Steroid resistant nephrotic syndrome causes

Noureddin Nourbakhsh, Robert H Mak

Division of Pediatric Nephrology, Rady Children’s Hospital San Diego, University of California, San Diego, La Jolla, CA, USA

Abstract: Patients with steroid-resistant nephrotic syndrome (SRNS) represent a challenging subset of patients with nephrotic syndrome who often fail standard immunosuppression and have a higher likelihood of progressing to end-stage renal disease. Appropriate treatment of SRNS requires an adequate understanding of the historical treatment, renal histopathology, and genetics associated with the disease. The aim of this review is to present a comprehensive appraisal of the history, role of renal biopsy, genetics, and treatment of SRNS.

Keywords: steroid-resistant nephrotic syndrome, focal segmental glomerulosclerosis

During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.

In addition to well studied epigenetic promoter methylation, more recently there have been substantial findings of epigenetic alterations in cancer due to changes in histone and chromatin architecture and alterations in the expression of microRNAs (microRNAs either cause degradation of messenger RNAs or block their translation ) [56] For instance, hypomethylation of the promoter for microRNA miR-155 increases expression of miR-155, and this increased miR-155 targets DNA repair genes MLH1, MSH2 and MSH6, causing each of them to have reduced expression. [57]

The obvious priority is immediate discontinuation of any further topical corticosteroid use. Protection and support of the impaired skin barrier is another priority. Eliminating harsh skin regimens or products will be necessary to minimize potential for further purpura or trauma, skin sensitivity, and potential infection. Steroid Atrophy [10] [11] is often permanent, though if caught soon enough and the topical corticosteroid discontinued in time, the degree of damage may be arrested or slightly improve. However, while the accompanying Telangectasias may improve marginally, the Striae is permanent and irreversible. [1]

Steroid resistant nephrotic syndrome causes

steroid resistant nephrotic syndrome causes

The obvious priority is immediate discontinuation of any further topical corticosteroid use. Protection and support of the impaired skin barrier is another priority. Eliminating harsh skin regimens or products will be necessary to minimize potential for further purpura or trauma, skin sensitivity, and potential infection. Steroid Atrophy [10] [11] is often permanent, though if caught soon enough and the topical corticosteroid discontinued in time, the degree of damage may be arrested or slightly improve. However, while the accompanying Telangectasias may improve marginally, the Striae is permanent and irreversible. [1]

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