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Diabetes mellitus carries a great burden on healthcare costs due to its growing population and high co-morbidity. This adverse effect sustains even when patients develop end-stage renal disease (ESRD). We here present data showing the effect of diabetes on economic costs in dialysis therapy in Taiwan. As of the end of 1997, we have 22 027 ESRD patients with a prevalence and incidence rate of 1013 and 253 per million populations, respectively. Diabetic nephropathy is the second most common cause of the underlying renal diseases, but accounts for 24.8% of the prevalent patients and 35.9% of the incident cases. The diabetic patients engendered 11.8% more expense for care of dialysis than the non-diabetic patients (US$26 988 vs. US$24 146 per patient-year). Higher inpatient cost mainly account for the difference. As compared to non-diabetic patients, the diabetic patients had 3.5 times more inpatients costs (US$1325 vs. US$4677 per patient-year), and higher proportion of inpatient-to-annualized cost ratio (5.5 vs. 17.3%) resulting from their more frequent hospitalization (0.59 vs. 1.13 times per patient-year) and longer hospital stay (6.7 vs. 18.9 days per patient-year). The major causes responsible for a more frequent hospitalization were cardiovascular disease, poorly controlled hyperglycemia, sepsis and failure of vascular access. The annualized costs for care of dialysis patients in Taiwan, including inpatient and outpatient costs, averaged US$25 576 per patient-year. This value is approximately half of that in most of the western countries and Japan. Thus, a more cost-effective way to achieve savings is to reduce the high incidence rate of dialysis population and to maximize the quality of dialysis treatment for avoiding hospitalization. Recent studies had shown that tight blood pressure control, intensive glycemic control, and use of angiotensin converting enzyme inhibitors in diabetic patients significantly reduced not only the rate of progressive renal failure, but also substantially reduced the cost of complications and led to higher cost effectiveness. Once diabetic patients reach stage of ESRD, an optimized pre-ESRD care and consideration of kidney transplantation are essential in terms of better patient survival and cost savings.

Ho-Han Wu, Szu-Yuan Li and Wu-Chang Yang Division of Nephrology, Department of Internal Medicine, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan; Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital and School of Medicine, National Yang-Ming University, Taipei, Taiwan and Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan

A 65-year-old female received a renal transplantation 3years ago, and her maintenance immunosuppressive regi-men included prednisolone 5 mg once daily (0.1 mg/kg/day), mycophenolate mofetil 1 g twice daily and cyclos-porin 125 mg twice daily (5 mg/kg/day) with averagetrough serum levels of cyclosporine between 200 and300 ng/mL since 3 months after renal transplantation.Her first episode of gouty arthritis developed more than10 years ago; however, the disease activity remained qui-escent, and there was no episode of gouty arthritis since 7years before renal transplantation. It was not until 2 yearsago, i.e. 1 year after transplantation, when the tophi firstappeared on the left hand during an episode of gouty ar-thritis, which was followed by frequent attacks since then.On admission, physical examination disclosed multiple to-phi on the left hand (Figure 1A) with exudation of white,chalky material from some tophi. Laboratory evaluationshowed a higher level of serum uric acid, up to 7.7 mg/dL,but the level of urinary uric acid excretion was lower, at175 mg/day (1 mmoL/day), and the creatinine clearancerate was 63 mL/min/1.73 m

A 52-year-old man with diabetic nephropathy-related endstage renal disease suffered from fever and pain with redness over the dorsum of his bilateral feet for 2 days. He had a history of liver cirrhosis caused by chronic hepatitis B. Physical examination revealed a temperature of up to 39.5°C, erythematous swelling with purple bullae formation and tenderness over bilateral feet (Figure 1A). Laboratory examination revealed a higher leukocyte count (24 200/mm), with 93% neutrophils and elevated serum levels, including C-reactive protein 193 mg/l (normal value

