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Journal articles on the topic 'Glomerulonephriti'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

Mukhtarova, A. V. Mukhtarova, M. M. Batyushin Batyushin, E. А. Sinelnik Sinelnik, N. V. Antipova Antipova, and A. V. Razina Razina. "Effect of VEGF a on the development of tubulointerstitial fibrosis and the probability of achieving complete remission in patients with primary chronic glomerulonephriti." Nephrology 4_2021 (December 29, 2021): 48–52. http://dx.doi.org/10.18565/nephrology.2021.4.48-52.

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2

Vanga, Amaresh, Sandeep Magoon, Jolanta Kowalewska, and Saad Mussarat. "Fibrilo-Tactoid Glomerulonephritis: A Possible Novel Morphological Variant." Case Reports in Nephrology and Dialysis 10, no. 3 (November 17, 2020): 154–62. http://dx.doi.org/10.1159/000510871.

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Fibrillary and immunotactoid glomerulonephritis are infrequent causes of primary nephrotic range proteinuria and are poorly understood. Recent significant developments include the discovery of DNA JB9 antigen in fibrillary glomerulonephritis. Here, we present a case of a middle-aged woman who presented with nephrotic range proteinuria, hematuria, and normal renal function. Renal biopsy revealed fibrils that were randomly arranged on electron microscopy. They were of small size and congo red negative similar to the ones found in fibrillary glomerulonephritis, but were also DNA JB 9 negative, and had a hollow core like in immunotactoid glomerulopathy. Though we try to classify these conditions into either immunotactoid glomerulonephropathy (ITGN) or fibrillary glomerulonephritis (FGN), there are scenarios such as this case where it does not fit into either and is probably an overlap or intermediate variant of these two conditions. Pathological features of these glomerulonephrites are discussed together with their clinical implications, treatment choices, and diagnostic importance.

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3

Manitius, J., B. Biedunkiewicz, J. Kustosz, and B. Rutkowski. "The Relationship between Insulin, Glucose and Serum Uric Acid and Their Contribution to the Progression of Renal Damage in Patients with Primary Glomerulonephritis." Journal of International Medical Research 24, no. 6 (November 1996): 449–53. http://dx.doi.org/10.1177/030006059602400601.

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It is known that some metabolic disturbances may modify the progression of renal disease including primary glomerulonephritis, but the role of purines in this process is still unknown. To investigate this, 13 untreated patients with primary glomerulonephritis were followed up for a mean of 17.6 months to analyze the changes in proteinuria and glomerular filtration rate. On entering the study, each patient was given an oral glucose tolerance test and an oral fructose load test. The areas under the glucose (PGA), insulin (PIA) and uric acid (PUAA, post-fructose) curves were calculated. Glomerulonephritic patients were found to have a statistically higher response to fructose than controls (782 ± 219 vs 518 ± 154, P < 0.005). Multiple regression analysis showed that PGA, PIA and PUAA were independently related to changes in proteinuria and glomerular filtration rate during the natural course of the disease. This preliminary study suggests that purine metabolism may modulate the progression of renal disease in proteinuric patients.

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4

Alaridhee, Hasanain, Azzah Alharbi, Zeayd Saeed, Róisín C. Thomas, and Cordula M. Stover. "Complement Properdin Determines Disease Activity in MRL/lpr Mice." Medicina 56, no. 9 (August 27, 2020): 430. http://dx.doi.org/10.3390/medicina56090430.

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Background and objects: In systemic lupus erythematosus, circulating immune complexes activate complement and, when trapped in renal capillaries, cause glomerulonephritis. Mouse models have been used in the preclinical assessment of targeting complement activation pathways to manage chronic inflammation in lupus. Properdin is the only known positive regulator of complement activation, but its role in the severity of lupus nephritis has not been studied yet. Materials and Methods: Fully characterized properdin-deficient mice were crossed with lupus prone MRL/lpr mice on C57Bl/6 background. Results: Compared to MRL/lpr properdin wildtype mice, MRL/lpr properdin-deficient mice had significantly lower anti-DNA antibody titres, TNFα and BAFF levels in serum. The qualitative glomerulonephritic score was less severe and there was significantly less serum creatinine in MRL/lpr properdin-deficient mice compared to MRL/lpr properdin wildtype littermate mice. Conclusion: Properdin plays a significant role in the severity of lupus overall and specifically in the extent of glomerulonephritis observed in MRL/lpr mice. Because MRL/lpr properdin-deficient mice had lower levels of anti-DNA antibodies, inflammatory mediators and markers of renal impairment, the study implies that properdin could constitute a novel therapy target in lupus disease.

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5

Wagner, J., S. Volk, C. C. Haufe, A. Ciechanowicz, M. Paul, and E. Ritz. "Renin gene expression in human kidney biopsies from patients with glomerulonephritis or graft rejection." Journal of the American Society of Nephrology 5, no. 7 (January 1995): 1469–75. http://dx.doi.org/10.1681/asn.v571469.

