OBJECTIVEThe aim of this study was to evaluate the association of urinary cystatin C, a tubular damage marker, with the progression of type 2 diabetic nephropathy.RESERCH DESIGN AND METHODSThe baseline values of serum and urinary cystatin C were measured as primary parameters and those of urinary nonalbumin protein (NAP) were measured as secondary parameters. In this prospective observational study, a total of 237 type 2 diabetic patients were followed up for 29 months (13–44 months).RESULTSBoth the urinary cystatin C-to-creatinine ratio (CCR) and NAP-to-creatinine ratio (NAPCR) were significantly different according to the degree of albuminuria. Both markers had strongly positive correlations at baseline. After adjusting for several clinical factors, both urinary CCR and NAPCR had significant associations with the decline of the estimated glomerular filtration rate (eGFR) (r = 0.160, P = 0.021; r = 0.412, P < 0.001, respectively). Urinary CCR had positive correlations with the decline of eGFR in the subpopulation of patients with eGFR ≥60 mL/min/1.73 m2. In patients with eGFR ≥60 mL/min/1.73 m2 and normoalbuminuria, only urinary NAPCR showed a significant association with the decline of eGFR; urinary CCR did not. In multivariate regression analysis, the number of patients who progressed to chronic kidney disease stage 3 or greater was higher in those in the upper tertiles of both the urinary levels of cystatin C and NAP than in those in the lower tertiles.CONCLUSIONSThe results of this study suggest that urinary cystatin C and NAP may be predictors of the progression of type 2 diabetic nephropathy.
This study showed that low T3 syndrome was highly prevalent in CKD and was a remarkable finding in early CKD. Furthermore, serum T3 levels were associated with severity of CKD even in the normal TSH level.
Background/Aims: The aim of this study was to examine the recent clinical trends and antibiotic susceptibilities of the causative microorganisms in renal and perirenal abscesses, and to elucidate the factors associated with treatment strategies.Methods: We retrospectively analyzed 56 patients who were diagnosed with renal and perirenal abscesses at our hospital from January 2000 to September 2007.Results: The mean age of the patients was 53.5 years, and a female predominance of patients (75%) was observed. Diabetes mellitus (44.6%) was the most common predisposing condition. The mean duration of symptoms before diagnosis was 11.6 days, and fever (75%) was the most common symptom. Escherichia coli (44%) and Klebsiella pneumoniae (28%) were common pathogens, and the rates of susceptibility of E. coli isolates to ampicillin, cephalothin, cefotaxime, trimethoprim-sulfamethoxazole, ciprofloxacin, gentamicin, and imipenem were 18.2%, 27.3%, 72.7%, 72.7%, 63.6%, 63.6%, and 100%, respectively. Abscesses were classified according to the location as follows: renal abscess (n=31, 55.4%) and perirenal abscess±renal abscess (n=25, 44.6%). In the renal abscess group, the infection rate of gram-negative organisms was higher than in the perirenal abscess group. Patients were also divided according to the treatment modality: antibiotics only (n=20, 35.7%) and percutaneous intervention or surgery (n=36, 64.3%). Patients who had a perirenal abscess or a large renal abscess required more invasive treatment.Conclusions: This study revealed somewhat different results from those of previous studies. Clinical and microbial differences were observed between the renal and perirenal abscess groups. Abscess location and the size of the renal abscess were the factors associated with treatment strategies.
Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.