In contrast to proteins and lipids, oxidative damage to DNA has not been well studied in patients undergoing hemodialysis (HD). We hypothesized that phagocytes are activated after blood-membrane contact during HD, and oxidants from metabolic activation can damage leukocyte DNA. To test this hypothesis, the 8-hydroxy-2'-deoxyguanosine (8-OHdG) content of leukocyte DNA was measured by high-performance liquid chromatography electrochemical detection method in 35 age- and sex-matched healthy subjects, 22 undialyzed patients with advanced renal failure, and 109 HD patients to assess the relation between oxidative DNA damage and complement-activating membranes, blood antioxidants, and iron status. Dialysis membranes were classified into complement-activating (cellulose; n = 55) and non-complement-activating (polymethylmethacrylate [PMMA]; n = 35; polysulfone [PS]; n = 19) membranes. We found increased oxidative stress in undialyzed and HD patients based on a decrease in plasma levels of ascorbate and alpha-tocopherol adjusted for blood lipid (alpha-tocopherol/lipid), serum albumin, and reduced glutathione levels in whole blood and an increase in oxidized glutathione levels in whole blood compared with controls (P < 0.001). The greatest 8-OHdG level in leukocyte DNA was in HD patients, followed by undialyzed patients and healthy controls (P < 0.001), and was significantly greater in HD patients using cellulose membranes than those using PMMA or PS membranes (P < 0.001). 8-OHdG levels correlated with plasma alpha-tocopherol/lipid (r = -0.314; P < 0.005), serum iron (r = 0. 446; P < 0.001), and transferrin saturation values (r = 0.202; P < 0.05) in the analysis of all HD patients. In a 6-week crossover study, 8-OHdG levels significantly decreased after the switch from cellulose to synthetic membranes for 2 weeks and increased after the shift from synthetic to cellulose membranes (P < 0.05). Iron metabolism indices and plasma alpha-tocopherol/lipid values did not change significantly in the study period. We conclude that 8-OHdG content in leukocyte DNA is a biomarker of oxidant-induced DNA damage in HD patients. Oxidative DNA damage is a consequence of uremia, further augmented by complement-activating membranes.

When Staphylococcus aureus is repeatedly positive in blood cultures even under effective antibiotics therapy (vancomycin, teicoplanin, or rifampin), computed tomography scan and sonography should be performed early to exclude mycotic aneurysm of the deeply seated arteries, especially in patients with abdominal aortic calcification. Before 1990, the most common causative organism of suprarenal aortic mycotic aneurysm was Salmonella; since 1990, it has been gram-positive cocci (i.e., Streptococcus and Staphylococcus) rather than gram-negative bacilli (i.e., Salmonella), possibly because of the more invasive procedures performed in clinical settings, but this hypothesis needs further investigation.

OBJECTIVE: To report an interaction between tacrolimus and rifampin with subsequent adverse effects on renal allograft function. CASE SUMMARY: A 61-year-old Chinese man received a cadaveric renal transplant in 1991. Progressive deterioration of allograft function developed during the following six years while the patient was receiving cyclosporine and prednisolone. In January 1998, tacrolimus was substituted for cyclosporine for late biopsy-proven graft rejection, with target trough blood concentrations between 5 and 8 ng/mL. After conversion, serum creatinine fell to 2.0 mg/dL; the nadir was reached within one year. At the same time, rifampin was instituted for controlling tuberculosis and empiric fluconazole was discontinued. Twelve days later, the patient's serum creatinine concentration rose to 2.9 mg/dL and tacrolimus concentration fell to 1.5 ng/mL, along with oliguria. These findings suggested acute rejection, which was successfully reversed by steroid therapy. However, more than a tenfold increase in the tacrolimus dosage was required to maintain the same concentrations during subsequent months, accompanied by an increase in serum creatinine (from 2.0 to 2.6 mg/dL) and decrease in urine excretion. Biopsy at this time demonstrated acute rejection (Banff I), chronic allograft nephropathy (Banff II), and suspected tacrolimus nephrotoxicity. After unsuccessful methylprednisolone recycling, mycophenolate mofetil was introduced to control rejection and facilitate reduction of the tacrolimus dosage to minimize its nephrotoxicity. CONCLUSIONS: As a potent CYP3A4 isoenzyme inducer, rifampin coadministration caused the abrupt decrease in tacrolimus blood concentrations, leading to an approximate tenfold increase in its daily dose, which may be important to subsequent allograft dysfunctions.

