Abstract: TH-PO089

Body Composition Parameters Do Not Contribute to Glomerular Hypertrophy

Session Information

Category: Glomerular

  • 1004 Clinical/Diagnostic Renal Pathology and Lab Medicine

Authors

  • Aoki, Satoshi, Japanese Red Cross Ishinomaki Hospital, Miyagi, Japan
  • Nagasawa, Tasuku, Japanese Red Cross Ishinomaki Hospital, Miyagi, Japan
Background

Glomerular hypertrophy is often observed in diabetic nephropathy and obesity-related glomerulopathy. A correlation between body-mass indices (BMI) and glomerulomegaly has been reported. However, specific contributing factors remain unknown. The aim of this study is to investigate relations between glomerular hypertrophy and clinical parameters.

Methods

We measured glomerular major axis length (GMAL) of 157 patients who underwent percutaneous renal biopsy from July 2013 to July 2015 in Japanese Red Cross Ishinomaki Hospital. Body composition parameters, subcutaneous fat area (cm2), visceral fat area (cm2), psoas major area (mm2/m2), and muscles of back proper area (mm2/m2) were calculated based on CT images. We performed a multiple regression analysis with GMAL as the dependent variable.

Results

157 cases were separated into 4 groups depending on the primary diseases: diabetic nephropathy (DN, n = 25), focal segmental glomerular sclerosis (FSGS, n = 20), hypertensive nephrosclerosis (HNS, n = 36) and the others (n = 76). Hypertrophic glomeruli (GMAL ≥ 250 μm) were observed in 76% of DN, 75% of FSGS, 66.7% of HNS and 56.6% of the others. The average GMAL was significantly greater in DN and FSGS. BMI, body weight, subcutaneous fat area, visceral fat area, psoas major area, and muscles of back proper area were not correlated with GMAL. As for blood and urine parameters, only eGFR had an inverse correlation (β = -0.657, p < 0.01). Glomerular density, the number of glomeruli that did not present global sclerosis per renal cortical area (/m2) was not interrelated to BMI.

Conclusion

eGFR was the significant contributor to enlargement of GMAL. Glomerular hypertrophy may arise as a result of compensatory mechanism to eGFR decline.