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Background: Recurrent focal segmental glomerular sclerosis (rFSGS) in renal transplant recipients (RTR) is difficult to predict and treat. Methods: We present the case of a 23-year-old white man who presented with rFSGS and acute renal failure, requiring dialysis 9-months after a 1-haplotype matched living-related transplant. Results: All biomarkers were abnormal at 1-year pre-transplant prior to initiation of dialysis and at the time of transplant. This study was approved by the Human Research Protection Office (HRPO) of Washington University School of Medicine. A renal allograft biopsy demonstrated 19 glomeruli, one of which was partially sclerosed and one was globally sclerosed (Figure 1A). Five-days after the initial presentation, the patient became anuric and he required hemodialysis (Figure 2). The role of suPAR in proteinuric renal disease is currently under active investigation (21). Some of the inconsistencies between reports may be related to the quality of the stored samples and the availability of all relevant clinical information including renal biopsy. Adrenocorticotropic hormone therapy provides transplant physicians with an additional therapeutic option for proteinuric kidney disease. Jochen Reiser is the inventor on pending and issued patents on novel anti-proteinuric therapies and technologies. Regarding this, I have seen several urines recently with a slightly low creatinine in the teens (e.g.
Renal biopsy is not immediately available here.  What management will you recommend?  How will you advise her and her parents? HIV is an important condition in this region.  An HIV test is important both because the condition could be a manifestion of HIV affecting the kidney, and because most active treatments for nephrotic syndrome involve immunosuppressive agents. A 25 year old woman is referred with a 6 month history of fatigue, joint pain, pleuritic chest pain and facial rash.
Ideal initial treatment according to WHO should be Artemisinin combination therapy, but it is not generally affordable so Quinine is still most commonly used. Treatment beyond this point is difficult, but almost certainly she has aggressive inflammatory disease in view of the creatinine changes, and will need cyclophosphamide. What type of disease process do you suspect?  What further features or investigations would you immediately seek? A key observation is the bland urinary sediment, showing little protein or blood, which essentially rules out severe glomerular pathology.  HIV nephropathy is a glomerulopathy, so it is an unlikely explanation.
Hope you had also written that vaginal examination is one of the things that you must do here.  She had advanced cervical cancer involving both ureters. She also had a CD4 count of 93 despite her anti-HIV therapy, with PCR showing 5,000 copies per ml, suggesting anti-retroviral failure.  In a well-resourced setting you would consider testing for drug resistance.
What do you think are the main diagnostic possibilities here?  What additional key questions would you like to ask? Further immunological tests are not possible, nor is a renal biopsy, but what simple tests are essential to your management? IPERTENSIONE ARTERIOSA LINEE GUIDA INQUADRAMENTO DIAGNOSTICO E TRATTAMENTO Universita degli Studi di Roma Tor Vergata U MARIA ADELAIDE MARINI.
Hypertension Prevalence Age Prevalence of Hypertension in the United States by Age Group * *Based on data from the 19992000 National Health and Nutrition Examination Survey. Availability, Prognostic Value and Cost of some markers of organ damage (scored from 0 to 4 pluses) ++++++++Microalbuminuria ++++++++ Est. Blood Pressure (BP) Measurement When measuring blood pressure, care should be taken to: Allow the patients to sit for several minutes in a quiet room before beginning blood pressure measurement Take at least two measurements spaced by 1-2 minutes, and additional measurements if the first two are quite different Use a standard bladder (12-13 cm long and 35 cm wide) but have a larger and a smaller bladder available for fat and thin arms, respectively. Blood Pressure (BP) Measurement Use phase I and V (disappearance) Korotkoff sounds to identify systolic and diastolic blood pressure, respectively Measure blood pressure in both arms at first visit to detect possible differences due to peripheral vascular disease.
Home BP Measurements Self-measurement of BP at home is of clinical value and its prognostic significance is now demonstrated. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button.