A 20-year-old Chinese male visited our outpatient department with bilateral flank pain and general malaise. Physical examination revealed pale conjunctiva and bilateral palpable flank mass. Laboratory evaluation showed an impairment of renal function (BUN 37 mg/dL, creatinine 2.9 mg/ dL) and pancytopaenia with white cell count 1300/μL, haemoglobin 6.5 g/dL and platelet count 33 000/μL. Sonogram showed bilateral nephromegaly and splenomegaly. Computed tomography (CT) revealed heterogeneous contrast enhancement of bilateral kidneys in an appearance of radiating striated infiltration similar to the surface of a cantaloupe, especially in the left kidney (Figure 1A). Bone marrow examination revealed numerous blasts, accounting for ∼90% of the lymphoid series (Figure 1B). The immunostains of these cells were positive for CD34, CD10, CD79a and CD 20, but negative for terminal deoxynucleotidyl transferase (TdT), CD117, MPO (myeloperoxidase), CD3 and CD7, which were compatible with the diagnosis of acute precursor B lymphoblastic leukaemia. Induction and consolidation chemotherapy were administered accordingly. Three months later, his renal function improved partially (BUN 28 mg/dL, creatinine 1.7 mg/dL), and the follow-up CT of the abdomen revealed a significant disappearance of the above-mentioned heterogeneous infiltration (Figure 1C). Because of very high risk of disease recurrence, this patient underwent allogenic haematopoietic stem-cell transplantation. One year later, another follow-up CT showed the normal pattern of contrast enhancement and regular size of kidneys (Figure 1D), when his disease remained in complete remission and his renal function was within normal range (BUN 12 mg/dL, serum creatinine 0.7 mg/dL). Nephromegaly is a common problem in clinical nephrology. Symmetrical enlargement of kidneys with a loss of the corticomedullary junction shown by imaging study indicates an infiltrating lesion that can be usually divided into either neoplastic or inflammatory type [1]. However, nephromegaly as an initial presentation of leukaemia is quite rare, with a frequency of only 3–5% [2]. Renal involvement usually occurs during the late stage of leukaemia, with an estimated frequency of ∼50% in paediatric patients and up to 65% in adults [3]. In summary, cantaloupelike kidney is a rare form of early infiltration of renal interstitium by leukaemic blasts. Thus, bone marrow examination is indicated when CT scan discloses infiltrative nephromegaly.

A 64-year-old man presented with progressive painless right lower leg swelling for 5 years. The patient had a history of surgical resection of similar lesions over his right forearm and abdominal wall 5 and 8 years ago, respectively. He had bilateral recurrent renal stones over the past 5 years. The physical examination was normal except for a painless stone-hard right lower leg swelling (Figure 1). He had no skin lesions or lymphadenopathy. His blood tests revealed a total white blood cell count of 4700/mm3 (78% neutrophils), hemoglobin 10.4 g/dL, blood urea nitrogen 57 mg/dL, creatinine 4.68 mg/dL, calcium 14.6 mg/dL (normal 8.4–10.6), and normal C-reactive protein and creatine kinase level. Serum electrophoresis was normal. He had a serum intact parathyroid hormone of 9.36 pg/dL (

To the Editor: In a recent issue of Kidney International, Ohtomo et al.1 showed that pioglitazone (PGZ), one of these currently used thiazolidinediones, could provide better renoprotection than insulin in an obese, hypertensive, type 2 diabetes mellitus rat model. However, a few questions should be considered for this animal study. First, many diabetic patients have insulin as their main treatment for glycemic control, as the author proved PGZ has better renoprotection, would combination treatment with insulin and PGZ be a better regimen for diabetic patients? If the answer is yes, why didn't the author add another group treated by both insulin and PGZ in their study design. Second, the glycemic control was not better in rats treated with PGZ than those with insulin. Is it possible that the dose of PGZ was too low to achieve a better glycemic status? Third, how could we explain the finding that insulin had a renoprotective effect in the first 8 weeks but it increased urine protein later gradually? According to Schena and Gesualdo,2 insulin can reduce oxidative stress with prevention of accumulation of toxic advanced glycation end products, which may provide renoprotection in the first 8 weeks. However, in the later period, insulin may induce production of matrix proliferation and results in glomerular sclerosis, thus renal function may decline with increased urine protein excretion.

A 64-year-old post-menopausal woman presented with dysuria, weakness and poor appetite that had lasted 3 months. A bilateral percutaneous nephrostomy (PCN) catheter was placed for bilateral hydroureteronephrosis at a local hospital, but malfunctioned due to blood clot formation. Physical examination revealed peritoneal signs. Laboratory test revealed leucocytosis, azotaemia with blood urea nitrogen (BUN) 93mg/dl, creatimine (Cr) 16.3mg/dl, and severe metabolic acidosis. Haemodialysis was initiated for uraemia. Computed tomography of the abdomen demonstrated the presence of ascites with peritoneal thickening in the lower peritoneal cavity, obstruction of the uterine outlet with intra-uterine fluid retention, tissue plane blurring between the uterine cervix and urinary bladder, and obstructive uropathy with the obstruction level at the bilateral uretero-vesical junction (Figures 1 and 2). Cervical cancer with pyometra was suspected and treated with dilation and curettage surgery, during which 150 c.c. of pus was drained out. Empiric antibiotics were given and sepsis resolved thereafter. A bilateral PCN catheter functioned well after repeated revisions. Haemodialysis was discontinued 3 weeks later (BUN 33mg/dl, Cr 2.8mg/dl). A biopsy of the cervix revealed squamous cell carcinoma with stromal invasion and the staging was IVA because of urinary bladder spreading. The patient recalled that she had suffered from intermittent vaginal spotting for the last 4 years, but had ignored it.

