Nephrogenic systemic fibrosis (NSF) is a rare and a debilitating disease noted uncommonly in patients with impaired renal function when exposed to low-stability gadolinium-based contrast agents (Gd-CAs). According to experimental studies, cytokines released by the stimulation of effector cells such as skin macrophages and peripheral blood monocytes activate circulating fibroblasts which play a major role in the development of NSF lesions. The presence of permissive factors, presumably, provides an environment conducive to facilitate the process of fibrosis. Multiple treatment modalities have been tried with variable success rates. More research is necessary to elucidate the underlying pathophysiological mechanisms which could potentially target the initial steps of fibrosis in these patients. This paper attempts to collate the inferences from the in vivo and in vitro experiments to the clinical observations to understand the pathogenesis of NSF. Schematic representations of receptor-mediated molecular pathways of activation of macrophages and fibroblasts by gadolinium and the final pathway to fibrosis are incorporated in the discussion.

Dietary approaches and medical treatment can prevent recurrence of urinary stones. Some interventions are appropriate for all types of stones, but there are particular risk factors that may need directed therapy.

Cardiovascular disease (CVD) is the leading cause of death in renal transplant recipients (RTRs). Clinical inertia (CI) is defined as “recognition of the problem, but failure to act.” The effect of educational interventions in minimizing CI in CVD risk factor management was assessed. Educational sessions were conducted among 201 RTRs to inform them about their goals for blood pressure (BP), low‐density lipoprotein cholesterol (LDL‐C) and glycated hemoglobin (HbA1c). Physicians were reminded about treatment goals using checklists. Pre‐intervention and post‐intervention CI was measured as “no action” or “appropriate action” by the physicians. Post‐intervention percentage of RTRs with “no clinical action” for BP, LDL‐C, and HbA1c control decreased from 10.8% to 3.8% (P=.02), 28.2% to 11.1% (P=.008), and 10.3% to 4.5% (P=.05), respectively, while those with “appropriate action” increased from 66.2% to 83.3% (P<.001), 68.7% to 79.4% (P=.008), and 85.1% to 93.2% (P=.03), respectively. Educational interventions and patient participation were shown to reduce CI.

Background Renin-angiotensin system (RAS) activation increases angiotensin II production which stimulates profibrotic factors especially in the setting of chronic kidney disease. Nephrogenic systemic fibrosis (NSF) is associated with gadolinium (Gd) exposure and renal failure. RAS involvement in NSF is unclear compared to transforming growth factor beta and Smad. RenTag mice were chosen to investigate the role of RAS in NSF-like dermal fibrosis because they demonstrated dermal fibrosis at birth, perturbations of RAS in subcutaneous tissue, and renal failure within 4 weeks of age. Methods Wild-type and RenTag mice were injected weekly with intravenous gadodiamide (3.0mmol/kg body weight) and sacrificed at 12 weeks of age for skin and kidney histology. Results RenTag mice had elevated BUN levels, pitted kidneys, and glomerular damage. RenTag mice skin revealed an increased density of fibroblasts, no mucopolysaccharide deposits, and increased collagen fibril density regardless of Gd exposure. Skin and kidney histopathology of wild-type mice were normal regardless of Gd exposure. CD34 positivity was higher in RenTag compared to wild-type. Conclusions Since RenTag’s dermal lesions remained unchanged after gadolinium exposure in the setting of renal failure this animal model suggests perturbations of subcutaneous RAS may be involved in Gd-naïve dermal fibrosis.