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Focal segmental glomerulosclerosis

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hyaline material inside of those. (D,E) Fluorescence microscopy (40×) shows, respectively, IgM and C3 trapping in areas of collapse/sclerosis. (F) Semi-fine stained in Toluidine Blue (63×) with collapse of the entire glomerular tuft and hyperplasia of podocytes and dilated Bowman's space. (G,H) Transmission electron microscopy contrasted with Osmium Tetroxide, Lead Citrate and Uranyl in block shows capillary loop collapse with hyalinosis in addition to diffuse fusion and flattening of the pedicels associated with microvillous transformation. (I) Electron microscopy tubes contrasted with osmium tetroxide, lead citrate, and uranyl in block with detail of disorganization of the cytoskeleton in the podocyte cytoplasm, with extensive effacement of the pedicels.
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glucocorticoids and other immune-modulatory drugs. Response to therapy is variable, with a significant portion of patients progressing to end-stage kidney failure. An American epidemiological study 20 years ago demonstrated that FSGS is estimated to occur in 7 persons per million, with cisgender male African-Americans at higher risk.
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Initial response to therapy also dictates long-term outcomes. Those defined as having a "complete response" typically manifest a proteinuria of <300 mg/day; those with a "partial response" manifest a sub-nephrotic range of proteinuria, <3.5 g/day. Either complete or partial response is
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is a common long-term complication of the disease. FSGS can be classified as primary, secondary, or genetic, depending on whether a particular toxic or pathologic stressor or genetic predisposition can be identified as the cause. Diagnosis is established by renal biopsy, and treatment consists of
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Histopathology of collapsing glomerulopathy. (A,B) Periodic Acid Schiff (PAS) and Jones Methenamine Silver (JMS) (40×), respectively show intense podocyte hyperplasia and glomerular tuft collapse. (C) JMS (20×) exhibits microcytic transformation of distal convoluted tubules with accumulations of
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Secondary FSGS is caused by an identifiable stress or toxin that injures podocytes. Many causes of secondary FSGS contribute to podocyte injury through hyperfiltration, which is a scenario of excess filtration by renal glomeruli. Hyperfiltration can be caused by obesity, diabetes or loss of the
466:, making it one of the most common causes of nephrotic syndrome in the United States. FSGS accounts for 2% of all cases of kidney failure. African American patients have four times the likelihood of developing FSGS. Men are about two times as likely to develop FSGS compared to women. 404:, whereas the glomerular tip lesion variant has a low rate of progression to end-stage renal disease in most patients. The cellular variant shows similar clinical presentation to collapsing and glomerular tip variant but has intermediate outcomes between the other two variants. 1720:
Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P, Friedman D, Briggs W, Dart R, Korbet S, Mokrzycki MH, Kimmel PL, Limou S, Ahuja TS, Berns JS, Fryc J, Simon EE, Smith MC, Trachtman H, Michel DM, Schelling JR, Vlahov D, Pollak M, Winkler CA (November 2011).
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FSGS can be classified by the putative cause of damage to podocytes. Primary FSGS involves cases in which no cause is readily identifiable. It is presumed that a set of unidentified circulating factors in the blood contribute to podocyte damage in these cases.
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Boute N, Gribouval O, Roselli S, Benessy F, Lee H, Fuchshuber A, Dahan K, Gubler MC, Niaudet P, Antignac C (April 2000). "NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome".
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from being filtered. FSGS involves damage to the renal podocytes such that larger molecules, most notably proteins, are filtered and lost through the kidney. Thus, many of the signs and symptoms of FSGS are related to protein loss.
450:-range (>3.5 g/day) proteinuria have over a 50% rate of progression to end-stage kidney disease at 10 years. Only 15% of patients with sub-nephrotic ranges of proteinuria progress to end-stage renal failure at 10 years. 2131: 2111: 1770:
Fuiano G, Comi N, Magri P, Sepe V, Balletta MM, Esposito C, Uccello F, Dal Canton A, Conte G (January 1996). "Serial morphometric analysis of sclerotic lesions in primary "focal" segmental glomerulosclerosis".
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Philippe A, Nevo F, Esquivel EL, Reklaityte D, Gribouval O, Tête MJ, Loirat C, Dantal J, Fischbach M, Pouteil-Noble C, Decramer S, Hoehne M, Benzing T, Charbit M, Niaudet P, Antignac C (October 2008).
