Sl Lui

Treatment of membranous lupus nephritis with nephrotic syndrome by sequential immunosuppression

The optimal therapy for pure membranous lupus nephritis (MLN) with nephrotic syndrome remains controversial. While the risk of progressive renal deterioration may be small, persistent heavy proteinuria leads to the complications of oedema, hypoalbuminaemia, hyperlipidaemia, hypercoagulability, and venous thrombosis. We examined prospectively the efficacy and tolerability of a sequential immunosuppressive regimen in a cohort of 20 patients with nephrotic syndrome due to pure MLN (WHO Class Va and Vb). Initial therapy comprised prednisolone (0.8 mg/kg/d p.o.) and cyclophosphamide (2–2.5 mg/kg/d p.o.). Prednisolone dosage was gradually tapered to 10 mg/d at 6 months, when cyclophosphamide was replaced by azathioprine (2 mg/kg/d p.o.) as maintenance therapy. Within 12 months of therapy 11(55%) patients had complete remission (CR), 7(35%) patients achieved partial remission (PR) (proteinuria reduced from 6.2 4.0 to 2.0 1.7 g =24 h, P < 0.01), and 2 patients failed to respond. Improvements in proteinuria and serum albumin level were observed after 3–6 months of treatment. Non-responders had lower baseline serum albumin compared to complete responders. Renal function remained stable during follow-up for 73.5 48.9 months. 8 patients had disease relapse at 47 15 months. Early complications (12 months) included herpes zoster (40%), minor respiratory or urinary tract infections (25%), mild leukopenia (15%), and transient amenorrhea (14.3%). 4 of the 20 patients developed pulmonary tuberculosis during follow-up, at 35 24 months after the diagnosis of MLN. 8 patients had hyperlipidaemia. Haemorrhagic cystitis, permanent amenorrhea, vascular complications, and mortality were not observed. We conclude that this sequential immunosuppressive regimen is effective in 90% of patients with MLN and heavy proteinuria. Prudent consideration of the benefits and potential side-effects is required to determine the optimal management for individual patients.

Star fruit intoxication in uraemic patients: case series and review of the literature

Abstract

A randomized prospective comparison of oral versus intraperitoneal ofloxacin as the primary treatment of CAPD peritonitis

Summary: Oral ofloxacin has been successfully used in our centres for the primary treatment of peritonitis complicating continous ambulatory peritoneal dialysis (CAPD). In view of the progressive rise in the resistance rate to ofloxacin among peritoneal bacterial isolates, a study was conducted to determine if oral ofloxacin remains a viable first line treatment for CAPD peritonitis in our centres and if the result can be improved by changing from an oral to an intraperitoneal (i.p.) route. In patients on three 2 L daily CAPD exchanges, ofloxacin given at the i.p. dosage of 200 mg loading followed by 25 mg/L of peritoneal dialysate achieved overnight trough peritoneal levels which are at least four times the minimal 90% inhibitory concentration (MIC90) of most bacterial pathogens without significant accumulation in the systemic circulation. This i.p. dosage was therefore chosen for the clinical study and the result was compared to that using ofloxacin given in the oral dosage of 400 mg loading followed by 300 mg once daily as maintenance. of all the recruited episodes, 35 were eligible for analysis. the overall primary cure rate including primary failures and relapses was 55.6% (10/18) in the oral treatment group and 70.6% (12/17) in the i.p. treatment group. the corresponding figures for gram positive bacterial (g +) infections were 36.4% and 50%, for gram negative bacterial (g ‐) infections were 66.7 and 80% and for culture negative infections were 75 and 80%. In culture positive cases, all treatment failures were due to resistant infections which were observed in 42.3% of all bacterial isolates, 47.1% of g + isolates and 33.3% of g ‐ isolates. Due to the high background level of bacterial resistance among our CAPD population, ofloxacin monotherapy given either by the oral or the i.p. route can no longer be recommended for the primary treatment of CAPD peritonitis.

Reactivation of systemic lupus erythematosus in a dialysis patient after tuberculous peritonitis

The disease activity of patients suffering from lupus nephritis usually becomes quiescent after the onset of end stage renal failure. Reactivation of lupus activity, especially after a long period of dialysis, is uncommon. Factors that might trigger off lupus reactivation after dialysis have not been well defined. We report a case of a 43-year-old Chinese woman on long-term peritoneal dialysis, who developed lupus reactivation with cerebral involvement 2 weeks after she was diagnosed to have tuberculous peritonitis. The close temporal relationship between the tuberculous peritonitis and the lupus reactivation raise the possibility that the tuberculous infection might have triggered off the lupus reactivation.