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The expression of renin mRNA was determined by a quantitative polymerase chain reaction assay in 27 human kidney samples: (1) 15 biopsies of patients with glomerulonephritis with or without angiotensin-converting enzyme inhibitor (ACEI) treatment; (2) biopsies of six renal allografts with graft rejection; and (3) six biopsy samples from unaffected parts of tumor nephrectomy specimens as controls. After isolation of RNA, 0.5 to 1 microgram of total RNA was used for reverse transcription to generate cDNA. The human renin gene was subsequently amplified by the use of two primers spanning the second and third exons. Renin expression was quantified with a renin cDNA mutant as the internal standard. It exhibited the same primer binding sites as the endogenous gene but carried a 155-basepair deletion, thus yielding a shorter amplification product. The number of glomeruli was counted by microscopic transillumination immediately after biopsy (median, 9 per biopsy; range, 2 to 23). Renin mRNA was expressed as femtograms of renin mRNA per glomerulus. Renin gene expression was lower in glomerulonephritic patients without ACEI treatment compared with that in control tumor nephrectomy samples, i.e., 63 +/- 20 (N = 7) versus 250 +/- 50 fg (N = 6) of renin mRNA/glomerulus, (P < 0.02), although plasma renin concentration in the glomerulonephritic patients was in the normal range. Significantly higher renin mRNA expression was found in glomerulonephritic patients treated with ACEI, i.e., 210 +/- 50 (N = 8) compared with 63 +/- 20 (N = 7) fg of renin mRNA/glomerulus in patient not treated with ACEI (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

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6

Werber, H. I., S. N. Emancipator, M. L. Tykocinski, and J. R. Sedor. "The interleukin 1 gene is expressed by rat glomerular mesangial cells and is augmented in immune complex glomerulonephritis." Journal of Immunology 138, no. 10 (May 15, 1987): 3207–12. http://dx.doi.org/10.4049/jimmunol.138.10.3207.

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Abstract Cultured rat mesangial cells have features of immune effector cells that may contribute to the derangements in glomerulonephritis. Recent reports have demonstrated that mesangial cells produce a cytokine similar to interleukin 1 (IL 1). We predicted rat mesangial cells could express a gene homologous to murine macrophage IL 1. Mesangial cells were cultured by explant and were used in the fourth through sixth passages. Antibodies to desmin and fibronectin but not cytokeratin stained the cytoskeleton of all mesangial cells examined; no Ia+, leukocyte common antigen+ mononuclear phagocytes were present. RNA from mesangial cells and P388D macrophages hybridized in dot blots with a 32P-probe nick-translated from the murine IL 1 cDNA. Mesangial cells but not Swiss 3T3 fibroblasts contained IL 1 mRNA transcripts that co-migrated with the 2.0 kb message from murine P388D macrophages by Northern analysis of poly(A) RNA. In situ hybridization of cultured cells demonstrated specific hybridization of 3H-IL 1 probe to cells with the morphology of contractile mesangial cells and P388D cells but not 3T3 cells. IL 1 release is an important mediator of local inflammation and injury. Therefore we compared the expression of the IL 1 gene in total RNA from kidneys of rats with immune complex glomerulonephritis with that extracted from kidneys of healthy rats. Glomerulonephritic kidneys contain a twofold to threefold increase in IL 1 mRNA compared with normals. We conclude that rat mesangial cells express mRNA with significant homology to murine macrophage IL 1 mRNA and further suggest that local production of the potent phlogistic mediator IL 1 may be important in the pathogenesis of glomerulonephritis.

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7

Peterson, O. W., L. C. Gushwa, C. B. Wilson, and R. C. Blantz. "Tubuloglomerular feedback activity after glomerular immune injury." American Journal of Physiology-Renal Physiology 257, no. 1 (July 1, 1989): F67—F71. http://dx.doi.org/10.1152/ajprenal.1989.257.1.f67.

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Tubuloglomerular feedback responses were examined in control euvolemic and glomerulonephritic rats 4 wk after administration of antiglomerular basement membrane antibody (AGBM). Single-nephron glomerular filtration rate (SNGFR) was reduced approximately 30% in AGBM rats. Tubuloglomerular feedback responses were also tested with both artificial and native tubular fluid. SNGFR was evaluated at 0, 10, 20, 30, and 40 nl/min. Tubuloglomerular feedback response was present in both control and AGBM rats, although there was a shift in turning point or perfusion rate down and leftward at which SNGFR decreased in the AGBM rats. No difference in tubuloglomerular feedback responses was observed between artificial and native tubular fluids. In this model of moderate glomerulonephritis, tubuloglomerular feedback activity appears to be appropriate and intact, and the composition of the fluid entering the loop of Henle does not appear to determine or to be a condition for the presence or absence of tubuloglomerular feedback activity.

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8

Horino, Taro, and Yoshio Terada. "5. Mesangial Proliferative Glomerulonephritis, Endocapillary Proliferative Glomerulonephritis, Crescentic Glomerulonephritis." Nihon Naika Gakkai Zasshi 98, no. 5 (2009): 1036–41. http://dx.doi.org/10.2169/naika.98.1036.

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9

Zarconi, Joseph, and Michael C. Smith. "Glomerulonephritis." Postgraduate Medicine 84, no. 1 (July 1988): 239–51. http://dx.doi.org/10.1080/00325481.1988.11700351.

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10

Dittrich, K. "Glomerulonephritis." Kinder- und Jugendmedizin 10, no. 04 (2010): 195–202. http://dx.doi.org/10.1055/s-0038-1628975.