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Deegens JK, Assmann KJ, Steenbergen EJ, Hilbrands LB, Gerlag PG, Jansen JL, Wetzels JF (November 2005). "Idiopathic focal segmental glomerulosclerosis: a favourable prognosis in untreated patients?".
332:, low blood protein levels (albumin, antibodies), and high blood cholesterol would support a diagnosis of FSGS, although these do not help to distinguish between FSGS and other causes of proteinuria. 807:
Haas M, Meehan SM, Karrison TG, Spargo BH (November 1997). "Changing etiologies of unexplained adult nephrotic syndrome: a comparison of renal biopsy findings from 1976–1979 and 1995–1997".
246:) to segments of glomeruli; moreover, only a portion of glomeruli are affected. The focal and segmental nature of disease seen on histology help to distinguish FSGS from other types of 420:-range proteinuria (>3.5 g/day). For patients who maintain nephrotic-range proteinuria despite glucocorticoids, or for patients who demonstrate glucocorticoid intolerance, 104:. This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss. FSGS is a leading cause of excess protein loss— 2058:
Troyanov S, Wall CA, Miller JA, Scholey JW, Cattran DC (April 2005). "Focal and segmental glomerulosclerosis: definition and relevance of a partial remission".
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Rydel JJ, Korbet SM, Borok RZ, Schwartz MM (April 1995). "Focal segmental glomerular sclerosis in adults: presentation, course, and response to treatment".
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Helal I, Fick-Brosnahan GM, Reed-Gitomer B, Schrier RW (February 2012). "Glomerular hyperfiltration: definitions, mechanisms and clinical implications".
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Kitiyakara C, Eggers P, Kopp JB (November 2004). "Twenty-one-year trend in ESRD due to focal segmental glomerulosclerosis in the United States".
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value in individuals with primary focal segmental glomerulosclerosis. The collapsing variant is associated with higher rate of progression to
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Schwartz MM, Korbet SM (December 1993). "Primary focal segmental glomerulosclerosis: pathology, histological variants, and pathogenesis".
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Korbet SM, Schwartz MM, Lewis EJ (June 1994). "Primary focal segmental glomerulosclerosis: clinical course and response to therapy".
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Raina R, Wang J, Sharma A, Chakraborty R (2020). "Extracorporeal Therapies in the Treatment of Focal Segmental Glomerulosclerosis".
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Five mutually exclusive variants of focal segmental glomerulosclerosis may be distinguished by the pathologic findings seen on
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Other tests helpful in the diagnosis include urine protein, urinalysis, serum albumin, and serum lipids. A clinical picture of
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gene. There is some data to suggest that HIV can infect tubular epithelial cells and podocytes, but much remains to be known.
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Brown EJ, Schlöndorff JS, Becker DJ, Tsukaguchi H, Tonna SJ, Uscinski AL, Higgs HN, Henderson JM, Pollak MR (January 2010).
325:(scarring) of a portion (average: 15%) of the glomerular space, with only a portion of glomeruli manifesting any sclerosis. 530: 2146: 1434:
Rennke HG, Klein PS (June 1989). "Pathogenesis and significance of nonprimary focal and segmental glomerulosclerosis".
218:. Large molecules, such as proteins, are usually too large to be filtered and instead are retained in the capillaries. 1507:
Dubrow A, Mittman N, Ghali V, Flamenbaum W (January 1985). "The changing spectrum of heroin-associated nephropathy".
424:(e.g., tacrolimus) are initiated. Successful treatment is defined as a drop in proteinuria to sub-nephrotic ranges. 291:
The pathogenesis of HIV-associated FSGS is unclear, but may be due to the presence of the G1/G2 risk alleles of the
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Nagata M, Kobayashi N, Hara S (August 2017). "Focal segmental glomerulosclerosis; why does it occur segmentally?".
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Kitiyakara C, Kopp JB, Eggers P (March 2003). "Trends in the epidemiology of focal segmental glomerulosclerosis".
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associated with 80% kidney survival at 10 years, compared with about 50% among non-responsive patients.
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Thomas DB, Franceschini N, Hogan SL, Ten Holder S, Jennette CE, Falk RJ, Jennette JC (March 2006).
