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1. Cluster analysis identifies distinct pathogenetic patterns in c3 glomerulopathies/immune complex–Mediated membranoproliferative GN

Author

Iatropoulos, P, Daina, E, Curreri, M, Piras, R, Valoti, E, Mele, C, Bresin, E, Gamba, S, Alberti, M, Breno, M, Perna, A, Bettoni, S, Sabadini, E, Murer, L, Vivarelli, M, Noris, M, Remuzzi, G, Bottanelli, L, Donadelli, R, Cuccarolo, P, Abbate, M, Carrara, C, Cannata, A, Ferrari, S, Gaspari, F, Stucchi, N, Bassani, C, Lena, M, Omati, G, Taruscia, D, Bellantuono, R, Giordano, M, Messina, G, Caruso, M, Gotti, E, Mescia, F, Perticucci, E, Schieppati, A, Verdoni, L, Berto, M, Baraldi, O, Montini, G, Pasini, A, Passler, W, Degasperi, T, Gaggiotti, M, Gregorini, G, Miglietti, N, Guarnieri, A, Cirami, L, Roperto, R, Di Giorgio, G, Barbano, G, Innocenti, M, Ghiggeri, G, Magnasco, A, Rolla, D, Casartelli, D, Lambertini, D, Maggio, M, Cosci, P, Conti, G, Amar, K, Ardissino, G, Marinosci, A, Sinico, R, Montoli, A, Bonucchi, D, Facchini, F, Furci, L, Ferretti, A, Nuzzi, F, Pecoraro, C, Visciano, B, Canavese, C, Radin, E, Stratta, P, Nordio, M, Benetti, E, Parolin, M, Alberici, F, Manenti, L, Brugnano, R, Manenti, F, Capitanini, A, Emma, F, Massella, L, Rosa, M, Mazzon, M, Basso, E, Besso, L, Lavacca, A, Mella, A, Bertero, M, Coppo, R, Peruzzi, L, Porcellini, M, Piccoli, G, Clari, R, Pasi, A, Gangemi, C, Alfandary, H, Dagan, A, Conceiçao, M, Sameiro, F, Croze, L, Malvezzi, P, Tsygin, A, Zelan, B, Nastasi, N, Iatropoulos, Paraskevas, Daina, Erica, Curreri, Manuela, Piras, Rossella, Valoti, Elisabetta, Mele, Caterina, Bresin, Elena, Gamba, Sara, Alberti, Marta, Breno, Matteo, Perna, Annalisa, Bettoni, Serena, Sabadini, Ettore, Murer, Luisa, Vivarelli, Marina, Noris, Marina, Remuzzi, Giuseppe, Bottanelli, L., Donadelli, R., Cuccarolo, P., Abbate, M., Carrara, C., Cannata, A., Ferrari, S., Gaspari, F., Stucchi, N., Bassani, C., Lena, M., Omati, G., Taruscia, D., Bellantuono, R., Giordano, M., Messina, G., Caruso, M., Gotti, E., Mescia, F., Perticucci, E., Schieppati, A., Verdoni, L., Berto, M., Baraldi, O., Montini, G., Pasini, A., Passler, W., Degasperi, T., Gaggiotti, M., Gregorini, G., Miglietti, N., Guarnieri, A., Cirami, L., Roperto, R. M., Di Giorgio, G., Barbano, G., Innocenti, M. L. D., Ghiggeri, G. M., Magnasco, A., Rolla, D., Casartelli, D., Lambertini, D., Maggio, M., Cosci, P. M., Conti, G., Amar, K., Ardissino, G., Marinosci, A., Sinico, R. A., Montoli, A., Bonucchi, D., Facchini, F., Furci, L., Ferretti, A., Nuzzi, F., Pecoraro, C., Visciano, B., Canavese, C., Radin, E., Stratta, P., Nordio, M., Benetti, E., Parolin, M., Alberici, F., Manenti, L., Brugnano, R., Manenti, F., Capitanini, A., Emma, F., Massella, L., Rosa, M., Mazzon, M., Basso, E., Besso, L., Lavacca, A., Mella, A., Bertero, M., Coppo, R., Peruzzi, L., Porcellini, M. G., Piccoli, G. B., Clari, R., Pasi, A., Gangemi, C., Alfandary, H., Dagan, A., Conceiçao, M., Sameiro, F. M., Croze, L., Malvezzi, P., Tsygin, A., Zelan, B., Nastasi, null, Iatropoulos, P, Daina, E, Curreri, M, Piras, R, Valoti, E, Mele, C, Bresin, E, Gamba, S, Alberti, M, Breno, M, Perna, A, Bettoni, S, Sabadini, E, Murer, L, Vivarelli, M, Noris, M, Remuzzi, G, Bottanelli, L, Donadelli, R, Cuccarolo, P, Abbate, M, Carrara, C, Cannata, A, Ferrari, S, Gaspari, F, Stucchi, N, Bassani, C, Lena, M, Omati, G, Taruscia, D, Bellantuono, R, Giordano, M, Messina, G, Caruso, M, Gotti, E, Mescia, F, Perticucci, E, Schieppati, A, Verdoni, L, Berto, M, Baraldi, O, Montini, G, Pasini, A, Passler, W, Degasperi, T, Gaggiotti, M, Gregorini, G, Miglietti, N, Guarnieri, A, Cirami, L, Roperto, R, Di Giorgio, G, Barbano, G, Innocenti, M, Ghiggeri, G, Magnasco, A, Rolla, D, Casartelli, D, Lambertini, D, Maggio, M, Cosci, P, Conti, G, Amar, K, Ardissino, G, Marinosci, A, Sinico, R, Montoli, A, Bonucchi, D, Facchini, F, Furci, L, Ferretti, A, Nuzzi, F, Pecoraro, C, Visciano, B, Canavese, C, Radin, E, Stratta, P, Nordio, M, Benetti, E, Parolin, M, Alberici, F, Manenti, L, Brugnano, R, Manenti, F, Capitanini, A, Emma, F, Massella, L, Rosa, M, Mazzon, M, Basso, E, Besso, L, Lavacca, A, Mella, A, Bertero, M, Coppo, R, Peruzzi, L, Porcellini, M, Piccoli, G, Clari, R, Pasi, A, Gangemi, C, Alfandary, H, Dagan, A, Conceiçao, M, Sameiro, F, Croze, L, Malvezzi, P, Tsygin, A, Zelan, B, Nastasi, N, Iatropoulos, Paraskevas, Daina, Erica, Curreri, Manuela, Piras, Rossella, Valoti, Elisabetta, Mele, Caterina, Bresin, Elena, Gamba, Sara, Alberti, Marta, Breno, Matteo, Perna, Annalisa, Bettoni, Serena, Sabadini, Ettore, Murer, Luisa, Vivarelli, Marina, Noris, Marina, Remuzzi, Giuseppe, Bottanelli, L., Donadelli, R., Cuccarolo, P., Abbate, M., Carrara, C., Cannata, A., Ferrari, S., Gaspari, F., Stucchi, N., Bassani, C., Lena, M., Omati, G., Taruscia, D., Bellantuono, R., Giordano, M., Messina, G., Caruso, M., Gotti, E., Mescia, F., Perticucci, E., Schieppati, A., Verdoni, L., Berto, M., Baraldi, O., Montini, G., Pasini, A., Passler, W., Degasperi, T., Gaggiotti, M., Gregorini, G., Miglietti, N., Guarnieri, A., Cirami, L., Roperto, R. M., Di Giorgio, G., Barbano, G., Innocenti, M. L. D., Ghiggeri, G. M., Magnasco, A., Rolla, D., Casartelli, D., Lambertini, D., Maggio, M., Cosci, P. M., Conti, G., Amar, K., Ardissino, G., Marinosci, A., Sinico, R. A., Montoli, A., Bonucchi, D., Facchini, F., Furci, L., Ferretti, A., Nuzzi, F., Pecoraro, C., Visciano, B., Canavese, C., Radin, E., Stratta, P., Nordio, M., Benetti, E., Parolin, M., Alberici, F., Manenti, L., Brugnano, R., Manenti, F., Capitanini, A., Emma, F., Massella, L., Rosa, M., Mazzon, M., Basso, E., Besso, L., Lavacca, A., Mella, A., Bertero, M., Coppo, R., Peruzzi, L., Porcellini, M. G., Piccoli, G. B., Clari, R., Pasi, A., Gangemi, C., Alfandary, H., Dagan, A., Conceiçao, M., Sameiro, F. M., Croze, L., Malvezzi, P., Tsygin, A., Zelan, B., and Nastasi, null