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ZusammenfassungGlomerulonephritiden sind relativ seltene Erkrankungen im Kindesalter, die resultierenden chronischen glomerulären Veränderungen führen jedoch dazu, dass in Deutschland jedes fünfte Kind mit chronischem Nierenersatzverfahren eine Glomerulonephritis als Grunderkrankung hat.Glomerulonephritiden manifestieren sich in dieser Altersgruppe überwiegend als akute Erkrankungen. Auch rapid progressive Verläufe mit plötzlicher Verschlechterung der Nierenfunktion sind bekannt, während schleichende Verläufe mit chronischer Hämaturie und/oder Proteinurie wesentlich seltener beobachtet werden.Die Langzeitprognose hängt stark von der rechtzeitigen Diagnosestellung und gezielten Behandlung ab. Deshalb sollte jeder Kinderarzt die klinischen Zeichen einer möglichen Glomerulonephritis kennen und die notwendigen diagnostischen Maßnahmen einleiten. Die rationale Diagnostik und die Besonderheiten typischer, im Kindesalter auftretender Glomerulonephritisformen werden in diesem Beitrag vorgestellt. Da die glomeruläre Entzündungsreaktion überwiegend immunologisch bedingt ist, besteht die Therapie neben symptomatischen auch aus immunsuppressiven Maßnahmen. Die Art der Behandlung ist jedoch von den in der Nierenbiopsie festgestellten spezifischen Veränderungen abhängig. Die kindernephrologische Mitbetreuung der betroffenen Kinder ist nicht nur bei chronischen Systemerkrankungen, sondern auch nach akuten Glomerulonephritiden notwendig.

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11

Floege, J., and A. Bienert. "Glomerulonephritis." DMW - Deutsche Medizinische Wochenschrift 138, no. 30 (July 16, 2013): 1515–28. http://dx.doi.org/10.1055/s-0033-1343239.

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12

Macanovic, Momir, and Peter Mathieson. "Glomerulonephritis." Medicine 31, no. 5 (May 2003): 36–42. http://dx.doi.org/10.1383/medc.31.5.36.27659.

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13

Hricik, Donald E., Moonja Chung-Park, and John R. Sedor. "Glomerulonephritis." New England Journal of Medicine 339, no. 13 (September 24, 1998): 888–99. http://dx.doi.org/10.1056/nejm199809243391306.

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14

Stahl, Rolf, and Elion Hoxha. "Glomerulonephritis." DMW - Deutsche Medizinische Wochenschrift 141, no. 13 (June 30, 2016): 960–68. http://dx.doi.org/10.1055/s-0042-107410.

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15

Couser, William G. "Glomerulonephritis." Lancet 353, no. 9163 (May 1999): 1509–15. http://dx.doi.org/10.1016/s0140-6736(98)06195-9.

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16

Durand, JM, and S. Burtey. "Glomerulonephritis." Lancet 354, no. 9176 (July 1999): 428–29. http://dx.doi.org/10.1016/s0140-6736(05)75849-9.

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17

Wardle, EN. "Glomerulonephritis." Lancet 354, no. 9176 (July 1999): 429. http://dx.doi.org/10.1016/s0140-6736(05)75850-5.

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18

Hohenstein, B., and C. Hugo. "Glomerulonephritis." Der Nephrologe 6, no. 3 (May 2011): 242–48. http://dx.doi.org/10.1007/s11560-010-0432-3.

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19

Mathieson, Peter W. "Glomerulonephritis." Seminars in Immunopathology 29, no. 4 (October 20, 2007): 315–16. http://dx.doi.org/10.1007/s00281-007-0095-y.

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20

Chadban, SJ, and RC Atkins. "Glomerulonephritis." Lancet 365, no. 9473 (May 2005): 1797–806. http://dx.doi.org/10.1016/s0140-6736(05)66583-x.

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21

Remuzzi, Giuseppe, Carla Zoja, and Tullio Bertani. "Glomerulonephritis." Current Opinion in Nephrology and Hypertension 2, no. 3 (May 1993): 465–74. http://dx.doi.org/10.1097/00041552-199305000-00015.

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22

Abbate, Mauro, and Giuseppe Remuzzi. "Glomerulonephritis." Current Opinion in Nephrology and Hypertension 4, no. 4 (July 1995): 374. http://dx.doi.org/10.1097/00041552-199507000-00016.

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23

Badr, Kamal F. "Glomerulonephritis." Current Opinion in Nephrology and Hypertension 6, no. 2 (March 1997): 111–18. http://dx.doi.org/10.1097/00041552-199703000-00001.

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24

Dendorfer, U., and J. Mann. "Glomerulonephritis." DMW - Deutsche Medizinische Wochenschrift 131, no. 3 (2006): 93–100. http://dx.doi.org/10.1055/s-2006-924931.

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25

Floege, J. "Glomerulonephritis." Der Nephrologe 10, no. 5 (August 26, 2015): 365–67. http://dx.doi.org/10.1007/s11560-014-0965-y.

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26

Hohenstein, B., and C. Hugo. "Glomerulonephritis." Der Nephrologe 11, no. 2 (November 18, 2015): 116–23. http://dx.doi.org/10.1007/s11560-015-0019-0.

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27

Floege, Jürgen. "Glomerulonephritis." Der Nephrologe 15, no. 6 (November 2020): 335. http://dx.doi.org/10.1007/s11560-020-00459-x.

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28

Haller, H., and W. L. Gross. "Glomerulonephritis." Der Internist 44, no. 9 (September 1, 2002): 1073–74. http://dx.doi.org/10.1007/s00108-003-1019-0.

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29

Haller, H., and W. L. Gross. "Glomerulonephritis." Der Internist 44, no. 11 (November 1, 2003): 1412. http://dx.doi.org/10.1007/s00108-003-1089-z.

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30

LAU, K. "Glomerulonephritis." Adolescent Medicine Clinics 16, no. 1 (February 2005): 67–85. http://dx.doi.org/10.1016/j.admecli.2004.09.008.