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Common signs are also due to loss of blood proteins by the glomerulus of the kidney, including:
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The treatment of secondary FSGS involves addressing the particular toxic or stress agent.
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Cutrim ÉMM, Neves PDMM, Campos MAG, Wanderley DC, Teixeira-Júnior AAL, Muniz MPR (2022).
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First-line treatment for primary FSGS consists of anti-inflammatory drugs. Specifically,
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Kasiske BL, Crosson JT (June 1986). "Renal disease in patients with massive obesity".
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Tucker JK (February 2002). "Focal segmental glomerulosclerosis in African Americans".
958:"Protecting Podocytes: A Key Target for Therapy of Focal Segmental Glomerulosclerosis" 820: 752: 664: 2075: 2037: 2010: 1972: 1918: 1877: 1826: 1788: 1752: 1710:
Chang, Anthony, Robbins & Cotran Pathologic Basis of Disease, Chapter 20, 895–952
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Secondary FSGS can also be caused by toxins, including anabolic steroids and heroin.
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that contribute to the filtration barrier, preventing molecules larger than 5 
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have also been proposed to play a role in the pathogenesis of this disease.
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of the collapsing variant of FSGS (collapsing glomerulopathy). A collapsed
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The most common symptoms are a result of abnormal loss of protein from the
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De Vriese AS, Sethi S, Nath KA, Glassock RJ, Fervenza FC (March 2018).
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Ichikawa I, Fogo A (June 1996). "Focal segmental glomerulosclerosis".
1164:"Mechanisms of glomerular albumin filtration and tubular reabsorption" 973: 2218: 2183: 475: 397: 352: 318: 235: 56: 1078:
Wallace MA (November 1998). "Anatomy and physiology of the kidney".
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consists of a set of capillaries from which blood is filtered into
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that includes at least fifteen serial cuts with at least eight
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A number of genes have been implicated in FSGS. These include:
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Nagata M (June 2016). "Podocyte injury and its consequences".
108:—in children and adults in the US. Signs and symptoms include 1248:
Wang CS, Greenbaum LA (February 2019). "Nephrotic Syndrome".
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focal glomerular sclerosis, focal nodular glomerulosclerosis
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Pollak MR, Quaggin SE, Hoenig MP, Dworkin LD (August 2014).
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The majority of untreated cases of FSGS will progress to
1719: 903: 806: 696: 187:(compensatory by the liver to compensate for low serum 609:"The many masks of focal segmental glomerulosclerosis" 51:
of focal segmental glomerulosclerosis, hilar variant.