Abstract

Membranoproliferative GN (MPGN) was recently reclassified as alternative pathway complement–mediated C3 glomerulopathy (C3G) and immune complex–mediated membranoproliferative GN (IC-MPGN). However, genetic and acquired alternative pathway abnormalities are also observed in IC-MPGN. Here, we explored the presence of distinct disease entities characterized by specific pathophysiologic mechanisms. We performed unsupervised hierarchical clustering, a data-driven statistical approach, on histologic, genetic, and clinical data and data regarding serum/plasma complement parameters from 173 patients with C3G/IC-MPGN. This approach divided patients into four clusters, indicating the existence of four different pathogenetic patterns. Specifically, this analysis separated patients with fluid-phase complement activation (clusters 1–3) who had low serum C3 levels and a high prevalence of genetic and acquired alternative pathway abnormalities from patients with solid-phase complement activation (cluster 4) who had normal or mildly altered serum C3, late disease onset, and poor renal survival. In patients with fluid-phase complement activation, those in clusters 1 and 2 had massive activation of the alternative pathway, including activation of the terminal pathway, and the highest prevalence of subendothelial deposits, but those in cluster 2 had additional activation of the classic pathway and the highest prevalence of nephrotic syndrome at disease onset. Patients in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous deposits. In addition, we provide a simple algorithm to assign patients with C3G/IC-MPGN to specific clusters. These distinct clusters may facilitate clarification of disease etiology, improve risk assessment for ESRD, and pave the way for personalized treatment.