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31

Shah, HH, J. Thakkar, JM Pullman, and AT Mathew. "Fibrillary glomerulonephritis presenting as crescentic glomerulonephritis." Indian Journal of Nephrology 27, no. 2 (2017): 157. http://dx.doi.org/10.4103/0971-4065.200521.

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32

Ishii, Masao, Yasunobu Hirata, Tokuichiro Sugimoto, Hiroaki Matsuoka, Kenjiro Kimura, Toshihiko Ishimitsu, Kazushige Fukui, et al. "Effect of α-Human Atrial Natriuretic Peptide on Proteinuria in Patients with Primary Glomerular Diseases." Clinical Science 77, no. 6 (December 1, 1989): 643–50. http://dx.doi.org/10.1042/cs0770643.

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1. The effects of synthetic α-human atrial natriuretic peptide (α-hANP) on urinary protein excretion were examined in nine healthy subjects and 20 patients with primary glomerular diseases who had proteinuria of 1.0 g or more per day. Synthetic α-hANP was intravenously infused into supine subjects at a rate of 8.3 pmol min−1 kg−1 for 40 min 2. Before α-hANP infusion, the plasma concentration of immunoreactive α-hANP was significantly higher in the patients with glomerulonephritis than in the normal subjects (44.3 ± 8.7 vs 19.4 ± 3.0 pmol/l, mean ± sem, P < 0.01) and it showed a positive correlation with mean arterial pressure (rs = 0.84, P < 0.001) and a negative correlation with creatinine clearance (rs = −0.50, P < 0.01) 3. During infusion of α-hANP, although the urinary excretion of protein did not change significantly in the normal subjects, it increased from 0.6 ± 0.2 to 3.0 ± 0.8 mg min−1 m−2 (P < 0.001) in the patients with glomerulonephritis. The urinary protein/creatinine ratio did not change significantly in the former (from 0.18 ± 0.05 to 0.22 ± 0.06; NS), whereas it rose from 3.25 ± 0.94 to 7.62 ± 1.31 (P < 0.001) in the latter 4. The urinary excretions of albumin and of α1-, α2-, β- and γ-globulins, which were electrophoretically analysed, all increased in eight nephrotic patients during or immediately after infusion of α-hANP 5. The α-hANP infusion increased urinary volume, urinary excretion of sodium and creatinine clearance in the glomerulonephritic patients, whereas the changes in urinary volume and creatinine clearance were not significant in the normal subjects. Renal blood flow did not show any significant changes in either group. Packed cell volume increased slightly, but significantly, in the two groups, whereas plasma renin activity did not show any significant changes in either group 6. These results suggest that α-hANP increases the transglomerular permeability to plasma protein in damaged glomeruli, most likely affecting the steric hindrance.

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33

Adey, D. B., B. R. MacPherson, and G. C. Groggel. "Glomerulonephritis with associated hypocomplementemia and crescents: an unusual case of fibrillary glomerulonephritis." Journal of the American Society of Nephrology 6, no. 2 (August 1995): 171–76. http://dx.doi.org/10.1681/asn.v62171.

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Fibrillary glomerulonephritis is an unusual, but not rare cause of glomerulonephritis. Hypocomplementemia in association with fibrillary glomerulonephritis has been reported only once previously. A patient with hypocomplementemia and fibrillary deposits as demonstrated by electronmicroscopy is reported. The clinical and pathologic features of fibrillary glomerulonephritis and immunotactoid glomerulopathy are reviewed.

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34

Samad, Tabassum, Wasim Md Mohosin Ul Haque, Muhammad Abdur Rahim, Mehruba Alam Ananna, and Sarwar Iqbal. "A Two Year Observation on Trend of Primary Glomerulonephritis in A Tertiary Care Hospital of Bangladesh." Bangladesh Journal of Medicine 27, no. 2 (August 3, 2016): 68–70. http://dx.doi.org/10.3329/bjmed.v27i2.29052.

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Aim: Glomerulonephritis remains the most probable underlying cause of end stage renal disease of uncertain aetiology in many developing countries, including Bangladesh. The pattern of glomerular disease varies widely from country to country. In Bangladesh, the incidence and histological pattern of glomerulonephritis is inadequately described. We performed a study, aiming to determine pattern of primary glomerulonephritis in a tertiary care hospital of our country.Material & Methods: It was a cross-sectional hospital based prospective study conducted at BIRDEM general hospital starting from from July 2013 to June 2015. It included all patients with primary glomerulonephritis and who underwent native kidney biopsy.Result: Total 67 biopsy were performed and among them primary glomerulonephritis was 42. Female and male ratio was 1.3:1 and mean age was 42.73±14 (14-75) years. Indications of biopsy were proteinuria (>1gm/day) and unexplained acute kidney injury. The commonest histopathological pattern in primary glomerulonephritis was membranoproliferative glomerulonephritis 33.33% (14/ 42) followed by mesangial proliferative glomerulonephritis 30.95% (13/42). Only three (7%) patient required blood transfusion for post biopsy bleeding. No one required nephrectomy.Conclusion: In conclusion, mesangial proliferative and membranoproliferative glomerulonephritis are the two most common causes of primary glomerulonephritis. Nephrotic range proteinuria was the main indication of biopsy. Post biopsy complication was negligible. Creation of a national renal registry is essential for obtaining more specific epidemiological data.Bangladesh J Medicine Jul 2016; 27(2) : 68-70

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35

Soliman, A. R., A. A. El Meligi, M. El Semari, M. El Shemi, and H. Mahmoud. "Possible new role for angiotensin-converting enzyme inhibitors in treating glomerulonephritis." Eastern Mediterranean Health Journal 9, no. 3 (September 1, 2021): 399–406. http://dx.doi.org/10.26719/2003.9.3.399.

