[A case report of hepatitis B virus reactivation in a hepatitis B core antibody-positive, hepatitis B surface antigen-negative hemodialysis patient].

Reactivation of the hepatitis B virus (HBV) has been reported in patients receiving immunosuppressive therapy or chemotherapy. We report a case of HBV reactivation in a patient negative for hepatitis B surface antigen (HBsAg), positive for hepatitis B core antibody (anti-HBc), and positive for hepatitis B surface antibody (anti-HBs), who was undergoing chronic maintenance hemodialysis without immunosuppressive therapy or chemotherapy. The patient was an 85-year-old woman with end-stage renal disease due to nephrosclerosis who had undergone maintenance hemodialysis for a year. She had been HBsAg-negative, anti-HBc- and anti-HBs-positive previously, but biannual routine surveillance for HBV showed positivity for HBsAg, negativity for anti-HBs, and positivity for HBV DNA (5.9 log copies/mL). She was asymptomatic, and transaminases were within normal limits. She was dialyzed in an isolated room with a dedicated staff member for the control of infection. HBV is a blood-borne pathogen, which is highly infectious. Hemodialysis is a procedure associated with high risk for blood-borne infection. We should recognize the risk of reactivation of HBV in HBsAg-negative, anti-HBc-positive patients, and consider how to incorporate anti-HBc screening and infection control in isolated anti-HBc-positive hemodialysis patients in clinical practice.

Glomerulonephritis induced by methicillin-resistant Staphylococcus aureus infection that progressed during puerperal period.

A 28-year-old Japanese woman developed fever, leg edema, purpura, and abdominal pain during the puerperal period, showing nephrotic syndrome with microscopic hematuria. At first she was thought to have Henoch-Shönlein purpura nephritis and was given steroids at another hospital. Because anasarca and massive urinary protein excretion developed, she was referred to our hospital. Renal biopsy specimens showed endocapillary proliferative glomerulonephritis with massive IgA and C3d deposition along the capillary loops and in the mesangium. A bacteriological study detected methicillin-resistant Staphylococcus aureus (MRSA) in cultures of vaginal secretions, urine, stool, and pharyngeal mucus samples. Based on the diagnosis of MRSA nephritis, anti-MRSA therapy with antibiotics was started, and MRSA became negative for each culture, and urinary protein decreased. Two months after the first renal biopsy, a second renal biopsy was performed, which revealed feeble endocapillary proliferation with mild IgA and C3d deposition in the mesangium. This case showed that the delivery procedure can cause MRSA nephritis after MRSA infection, and that steroid therapy should be avoided in the early phase of this type of nephritis.

Chromosomal mapping of hyperserum IgA and glomerular IgA deposition in a high IgA (HIGA) strain of DdY mice.

BACKGROUND: The high IgA (HIGA) strain of ddY mice is an inbred model of IgA nephropathy (IgAN), established by selective mating of outbred ddY mice. HIGA mice show high levels of serum IgA and glomerulonephritis with mesangial IgA deposition. To identify the genetic loci responsible for hyperserum IgA and glomerular IgA deposition in this strain, quantitative trait loci analysis was carried out. METHODS: By crossing HIGA with BALB/c mice, 244 F2 generations were produced. Serum IgA levels and glomerular IgA deposition were examined at 40 weeks of age. Genetic markers were typed at 105 microsatellites and the quantitative trait loci of hyperserum IgA and glomerular IgA deposition were confirmed using Map Manager QTX software. RESULTS: Two significant quantitative trait loci of hyperserum IgA were identified on chromosome 2 [logarithm of odds (LOD) = 5.01] and chromsome 4 (LOD = 4.45), and a suggestive quantitative trait locus of hyperserum IgA was located on chromosome 1 (LOD = 3.49). On chromosome 15, a significant quantitative trait locus of glomerular IgA deposition was identified (LOD = 4.40) without the hyperserum IgA locus. Serum IgA level was weakly correlated with the intensity of glomerular IgA in 244 F2 mice; however, the quantitative trait loci of hyperserum IgA were not significantly associated with glomerular IgA deposition. CONCLUSION: These findings indicate that, in HIGA mice, glomerular IgA deposition is mainly regulated by a quantitative trait locus on chromosome 15, and hyperserum IgA synergistically but weakly affect glomerular IgA deposition. The immune disturbance similar to IgAN was revealed to be under multigenic control in HIGA mice.