Published
2018

2. Cluster Analysis Identifies Distinct Pathogenetic Patterns in C3 Glomerulopathies/Immune Complex–Mediated Membranoproliferative GN

Author

Iatropoulos, Paraskevas, Daina, Erica, Curreri, Manuela, Piras, Rossella, Valoti, Elisabetta, Mele, Caterina, Bresin, Elena, Gamba, Sara, Alberti, Marta, Breno, Matteo, Perna, Annalisa, Bettoni, Serena, Sabadini, Ettore, Murer, Luisa, Vivarelli, Marina, Noris, Marina, Remuzzi, Giuseppe, Bottanelli, L., Donadelli, R., Cuccarolo, P., Abbate, M., Carrara, C., Cannata, A., Ferrari, S., Gaspari, F., Stucchi, N., Bassani, C., Lena, M., Omati, G., Taruscia, D., Bellantuono, R., Giordano, M., Messina, G., Caruso, M., Gotti, E., Mescia, F., Perticucci, E., Schieppati, A., Verdoni, L., Berto, M., Baraldi, O., Montini, G., Pasini, A., Passler, W., Degasperi, T., Gaggiotti, M., Gregorini, G., Miglietti, N., Guarnieri, A., Cirami, L., Roperto, R. M., Di Giorgio, G., Barbano, G., Innocenti, M. L. D., Ghiggeri, G. M., Magnasco, A., Rolla, D., Casartelli, D., Lambertini, D., Maggio, M., Cosci, P. M., Conti, G., Amar, K., Ardissino, G., Marinosci, A., Sinico, R. A., Montoli, A., Bonucchi, D., Facchini, F., Furci, L., Ferretti, A., Nuzzi, F., Pecoraro, C., Visciano, B., Canavese, C., Radin, E., Stratta, P., Nordio, M., Benetti, E., Parolin, M., Alberici, F., Manenti, L., Brugnano, R., Manenti, F., Capitanini, A., Emma, F., Massella, L., Rosa, M., Mazzon, M., Basso, E., Besso, L., Lavacca, A., Mella, A., Bertero, M., Coppo, R., Peruzzi, L., Porcellini, M. G., Piccoli, G. B., Clari, R., Pasi, A., Gangemi, C., Alfandary, H., Dagan, A., Conceiçao, M., Sameiro, F. M., Croze, L., Malvezzi, P., Tsygin, A., Zelan, B., Nastasi, null, Iatropoulos, P, Daina, E, Curreri, M, Piras, R, Valoti, E, Mele, C, Bresin, E, Gamba, S, Alberti, M, Breno, M, Perna, A, Bettoni, S, Sabadini, E, Murer, L, Vivarelli, M, Noris, M, Remuzzi, G, Bottanelli, L, Donadelli, R, Cuccarolo, P, Abbate, M, Carrara, C, Cannata, A, Ferrari, S, Gaspari, F, Stucchi, N, Bassani, C, Lena, M, Omati, G, Taruscia, D, Bellantuono, R, Giordano, M, Messina, G, Caruso, M, Gotti, E, Mescia, F, Perticucci, E, Schieppati, A, Verdoni, L, Berto, M, Baraldi, O, Montini, G, Pasini, A, Passler, W, Degasperi, T, Gaggiotti, M, Gregorini, G, Miglietti, N, Guarnieri, A, Cirami, L, Roperto, R, Di Giorgio, G, Barbano, G, Innocenti, M, Ghiggeri, G, Magnasco, A, Rolla, D, Casartelli, D, Lambertini, D, Maggio, M, Cosci, P, Conti, G, Amar, K, Ardissino, G, Marinosci, A, Sinico, R, Montoli, A, Bonucchi, D, Facchini, F, Furci, L, Ferretti, A, Nuzzi, F, Pecoraro, C, Visciano, B, Canavese, C, Radin, E, Stratta, P, Nordio, M, Benetti, E, Parolin, M, Alberici, F, Manenti, L, Brugnano, R, Manenti, F, Capitanini, A, Emma, F, Massella, L, Rosa, M, Mazzon, M, Basso, E, Besso, L, Lavacca, A, Mella, A, Bertero, M, Coppo, R, Peruzzi, L, Porcellini, M, Piccoli, G, Clari, R, Pasi, A, Gangemi, C, Alfandary, H, Dagan, A, Conceiçao, M, Sameiro, F, Croze, L, Malvezzi, P, Tsygin, A, Zelan, B, and Nastasi, N

