nephropathy. For this patient, there was pathological proof of the combination of diabetic nephropathy and ANCA-associated vasculitis.

Thalidomide prevents the progression of peritoneal fibrosis in mice.

Thalidomide is clinically recognized as a therapeutic agent for multiple myeloma and has been known to exert anti-angiogenic actions. Recent studies have suggested the involvement of angiogenesis in the progression of peritoneal fibrosis. The present study investigated the effects of thalidomide on the development of peritoneal fibrosis induced by injection of chlorhexidine gluconate (CG) into the mouse peritoneal cavity every other day for 3 weeks. Thalidomide was given orally every day. Peritoneal tissues were dissected out 21 days after CG injection. Expression of CD31 (as a marker of endothelial cells), proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), α-smooth muscle actin (as a marker of myofibroblasts), type III collagen and transforming growth factor (TGF)-ß was examined using immunohistochemistry. CG group showed thickening of the submesothelial zone and increased numbers of vessels and myofibroblasts. Large numbers of VEGF-, PCNA-, and TGF-ß-positive cells were observed in the submesothelial area. Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-ß-positive cells. Moreover, thalidomide attenuated peritoneal permeability for creatinine, compared to the CG group. Our results indicate the potential utility of thalidomide for preventing peritoneal fibrosis.

Diffuse liver metastasis of small cell lung cancer causing marked hepatomegaly and fulminant hepatic failure.

A 62-year-old female was admitted for examination of an abnormal liver function. Plain CT and MRI of the abdomen showed marked hepatomegaly but no visible nodular lesion in the liver. On the 3rd hospital day she had hepatic encephalopathy and was treated with a course of high-dose steroids, but ultimately died of disease progression on the 7th hospital day. An autopsy revealed a small pulmonary nodule with the histological findings showing small cell carcinoma. There was almost complete parenchymal replacement with metastatic tumor in the liver. Neoplastic involvement of the liver should be considered in the differential diagnosis of fulminant hepatic failure of unknown etiology.