Patients with gouty arthritis were examined at Veterans General Hospital to evaluate whether their renal function is impaired and to define the factor(s), if any, of renal function deterioration. A total of 152 cases were included in the study, and the patients were divided into two groups. One group (n = 80) exhibited pure gout without any associated medical problems or preexisting renal disorders. The second group (n = 72) included patients with gout and hypertension. The group with pure gout was further stratified into patients with tophi (n = 21) and those without (n = 59). Seventy-two sex- and age-matched normal adults served as the control group. We found (1) that the renal function was impaired in the pure-gout group when compared with sex- and age-matched normal individuals (serum creatinine 1.56 +/- 0.64 vs. 0.90 +/- 0.16 mg/dl, p = 0.0001; creatinine clearance 59.91 +/- 30.90 vs. 97.10 +/- 27.19 ml/min, p = 0.0001); (2) that the renal function was significantly more aggravated in patients with clinically visible tophi than in those without (gout with tophi vs. gout without tophi: serum creatinine 1.89 +/- 0.90 vs. 1.44 +/- 0.48 mg/dl, p = 0.040; creatinine clearance 47.27 +/- 31.90 vs. 64.40 +/- 29.53 ml/min, p = 0.030), and (3) that a further significant decline of the renal function was noted in gouty patients with an associated medical illness, i.e., hypertension (gout with hypertension vs. pure gout: serum creatinine 2.10 +/- 0.97 vs. 1.56 +/- 0.64 mg/dl, p = 0.0001; creatinine clearance 45.06 +/- 24.69 vs. 59.91 +/- 30.90 ml/min, p = 0.0029).(ABSTRACT TRUNCATED AT 250 WORDS)

Background The renin-angiotensin-aldosterone system (RAAS) plays an important role in the progression of chronic kidney disease (CKD). Although dual RAAS inhibition results in worse renal outcomes than monotherapy in high risk type 2 diabetes patients, the effect of dual RAAS inhibition in patients with non-DM CKD is unclear. The aim of this study was to evaluate the potential renoprotective effect of add-on direct renin inhibitor in non-DM CKD patients. Methods We retrospectively enrolled 189 non-DM CKD patients who had been taking angiotensin II receptor blockers (ARBs) for more than six months. Patients were divided into an add-on aliskiren group and an ARB monotherapy group. The primary outcomes were a decline in glomerular filtration rate (GFR) and a reduction in urinary protein-to-creatinine ratio at six months. Results The baseline characteristics of the two groups were similar. Aliskiren 150 mg daily reduced the urinary protein-to-creatinine ratio by 26% (95% confidence interval, 15 to 37%; p Conclusion Add-on direct renin inhibitor aliskiren (150 mg daily) safely reduced proteinuria and attenuated the decline in GFR in the non-DM CKD patients who were receiving ARBs.

Refractory ascites can occur in patients with various conditions. Although several procedures based on the reinfusion of ascitic fluid have been reported after the failure of bed rest, salt and water restriction, diuretics, intravenous administration of albumin, and repeated paracentesis, these procedures are performed for ascitic fluid removal without dialytic effect. In this study, a flow control reinfusion of ascites during hemodialysis (HD) was performed to demonstrate the efficacy of this method in a lupus patient with massive refractory ascites and respiratory and acute renal failure (ARF). The alleviation of ascites and ARF attests to the success of the flow control reinfusion of ascites during HD. This procedure can control the rate of ascites and body fluid removal simultaneously during HD using the roller pump. In conclusion, with a normal coagulation profile, the procedure of flow control reinfusion of ascites during HD is an effective alternative treatment for the alleviation of refractory ascites with renal failure.

