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Glomerulonephritis Research Paper

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Glomerulonephritis Research Paper
Glomerulonephritis and Glomerulosclerosis of Kidneys and Nursing Considerations
Mark Greiner
Liberty University

Abstract
Glomerulosclerosis or nephropathy is a major cause of chronic kidney disease that can lead to future total kidney failure. One of precursors is glomerulonephritis, this inflammation of the glomeruli has many possible causes. People with either type of uncontrolled diabetes mellitus are at higher risk. A clinical indicator of early glomerulosclerosis is a change in renal function and is measured by the amount of albumin present in the urine. Microalbuminuria, or urinary albumin levels are checked and monitored in diabetic patient as a forecaster of possible future diabetic nephropathies. It is essential to educate
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2400-2401). This filtrate travels through nephron tubules where up to two-thirds of the water and soluble substances such as potassium and glucose are reabsorbed for use, the rest is excreted through the urine (Britt MD, Peitzman MD, Barie MD, & Jurkovich MD, 2012, p. 494). Another element important to the glomerulus is the different membrane areas within, each are important to glomerular filtration. The epithelial layer made of podocyte cells lines the Bowman capsule that form slit pores to prevent red blood cells and proteins from entering the filtrate, and the mesangium layer which help regulate the amount of blood flow through the glomerulus with a muscle like contractibility (Grossman & Mattson-Porth, p. 1002). Glomerular disease affects the function of the kidney. Depending on source, it may manifest with either increased or decreased permeability causing imbalances that can disturb the whole body. Typically the five categories of the clinical manifestation of this disease are:
1. Nephritic
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B. (2006, June). Can Glomerulosclerosis be Reversed? Nature Clinical Practice Nephrology, 2(6), 290.
Gross, J. L., de Azevedo, M. J., Silveiro, S. P., & Canani, L. H. (2005, January). Diabetic Nephropathy: Diagnosis, Prevention, and Treatment. Diabetes Care, 28(1), 164-176. Retrieved from http://search.proquest.com/docview/223061929?accountid=12085
Grossman, S., & Mattson-Porth, C. (2014). Porth 's Pathophysiology (9th ed.). Philadelphia: Lippincott Williams and Wilkins.
Ma, L.-J., & Fogo, A. B. (2007, November). Modulation of glomerulosclerosis. Seminars in Immunopathology, 29(4), 385-395.
Nasr, S. H., Satoskar, A., Markowitz, G. S., Valeri, A. M., Appel, G. B., Stokes, M. B., . . . Nadasdy, T. (2009). Proliferative Glomerulonephritis with Monoclonal IgG Deposits. Journal of the American Society of Nephrology, 20(9), 2055-2064.
Nichols, G., Vupputuri, S., & Lau, H. (2011). Medical Care Costs Assoiciated With Progression of Diabetic Nephropathy. Diabetes Care, 2374-2378.
Tan, L. (1994). Nursing care of a child with acute glomerulonephritis. British Journal Of Nursing, 3(4), 175-179.
Wasserstein, A. G. (1997, April 1). Membranous Glomerulonephritis. Journal of the American Society of Nephrology, 8(4),

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