Adrenal Insufficiency in a Peritoneal Dialysis Patient Taking Megestrol Acetate

Two months before presentation, she had experienced 1 episode of peritonitis caused by Prevotella species, which was adequately eradicated by intravenous cefmetazole, as evidenced by white cell counts of less than 100/mm3 in effluent after treatment. At her current admission, she presented with fatigue, abdominal pain, fever, and turbid effluent. The physical examination revealed a painful abdomen with rebounding tenderness. The exit of the peritoneal dialysis catheter looked clean, without apparent sign of tunnel infection. Peritoneal effluent contained white cells 185/ mm3, with 98% polymorphonuclear leukocytes. Gram stain of the effluent failed to show any micro-organisms. Computed tomography imaging of the abdomen revealed no significant intra-abdominal lesions. We diagnosed CAPD-related peritonitis and gave empiric antibiotic therapy (intravenous cefmetazole 2000 mg once daily) after peritoneal fluid and blood cultures had been taken. Cultures of the peritoneal fluid subsequently yielded M. morganii on 2 occasions. The antibiotic regimen was then replaced with intraperitoneal ceftazidime 500 mg, 4 times daily. The woman’s abdominal pain, nausea, and vomiting steadily subsided. Peritoneal effluent cell counts returned to 5/mm3 by day 10. She was discharged and did not relapse. M. morganii has recently become an important opportunistic pathogen (2–6), being frequently encountered in the intensive care unit, partly because of its preponderance in immunocompromised individuals and also because of various invasive procedures (7). As first reported by Atalay et al. (1), M. morganii caused peritonitis in a polymicrobial fashion (with Providencia rettgeri). However, in the present patient, it was isolated as a single pathogen in CAPD-related peritonitis. To our knowledge, this case is probably the first of CAPD-related peritonitis attributable to M. morganii in a monobacterial setting. Another unique feature is that M. morganii was able to cause severe infection in an immunocompetent patient such as ours. Fortunately, the microbe was sensitive to amikacin, ceftazidime, cefepime, quinolone, imipenem, and piperacillin–tazobactam, as has been reported in the literature (8). Our patient recovered completely after the use of ceftazidime. In conclusion, M. morganii is a rare cause of CAPDrelated peritonitis, and our patient may be the second case of M. morganii peritonitis and the first of monobacterial infection with that organism.

Ruptured Abdominal Aortic Aneurysm As a Cause of Spontaneous Hemoperitoneum in a Patient on Peritoneal Dialysis

patients, 1-year survival was 56% in those with severe LVH and 91% in those without LVH (4). Moreover, in a previous cohort of HD patients, it was demonstrated that a 10% decrease in left ventricular mass was associated with a 22% reduction in the relative risk for all-cause death and a 28% reduction for cardiovascular death (7). The 17% decrease in LVMI in our patients might have a significant impact on their survival. In patients with decreased RRF, PD+HD has several advantages. First, PD+HD may achieve PD prolongation with a minimal change in lifestyle (2,3). The combined modality is suitable for those who prefer PD, a home-based continuous therapy. Second, PD+HD may be indicated for patients with hemodynamic instability, because it reduces the frequency of HD sessions (3). Third, PD+HD may prevent excessive use of hypertonic glucose solutions, which accelerate peritoneal membrane deterioration and increase the risk of encapsulating peritoneal sclerosis (3). In addition, the combined modality may permit a “PD holiday” with peritoneal rest, which can improve quality of life and might be beneficial for maintaining peritoneal function (3). The limitations of the present study include a lack of controls, a small number of patients, and a short follow-up period. In addition, the prognosis and longterm safety of PD+HD have yet to be established. Further studies are needed to shed light on these issues. In our patients, PD+HD improved LVH, volume status, and solute removal. Combined therapy with PD+HD might be useful for patients with decreased RRF and might permit the safe prolongation of PD.

Peritoneal Dialysis-Related Peritonitis Caused by Erosion of Umbilical Abscess into the Peritoneal Cavity

access and all-cause mortality: a propensity score analysis. J Am Soc Nephrol 2004; 15:477–86. 3. Brown PA, McCormick BB, Knoll G, Su Y, Doucette S, Fergusson D, et al. Complications and catheter survival with prolonged embedding of peritoneal dialysis catheters. Nephrol Dial Transplant 2008; 23:2299–303. 4. McCormick BB, Brown PA, Knoll G, Yelle JD, Page D, Biyani M, et al. Use of the embedded peritoneal dialysis catheter: experience and results from a North American Center. Kidney Int Suppl 2006; (103):S38–43. 5. Rambausek M, Zeier M, Weinreich T, Ritz E, Rau J, Pomer S. Bowel perforation with unused Tenckhoff catheters. Perit Dial Int 1989; 9:82. 6. Brady HR, Abraham G, Oreopoulos DG, Cardella CJ. Bowel erosion due to dormant peritoneal catheter in immunosuppressed renal transplant recipients. Perit Dial Int 1988; 8:163–5. doi:10.3747/pdi.2011.00016