Effect of Corticotropin (Acth) on Children With the Nephrotic Syndrome

Rapoport, Milton; Ww, McCrory; Barbero, Giulio J.; Hl, Barnett; Cw, Forman

doi:10.1001/jama.1951.03670290009004

Cited by 43 publications

(20 citation statements)

References 5 publications

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“…The institutional review board on human research at both centers approved the study. Sixteen patients (patients 4, 7, 9, 10, and [13][14][15][16][17][18][19][20][21][22][23][24] were studied prospectively as part of two distinct clinical investigator-initiated studies for the use of ACTH gel in the nephrotic syndrome (National Institutes of Health Clinical Trial numbers NCT01155141 and NCT01129284), and four patients (patients 4, 7, 9, and 10) have been described previously with shorter-term results (30,32). The remaining patients were evaluated retrospectively on the basis of chart reviews.…”

Section: Methodsmentioning

confidence: 99%

“…The 12 Stanford patients (patients [13][14][15][16][17][18][19][20][21][22][23][24] were treated with an identical treatment regimen as part of a clinical trial: 40 units subcutaneously (SC) weekly for 2 weeks, 80 units SC weekly for 2 weeks, then 80 units SC twice weekly to complete 16 weeks of therapy. This is referred to as the Stanford regimen, with a cumulative drug exposure of 2160 units.…”

Section: Patient Characteristicsmentioning

confidence: 99%

“…ACTH injections were one of the first therapies used for the nephrotic syndrome in children (24,25) but fell out of favor when oral prednisone became an inexpensive and easy-to-use alternative. There has been recent interest in the role of ACTH in treating the nephrotic syndrome and in the noncorticosteroid actions of this drug (26).…”

Section: Introductionmentioning

confidence: 99%

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Treatment of Idiopathic FSGS with Adrenocorticotropic Hormone Gel

Hogan

Bomback

Mehta

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Adrenocorticotropic hormone (ACTH) has shown efficacy as primary and secondary therapy for nephrotic syndrome due to membranous nephropathy. The data on using ACTH to treat idiopathic FSGS are limited. This report describes our experience using ACTH for nephrotic syndrome due to idiopathic FSGS in the United States.Design, setting, participants, & measurements Twenty-four patients with nephrotic syndrome from idiopathic FSGS were treated with ACTH gel at two academic medical centers between 2009 and 2012, either as part of investigator-initiated pilot studies (n=16) or by prescription for treatment-resistant FSGS (n=8). The primary outcome was remission of proteinuria. The median dose of ACTH was 80 units injected subcutaneously twice weekly. Treatment durations were not uniform.Results Twenty-two patients had received immunosuppression (mean, 2.2 medications) before ACTH therapy. Six patients had steroid-dependent and 15 had steroid-resistant FSGS. At the time of ACTH initiation, the median serum creatinine (interquartile range) was 2.0 (1.1-2.7) mg/dl, estimated GFR was 36 (28-78) ml/min per 1.73 m 2 , and urine protein-to-creatinine ratio was 4595 (2200-8020) mg/g. At the end of ACTH therapy, 7 of 24 patients (29%) experienced remission (n=2 complete remissions, n=5 partial remissions). All remitters had steroid-resistant (n=5) or steroid-dependent (n=2) FSGS. Two responders relapsed during the follow-up period (mean 6 SD, 70631 weeks). Adverse events occurred in 21 of 24 patients, including one episode of new-onset diabetes that resolved after stopping ACTH and two episodes of AKI.Conclusions Response to ACTH treatment among steroid-resistant or steroid-dependent patients with FSGS is low, but ACTH gel may be a viable treatment option for some patients with resistant nephrotic syndrome due to idiopathic FSGS. Further research is necessary to determine which patients will respond to therapy.

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Section: Methodsmentioning

confidence: 99%

Section: Patient Characteristicsmentioning

confidence: 99%

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Treatment of Idiopathic FSGS with Adrenocorticotropic Hormone Gel

Hogan

Bomback

Mehta

et al. 2013

Clinical Journal of the American Society of Nephrology

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“…In many patients with the nephrotic syndrome, proteinuria diminished during or after treatment with corticotropin (ACTH) or Cortisone (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Further, in most patients so treated GFR increased (6)(7)(8)12).…”

mentioning

confidence: 99%

The Effect of Corticotropin (ACTH) on Glomerular Permeability to Albumin in Children with the Nephrotic Syndrome 12

Lauson¹,

Forman²,

McNamara³

et al. 1954

J. Clin. Invest.

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Present evidence indicates that proteinuria in patients with the nephrotic syndrome is the result of increased permeability of the glomerular capillary walls to proteins, particularly to albumin (1, 2). A rough indication of the permeability to albumin, relative to permeability to water, is provided by the ratio of the concentration of albumin in glomerular fluid to that in plasma. Assuming that no albumin is excreted by the tubules, the rate of albumin excretion (in mg. per min.) divided by the rate of glomerular filtration of water (GFR, in ml. per min.) represents the lowest possible concentration of albumin in glomerular fluid (in mg. per ml.) ; if some albumin is reabsorbed by the tubules, as seems likely, the actual concentration of albumin in glomerular fluid would be greater than this calculated value. If it is accepted that the clearance of inulin (CIN) is equivalent to GFR in children with the nephrotic syndrome (3), it follows that the renal clearance of albumin (CALB) divided by CIN, i.e., CALB/CIN, represents the minimum ratio of the albumin concentration in glomerular fluid to that in plasma. Chinard, Lauson, and Eder (4) showed that in patients with the nephrotic syndrome the renal clearance of the blue dye, T-1824 (CT_1824), was somewhat less than but approximately proportional to CALB. It would appear, therefore, that where large changes in permeability are expected CT_1824should be a satisfactory substitute for CALB. The

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“…If excessive potassium excretion depended upon excessive sodium reabsorption as a result of "glomerulo-tubular imbalance," this effect might be expected to disappear during and following diuresis when glomerular filtration rate rises and sodium excretion is abundant. Accordingly, observations on effects of intravenous sodium loading were made over a threeweek period in the same nephrotic children during accumulating edema; during administration of a ten-day course of adrenocorticotrophic hormone (ACTH) which produces an almost predictable diuresis in a large proportion of nephrotic children (20,21 ); at the onset of diuresis; and finally, when non-edematous. The studies were designed: 1) To compare the excretions of sodium, potassium, and water in the nephrotic with those observed in normal subjects under similar loading conditions; 2) to determine whether the tendency to excessive potassium excretion was the result of increased sodium reabsorption; 3) to relate renal and extrarenal transfers of potassium; and 4) to determine whether alterations of ion transport by the kidney might represent either (a) effective function in defense of body composition in the presence of a primary glomerular membrane lesion, plasma albumin loss, and simultaneous changes in body tissue cell structure and function, or (b) impaired kidney function.…”

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confidence: 99%