Volume : 09, Issue : 10, October – 2022

Title:

86.RESEARCH ON THE FORMATION OF EDEMA IN NEPHROTIC PATIENTS WITH SYMPTOMS WITH MINIMAL LESIONS
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Authors :

Dr.Aqsa Shahbaz, Dr. Iqra Arshad, Dr.samia Munir

Abstract :

Aim: It has lately been demonstrated that children with nephrotic syndrome induced by the minimal modifying disease can have excessive salt retention, triggered vasoactive hormone, and long-term edema.
Methods: The current study looks at these problems in kids who do not have MCD and have nephrotic syndrome. Significant sodium retention (fractional sodium excretion, FENa, 0.3 7 0.3%) was detected in three kids having hypovolemic complaints. The suppression of lithium elimination in addition to maximum water excretion suggests ardent sodium reabsorption throughout the nephron. The levels of aldosterone, renin, and norepinephrine have all been high. Sixteen additional non-MCD kids had stable edema. FENa was 1.9 7 1.2%, whereas FELi, Vmax, and hormones were mostly normal and comparable to information from 37 nonproteinuric youngsters.
Results: Thirteen kids having MCD had hypovolemic signs and significant sodium retention (FENa 0.4 7 0.4%), while 16 were normal (FENa 1.2 7 0.8%). In terms of tubular salt processing and hormones, the very same differential might be established for non-MCD youngsters. Furthermore, hypoproteinemia was distinct. Plasma colloid osmotic pressure was considerably less in children having non-MCD lesions (4.3 7 0.5 mmHg) than among those who had stable edema (14.1 7 4.7 mmHg; P, 0.06); really no variation observed in MCD (corresponding, 8.2 6 4.1 and 9.8 7 2.3 mmHg).
Conclusion: In conclusion, whether they have non-MCD or MCD, kids having renal disease can appear to have pathophysiologic images of reduced effective circulation volume or constant edema. The pathophysiology of the hypovolemic picture appears to remain distinct, given that this is linked to severe hypoproteinemia exclusively in non-MCD kids.
Keywords: Nephrotic Syndrome, Ardent Salt Retention, Vasoactive Hormone, Sustained Edema.

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References:

1. Herbowski L. The maze of the cerebrospinal fluid discovery. Anat Res Int 2013; 2013: 596027–592014.
2. Brinker T, Stopa E, Morrison J, et al. A new look at cerebrospinal fluid circulation. Fluids Barriers CNS 2014; 11: 1
3. Johanson CE, Duncan JA3rd, Klinge PM, et al. Multiplicity of cerebrospinal fluid functions: New challenges in health and disease. Cerebrospinal Fluid Res 2008; 5: 10.
4. Louveau A, Smirnov I, Keyes TJ, et al. Structural and functional features of central nervous system lymphatic vessels. Nature 2015; 523: 337–341.
5. Rasmussen MK, Mestre H, Nedergaard M. The glymphatic pathway in neurological disorders. Lancet Neurol 2018; 17: 1016–1024.
6. Jessen NA, Munk AS, Lundgaard I, et al. The glymphatic system: a beginner’s guide. Neurochem Res 2015; 40: 2583–2599.
7. Wright BL, Lai JT, Sinclair AJ. Cerebrospinal fluid and lumbar puncture: a practical review. J Neurol 2012; 259: 1530–1545.
8. Sakka L, Coll G, Chazal J. Anatomy and physiology of cerebrospinal fluid. Eur Ann Otorhinolaryngol Head Neck Dis 2011; 128: 309–316.
9. Bothwell SW, Janigro D, Patabendige A. Cerebrospinal fluid dynamics and intracranial pressure elevation in neurological diseases. Fluids Barriers CNS 2019; 16: 9.
10. Plog BA, Nedergaard M. The glymphatic system in Central nervous system health and disease: past, present, and future. Annu Rev Pathol 2018; 13: 379–394.
11. Abbott NJ, Pizzo ME, Preston JE, et al. The role of brain barriers in fluid movement in the CNS: is there a ‘glymphatic’ system? Acta Neuropathol 2018; 135: 387–407.
12. Lovelock CE, Rinkel GJ, Rothwell PM. Time trends in outcome of subarachnoid hemorrhage: population-based study and systematic review. Neurology 2010; 74: 1494–1501.
13. Nieuwkamp DJ, Setz LE, Algra A, et al. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a meta-analysis. Lancet Neurol 2009; 8: 635–642.
14. Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet 2017; 389: 655–666.
15. Fujii M, Yan J, Rolland WB, et al. Early brain injury, an evolving frontier in subarachnoid hemorrhage research. Transl Stroke Res 2013; 4: 432–446.
16. Tso MK, Macdonald RL. Subarachnoid hemorrhage: a review of experimental studies on the microcirculation and the neurovascular unit. Transl Stroke Res 2014; 5: 174–189.
17. Fang Y, Shi H, Ren R, et al. Pituitary adenylate cyclase-activating polypeptide attenuates brain edema by protecting blood-brain barrier and glymphatic system after subarachnoid hemorrhage in rats. Neurotherapeutics 2020; 17: 1954–1972.
18. Zhang Z, Liu J, Fan C, et al. The GluN1/GluN2B NMDA receptor and metabotropic glutamate receptor 1 negative allosteric modulator has enhanced neuroprotection in a rat subarachnoid hemorrhage model. Exp Neurol 2018; 301: 13–25.
19. Fumoto T, Naraoka M, Katagai T, et al. The role of oxidative stress in microvascular disturbances after experimental subarachnoid hemorrhage. Transl Stroke Res 2019; 10: 684–694.
20. Coulibaly AP, Provencio JJ. Aneurysmal subarachnoid hemorrhage: an overview of inflammation-induced cellular changes. Neurotherapeutics 2020; 17: 436–445.
21. Staykov D, Schwab S. Clearing bloody cerebrospinal fluid: clot lysis, neuroendoscopy and lumbar drainage. Curr Opin Crit Care 2013; 19: 92–100.