Subjects
0301 basic medicine, Complement system, Glomerulonephritis, Membranoproliferative, membranoproliferative glomerulonephritis (MPGN), 030232 urology & nephrology, Disease, Antigen-Antibody Complex, Biology, Kidney, 03 medical and health sciences, 0302 clinical medicine, Glomerulopathy, Clinical Research, medicine, Dense Deposit Disease, Humans, C3 glomerulopathy, General Medicine, Complement System Proteins, C3 glomerulonephriti, medicine.disease, C3-convertase, Immune complex, 030104 developmental biology, Nephrology, Immunology, Alternative complement pathway, Nephrotic syndrome, Rare disease
Abstract

Membranoproliferative GN (MPGN) was recently reclassified as alternative pathway complement–mediated C3 glomerulopathy (C3G) and immune complex–mediated membranoproliferative GN (IC-MPGN). However, genetic and acquired alternative pathway abnormalities are also observed in IC-MPGN. Here, we explored the presence of distinct disease entities characterized by specific pathophysiologic mechanisms. We performed unsupervised hierarchical clustering, a data-driven statistical approach, on histologic, genetic, and clinical data and data regarding serum/plasma complement parameters from 173 patients with C3G/IC-MPGN. This approach divided patients into four clusters, indicating the existence of four different pathogenetic patterns. Specifically, this analysis separated patients with fluid-phase complement activation (clusters 1–3) who had low serum C3 levels and a high prevalence of genetic and acquired alternative pathway abnormalities from patients with solid-phase complement activation (cluster 4) who had normal or mildly altered serum C3, late disease onset, and poor renal survival. In patients with fluid-phase complement activation, those in clusters 1 and 2 had massive activation of the alternative pathway, including activation of the terminal pathway, and the highest prevalence of subendothelial deposits, but those in cluster 2 had additional activation of the classic pathway and the highest prevalence of nephrotic syndrome at disease onset. Patients in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous deposits. In addition, we provide a simple algorithm to assign patients with C3G/IC-MPGN to specific clusters. These distinct clusters may facilitate clarification of disease etiology, improve risk assessment for ESRD, and pave the way for personalized treatment.

Published
2017

3. Childhood Hypercalciuric Hypercalcemia With Elevated Vitamin D and Suppressed Parathyroid Hormone: Long-Term Follow Up.

Author

Gurevich E, Levi S, Borovitz Y, Alfandary H, Ganon L, Dinour D, and Davidovits M

Abstract

Purpose: Hypercalcemia with low parathyroid hormone (PTH) level, hypercalciuria, nephrocalcinosis, or nephrolithiasis, was recently reported as caused by mutations in CYP24A1 and SLC34A genes. These encode for vitamin D-24A-hydroxylase and for the renal phosphate transporters NaPiIIa and NaPiIIc, respectively. We aimed to describe the clinical course of these monogenic disorders in patients with and without found mutations during long-term follow-up. Methods: Ten patients with hypercalcemia, hypercalciuria, elevated 1,25-(OH) 2 D levels and suppressed PTH were followed in our center during 1998-2019. Relevant laboratory and imaging data and results of genetic evaluation were retrieved from medical files. Results: The median age at presentation was 9.5 months (range 1 month-11 years), six were males, and the median follow-up time was 3.8 (1.1-14) years. Mutations in CYP24A1 and SLC34A3 were identified in three and one patients, respectively. Five patients presented with nephrocalcinosis, three with nephrolithiasis, and two had normal renal ultrasound. High blood calcium and 1,25-(OH) 2 D levels at presentation decreased during follow-up [11.1 ± 1 vs. 9.9 ± 0.5 mg/dl ( p = 0.012), and 307 ± 130 vs. 209 ± 65 pmol/l ( p = 0.03), respectively]; this paralleled an increase in suppressed PTH levels (5.8 ± 0.9 vs. 11.8 ± 7.3 pg/ml, p = 0.2). Substantial improvements in hypercalciuria and renal sonography findings were not observed. Two patients had impaired renal function (eGFR 84-88 ml/min/1/73 m 2 ) at the last follow up. Interventions included appropriate diet, citrate supplementation, and thiazides. Conclusion: Despite improvement in hypercalcemia and 1,25-(OH) 2 D levels, not all the patients showed improvements in hypercalciuria and nephrocalcinosis. Deterioration of renal function was also observed. Long-term follow up and intervention to prevent nephrocalcinosis and nephrolithiasis are recommended in these children., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Gurevich, Levi, Borovitz, Alfandary, Ganon, Dinour and Davidovits.)

Published
2021
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