“…Settings in Which PRES May Be Likely to Develop
- Autoimmune disorders: Systemic Lupus Erythematous, antiphospholipid syndrome, polyarteritis nodosa, cryoglobulinemia, thrombotic thrombocytopenic purpura, scleroderma, polyangiitis, antiglomerular basement membrane antibody disease, rheumatoid arthritis, Sjögren syndrome, Crohn's disease, ulcerative colitis, autoimmune hepatitis, type 1 diabetes mellitus, Grave's disease, Hashimoto thyroiditis, and neuromyelitis optica [2, 16–20]
- Essential hypertension
- Preeclampsia and eclampsia [21, 22]
- Acute or chronic renal failure and dialysis (55%)[23–27]
- Septicemia and severe infections (predominantly gram positive organisms) [4, 28]
- Immunosuppressive therapy (despite normal levels): cisplatin, cyclosporine, tacrolimus, intravenous globulin, rituximab, methotrexate, bevacizumab, sunitinib, and sorafenib [15, 29–33]
- Others: blood transfusion, contrast exposure, hypercalcemia, cocaine, and methamphetamine
The incidence has been variably reported, with a study from Ireland showing an occurrence of 0.84% [34]. Patients with CKD and end stage renal disease (ESRD) have the perfect setup for the development of PRES such as a higher MAP, volume overload, electrolyte abnormalities, and underlying chronic vascular disease.…”