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Serum transforming growth factor-beta [TGF-beta1] production was estimated for 10 patients with essential hypertension, 12 patients with glomerulonephritis [5 hypertensive and 7 normotensive] and 10 healthy controls. The glomerulonephritis group received angiotensin-converting enzyme inhibitor captopril 25-75 mg/day for 4 weeks. Blood urea, serum creatinine, 24-hour urinary protein and serum TGF-beta1 were then re-estimated. Urea and creatinine were significantly higher in the hypertension and glomerulonephritis groups than in the controls and also higher in the glomerulonephritis group than the hypertension group. TGF-beta1 was significantly higher in the glomerulonephritis groups than in the control and hypertension groups. TGF-beta1 and 24-hour urinary protein were significantly reduced in the glomerulonephritis group

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36

Stoian, Marilena, Gabriel Scarlat, Bassil Dona, Bianca Procopiescu, and Claudia Ciofu. "Clinico-Pathological Correlations of Poststreptococcal Glomerulonephritis." Internal Medicine 19, no. 2 (February 1, 2022): 63–70. http://dx.doi.org/10.2478/inmed-2022-0208.

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Abstract Postinfectious glomerulonephritis is associated with bacterial, viral, fungal, and parasitic infectious agents and histologically appears most often as acute diffuse endocapillary or proliferative glomerulonephritis secondary infection with: group A streptococcus, streptococcus viridans, staphilococus aureus, diploccocus pneumoniae, Brucella melitensis, Salmonella typhi, Yershinia enterocolitica, Plasmodium falciparum, meningococcus, Mycoplasma, Klebsiella, varicella, variola, mumps. Less commonly, it appears as diffuse crescentic glomerulonephritis and a lot of infectious causes are incriminated like: streptococcus, legionella, varicella, Treponema pallidum or as focal crescentic glomerulonephritis: streptococcus A. It rarely appears as mesangiocapillary glomerulonephritis secondary infection with: streptococcus viridans, hepatitis C virus; diffuse or focal mesangial proliferative glomerulonephritis: hepatitis B virus, salmonella, adenovirus, influenza virus, salmonella; focal segmental, necrotizing and sclerosing glomerulonephritis: bacterial endocarditis; membranous glomerulonephritis: hepatitis B virus, syphilis, filarial, Mycobacterium, plasmodium falciparum; focal proliferative: Mycoplasma; mesangiolytic glomerulonephritis :Echo virus. Poststreptococcal glomerulonephritis (PSGN) is caused by prior infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The clinical presentation of PSGN varies from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury. The prognosis is generally favorable, especially in children, but in some cases, the long-term prognosis is not benign. Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patients.

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37

Bhardwaj, Parul, Anju Bala, and Parvinder Singh. "Viral Hepatitis A and B as Differential in Children Presenting with Acute Glomerulonephritis." International Journal of Science and Healthcare Research 6, no. 3 (August 11, 2021): 154–57. http://dx.doi.org/10.52403/ijshr.20210725.

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Hepatitis A and B presenting as acute glomerulonephritis is rare in pediatric age group. In children it is necessary to recognize glomerulonephritis early in the course of disease so as to prevent long term morbidity. Cases described in this report indicate that children presenting with acute glomerulonephritis must be investigated for viral hepatitis. Keywords: Glomerulonephritis, Hepatitis A, Hepatitis B.

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38

Sharma, Purva, Michael Kuperman, Lorraine Racusen, and Duvuru Geetha. "Fibrillary Glomerulonephritis Presenting as Rapidly Progressive Glomerulonephritis." American Journal of Kidney Diseases 60, no. 1 (July 2012): 157–59. http://dx.doi.org/10.1053/j.ajkd.2011.12.024.

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39

Kawamorita, Yosuke, Yoshihide Fujigaki, Atsuko Imase, Shigeyuki Arai, Yoshifuru Tamura, Masayuki Tanemoto, Hiroshi Uozaki, Yutaka Yamaguchi, and Shunya Uchida. "Successful Treatment of Infectious Endocarditis Associated Glomerulonephritis Mimicking C3 Glomerulonephritis in a Case with No Previous Cardiac Disease." Case Reports in Nephrology 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/569047.

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We report a 42-year-old man with subacute infectious endocarditis (IE) with septic pulmonary embolism, presenting rapidly progressive glomerulonephritis and positive proteinase 3-anti-neutrophil cytoplasmic antibody (PR3-ANCA). He had no previous history of heart disease. Renal histology revealed diffuse endocapillary proliferative glomerulonephritis with complement 3- (C3-) dominant staining and subendothelial electron dense deposit, mimicking C3 glomerulonephritis. Successful treatment of IE with valve plastic surgery gradually ameliorated hypocomplementemia and renal failure; thus C3 glomerulonephritis-like lesion in this case was classified as postinfectious glomerulonephritis. IE associated glomerulonephritis is relatively rare, especially in cases with no previous history of valvular disease of the heart like our case. This case also reemphasizes the broad differential diagnosis of renal involvement in IE.

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Adhikari, Sudhir, Deekshanta Sitaula, Shanti Regmi, Biraj Parajuli, and Sumita Poudel. "ACUTE GLOMERULONEPHRITIS IN CHILDREN: A HOSPITAL-BASED STUDY IN A TERTIARY CARE CENTRE IN NEPAL." Journal of Chitwan Medical College 12, no. 1 (March 15, 2022): 9–12. http://dx.doi.org/10.54530/jcmc.548.

