Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kidney transplant glomerulopathy (TG) has a poor outcome as there are no known effective therapies. Therefore, we investigated whether rituximab therapy (RTx) could halt progression of established TG. Fourteen kidney-transplant patients (nine of whom were men), with median age of 54 (range: 30-74) years, of whom seven had biologic markers for HCV infection, underwent a kidney biopsy (KB) at 118 months post-transplant because of impaired allograft function, associated with albuminuria (95-13430 mg/day), within nephrotic-range albuminuria in seven patients. KBs showed no evidence of acute cellular rejection but showed TG. Donor-specific anti-HLA antibodies were present in six cases. When diagnosis of TG was made, patients were placed on rituximab therapy (RTx) (2-4 injections of 375 mg/m2 week), and other concurrent immunosuppression treatments were not modified. By last follow up post-RTx (30 months), seven (50%) patients had lost their kidney within 6-26 months and the other seven had stable creatinine (182 vs. 161 micromol/l; NS), and albuminuria had decreased from 2660 to 500 mg/day (P = 0.03). There was prolonged B-cell lymphopenia (from 71 to 0/mm3) whereas immunoglobulin G, A, M levels remained stable, and four patients (28.5%) experienced severe infectious complications. We conclude that long-term RTx in kidney-transplant patients with TG is associated with allograft function/stabilization in 50% of cases.
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PMID:Treatment of symptomatic transplant glomerulopathy with rituximab. 1945 96

We describe a case of an adult female who presented with nephrotic syndrome. She was diagnosed with systemic lupus erythematosus with serum antinuclear antibodies, leucopenia with lymphopenia, butterfly erythema, and nephrotic syndrome. Renal biopsy revealed normal glomeruli with diffuse effacement of the foot processes, consistent with lupus podocytopathy. Although human albumin replacement was performed initially, acute renal failure developed rapidly. Therefore, she was treated with double filtration plasmapheresis (DFPP) in addition to oral steroid. After steroid therapy combined with DFPP, the renal function and proteinuria improved rapidly. Although the impact of DFPP on the treatment of lupus nephritis remains to be delineated, our observations suggest that DFPP in lupus podocytopathy played a pivotal role in facilitating the early recovery from renal injuries. Because of the rapid improvement of renal function without any change in body weight by DFPP, acute renal failure in the setting of lupus podocytopathy might contribute to an alternative pathophysiological factor for the diminished glomerular filtration rate, similar to that observed in the setting of idiopathic minimal change glomerulopathy.
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PMID:Accelerated recovery from nephrotic syndrome with acute renal failure by double filtration plasmapheresis in a patient with lupus podocytopathy. 2235 Apr 66

The novel coronavirus (SARS-CoV-2) has turned into a life-threatening pandemic disease (Covid-19). About 5% of patients with Covid-19 have severe symptoms including septic shock, acute respiratory distress syndrome, and the failure of several organs, while most of them have mild symptoms. Frequently, the kidneys are involved through direct or indirect mechanisms. Kidney involvement mainly manifests itself as proteinuria and acute kidney injury (AKI). The SARS-CoV-2-induced kidney damage is expected to be multifactorial; directly it can infect the kidney podocytes and proximal tubular cells and based on an angiotensin-converting enzyme 2 (ACE2) pathway it can lead to acute tubular necrosis, protein leakage in Bowman's capsule, collapsing glomerulopathy and mitochondrial impairment. The SARS-CoV-2-driven dysregulation of the immune responses including cytokine storm, macrophage activation syndrome, and lymphopenia can be other causes of the AKI. Organ interactions, endothelial dysfunction, hypercoagulability, rhabdomyolysis, and sepsis are other potential mechanisms of AKI. Moreover, lower oxygen delivery to kidney may cause an ischaemic injury. Understanding the fundamental molecular pathways and pathophysiology of kidney injury and AKI in Covid-19 is necessary to develop management strategies and design effective therapies.
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PMID:Covid-19 and kidney injury: Pathophysiology and molecular mechanisms. 3302 18