Activation of the alternative complement pathway occurs in obese T2DM patients and is enhanced in the post-prandial hyperchylomicronic condition, which induces overproduction of ASP and C3a-mediated tissue inflammation. Therefore, complement-mediated inflammation may contribute to the acceleration of diabetic microangiopathy in addition to the development of macroangiopathy.

A 23 year-old male was investigated for hypertension, moderate renal insufficiency, persistent proteinuria and bilateral small kidneys. The renal pathological features were diagnostic with greatly enlarged glomeruli (the mean diameter was 325 μm, which was approximately two times larger than normal glomeruli), indicating oligomeganephronia (OMN). He also showed malrotated kidneys, expanded extrarenal pelvis, and hearing loss. Thus, these clinical and pathological features aided in diagnosing the renal disorder as OMN. This is a very rare case of OMN, which did not advance to end-stage renal failure as an adult. We believe that multiple anomalies might be suggestive findings of OMN in patients, such as renal insufficiency, persistent proteinuria, and bilateral small kidneys.

Our results indicate that CsA does not accelerate GC-induced osteoporosis in patients with nephrotic syndrome. We conclude that CsA is appropriate for the treatment of GC-dependent nephrotic syndrome, because it does not adversely affect bone metabolism and has favorable glomerular effects.

A 17-year-old man presented with a decreased renal function (creatinine clearance 66.0 ml/min/1.73 m 2 ) and proteinuria (1.25 g/24 hrs). He was born weighing 1,065 g 26 weeks of pregnancy. He was mildly overweight (BMI 26.9 kg/m 2 ) due to an increased weight gain (10 kg) over the past year. Renal biopsy showed perihilar sclerosing lesions in three of eleven glomeruli, low glomerular density, enlarged glomeruli, and limited fusions of foot processes, thus indicating secondary focal segmental glomerulosclerosis (FSGS). We speculated that the patient's overweight status may have caused a worsening of glomerular hyperfiltration due to the fewer number of nephrons leading to the development of secondary FSGS.

Insulin resistance is a major player in the pathogenesis of type 2 diabetes. C3 converts to C3a and acylation stimulating protein (ASP) by complement activation. ASP activates adipose tissue macrophages and accelerates continuous inflammation. Tissuebound C3a is known to induce insulin resistance. We examined the relationship between insulin resistance and complement activation by the in vivo alteration of ASP. The levels of ASP and parameters of insulin resistance and inflammation were measured in plasma from 25 patients with type 2 diabetes. A selective peroxisome proliferator-activated receptor gamma (PPAR) agonist was administered to these 25 patients for three months, and then ASP and the parameters were measured again. The alterations of ASP and the parameters were examined in the pathophysiological state. Plasma levels of ASP and complement activation products were significantly higher in diabetes. Parameters of insulin resistance were also significantly increased. The ASP level significantly improved after PPAR agonist administration. The improvement in ASP level correlated with improvements in parameters of insulin resistance and inflammation. The levels of other relevant adipocytokines by insulin resistance correlated with the degree of inflammation. ASP and complement activation were associated with insulin resistance and chronic inflammation in diabetes.