Renal biopsy findings by electron microscopy in nutcracker syndrome complicated with proteinuria did not exhibit podocyte foot process effacement, although the small number of case reports with available electron microscopy reports and the intermittent nature of renal vein compression do not allow us to draw any definite conclusions [16, 17]

Renal biopsy findings by electron microscopy in nutcracker syndrome complicated with proteinuria did not exhibit podocyte foot process effacement, although the small number of case reports with available electron microscopy reports and the intermittent nature of renal vein compression do not allow us to draw any definite conclusions [16, 17]. The exact Chloroprocaine HCl pathogenesis of idiopathic MCD has not been fully elucidated. should Chloroprocaine HCl be considered and explored. 1. Introduction Minimal change disease (MCD) is a disease of the podocyte that manifests with sudden onset nephrotic syndrome. Isolated diffuse effacement of the epithelial foot processes on electron microscopy is the defining feature of MCD. Clinically, it is characterized by the development of massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Although the majority of patients have idiopathic or primary MCD, some may exhibit MCD secondary to another disease process or exposure to drugs. Examining patients with Chloroprocaine HCl secondary MCD allows us to investigate shared mechanisms of pathogenesis [1]. Herein, we report a lupus patient with a renal transplant who developedde novoMCD associated with right external iliac vein stenosis. 2. Case Presentation A 27-year-old Latina woman received a living related transplant from her mother for end stage renal disease (ESRD) secondary to advanced lupus nephritis and presented with nephrotic range proteinuria 6 months after transplantation. The patient was diagnosed with systemic lupus erythematosus (SLE) at age of 17. During the course of the disease she fulfilled the American College of Rheumatology (ACR) criteria including malar rash, arthritis, pericarditis, class IV/V lupus nephritis, leucopenia, lymphopenia, and positive antinuclear (ANA) and anti-double-stranded DNA (anti-dsDNA) antibodies. The patient’s lupus nephritis was treated with glucocorticoids, multiple doses of cyclophosphamide, mycophenolate mofetil, and rituximab. Despite aggressive treatment, she progressed to ESRD and required renal transplantation. She received a PLA2G10 kidney from her mother, which was donor/recipient CMV +/?. The patient has been negative for anti-Ro, anti-La, anti-Sm, anti-RNP, de novoMCD. Her disease occurred 6 months after transplantation and was characterized by unresponsiveness to high-dose glucocorticoids but immediate and sustained remission of proteinuria and renal failure with restoration of normal venous blood flow at the anastomosis. We hypothesize that the mechanical forces generated by the increase in venous blood pressure at the level of the glomerular tuft due to the iliac vein stenosis may have inflicted or predisposed the foot process effacement of the podocytes covering the glomerular basement membrane (GBM) and resulted in the appearance of MCD on renal biopsy and proteinuria. Our hypothesis may be supported by the fact that two doses of pulse methylprednisolone achieved only partial remission and a subsequent course of oral prednisone did not prevent the development of acute renal failure with persistently increased proteinuria and serum creatinine levels. Nevertheless, once the iliac vein stenosis was visualized and repaired, normal renal function was recovered. Podocytes are highly specialized cells of epithelial origin that attach to the GBM through their foot processes. These foot processes interdigitate with one another and the filtration slits that are created between them are covered with an extracellular structure, the slit diaphragm [2]. The latter serves as a size- and charge-selective barrier of macromolecule filtration establishing selective permeability [3], while the foot processes with their contractile system stabilize the GBM and counteract local elastic distension caused by high capillary pressures [4]. Our hypothesis is based on observations suggesting that podocytes may respond to stress caused by increases in intracapillary pressures or exposure to toxins with foot process effacement and rearrangement of their actin cytoskeleton [5C7]. This process has been associated temporally with the emergence of proteinuria [8]. In order to explore the consequences of renal vein stenosis on the kidney and whether it has been previously associated with MCD in other instances, we examined cases of the nutcracker syndrome. This syndrome is characterized by anatomical stenosis of the left renal vein inflicted by its compression between the aorta and proximal superior mesenteric artery. The left renal vein stenosis, which sometimes can be intermittent, causes congestion of the left kidney and leads to the formation of collateral veins. The clinical characteristics of this syndrome include flank pain, hematuria [9C11], and proteinuria [12C15], particularly of orthostatic type, on urine analysis. The onset of proteinuria in this syndrome may demonstrate a similar mechanism of mechanical forces developing at the glomerulus due to renal or iliac vein stenosis in the posttransplant period that can act as a stress signal to the podocytes and cause foot process retraction in order to avoid further damage [6, 7]. Renal biopsy findings by electron microscopy in nutcracker syndrome complicated with Chloroprocaine HCl proteinuria did not exhibit podocyte foot process effacement, although the small number of case reports with available electron microscopy reports and Chloroprocaine HCl the intermittent nature of renal vein compression.