Relapsing Tubulointerstitial Nephritis with Antimitochondrial M2 Antibody Accompanied by Pulmonary Involvement.

We herein report a 50-year-old woman who suffered from tubulointerstitial nephritis with antimitochondrial M2 antibody, distal renal tubular acidosis, and Fanconi syndrome. Our case also had interstitial pneumonia. After initially successful glucocorticoid therapy, tubulointerstitial nephritis and interstitial pneumonia relapsed.

Prediction of Acute Glomerular Filtration Rate Reductions Following Renin-angiotensin System Blockade in Chronic Kidney Disease: A Possible Application of Ultrasonography in Clinical Practice.

Objective Renal arteriolosclerosis is a risk factor for acute reductions in the glomerular filtration rate (GFR) when renin-angiotensin system (RAS) inhibitors are administered. Renal arteriolosclerosis can be detected by an increase in the resistive index (RI) on Doppler ultrasonography. The purpose of the present study is to determine whether or not the RI can predict acute GFR reductions following RAS blockade in chronic kidney disease (CKD).

Chronological renal resistive index increases related to atherosclerotic factors, and effect of renin-angiotensin system inhibitors.

Background: Renal resistive index (RI) calculated using renal Doppler ultrasonography (RDU) has recently been considered a clinically important indicator of renal outcome, survival, and systemic arteriosclerotic disorders. However, the cause of RI elevation remains unclear. The present study was an effort to first, identify the factors related to RI elevation, and second, understand the effect of renin-angiotensin system inhibitors (RAS-Is) on renal RI elevation.

Nephrotic Syndrome with Thrombocytopenia, Lymphadenopathy, Systemic Inflammation, and Splenomegaly.

Nephrotic syndrome can be caused by various diseases, from primary kidney diseases to systemic diseases. A kidney biopsy is useful for confirming the causes of nephrotic syndrome and in its management. We herein describe a case of nephrotic syndrome with thrombocytopenia, lymphadenopathy, systemic inflammation, splenomegaly, kidney enlargement, and progressive renal insufficiency.

Delayed progression of edema formation around a hematoma expressing high levels of VEGF and mmp-9 in a patient with traumatic brain injury: case report.

The mechanisms accounting for the development of tissue damage following traumatic brain injury (TBI) have been studied for several decades. A variety of mediators, such as vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9), which play a crucial role in edema formation after TBI, have been identified. We experienced a case of brain edema that progressed continuously at least until 13 days after head injury.