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Background: Acute glomerulonephritis is a common pediatric kidney disease which places a huge burden in developing countries. This study aimed to evaluate causes, clinical manifestations, laboratory findings and complications of acute glomerulonephritis in children presented to a tertiary care center of Nepal. Methods: This was a retrospective review of records of children admitted with acute glomerulonephritis at Chitwan Medical College from April 2018 to February 2021. Socio-demographic data, clinic-laboratory profile and outcomes were obtained from medical records and descriptive analysis was carried out. Results: Among 48 recruited children with acute glomerulonephritis, 60.4% were male and the mean age was 9.5 ± 3.7 years. Post infectious glomerulonephritis including post streptococcal glomerulonephritis (48%) was the main cause of acute glomerulonephritis. The major clinical features were edema (81.3%), hypertension (72.9%), dyspnea (29.2%) and hematuria (25%). ASO titer was positive in 45.8%. The complications noted were acute kidney injury (6.3%), hypertensive emergency (6.3%) and congestive cardiac failure (2.1%). Conclusions: Most of the patients were above 5 years of age and presented most commonly during autumn and summer season. The complications of acute glomerulonephritis were acute kidney injury, hypertensive emergency and congestive cardiac failure.

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Konstantinov, Konstantin N., Suzanne N. Emil, Marc Barry, Susan Kellie, and Antonios H. Tzamaloukas. "Glomerular Disease in Patients with Infectious Processes Developing Antineutrophil Cytoplasmic Antibodies." ISRN Nephrology 2013 (February 19, 2013): 1–18. http://dx.doi.org/10.5402/2013/324315.

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To identify differences in treatment and outcome of various types of glomerulonephritis developing in the course of infections triggering antineutrophil cytoplasmic antibody (ANCA) formation, we analyzed published reports of 50 patients. Immunosuppressives were added to antibiotics in 22 of 23 patients with pauci-immune glomerulonephritis. Improvement was noted in 85% of 20 patients with information on outcomes. Death rate was 13%. Corticosteroids were added to antibiotics in about 50% of 19 patients with postinfectious glomerulonephritis. Improvement rate was 74%, and death rate was 26%. Two patients with mixed histological features were analyzed under both pauci-immune and post-infectious glomerulonephritis categories. In 9 patients with other renal histology, treatment consisted of antibiotics alone (7 patients), antibiotics plus immunosuppressives (1 patient), or immunosuppressives alone (1 patient). Improvement rate was 67%, permanent renal failure rate was 22%, and death rate was 11%. One patient with antiglomerular basement disease glomerulonephritis required maintenance hemodialysis. Glomerulonephritis developing in patients who became ANCA-positive during the course of an infection is associated with significant mortality. The histological type of the glomerulonephritis guides the choice of treatment. Pauci-immune glomerulonephritis is usually treated with addition of immunosuppressives to antibiotics.

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Ramos, Eduardo Antonio Gonçalves, and Zilton A. Andrade. "Chronic glomerulonephritis associated with hepatosplenic schistosomiasis mansoni." Revista do Instituto de Medicina Tropical de São Paulo 29, no. 3 (June 1987): 162–67. http://dx.doi.org/10.1590/s0036-46651987000300008.

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In a series of 36 cases of renal disease associated with hepatosplenic schistosomiasis the following morphologic types of glomerulonephritis were found: mesangio-capillary (33.2%), mesangial proliferative (25.0%), focal glomerular sclerosis (16.7%) and sclerosing glomerulonephritis (8.3%). No significant statistical differences were found when these results were compared with those from 36 cases of glomerulonephritis not associated with hepatosplenic disease. On the other hand, endocapillary glomerulonephritis was found to be predominant in the latter group of cases. These results did not substantiate the assumption that mesangio-capillary glomerulonephritis is specifically related to hepatosplenic schistosomiais. However, if the types of glomerulonephritis that predominantly involve the me-sangium are considered together, they are significantly associated with hepatosplenic schistosomiasis. Mesangial involvement is known to occur in other parasitic diseases and that may be related to a common immunopathogenesis.

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Lhotta, K., H. P. Neumayer, M. Joannidis, D. Geissler, and P. KöNig. "Renal expression of intercellular adhesion molecule-1 in different forms of glomerulonephritis." Clinical Science 81, s25 (October 1, 1991): 477–81. http://dx.doi.org/10.1042/cs0810477.

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1. Expression of intercellular adhesion molecule-1 was investigated in five normal kidneys and 47 renal biopsies with the use of monoclonal antibody 7F7 and immunoperoxidase staining. 2. In the normal kidney, intercellular adhesion molecule-1 was expressed on endothelial cells of glomerular and peritubular capillaries, on Bowman's capsule, on some interstitial cells and weakly in the mesangium. 3. Increased glomerular staining was detected in early cases of rapidly progressing glomerulonephritis (5/8) and in some cases of non-IgA mesangioproliferative glomerulonephritis (5/9), IgA nephropathy (3/5), Henoch-Schoenlein purpura (2/2), lupus nephritis (5/6) and focal segmental glomerulosclerosis (1/3). A decrease in intercellular adhesion molecule-1 expression was noted in advanced rapidly progressive glomerulonephritis (3/8), two cases of membraneous nephropathy, one severe mesangioproliferative glomerulonephritis biopsy, the two membranoproliferative glomerulonephritis biopsies and in sclerotic loops in focal segmental glomerulosclerosis. 4. Expression de novo on tubular epithelial cells occurred in rapidly progressive glomerulonephritis, in membranoproliferative glomerulonephritis, and to a lesser extent in some cases of membranous nephropathy, minimal change disease, IgA nephropathy, focal segmental glomerulosclerosis, a severe case of mesangioproliferative glomerulonephritis and in the mixed essential cryoglobulinaemia case. In 63% of positive tubuli, intraluminal cells which expressed CD18, the common β-chain of leucocyte-function-associated antigen-1, Mac-1 and p150,95, were present. 5. Intercellular adhesion molecule-1 was also found on the majority (59%) of infiltrating mononuclear cells in all forms of glomerulonephritis.

