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7/27/2019 Abbot, diabetes management
1/1
A-416Trinity University of Asia
Serum Beta 2-Microglobulin and Cystatin C AsEarly Markers for Renal DysfunctionMaria Teresa T. Rodriguez, RMT, MAEd, MSMT1 Geraldine B. Dayrit, RMT, MS Micro, Dip R&DM1
Suzzette V. Lumanga, RMT, MSMT1 Raymundo W. Lo, MD2
Affiliations:1. Trinity University of Asia College of Medical Technology, 275 E. Rodriguez Sr. Blvd., Cathedral Heights, Quezon City, PHILIPPINES;
2. St. Lukes Medical Center Institute of Pathology, 279 E. Rodriguez Sr. Blvd., Cathedral Heights, Quezon City, PHILIPPINES;
BACKGROUND: Nephropathy is one of the major complications of diabetes mellitus and causes premature deaths
among diabetic patients. The alarming rise in the mortality rate of diabetics globally due to this complication is the
foremost concern of this undertaking. This study aimed to determine the serum levels of beta 2-microglobulin and
Cystatin C among diabetics, as early markers of kidney dysfunction. It sought to find if Cystatin C, a low molecular
weight plasma protein which is normally being filtered by the glomeruli, totally reabsorbed and catabolized in the
proximal convoluted tubule of the kidneys, can detect renal insufficiency earlier than blood urea nitrogen and serum
creatinine. Beta 2-microglobulin (b2m), another protein in which plasma level is also being maintained by the
kidneys, was also included in this study. Pearson coefficient correlation was used for statistical analysis.
METHODS: One hundred diabetic participants without renal dysfunction were selected by purposive sampling. A
control group composed of nondiabetics with the same gender and age bracket as the test group was also included.
Fasting blood glucose, blood urea nitrogen (BUN), serum creatinine, b2m and Cystatin C were measured using the
reagents from Abbott Diagnostics and its equipment, the Architect c4000.
RESULTS: Computed r-values of -0.118 (0.224) for fasting glucose and 0.195 (0.052) for urea nitrogen imply that
the two parameters are not significantly related to the level of serum cystatin. However, computed r-value of 0.526
(0.000) for creatinine indicates that when creatinine level increases cystatin also increases, while the 0.766 (0.000)
for b2m shows that there is a great possibility that when b2m is elevated, the cystatin of diabetic patients is also
high. Also, serum levels of cystatin were elevated in 27% of the total diabetic participants, while 19% have increased
beta 2-microglobulin, that is, in the presence of normal blood urea nitrogen and serum creatinine. Moreover, using
Bevc formula (90.63 x cystatin C-1.192), 25% of the diabetic participants have eGFR below 90 mL/min/1.73m2, a
vivid reflection of mild to moderate decrease in renal function.
CONCLUSION: The findings suggest that serum beta 2-microglobulin and cystatin C are early markers for kidney
dysfunction in cases of incipient diabetic nephropathy, as seen in increased levels of these serum proteins, withnormal levels of the routine kidney markers BUN and creatinine. Further, the results also imply that the inclusion of
new B (beta 2-microglobulin) and C (cystatin C) kidney function tests which could identify mild renal insufficiency
would surely become a cornerstone of diabetes care.