The Na+-excreting efficacy of indapamide in combination with furosemide in massive edema.

BACKGROUND: Massive systemic edema is often observed in patients with severe nephrotic syndrome, including diabetic nephropathy. Although furosemide, a loop diuretic, is often administered to these patients, some patients do not respond to this treatment, still showing massive edema. METHODS: The efficacy of indapamide which has a thiazide-like effect on distal convoluted tubules in combination with furosemide, was evaluated in eight patients with massive edema, in regard to both Na+ excretion and diuresis. Indapamide 2 mg was administered once a day, in the morning, to patients in whom it was considered that furosemide treatment of 40-120 mg a day for 1 week was ineffective. RESULTS: Urinary Na+ excretion was markedly increased, from 83.7 +/- 82.2 mEq/day to 140.7 +/- 33.8 mEq/day after 1 week of the combination therapy compared with furosemide alone (P < 0.01); urine volume was also increased, from 1070 +/- 230 ml to 1359 +/- 296 ml after 1 week of the combination therapy (P < 0.05). In this context, body weight was significantly decreased, from 57.2 +/- 12.3 kg to 53.4 +/- 12.8 kg, after the combination therapy (P = 0.01). Indapamide in combination with furosemide was well tolerated, and no significant changes in serum levels of creatinine and potassium were observed. CONCLUSIONS: This combination therapy appears to be effective in patients with massive edema, as it increased diuresis, and achieved potent Na+ excretion.

Role of coagulation factor Xa and protease-activated receptor 2 in human mesangial cell proliferation.

BACKGROUND: Fibrin deposition and mesangial cell proliferation are frequently observed in the active type of mesangioproliferative glomerulonephritis. Coagulation factors, such as factor V and factor Xa are colocalized with fibrin in the mesangial areas in active type of IgA nephropathy with mesangial cell proliferation. In this study, therefore, we studied the role of factor Xa and its receptor, protease-activated receptor 2 (PAR2) in mesangial cell proliferation and fibrin deposition, and examined ant-proliferative effects of a specific factor Xa inhibitor, DX-9065a, in cultured human mesangial cells. METHODS: To examine the effect of DX-9065a on the factor Xa-induced proliferation of cultured human mesangial cells, we measured thymidine incorporation and cell numbers. We also examined the effect of DX-9065a on extracellular regulated kinase (ERK) activation and fibrin production induced by factor Xa in human mesangial cells. RESULTS: Factor Xa increased [(3)H]-thymidine incorporation and cell numbers in a dose-dependent manner in mesangial cells, which was inhibited by DX-9065a. DX-9065a also suppressed factor Xa-triggered fibrin deposition on mesangial cell surface. Factor Xa induced the activation of ERK in mesangial cells and this activation was also completely inhibited by DX-9065a, but not inhibited by PAR1 antagonist. Factor Xa-induced cell proliferation and ERK activation were inhibited by PD98059. CONCLUSION: There results suggest that factor Xa can induce mesangial cell proliferation through the activation of ERK via PAR2 in mesangial cells and that PAR2 may play a crucial role in the cell proliferation induced by factor Xa. Our results implicate that DX-9065a may be a promising agent to regulate proliferation of mesangial cellss and inhibit the coagulation process in mesangium.

Quantitative trait loci (QTL) analysis reveals a close linkage between the hinge region and trimeric IgA dominancy in a high IgA strain (HIGA) of ddY mice.