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Takayasu, Mamiko, Kouichi Hirayama, Homare Shimohata, Masaki Kobayashi, and Akio Koyama. "Staphylococcus aureus Infection-Related Glomerulonephritis with Dominant IgA Deposition." International Journal of Molecular Sciences 23, no. 13 (July 5, 2022): 7482. http://dx.doi.org/10.3390/ijms23137482.

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Since 1995, when we reported the case of a patient with glomerulonephritis with IgA deposition that occurred after a methicillin-resistant Staphylococcus aureus (MRSA) infection, many reports of MRSA infection-associated glomerulonephritis have accumulated. This disease is being systematized as Staphylococcus infection-associated glomerulonephritis (SAGN) in light of the apparent cause of infection, and as immunoglobulin A-dominant deposition infection-related glomerulonephritis (IgA-IRGN) in light of its histopathology. This glomerulonephritis usually presents as rapidly progressive glomerulonephritis or acute kidney injury with various degrees of proteinuria and microscopic hematuria along with an ongoing infection. Its renal pathology has shown several types of mesangial and/or endocapillary proliferative glomerulonephritis with various degrees of crescent formation and tubulointerstitial nephritis. IgA, IgG, and C3 staining in the mesangium and along the glomerular capillary walls have been observed on immunofluorescence examinations. A marked activation of T cells, an increase in specific variable regions of the T-cell receptor β-chain-positive cells, hypercytokinemia, and increased polyclonal immune complexes have also been observed in this glomerulonephritis. In the development of this disease, staphylococcal enterotoxin may be involved as a superantigen, but further investigations are needed to clarify the mechanisms underlying this disease. Here, we review 336 cases of IgA-IRGN and 218 cases of SAGN.

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Kimmel, Martin. "Infekt-assoziierte Glomerulonephritiden." DMW - Deutsche Medizinische Wochenschrift 145, no. 04 (February 2020): 240–47. http://dx.doi.org/10.1055/a-0974-9420.

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AbstractGlomerulonephritis, secondary to bacterial, or, more rarely, viral or parasitic infections, is called infection-associated. The epidemiology of infection-associated glomerulonephritis has changed in recent decades. For a long time, the classic form has been acute poststreptococcal glomerulonephritis (APGN), but in developed countries its incidence has declined sharply. However, there is an increase in staphylococcal associated glomerulonephritis (SAGN). The clinical manifestations of APGN and SAGN are different: APGN typically presents with a glomerulonephritis after an infectious latency period (post-infectious), while SAGN typically shows an immune complex glomerulonephritis concomitant with infection (para-infectious). SAGN often presents with an occult infections in older patients with multiple comorbidities.

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Niles, J. L., G. L. Pan, A. B. Collins, T. Shannon, S. Skates, R. Fienberg, M. A. Arnaout, and R. T. McCluskey. "Antigen-specific radioimmunoassays for anti-neutrophil cytoplasmic antibodies in the diagnosis of rapidly progressive glomerulonephritis." Journal of the American Society of Nephrology 2, no. 1 (July 1991): 27–36. http://dx.doi.org/10.1681/asn.v2127.

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Circulating anti-neutrophil cytoplasmic antibodies (ANCA) have been described in most patients with "pauci-immune" necrotizing and crescentic glomerulonephritis. A 29-kDa serine protease (p29 or proteinase 3) and myeloperoxidase are the two best characterized antigens recognized by ANCA. The study presented here was conducted to define the diagnostic value of assays for antibodies against these two antigens in rapidly progressive glomerulonephritis. Radioimmunoassays were developed for anti-p29 and anti-myeloperoxidase antibodies, with purified antigens, and the results of the radioimmunoassays were compared with those obtained by immunofluorescence tests for ANCA. We performed assays on serum samples from 123 patients with the syndrome of rapidly progressive glomerulonephritis, as well as from 200 blood bank donors and from 717 additional control patients. Without knowledge of the results of ANCA tests, the renal pathologic findings in the 123 patients with rapidly progressive glomerulonephritis were analyzed, and 42 were classified as pauci-immune necrotizing and crescentic glomerulonephritis, 18 were classified as anti-glomerular basement membrane nephritis and 63 were classified as other forms of renal disease. We found radioimmunoassays to be more reliable in the diagnosis of pauci-immune necrotizing and crescentic glomerulonephritis than immunofluorescence testing. By radioimmunoassay, ANCA were found in 40 of 42 patients (95% sensitivity) with pauci-immune necrotizing and crescentic glomerulonephritis (14 with anti-p29 and 26 with anti-myeloperoxidase antibodies). The tests for antibodies to p29 and myeloperoxidase were 99.9 and 99.5% specific for pauci-immune necrotizing and crescentic glomerulonephritis, respectively. In the setting of rapidly progressive glomerulonephritis, a positive radioimmunoassay for anti-p29 or anti-myeloperoxidase antibodies (together with a negative test for anti-GBM antibodies) gives a probability of pauci-immune necrotizing and crescentic glomerulonephritis of over 99%.