To the Editor: We read with great interest the article by Santiago et al. The continuous renal replacement therapy (CRRT) device functioned correctly after connecting with the extracorporeal membrane oxygenation (ECMO) circuit in parallel, not in series. Previously we observed different problematic pressures in connecting the CRRT device with the ECMO circuit in adults and children. It is clear from this article that the low blood flow rate of the CRRT device drained from the ECMO circuit will trigger the ‘arterial line disconnection’ alarm, owing to the positive inlet pressure exceeding the normal range. How can we ignore a prior warning of the Food and Drug Administration in 2005 on the potential risk of fluid imbalance in a Prisma device by allowing the alarm to be silenced repeatedly? Therefore, the real fluid removal from the CRRT device should be measured to make sure an accurate balance. When we tried the same connection system in adults, the normal blood flow (150ml/min) of the CRRT device avoided alarm because of difficulty in blood extraction, but not in blood return. Actually, the high resistance within the ECMO circuit following the centrifugal pump hindered the outlet flow of the CRRT device. Again, the on-line monitoring of pressure became an obstacle. It is not recommended to override the alarm, owing to the potential risks of hemolysis and filter clotting. Difficulty in finding vascular access for renal replacement therapy is a common problem in critically ill patients, especially in children. Thus, the utility of the ECMO circuit might be an alternative solution. However, it is inappropriate to conclude that inclusion of the CRRT device in the ECMO circuit is safe and effective without any complications in all patients.

To the Editor: In a recent issue of Kidney International, Chen et al.1 suggested that patients with myeloperoxidase (MPO)-antineutrophil cytoplasmic autoantibodies (ANCA) positive Wegener's granulomatosis were not rare in Chinese, and the prevalence of elevated initial serum creatinine was significantly higher in patients with MPO-ANCA than that in patients with PR3-ANCA. However, the possible contributors for more prevalent elevated serum creatinine in patients with MPO-ANCA were not clarified. First, the common confounding factors associated with chronic kidney diseases (e.g. diabetes mellitus, hypertension, advanced age, nephrotoxic agents (e.g. non-steroid anti-inflammation drugs) use, etc.) and acute renal failure (e.g. prerenal and postrenal types) should be excluded in patients with elevated initial serum creatinine. Second, the serum ANCA titer, a plausible indicator of disease activity, might be further determined in both groups. Third, the significantly lower prevalence of extra-renal involvement (e.g. arthralgia, skin rash, ophthalmic, and ear involvement) in the MPO-ANCA group1 may lead to a longer insidious inflammation process, resulting in more severe renal damages with elevated serum creatinine. It was speculated that MPO-ANCA-positive Wegener's granulomatosis was somewhat more like microscopic polyangiitis, which was more likely to have a greater degree and severity of glomerulosclerosis, interstitial fibrosis, and tubular atrophy on initial renal biopsy.2 In addition, the differences in histopathology between MPO-ANCA and PR3-ANCA glomerulonephritis could be explained by the observation that in patients with MPO-ANCA, kidney biopsy was carried out late in the course of the disease, and diffuse chronic sclerotic lesions predominated.3

To the Editor: With the article by Tang et al.,1 recently published in Kidney International, we anticipate that the lamivudine-resistant mutation and hepatitis flares will occur in their patients with hepatitis B virus-associated membranous nephropathy under further long-term lamivudine treatment. Although, hepatitis B virus variants with mutations at the YMDD motif of DNA polymerase have not been observed in their cohort, the proportion of patients with a documented lamivudine-resistant mutation increased from 23% in year 1 to 65% in year 5 was reported by Chayama et al.2 and Lok et al.3

Acute renal failure (ARF) is an unusual complication of wasp stings and mostly results from toxic-ischemic acute tubular necrosis. This patient, who was stung by a swarm of wasps, experienced an allergic reaction, rhabdomyolysis, intravascular hemolysis, and subsequent ARF. The originality of this case report is related to the finding of combined lesions of acute tubulointerstitial nephritis and acute tubular nephropathy. From our extensive literature review, it is the first case of a patient developing this type of injury after wasp stings, and the complications have been documented previously only in one form or another. Renal biopsy should be encouraged, especially for a patient with delayed recovery of renal function after wasp stings, to facilitate early steroid treatment for the patient with the histological change of acute interstitial nephritis. Early use of steroid therapy may hasten renal recovery by preventing the development of interstitial fibrosis.

Hypercalcemia occurs frequently after renal transplantation. Preexisting hyperparathyroidism is the most common cause of post-transplantation hypercalcemia. We describe a renal transplant recipient infected with Pneumocystis carinii pneumonia (PCP) who developed hypercalcemia, elevated 1,25-dihydroxyvitamin D, and suppressed parathyroid hormone levels. This phenomenon mimics the extrarenal production of 1,25-dihydroxyvitamin D by activated alveolar macrophages in granulomatous diseases with hypercalcemia. To the best of our knowledge, this is the first report of 1,25-dihydroxyvitamin D-mediated hypercalcemia caused by PCP in a renal transplant recipient. This entity should be included in the differential diagnosis for renal transplant recipients with hypercalcemia, especially in patients who develop lung infections.