OBJECTIVE:Colistin is a cationic polypeptide antibiotic with a cyclic structure that belongs to the polymyxin group. It was banned from clinical use because of its significant renal side effects, such as nephrotoxicity. However, the administration of colistin has recently been initiated again in the treatment of multi-drug resistant pathogens, such as Acinetobacter baumannii and Pseudomonas aeruginosa. Nephrotoxicity and neurotoxicity are the main problems encountered in the clinical use of polymyxins. The aim of this study was to determine the frequency and risk factors of colistin-related nephrotoxicity in the adult intensive care unit (ICU).METHODS:In this study, a retrospective review of patients who were followed up between January 1 and December 31, 2016 and who received colistin treatment in the adult ICU was performed. Retrospective computer records of age, sex, site of infection and microorganism breeding, daily creatinine values, and additional diseases were recorded and examined. Nephrotoxicity was assessed using the Risk, Injury, Failure, Loss, and End-stage kidney disease criteria.RESULTS:A total of 48 patients were included in the study. Of these, 50% were male. The mean age of the patients with nephrotoxicity was 59.73±22.38 years, and the mean age of those without nephrotoxicity was 58.00±22.39 years. A. baumanni was observed to be the causative microorganism in all patients, and the most frequent infection was pneumonia. Nephrotoxicity was investigated in 54.2% (n=26) of the patients. In this study, when risk factors for nephrotoxicity were evaluated, it was found that the presence of nephrotoxicity was greater in cases with chronic obstructive pulmonary disease, malignancy, or abdominal surgery in patients older than 65 years. In addition, mortality was greater in those who developed nephrotoxicity, although it was not statistically significant.CONCLUSION:In this study, the rate of nephrotoxicity was 54.2% in patients who received colistin in the ICU. Therefore, patients in the adult ICU receiving colistin therapy should be carefully monitored for the development of nephrotoxicity as a side effect.

Increased activity of urinary N-acetyl-beta-D-glucosaminidase (NAG) can be used as an early indicator of damage to the tubular epithelium. Systemic lupus erythematosus (SLE) is a multisystem autoimmune rheumatic disease. Nephritis is known as the most serious complication of SLE and the strongest predictor of poor outcome. In this study urinary NAG excretion was investigated in 24 SLE patients with normal renal function (serum creatinine < or =1.2 mg/dL) and the results were compared with those from 26 untreated patients with rheumatoid arthritis (RA) and 27 healthy controls. The SLE patients were divided into two groups according to their urinary total protein levels: group A consisted of 16 patients with < or =3.5 g/day proteinuria, and group B consisted of eight patients with nephrotic-range proteinuria (>3.5 g/day). Serum and urinary creatinine, total urinary protein levels, and urinary NAG excretion were measured in patients with SLE and RA. In addition, serum C3 and C4 levels were determined in the SLE patients. Renal biopsies were performed in all of the SLE patients. Glomerular lesions were classified according to WHO criteria for lupus nephritis (LN) I-V. The Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) was used to assess disease activity. Urinary NAG excretion was significantly higher in the SLE groups than in the healthy controls (P<0.001). In urinary NAG excretion there was also significant difference between SLE groups and RA patients (P<0.001). However, there was no significant difference in NAG excretion between the RA and control groups (P=0.062). Urinary NAG excretion was significantly higher (P<0.05) in group B compared to group A. There were no differences in SLEDAI scores, ages, and serum creatinine levels between study groups (P=0.601, P=0.285, P=0.669, respectively). Elevated SLEDAI values and hypocomplementemia were detected more often in younger patients (P<0.010, r=-0.529 and P<0.010, r=-0.569, respectively). There was a strong positive correlation between proteinuria and urinary NAG activity (P<0.001, r=0.759). These results suggest that the determination of urinary NAG activity may be a useful supplement to the routine biochemical analysis performed on the urine in cases of SLE.

BACKGROUND:The aim of the present study was to evaluate the effectiveness of the Simplified Acute Physiology Score (SAPS) III and the Acute Physiology and Chronic Health Evaluation (APACHE) IV in the prediction of in-hospital mortality in surviving multitrauma patients. METHODS:This study was conducted in the 13-bed intensive care unit (ICU) of a tertiary hospital. A retrospective review of multitrauma patients whose care was managed in the ICU was performed. Data collection included details of age, gender, ICU admission, and outcome. APACHE IV and SAPS III scores, as well as the predicted mortality rate (PMR), were calculated using web-based calculators. RESULTS:Of the 90 patients 20% (n=18) were female and 80% (n=72) were male. The overall mortality rate was 25.6%. The mean APACHE IV, Acute Physiology Score (APS) and SAPS III score was 69.27±34.51, 66.42±33.72, and 26.36±27.14, respectively. The mean PMR according to the APACHE IV and the SAPS III was 26.36±27.14 and 17.07±24.88, respectively. The area under the curve result of receiver operating characteristic curve analysis was 0.87 for the APACHE IV and 0.93 for the SAPS III. CONCLUSION:The performance of the SAPS III was more sensitive and discriminative than the APACHE IV scoring system for multi-trauma ICU patients.

Urinary glycosaminoglycans (GAG) and heparan sulfate (HS) are considered to be markers of early renal involvement. This study was undertaken to demonstrate their excretion patterns in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) with and without arthritis. Serum creatinine and urinary GAG, HS, microalbumin, and creatinine measurements were made in 51 biopsy-proven lupus nephritis (LN) cases, 12 RA patients, and 21 healthy controls. Urinary GAG and HS levels were higher in the LN and RA groups than in controls. Heparan sulfate excretions and SLE disease activity index (SLEDAI) scores were no different between SLE patients with classes 1 and 2 (group A) and those with classes 3, 4, and 5 (group B) renal involvement. However, GAG and microalbumin excretions were significantly high in the latter. There were no differences in GAG and HS excretions between normoalbuminuric, microalbuminuric, and macroproteinuric SLE patients or between those with and without arthritis. In conclusion, urinary GAG and HS, being unrelated to the presence of arthritis, are independent markers of LN. Extrarenal causes or subclinical renal involvement may be responsible in RA due to their increased excretion in these patients.