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Kiffel J, Rahimzada Y, Trachtman H (September 2011).
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Important prognostic factors include the degree of 2265: 2093: 1042: 650: 1769: 1344: 738: 151:Susceptibility to infection (due to loss of serum 2503: 197:in the urine (secondary to hypercholesterolemia) 602: 600: 1808: 1541: 955: 646: 644: 226:, the site of filtration of ions and solutes. 2466:Eosinophilic granulomatosis with polyangiitis 2251: 2053: 2051: 1804: 1802: 1247: 951: 949: 554: 550: 548: 546: 544: 542: 540: 1306: 1161: 597: 272:that contributes to the filtration barrier; 1433: 1340: 1338: 1284:"Focal Segmental Glomerulosclerosis (FSGS)" 1003: 1001: 899: 897: 895: 780:"Focal segmental glomerulosclerosis (FSGS)" 641: 606: 92:) is a histopathologic finding of scarring 2258: 2244: 2048: 1988: 1986: 1938: 1799: 1467: 1465: 1380: 1378: 1376: 946: 734: 732: 730: 728: 537: 524: 522: 284:, which encodes the actin-binding protein 258:contralateral kidney, among other causes. 242:On histology, FSGS manifests as scarring ( 74: 38: 1966: 1956: 1934: 1932: 1912: 1871: 1861: 1746: 1687: 1602: 1410: 1189: 1179: 1138: 1115:"The glomerulus: the sphere of influence" 981: 929: 875: 692: 690: 688: 686: 684: 682: 624: 580: 222:FSGS is primarily a disease of the renal 1335: 998: 892: 842: 840: 838: 802: 800: 528:"focal segmental glomerulosclerosis" at 362: 339: 205: 2332:Membranoproliferative/mesangiocapillary 1983: 1462: 1373: 1077: 846: 725: 519: 416:are begun in patients manifesting with 396:Recognition of these variants may have 2504: 1929: 1888: 1212: 1086:(5): 800, 803–16, 819–20, quiz 821–4. 1007: 679: 462:FSGS accounts for 35% of all cases of 2239: 835: 797: 774: 772: 770: 392:Not otherwise specified (NOS) variant 351:is seen at the top, right-of-centre. 124: 1556:10.1001/archinte.1986.00360180095016 557:"Focal Segmental Glomerulosclerosis" 555:Rosenberg AZ, Kopp JB (March 2017). 137:Frothy urine (due to excess protein) 13: 767: 201: 86:Focal segmental glomerulosclerosis 25:Focal segmental glomerulosclerosis 14: 2533: 2089: 443:and initial response to therapy. 335: 230:are specialized cells lining the 2456:Granulomatosis with polyangiitis 2267:Disease of the kidney glomerules 1022:10.1097/00000441-200202000-00006 469: 140:Excess water retention (pitting 2021: 1939:Chen YM, Liapis H (July 2015). 1837: 1763: 1713: 1704: 1655: 1619: 1570: 1535: 1500: 1427: 1300: 1276: 1241: 1206: 1155: 1106: 1071: 1036: 956:Campbell KN, Tumlin JA (2018). 457: 321:. Histologic features include 1: 1823:10.1016/s0272-6386(12)70349-9 1521:10.1016/s0272-6386(85)80133-5 1448:10.1016/s0272-6386(89)80001-0 1092:10.1016/s0001-2092(06)62377-6 821:10.1016/s0272-6386(97)90485-6 753:10.1016/s0272-6386(12)80128-4 665:10.1016/S0272-6386(04)01081-9 513: 383:Glomerular tip lesion variant 313:Diagnosis of FSGS is made by 711:10.1016/0272-6386(95)90120-5 531:Dorland's Medical Dictionary 430: 407: 308: 276:, which encodes the protein 268:, which encodes the protein 133:of the kidney, and include: 7: 2327:Endocapillary proliferative 1162:Tojo A, Kinugasa S (2012). 496: 10: 2538: 1227:10.1016/j.kint.2016.01.012 922:10.1053/j.ackd.2011.03.005 607:D'Agati V (October 1994). 