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Majumdar, Avirup, Virendra Atam, and Mayank Mishra. "Rare case of post-varicella membranoproliferative glomerulonephritis presenting with massive proteinuria." BMJ Case Reports 13, no. 3 (March 2020): e233084. http://dx.doi.org/10.1136/bcr-2019-233084.

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Chicken pox caused by varicella zoster virus is usually a self-limiting disease causing rare life-threatening complications. Involvement of the kidneys is infrequent during the course of the illness. Literature shows rare reports of acute glomerulonephritis following varicella infection. We report a case of 16-year-old boy presenting with anasarca with characteristic healed rashes of chicken pox. His urinalysis revealed a ‘massive’ nephrotic range proteinuria (16 g/24 hours), gross hematuria and pyuria. A percutaneous renal biopsy showed membranoproliferative glomerulonephritis. Most cases of post-varicella glomerulonephritis have been described in children, massive proteinuria of this range in an immunocompetent adolescent, being an extremely rare entity. Acute proliferative glomerulonephritis in such cases is usually an immune complex hypocomplementaemic glomerulonephritis in response to the zoster infection. Proteinuria in most patients is benign and self-limiting with few fatal reports of crescentic glomerulonephritis progressing to acute renal failure.

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Torffvit, O., H. Thysell, and L. Nässberger. "Occurrence of Autoqntibodies Directed Against Myeloperoxidase and Elastase in Patients Treated with Hydralazine and Presenting with Glomerulonephritis." Human & Experimental Toxicology 13, no. 8 (August 1994): 563–67. http://dx.doi.org/10.1177/096032719401300810.

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We have undertaken an investigation retrospectively of 21 patients with positive antinuclear antibodies, who had been on hydralazine treatment and developed a glomerulonephritis. Four patients had circulating antimyeloperoxidase (MPO) and two of them were concluded to have a hydralazine-induced glomerulonephritis, corresponding to a frequency of 10%. These two patients had antibodies of IgG and IgM class directed against myeloperoxidase (MPO), and also antibodies against elastase. These two patients had also a biopsy proven extracapillary glomerulonephritis with focal segmental necrosis. Antibodies against elastase were furthermore seen in three patients with proliferative glomerulonephritis and in one patient with membranoproliferative glomerulonephritis. This study confirms an association between circulating anti-MPO and a histopathological picture compatible with extracapillary proliferation and focal segmental necrosis. From a clinical, histopathological and serological point of view it can be concluded that in two patients the glomerulonephritis was associated with antibody evidence of an autoimmune side effect.

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Andeen, Nicole K., Megan L. Troxell, Maziar Riazy, Rupali S. Avasare, Jessica Lapasia, J. Ashley Jefferson, Shreeram Akilesh, et al. "Fibrillary Glomerulonephritis." Clinical Journal of the American Society of Nephrology 14, no. 12 (November 4, 2019): 1741–50. http://dx.doi.org/10.2215/cjn.03870319.

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Background and objectivesFibrillary GN has been defined as an immune complex-mediated GN with amyloid-like fibrils larger than amyloid which are IgG positive and Congo red negative. With discovery of DNAJB9 as a highly sensitive and specific marker for fibrillary GN, the specificity of the morphologic criteria for establishing the diagnosis of fibrillary GN has come into question.Design, setting, participants, & measurementsWe sought to (1) determine anatomic characteristics that best define fibrillary GN and (2) identify clinical and pathologic features that predict outcomes.ResultsWe retrospectively reviewed kidney biopsies from patients diagnosed with fibrillary GN or suspected fibrillary GN between 1997 and 2017 (n=266, 65% female, median age 61). Approximately 11% of kidney biopsies had one or more unusual feature including monotypic deposits, Congo red positivity, or unusual fibril diameter. Fibrillary GN as a possible monoclonal gammopathy of renal significance represented <1% of cases. Immunostaining for DNAJB9 confirmed fibrillary GN in 100% of cases diagnosed as fibrillary GN and 79% of atypical cases diagnosed as possible fibrillary GN. At a median time of 24 months (interquartile range, 8–46 months) after biopsy (n=100), 53% of patients reached the combined primary outcome of ESKD or death, 18% had CKD, and 18% had partial remission. On multivariable analysis, male sex (adjusted hazard ratio [aHR], 3.82; 95% confidence interval [95% CI], 1.97 to 7.37) and eGFR were the most significant predictors of primary outcome (aHR of 8.02 if eGFR <30 ml/min per 1.73 m2 [95% CI, 1.85 to 34.75]; aHR of 6.44 if eGFR 30 to <45 ml/min per 1.73 m2 [95% CI, 1.38 to 29.99]). Immunosuppressive therapy with rituximab was significantly associated with stabilization of disease progression.ConclusionsDetection of DNAJB9 is a useful diagnostic tool for diagnosing atypical forms of fibrillary GN. The outcomes for fibrillary GN are poor and progression to ESKD is influenced predominantly by the degree of kidney insufficiency at the time of diagnosis and male sex. Rituximab may help preserve kidney function for select patients with fibrillary GN.PodcastThis article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2019_11_04_CJN03870319.mp3

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YOSHIZAWA, Nobuyuki. "Acute Glomerulonephritis." Internal Medicine 39, no. 9 (2000): 687–94. http://dx.doi.org/10.2169/internalmedicine.39.687.

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