Polymerization of IgA has been suggested as one of the causes of mesangial deposition in IgA nephropathy. HIGA mice are an inbred model of IgA nephropathy, established by selective mating of ddY mice. This strain is characterized by a unique profile of the IgA molecule that is dominantly polymeric and has high serum levels with intense IgA deposition on the mesangium. We carried out quantitative trait loci (QTL) analysis, using F2 generations by crossing HIGA with BALB/c mice. Significant linkage of polymeric IgA in serum samples was identified around D12Mit263, which is close to the gene of the immunoglobulin heavy chain on chromosome 12. The amino acid sequence of the alpha heavy chain revealed marked differences between BALB/c and HIGA mice. Furthermore, most differences were focussed on the hinge region. The DBA/2J strain, which has the same amino acid sequence in the hinge region as the HIGA strain, also showed polymeric IgA dominance but low IgA levels in sera. Size fraction analysis revealed that these polymeric IgA showed trimer dominance in both DBA/2J and HIGA mice. In conclusion, the hinge region plays a key role in trimeric IgA formation in HIGA mice.

A case of normoreninemic aldosterone-producing adenoma associated with chronic renal failure: case report and literature review.

The diagnosis of aldosterone-producing adenoma (APA) is challenging for endocrinologists, as APA does not always present with the typical constellation of clinical and laboratory features, such as hypertension, hypokalemia, suppressed plasma renin activity (PRA), and high plasma aldosterone concentration (PAC). Very recently, several studies have indicated that APA can be discovered even in normokalemic subjects with normal PRA more frequently than previously considered. Here we report a case of APA associated with chronic renal failure, which showed normokalemia and normal PRA. The patient was referred to our clinic for evaluation of an incidentally discovered adrenal mass with abnormally high PAC. After 6 yr, it was found that the right adrenal tumor showed a marked increase in size. Endocrinological examinations indicated normal PRA and markedly high PAC. Aldosterone showed a better response to the upright posture test than that to ACTH stimulation test. The diagnosis of APA was made based on the markedly high PAC to PRA ratio and the adrenocortical scintigraphy, which showed unequivocal uptake into the tumor. Right laparoscopic adrenalectomy was performed, revealing a right adrenocortical adenoma with massive hemorrhage. Histopathological examinations revealed the presence of two independent adrenocortical adenomas, one APA with predominant clear tumor cells and few c17 (17alpha-hydroxylase) immunoreactivity and the other, cortisol producing adenoma with compact cytoplasm and abundant C17 immunoreactivity. This case indicates a difficulty of diagnosis of "normoreninemic APA" with renal failure. This case is in line with the recent concept that APA is a continuous condition in which only a minority of patients have the classical clinical picture of primary aldosteronism such as hypokalemia. It is possible that normokalemic APA constitutes the most common presentation of the disease.

[Anesthesia for living-donor liver transplantation in a patient with adult polycystic liver disease].

Anesthesia for living-donor liver transplantation (LDLT) was performed for two patients with adult polycystic liver disease (APLD). APLD is characterized by gradual cystic transformation of both lobes of the liver. Abdominal enlargement, poor appetite, abdominal pain, infection of liver cysts and portal hypertension are symptoms of this disease. Liver transplantation is indicated as the final therapy. Our two patients had very large livers (7400 g and 9500 g). The second patient had suffered renal failure due to a polycystic kidney so that continuous hemodiafiltration had to be performed after surgery. In both cases, sudden hypotension frequently occurred during manipulation of the enlarged liver. In the first case, sudden massive bleeding occurred as a result of laceration of the middle and left hepatic vein when the liver was dropped from the surgeon's hand. In both cases, the position of endotracheal tube became 2 cm shallower after surgery probably because of the shift in the position of the mediastinum after elimination of abdominal compression caused by the enlarged liver. One patient was discharged 39 days and the other 115 days after surgery. Anesthesiologists should pay special attention to the features reported here during LDLT for patients with APLD.