299:Gain of function mutations 2478: 2442: 2409:Type III hypersensitivity 2403: 2381: 2365: 2340: 2312: 2284: 2273: 2198: 2097: 1958:10.1186/s12882-015-0090-9 1359:10.1007/s00424-017-2023-x 1262:10.1016/j.pcl.2018.08.006 63: 46: 37: 29: 24: 2461:Microscopic polyangiitis 2387:Type II hypersensitivity 1863:10.3389/fmed.2022.846173 437:end-stage kidney disease 280:found in podocytes; and 170:-range of >3.5 g/day) 2522:Disorders causing edema 2322:Mesangial proliferative 1057:10.1053/snep.2003.50025 868:10.1038/nrneph.2014.216 402:end-stage renal disease 144:, due to loss of serum 2072:10.1681/ASN.2004070593 1739:10.1681/ASN.2011040388 1595:10.1681/ASN.2008010059 1486:10.1038/nrneph.2012.19 1403:10.1681/ASN.2017090958 910:Adv Chronic Kidney Dis 422:calcineurin inhibitors 369: 360: 219: 185:High serum cholesterol 2427:diffuse proliferative 1914:10.1038/sj.ki.5000160 1250:Pediatr Clin North Am 1119:Clin J Am Soc Nephrol 561:Clin J Am Soc Nephrol 366: 343: 209: 2395:Goodpasture syndrome 1850:Front Med (Lausanne) 1131:10.2215/CJN.09400913 573:10.2215/CJN.05960616 248:glomerular sclerosis 180:Low serum antibodies 164:Protein in the urine 100:and damage to renal 1181:10.1155/2012/481520 626:10.1038/ki.1994.388 2491:glomerulonephrosis 2486:glomerulonephritis 2417:Post-streptococcal 2199:External resources 1321:10.1007/BF00866790 968:(Suppl 1): 14–29. 784:www.kidneyfund.org 508:Nephrotic syndrome 503:Glomerulonephritis 464:nephrotic syndrome 380:Collapsing variant 370: 361: 220: 168:nephrotic syndrome 125:Signs and symptoms 106:nephrotic syndrome 2499: 2498: 2474: 2473: 2361: 2360: 2286:Non-proliferative 2233: 2232: 2007:10.1159/000506277 1785:10.1681/ASN.V7149 974:10.1159/000481634 850:(February 2015). 389:Perihilar variant 174:Low serum albumin 83: 82: 19:Medical condition 2529: 2379: 2378: 2282: 2281: 2260: 2253: 2246: 2237: 2236: 2127:(with .1 suffix) 2095: 2094: 2084: 2083: 2060:J Am Soc Nephrol 2055: 2046: 2045: 2025: 2019: 2018: 1990: 1981: 1980: 1970: 1960: 1936: 1927: 1926: 1916: 1892: 1886: 1885: 1875: 1865: 1841: 1835: 1834: 1806: 1797: 1796: 1773:J Am Soc Nephrol 1767: 1761: 1760: 1750: 1727:J Am Soc Nephrol 1717: 1711: 1708: 1702: 1701: 1691: 1659: 1653: 1652: 1623: 1617: 1616: 1606: 1583:J Am Soc Nephrol 1574: 1568: 1567: 1539: 1533: 1532: 1504: 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2337: 2335: 2334: 2329: 2324: 2318: 2316: 2310: 2309: 2307: 2306: 2301: 2296: 2294:Minimal change 2290: 2288: 2279: 2271: 2270: 2263: 2262: 2255: 2248: 2240: 2231: 2230: 2227: 2226: 2215: 2203: 2202: 2200: 2196: 2195: 2192: 2191: 2180: 2169: 2143: 2128: 2107: 2102: 2101: 2099: 2098:Classification 2091: 2090:External links 2088: 2086: 2085: 2047: 2020: 2001:(5): 513–523. 1982: 1928: 1887: 1836: 1798: 1762: 1712: 1703: 1680:10.1038/ng.505 1654: 1618: 1589:(10): 1871–8. 1569: 1534: 1499: 1480:(5): 293–300. 1461: 1426: 1397:(3): 759–774. 1372: 1353:(7–8): 983–8. 1334: 1299: 1275: 1240: 1221:(6): 1221–30. 1205: 1154: 1105: 1070: 1035: 997: 945: 891: 834: 796: 766: 724: 678: 640: 619:(4): 1223–41. 596: 567:(3): 502–517. 