The role of host factors and bacterial virulence genes in the development of pyelonephritis caused by Escherichia coli in renal transplant recipients.

BACKGROUND AND OBJECTIVES: The aim of this study was to determine the role of host factors and bacterial virulence genes in the development of pyelonephritis caused by Escherichia coli in renal transplant (Tx) recipients. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: A total of 328 E. coli isolates from cases of cystitis (Cys; n=239) or pyelonephritis (PN; n=89), with 169 from renal Tx recipients, were subjected to molecular analyses to identify P-fimbria subunits (PapC, PapG II, and PapGIII), G- and M-fimbriae, and aerobactin. The presence of antibiotic resistance was also determined. Parameters such as gender, age, immunosuppression regimens, causes of ESRD, kidney donor, intraoperative anastomosis, use of double J stent, trimethoprim/sulfamethoxazole (TMP/SMZ) prophylaxis, and time after Tx were evaluated. RESULTS: A multivariate analysis showed a significant association between PN and renal Tx. In renal Tx recipients, the risk of occurrence of PN was significantly higher among males and for those no longer receiving TMP/SMZ prophylaxis. E. coli strains isolated from PN presented a lower prevalence of papGIII and lower rates of resistance to pipemidic acid. Although papGII was more prevalent in PN than in Cys, it was not independently associated with PN. CONCLUSIONS: These findings suggested that renal Tx increases the risk for PN, and the male sex represented a host factor independently associated with risk, whereas the prophylaxis with TMP/SMZ was protective. The lack of papGIII and low resistance to first-generation quinolones were bacterial-independent risk factors for PN in Tx.

Effects of Lactobacillus casei and Bifidobacterium breve on urinary oxalate excretion in nephrolithiasis patients.

It had been suggested that lactic acid bacteria (LAB) may degrade oxalate in the intestinal lumen, reducing urinary oxalate excretion. We aimed to evaluate the effect of a LAB mixture containing Lactobacillus casei (LC) and Bifidobacterium breve (BB) (LC + BB) upon urinary oxalate reduction in stone-forming (SF) patients without hyperoxaluria under conditions of an oxalate-rich diet. After an oxalate restriction period (7 days washout), 14 SF patients consumed an oxalate-rich diet during 4 weeks (200 mg/day) and a lyophilized LC + BB preparation was given t.i.d. after meals during the last 2 weeks. Twenty-four-hour urine samples were collected for determination of oxalate, calcium, magnesium, citrate, sodium, potassium and creatinine at baseline, after 2 weeks (DIET) and 4 weeks (DIET + LC + BB). The mean urinary oxalate excretion was significantly higher after DIET versus baseline (27 +/- 8 vs. 35 +/- 11 mg/24 h), but the mean decrease was not significant between DIET + LC + BB and DIET periods (35 +/- 11 vs. 33 +/- 10 mg/24 h). Seven out of 14 patients presented a reduction in oxaluria after LC + BB versus DIET, being the reduction higher than 25% in 4, and up to 50% in 2 of them. The latter two patients were those who had presented the greatest increase in oxaluria in response to dietary oxalate. In conclusion, this mixture of L. casei and B. breve was shown to possess a variable lowering effect upon urinary oxalate excretion that may be dependent on dietary oxalate intake.

Preservation of urine samples for metabolic evaluation of stone-forming patients.

Metabolic evaluation of stone-forming (SF) patients is based on the determination of calcium, oxalate, citrate, uric acid and other parameters in 24-h urine samples under a random diet. A reliable measurement of urinary oxalate requires the collection of urine in a receptacle containing acid preservative. However, urinary uric acid cannot be determined in the same sample under this condition. Therefore, we tested the hypothesis that the addition of preservatives (acid or alkali) after urine collection would not modify the results of those lithogenic parameters. Thirty-four healthy subjects (HS) were submitted to two non-consecutive collections of 24-h urine. The first sample was collected in a receptacle containing hydrochloric acid (HCl 6 N) and the second in a dry plastic container, with HCl being added as soon as the urine sample was received at the laboratory. Additionally, 34 HS and 34 SF patients collected a spot urine sample that was divided into four aliquots, one containing HCl, another containing sodium bicarbonate (NaHCO(3 )5 g/l), and two others in which these two preservative agents were added 24 h later. Urinary oxalate, calcium, magnesium, citrate, creatinine and uric acid were determined. Urinary parameters were also evaluated in the presence of calcium oxalate or uric acid crystals. Mean values of all urinary parameters obtained from previously acidified 24-h urine samples did not differ from those where acid was added after urine collection. The same was true for spot urine samples, with the exception of urinary citrate that presented a slight albeit significant change of 5.9% between samples in HS and 3.1% in SF. Uric acid was also not different between pre- and post-alkalinized spot urine samples. The presence of crystals did not alter these results. We concluded that post-delivery acidification or alkalinization of urine samples does not modify the measured levels of urinary oxalate, calcium, magnesium, creatinine and uric acid, and that the change on citrate was not relevant, hence allowing all parameters to be determined in a single urine sample, thus avoiding the inconvenience and cost of multiple 24-h urine sample collections.