Israel Medical Association Journal

Background: Low serum albumin is known to be associated with mortality in sepsis, as it reflects effects of nutrition, catabolism, and edema.

Objectives: To examine the association of albumin levels with in-hospital mortality in adults with sepsis, stratified by age groups.

Methods: This nationwide retrospective cohort study comprised patients admitted with sepsis to intensive care units in seven tertiary hospitals during 2003–2011. Only patients with available serum albumin levels at hospital admission and one week after were included. Patients with an intra-abdominal source of sepsis were excluded. The association between sepsis and mortality was analyzed using multivariate logistic regression models.

Results: The study included 3967 patients (58.7% male, median age 69 years). Mean serum albumin levels were 3.1 ± 0.7 g/dl at admission and 2.4 ± 0.6 g/dl one week later. In a multivariate logistic regression model, serum albumin one week after admission was inversely associated with in-hospital mortality (odds ratio [OR] 0.64, 95% confidence interval 0.55–0.73 per 1 g/dl). In an age-stratified analysis, the association was stronger with younger age (OR 0.44 for patients aged < 45 years, 0.60 for patients aged 45–65 years, and 0.67 for patients aged > 65 years). Serum albumin on admission was not associated with in-hospital mortality.

Conclusions: The decline in serum albumin one week after admission is a stronger predictor of mortality in younger patients. Older patients might have other reasons for low serum albumin, which reflect chronic co-morbidity rather than acuity of disease.

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. 

 

Fish is a common cause of food allergy. The reactions usually occur after its ingestion. In most immunoglobulin E-mediated reactions, the allergens are gastroresistant and heat-stable proteins of low molecular weight (parvalbumin). On the other hand, isolated contact urticaria following the handling of raw fish but without symptoms after its ingestion was found among cooks and professional fish handlers. In these cases, the fish allergens are gastrosensitive and thermolabile, as demonstrated by the decrease in the diameter of the wheal in the skin-prick test using cooked fish. To the best of our knowledge isolated fish contact urticaria in children has not been previously reported. We analyze the features of three pediatric cases of contact urticaria from cod (one of them was sensitized to parvalbumin), with tolerance after ingestion of this fish on oral food challenge.

Background: Alternatives to cow’s milk and soy milk are often necessary for children with food allergies. Although hydrolyzed and elemental formulas are appropriate replacements, other milk products such as rice and almond milk are insufficient protein sources for children under 2 years of age. A chart review on three patients treated for protein malnutrition in association with multiple diagnosed food allergies that resulted in refractory eczema revealed adverse outcomes that resulted from elimination diets. The use of rice milk resulted in hypoalbuminemia and poor weight gain in all cases, and multiple secondary infections in one patient. These cases illustrate the need for careful nutritional guidance in the management of food allergy, as well as the importance of cautious use and interpretation of testing for food allergies in the absence of a clear clinical history of reaction.

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