OB-FSG indicates a poor prognosis with almost one-half of patients developing advanced renal failure. Knowledge of the clinico-pathological features of this entity (obesity, FSG lesions with glomerulomegaly, absence of nephrotic syndrome despite nephrotic-range proteinuria) should be helpful in establishing an accurate and early diagnosis.

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We have identified 17 obese patients (body mass index, BMI, 37.9 ± 4.1)with proteinuria > 1 g/day (1.3-6.4 g/24 h, mean 3.1 ± 1.7). Their age was 34-70 years (48.3 ± 10); 11 were females and 6 males. Six patients had only one functioning kidney and a sleep apnea syndrome had been diagnosed in 5. Renal biopsies, obtained in 5 cases, showed focal glomerulosclerosis in 2 cases, minimal changes in 2 and mesangial proliferation in 1. Nine patients (group 1) were treated with hypocaloric diets; body weight significantly decreased (BMI 37.1 ± 3, 34 ± 3.5 and 32.6 ± 3.2 at 0, 6 and 12 months, respectively) as well as proteinuria (2.9 ± 1.7, 1.2 ± 1 and 0.4 ± 0.6 g/24 h). There was a significant correlation between body weight loss and decrease in proteinuria (r = 0.69, p < 0.05). Eight patients (group 2) were treated with captopril, without dietary changes. BMI remained stable but proteinuria showed a dramatic decrease, similar to that in group 1 (3.4 ± 1.7, 1.2 ± 0.9 and 0.7 ± 1 g/24 h, respectively). Renal function remained stable in both groups. In summary, both body weight loss and captopril treatment can induce a sharp decrease in obesity-related proteinuria.

H pylori-infected pediatric patients from Chile show high prevalence of the mutation responsible for clarithromycin resistance. The failure to eradicate H pylori can be attributed to the presence of the A2143G mutation.

The administration of voriconazole by the intravenous (i.v.) route in patients with moderate or severe renal failure is limited because of potential toxic effects of the accumulation of the solvent vehicle sulphobutylether beta cyclodextrin sodium. This study aimed to assess the impact of intravenous voriconazole administration on renal and liver function in critically ill patients with impaired renal function treated with this antifungal drug. The study population consisted of a retrospective cohort of patients admitted to medical-surgical intensive care units (ICUs) who were treated with i.v. voriconazole for more than 3 days. Patients with impaired renal function were those with serum creatinine concentration >1.5 mg/dL, creatinine clearance <50 mL/min, or under any extrarenal depuration procedure. Renal damage was defined as an increase of at least = 2 times initial serum creatinine level or starting of an extrarenal depuration procedure during voriconazole therapy. Liver damage was defined as an increase of = 4 times the initial serum concentration of liver enzymes, or = 2 times in patients with previous impaired liver function. A total of 69 patients was included in the study of which 26 (37.7%) had impaired renal function at the beginning of voriconazole treatment (serum creatinine >2.5 mg/dL in 10 patients). Mean (SD) duration of voriconazole treatment was 13.0 (9.5) days in patients with normal renal function and 11.2 (6.3) days in those with altered renal function. Renal damage during voriconazole therapy occurred in 13 (30.2%) patients with initial normal renal function and in 4 (15.4%) in patients with impaired renal function (P = 0.257). Liver damage during treatment with voriconazole was observed in 12 (27.9%) patients with normal initial renal function and in 3 (11.5%) patients with impaired renal function (P = 0.281). Renal failure developing during voriconazole treatment was associated with a significantly higher mortality rate (82.4% vs. 44.%, P = 0.01), except in the subgroup of patients with altered renal function before starting i.v. voriconazole (60% size=1>vs. 75%, P = 0.385). The use of i.v. voriconazole in ICU patients with pretreatment impaired renal function was not associated with renal or liver damage nor with an increase in ICU mortality.