This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. After initiation of hemodialysis, β3 integrin activity on human podocytes, in response to patient serum, as well as AT1R-Ab were further elevated. Recurrent FSGS has been reported within 1 week after transplant (4); and it has been hypothesized that a circulating factor is responsible (5, 6).
Adrenocorticotropic hormone Acthar® (Acthar Gel, Questcor, Anaheim Hills, CA, USA) has been shown to induce complete or partial remission in a percentage of patients with treatment-resistant FSGS in native kidneys, with 2 of 5 responders in one study and 8 of 24 responders in another (10, 11).
A 23-year-old white male with a history of end stage renal disease (ESRD) secondary to FSGS presented 9-months after undergoing a one-haplotype matched renal transplant on 24 July 2012 from his father with a low-grade fever consistent with a non-descript viral illness, malaise, progressive edema, acute kidney injury, and nephrotic range proteinuria.
Plasmapheresis with 1.5 plasma volume exchanges with fresh frozen plasma followed by 10 g of IVIG the day of his renal biopsy was attempted.
Time course of events, treatments, and responses in serum albumin and urine protein excretion. One-month after initiation of ACTH treatment, the urine output increased, creatinine improved, and the patient was able to discontinue dialysis. It is also likely that different suPAR fragments exist and that all of those may not be readily measured with current ELISA, and thus the need to detect the activating capacity of suPAR at the level of the podocyte. Podocytes express AT-1R (27, 28), and antibodies against the AT1R have been hypothesized to play a role in many kidney diseases. Adrenocorticotropic hormone is a drug which has been approved for infantile spasms, but also carries the indication for nephrotic syndrome (32). Given the success in this case, the relationship of adrenocorticotropic hormone therapy and suPAR needs to be better defined on a molecular level as well as in controlled trials, possibly as an ad hoc to the trial currently underway for transplant glomerulopathy (34).
Some kind of antimicrobial was prescribed a month ago, but the swelling was present then and has increased since.
The level of HIV positivity in the region is high, but in sick patients, in particular medical inpatients, it is much higher (up to 80%). Some might argue for MMF in a young woman, but it is less well tested, and much more expensive. Injecting laboratory animals with serum from patients with FSGS caused proteinuria and glomerular lesions reminiscent of FSGS (7). The complement dependent cytotoxicity (CDC) and flow cross-match were negative pre-transplant.
He developed low-level cytomegalovirus (CMV)-viremia (Table 1) and leukopenia 4-months after transplantation, and his MPA was discontinued and the valganciclovir (VGCV) dose increased from 450 to 900 mg daily for treatment. There were no donor specific antibodies identified by single antigen bead assay (Luminex, One-lambda, Los Angeles, CA, USA). With this assay, strong integrin activation is indicative of the presence of pathologic suPAR forms, but not physiologic or inflammatory suPAR that accumulated from decreased clearance (12).
However, shortly after commencement, the patient developed wheezing, shortness of breath, and an erythematous rash on his trunk, and extremities suggestive of an allergic reaction, and plasmapheresis was discontinued. We attempted to treat him with galactose (15 g of galactose twice a day for 6 weeks) in view of previously published data on possible benefit (17, 18).
In addition, urinary suPAR was recently shown to be highly specific for FSGS and FSGS-urine strongly activated β3 integrin on human podocytes (25, 26). The permeability activity (termed Palb activity or Palb) is used to infer the presence of a circulating factor.
They have been shown to be elevated in vascular rejection (29), pre-eclampsia (30), and systemic sclerosis (31).
Its use in renal transplant patients has not been reported for recurrent nephrotic syndrome. However, the case also demonstrates the difficulty in understanding the precise cause as well as the course of rFSGS. One week after therapy with aborted plasmapheresis (secondary to intolerance), and high dose steroids, the Palb and suPAR-β3 integrin activity remained significantly positive. Serum from FSGS patients induced increased glomerular albumin permeability (Palb) in isolated glomeruli ex vivo (5). The next day we attempted plasmapheresis with albumin, and again the patient developed similar symptoms.

These biomarkers identified the patients as high risk for rFSGS despite the fact that he remained recurrence free for the first 9-months following his transplant.
In the future, urinary suPAR measurements in urine may provide valuable information in assaying the suPAR forms that are most relevant to FSGS. Palb is calculated from the ratio of capillary expansion of experimental and control glomeruli.
Although not completely defined, ACTH, either alone or via its breakdown product α-melanocyte-stimulating hormone, may induce a potent anti-inflammatory effect by reducing B- and T-cell activity and may also have a direct, podocyte-sparing effect within the glomerulus (33). We also did not have sufficient serum to assess our complete biomarker panel between transplant and recurrence and we did not have samples for biomarker assessment at the time of ACTH effectiveness. Our patient developed recurrence 9-months later when serum suPAR increased by more than 50%.
The results of this paper have not been published previously in whole or part, except in abstract form. After 12-weeks of treatment with high-dose steroids, rituximab, and galactose, the patient remained hemodialysis-dependent. His CMV-viremia resolved within 4 weeks (Table 1) and he was treated with consolidation therapy with VGCV, 900 mg daily, which he was still taking at presentation. Periodic acid-Schiff and trichrome stains confirmed acute tubular injury and highlighted minimal interstitial fibrosis. We considered plasmapheresis with a hypoallergenic dialyzer column, but he refused this treatment.
He subsequently received oral prednisone 100 mg daily as he had responded to a similar dose during his previous four FSGS recurrences as a child prior to his renal transplantation.
It will require further studies to understand why the patient was disease free for the first 9-months after transplant. Values range from 0, indicating no activity, to 1, indicating complete loss of the permeability barrier. In one case report of rFSGS, AT1R-Ab level was elevated and the patient was treated successfully with plasmapheresis and angiotensin converting enzyme inhibitors (ACEI) (9).
This would be consistent with the observation that serum suPAR and the integrin activation profile were decreasing. This could have been the initiating injury that caused a point of no return for podocyte injury.
Three-months after his initial presentation, we commenced adrenocorticotropic hormone (ACTH, Acthar® Gel), 80 units subcutaneously twice weekly.
At the end of 8-weeks, the patient was still hemodialysis-dependent and the prednisone was gradually tapered to 10 mg daily over 2 months.
While the clinical improvement of the patient after plasmapheresis suggests removal of antibodies, it does not prove the pathogenicity of AT1R-Ab in this case.
We were able to discontinue the ACTH after 8-months of therapy without evidence of recurrence 8-months after discontinuation. The authors would also like to acknowledge the laboratory expertise of Mukut Sharma and Dr.
The approximate 50 kD sized serum soluble urokinase receptor (suPAR) is one of the leading candidates. This low-dose was chosen because of our experience with efficacy with this dose for other recurrent glomerulonephritidies and others have reported that even 100 mg can successfully treat recurrent FSGS (13–16). This permeability factor has a high affinity for galactose and Palb activity was lost after galactose infusion in a RTR with rFSGS (17).
A recent report suggested antibodies to the angiotensin II type 1 receptor (AT1R-Ab) may contribute to development of rFSGS in renal transplant recipients (RTR) by causing podocyte injury and severe podocyte foot process effacement (9). Electron microscopy showed extensive foot process effacement and detached podocytes with reactive cytoplasmic changes and villiform transformation (Figure 1B).

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