Israel Medical Association Journal

Background: Tunneled hemodialysis catheters are frequently used and are a major source of catheter-related bloodstream infections (CRBSI), which result in significant morbidity.

Objectives: To examine the adverse outcomes associated with CRBSIs, including hospitalization, recurrence, 1-year mortality, and catheter outcomes in a hemodialysis setting that uses modern preventive catheter-care practices.

Methods: We conducted a retrospective cohort study of adults with jugular tunneled hemodialysis catheters who met criteria for CRBSI from 1 January 2015 to 31 December 2020 at a tertiary referral center.

Results: Of 380 hemodialysis patients, 75 experienced CRBSI events. The average rate was 1.55 CRBSIs per 100 patient months. The median time from catheter insertion to CRBSI was 179 days; and 68% required inpatient management. Gram-positive bacteria accounted for 53% of isolates, with Gram-negative organisms also being common. Recurrence occurred in 16% of cases and was independently associated with ferritin levels over 500 ng/ml (P = 0.02), albumin levels below 3.5 g/dl (P = 0.011), and uric acid levels under 2.5 mg/dl (P = 0.04). Catheters were removed in 61.3%, exchanged over a guidewire in 24%, and salvaged in 18.6%. The 1-year mortality rate was 28% and was associated with lower weight, catheter salvage, neutrophilia, hypoalbuminemia, and hypokalemia. Using chlorhexidine exit-site dressings was associated with fewer hospital admissions.

Conclusions: Among hemodialysis patients with CRBSI, recurrence and mortality might be linked to a patient's nutritional and inflammatory status. Current preventive measures might reduce hospitalization rates, but in this cohort, they were not associated with lower recurrence or mortality rate.

Background: Proteinuria and albuminuria are markers of kidney injury and function, serving as a screening test as well as a means of assessing the degree of kidney injury and risk for cardiovascular disease and death in both the diabetic and the non-diabetic general population.

Objectives: To evaluate the association between proteinuria below 300 mg/24 hours and albuminuria, as well as a possible association with kidney function in patients with diabetes mellitus (DM).

Methods: The medical files of patients with type 1 and type 2 DM with proteinuria below 300 mg/24 hours at three different visits to the Diabetic Nephropathy Clinic were screened. This involved 245 patient files and 723 visits. The data collected included demographics; protein, albumin and creatinine levels in urine collections; blood biochemistry; and clinical and treatment data. 

Results: The association between proteinuria and albuminuria is non-linear. However, proteinuria in the range of 162–300 mg/24 hours was found to be linearly and significantly correlated to albuminuria (P < 0.001, r = 0.58). Proteinuria cutoff, based on albuminuria cutoff of 30 mg/24 hours, was found to be 160.5 mg/24 hr. Body mass index (BMI) was the sole independent predictor of proteinuria above 160.5 mg/24 hr. Changes in albuminuria, but not proteinuria, were associated with changes in creatinine clearance. 

Conclusions: A new cutoff value of 160.5 mg/hr was set empirically, for the first time, for abnormal proteinuria in diabetic patients. It appears that proteinuria below 300 mg/24 hr is not sufficient as a sole prognostic factor for kidney failure. 

 

Background: Decreased heparan sulfate proteoglycan content of the glomerular basement membrane has been described in proteinuric patients with diabetic nephropathy. Heparanase is an endo-b-D-glucuronidase that cleaves negatively charged heparan sulfate side chains in the basement membrane and extracellular matrix.

Objectives: To investigate whether urine from type I diabetic patients differs in heparanase activity from control subjects and whether resident glomerular cells could be the source of urinary heparanase.

Methods: Using soluble ³⁵S-HSPG[1] and sulfate-labeled extracellular matrix we assessed heparanase activity in human glomerular epithelial cells, rat mesangial cells, and urine from 73 type I diabetic patients. Heparanase activity resulted in the conversion of a high molecular weight sulfate-labeled HSPG into heparan sulfate degradation fragments as determined by gel filtration analysis.

Results: High heparanase activity was found in lysates of both epithelial and mesangial cells. Immunohistochemical staining localized the heparanase protein to both glomeruli capillaries and tubular epithelium. Heparanase activity was detected in the urine of 16% and 25% of the normoalbuminuric and microalbuminuric diabetic patients, respectively. Urine from 40 healthy individuals did not posses detectable heparanase. Urinary heparanase activity was associated with worse glycemic control.

Conclusion: We suggest that heparanase enzyme participates in the turnover of glomerular HSPG. Hyperglycemia enhances heparanase activity and/or secretion in some diabetic patients, resulting in the loss of albumin permselective properties of the GBM[2].

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[1] HSPG = heparan sulfate proteoglycan

[2] GBM = glomerular basement membrane