536: 517: 515: 512: 511: 510: 505: 498: 495: 494: 493: 488: 483: 478: 471: 468: 459: 456: 446:Patients with 432: 429: 409: 406: 394: 393: 390: 387: 384: 381: 337: 336:Classification 334: 310: 307: 216:Bowman's space 203: 200: 199: 198: 192: 182: 177: 176:(<3.5 g/dl) 171: 166:(often in the 157: 156: 149: 138: 126: 123: 118:Kidney failure 81: 80: 67: 61: 60: 44: 43: 35: 34: 31: 27: 26: 18: 16:Kidney disease 15: 9: 6: 4: 3: 2: 2534: 2523: 2520: 2518: 2515: 2513: 2510: 2509: 2507: 2492: 2489: 2487: 2484: 2483: 2481: 2477: 2467: 2464: 2462: 2459: 2457: 2454: 2453: 2451: 2449: 2445: 2441: 2435: 2432: 2428: 2425: 2424: 2423: 2420: 2418: 2415: 2414: 2412: 2410: 2406: 2402: 2396: 2393: 2392: 2390: 2388: 2384: 2380: 2377: 2375: 2370: 2364: 2354: 2351: 2349: 2346: 2345: 2343: 2339: 2333: 2330: 2328: 2325: 2323: 2320: 2319: 2317: 2315: 2314:Proliferative 2311: 2305: 2302: 2300: 2297: 2295: 2292: 2291: 2289: 2287: 2283: 2280: 2278: 2272: 2268: 2261: 2256: 2254: 2249: 2247: 2242: 2241: 2238: 2225: 2221: 2220: 2216: 2214: 2210: 2209: 2205: 2204: 2201: 2197: 2190: 2186: 2185: 2181: 2179: 2175: 2174: 2170: 2168: 2165: 2162: 2159: 2156: 2153: 2149: 2148: 2144: 2142: 2138: 2137: 2133: 2129: 2126: 2122: 2118: 2117: 2113: 2109: 2108: 2105: 2100: 2096: 2081: 2077: 2073: 2069: 2066:(4): 1061–8. 2065: 2061: 2054: 2052: 2043: 2039: 2036:(10): 393–8. 2035: 2031: 2024: 2016: 2012: 2008: 2004: 2000: 1996: 1989: 1987: 1978: 1974: 1969: 1964: 1959: 1954: 1950: 1946: 1942: 1935: 1933: 1924: 1920: 1915: 1910: 1906: 1902: 1898: 1891: 1883: 1879: 1874: 1869: 1864: 1859: 1855: 1851: 1847: 1840: 1832: 1828: 1824: 1820: 1817:(6): 874–83. 1816: 1812: 1805: 1803: 1794: 1790: 1786: 1782: 1778: 1774: 1766: 1758: 1754: 1749: 1744: 1740: 1736: 1732: 1728: 1724: 1716: 1707: 1699: 1695: 1690: 1685: 1681: 1677: 1673: 1669: 1665: 1658: 1650: 1646: 1642: 1641:10.1038/74166 1638: 1635:(4): 349–54. 1634: 1630: 1622: 1614: 1610: 1605: 1600: 1596: 1592: 1588: 1584: 1580: 1573: 1565: 1561: 1557: 1553: 1550:(6): 1105–9. 1549: 1545: 1538: 1530: 1526: 1522: 1518: 1514: 1510: 1503: 1495: 1491: 1487: 1483: 1479: 1475: 1468: 1466: 1457: 1453: 1449: 1445: 1442:(6): 443–56. 1441: 1437: 1430: 1422: 1418: 1413: 1408: 1404: 1400: 1396: 1392: 1388: 1381: 1379: 1377: 1368: 1364: 1360: 1356: 1352: 1348: 1347:Pflugers Arch 1341: 1339: 1330: 1326: 1322: 1318: 1315:(3): 374–91. 1314: 1310: 1303: 1289: 1285: 1279: 1271: 1267: 1263: 1259: 1255: 1251: 1244: 1236: 1232: 1228: 1224: 1220: 1216: 1209: 1201: 1197: 1192: 1187: 1182: 1177: 1173: 1169: 1168:Int J Nephrol 1165: 1158: 1150: 1146: 1141: 1136: 1132: 1128: 1125:(8): 1461–9. 1124: 1120: 1116: 1109: 1101: 1097: 1093: 1089: 1085: 1081: 1074: 1066: 1062: 1058: 1054: 1051:(2): 172–82. 1050: 1046: 1045:Semin Nephrol 1039: 1031: 1027: 1023: 1019: 1015: 1011: 1004: 1002: 993: 989: 984: 979: 975: 971: 967: 963: 959: 952: 950: 941: 937: 932: 927: 923: 919: 915: 911: 907: 900: 898: 896: 887: 883: 878: 873: 869: 865: 861: 857: 853: 849: 843: 841: 839: 830: 826: 822: 818: 815:(5): 621–31. 814: 810: 803: 801: 785: 781: 775: 773: 771: 762: 758: 754: 750: 747:(6): 773–83. 746: 742: 735: 733: 731: 729: 720: 716: 712: 708: 705:(4): 534–42. 704: 700: 693: 691: 689: 687: 685: 683: 674: 670: 666: 662: 659:(5): 815–25. 