Acute tubulointerstitial nephritis associated with infliximab therapy in a patient with Crohn's disease: a case report.

We report the case of a 39-year-old man who presented with a history of generalized fatigue, nausea, subjective fever with rigors, and renal dysfunction after receiving infliximab (IFX) therapy for Crohn's disease. A renal biopsy revealed acute tubulointerstitial nephritis (ATIN). After other causes of acute kidney injury were excluded, steroid therapy was initiated, his fever subsided, and kidney function improved.

Prevalence and 20-year epidemiological trends of glomerular diseases in the adult Saudi population: a multicenter study.

Background: Recent international reports have shown significant changes in the incidence of different glomerular diseases.

Objective: Examine temporal and demographic trends of biopsy-diagnosed glomerular diseases in the adult population of Saudi Arabia over the last two decades.

Design: Medical record review.

Rituximab as a rescue therapy in patients with glomerulonephritis.

To evaluate the use of rituximab in the treatment of severe glomerulonephritis (GN) in order to prevent progression of kidney disease toward the end stage, we designed a multicenter, retrospective study in Saudi Arabia about the efficacy and safety of the use of "off label" rituximab in a variety of severe refractory GN to conventional treatment and the progression of kidney disease for at least one year of follow-up. All the patients had kidney biopsies before treatment with rituximab, and proteinuria and glomerular filtration rate (GFR) were followed-up for the period of the study. The immediate side-effect at the time of administration of rituximab included itching in three patients, hypotension in one patient and anaphylaxis in one patient (dropped out from the study).

Mitochondrial reactive oxygen species generation triggers inflammatory response and tissue injury associated with hepatic ischemia-reperfusion: therapeutic potential of mitochondrially targeted antioxidants.

Mitochondrial reactive oxygen species generation has been implicated in the pathophysiology of ischemia-reperfusion (I/R) injury; however, its exact role and its spatial-temporal relationship with inflammation are elusive. Herein we explore the spatial-temporal relationship of oxidative/nitrative stress and inflammatory response during the course of hepatic I/R and the possible therapeutic potential of mitochondrial-targeted antioxidants, using a mouse model of segmental hepatic ischemia-reperfusion injury. Hepatic I/R was characterized by early (at 2 h of reperfusion) mitochondrial injury, decreased complex I activity, increased oxidant generation in the liver or liver mitochondria, and profound hepatocellular injury/dysfunction with acute proinflammatory response (TNF-α, MIP-1α/CCL3, MIP-2/CXCL2) without inflammatory cell infiltration, followed by marked neutrophil infiltration and a more pronounced secondary wave of oxidative/nitrative stress in the liver (starting from 6 h of reperfusion and peaking at 24 h).