658: 654: 647: 645: 636: 632: 627: 622: 618: 614: 610: 603: 601: 592: 588: 583: 578: 574: 570: 566: 562: 558: 551: 549: 547: 545: 543: 541: 534: 532: 525: 523: 518: 509: 506: 504: 501: 500: 492: 489: 487: 484: 482: 479: 477: 474: 473: 470:Notable cases 467: 465: 455: 451: 449: 444: 442: 438: 428: 425: 423: 419: 415: 405: 403: 399: 391: 388: 385: 382: 379: 378: 377: 375: 365: 358: 357:Kidney biopsy 354: 350: 346: 342: 333: 331: 326: 324: 320: 316: 306: 304: 300: 296: 294: 289: 287: 283: 279: 275: 271: 267: 262: 259: 255: 251: 249: 245: 240: 237: 233: 229: 225: 217: 213: 208: 196: 193: 190: 186: 183: 181: 178: 175: 172: 169: 165: 162: 161: 160: 154: 150: 147: 143: 139: 136: 135: 134: 132: 122: 119: 115: 111: 107: 103: 99: 95: 91: 87: 77: 71: 68: 66: 62: 58: 54: 53:Kidney biopsy 50: 45: 41: 36: 32: 28: 23: 2448:Pauci-immune 2444:Type III RPG 2341:By condition 2298: 2217: 2206: 2182: 2171: 2145: 2130: 2110: 2063: 2059: 2033: 2029: 2023: 1998: 1994: 1948: 1944: 1907:(5): 920–6. 1904: 1900: 1890: 1853: 1849: 1839: 1814: 1810: 1779:(1): 49–55. 1776: 1772: 1765: 1730: 1726: 1715: 1706: 1671: 1667: 1657: 1632: 1628: 1621: 1586: 1582: 1572: 1547: 1543: 1537: 1515:(1): 36–41. 1512: 1508: 1502: 1477: 1473: 1439: 1435: 1429: 1394: 1390: 1350: 1346: 1312: 1308: 1302: 1291:. 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Retrieved 786:. 2021-10-28 783: 744: 740: 702: 698: 656: 652: 616: 612: 564: 560: 529: 486:Sean Elliott 481:Gary Coleman 461: 458:Epidemiology 452: 445: 434: 426: 411: 395: 374:renal biopsy 371: 327: 315:renal biopsy 312: 297: 290: 281: 273: 265: 263: 260: 256: 252: 241: 221: 158: 128: 89: 85: 84: 2405:Type II RPG 2353:Amyloidosis 2208:MedlinePlus 1995:Blood Purif 1945:BMC Nephrol 1674:(1): 72–6. 1016:(2): 90–3. 441:proteinuria 330:proteinuria 195:Fatty casts 110:proteinuria 94:(sclerosis) 30:Other names 2506:Categories 2383:Type I RPG 2304:Membranous 2030:Neth J Med 1901:Kidney Int 1856:: 846173. 1293:2022-06-30 1215:Kidney Int 1174:: 481520. 790:2023-11-14 613:Kidney Int 514:References 398:prognostic 349:glomerulus 345:Micrograph 224:glomerulus 212:glomerulus 210:The renal 153:antibodies 131:glomerulus 70:Nephrology 49:micrograph 2369:nephritic 2366:Primarily 2277:nephrotic 2274:Primarily 2219:eMedicine 2189:236403004 2184:SNOMED CT 1668:Nat Genet 1629:Nat Genet 476:Andy Cole 448:nephrotic 431:Prognosis 418:nephrotic 408:Treatment 353:PAS stain 323:sclerosis 319:glomeruli 309:Diagnosis 244:sclerosis 228:Podocytes 102:podocytes 98:glomeruli 65:Specialty 57:PAS stain 2348:Diabetic 2224:med/2944 2080:15716334 2042:16301760 2015:32074606 1977:26156092 1923:16518352 1882:35308512 1757:21997394 1698:20023659 1649:10742096 1613:18614772 1494:22349487 1421:29321142 1367:28664408 1270:30454752 1235:27165817 1200:22685655 1149:24875196 1065:12704577 1030:11863085 992:29852493 940:21896374 886:25447132 673:15492947 591:28242845 497:See also 2479:General 2178:D005923 1968:4496884 1951:: 101. 1873:8927620 1831:8250036 1793:8808109 1748:3231787 1689:2980844 1604:2551572 1564:3718096 1529:3966467 1456:2658558 1412:5827609 1329:8792409 1191:3363986 1140:4123398 1100:9829131 983:6589822 931:3709971 877:4772430 848:Fogo AB 829:9370176 761:8203357 719:7702047 635:7861720 582:5338705 278:podocin 270:nephrin 146:albumin 2213:000478 2167:600995 2164:613237 2161:612551 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Index


micrograph
Kidney biopsy
PAS stain
Specialty
Nephrology
Edit this on Wikidata
(sclerosis)
glomeruli
podocytes
nephrotic syndrome
proteinuria
edema
Kidney failure
glomerulus
edema
albumin
antibodies
Protein in the urine
nephrotic syndrome
Low serum albumin
Low serum antibodies
High serum cholesterol
oncotic pressure
Fatty casts

glomerulus
Bowman's space
glomerulus
Podocytes

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