Glomerulonephritis: Understanding Of Glomerular Damage Mechanism - Essay Example

Glomerulonephritis: Understanding Of Glomerular Damage Mechanism Abstract Gaining an understanding of glomerular damage mechanism is crucial in effective management of all glomerular diseases in children and adults. Glomerular mechanism differs from one disease to the other. The diverse causes of glomerular diseases include hemodynamic injury, abnormal metabolism, toxins, hypoxia, and the most common immune-mediated injury. In most cases, disease progression commences with minor injury to end-stage renal disease. The glomerular vessels have unique structures referred as Bowman’s capsule that filters blood as it passes through the glomerular basement membrane to form urine. Glomeruli comprises of three types of cells that all of which are vulnerable to injury for varying reasons. Introduction There are millions of minute filters exclusive to the human kidney. The fundamental responsibility of these filters is to clean the blood by eliminating any waste products which form urine. During filtration, the waste products do not include any relevant cells or proteins as they are kept in the blood. Within the kidney, glomeruli structures take the form of vessel knots that assist also in the elimination of excess fluid. Upon any damage of the glomeruli structures, the role of human kidneys in blood filtration ends and the kidneys malfunction. In severe glomeruli structures’ damage, the human body can get into kidney failure. Consequently, any glomerulonephritis includes all conditions that damage or causes inflammations on the glomeruli. Glomerulonephritis is also referred to as glomerular disease and can either be active or chronic. Thesis Understanding glomerulonephritis requires defining glomerulonephritis, and understanding the causes, symptoms and signs, and treatment and management?” Definition According to Ponticelli & Glassock [Pon09] glomerulonephritis is not a single disease, but a collective name referring to numerous renal diseases. These diseases are associated with the inflammation of the glomeruli or kidney’s small blood vessels. Between the two commonly known types of glomerulonephritis, acute and chronic, some identifiable characteristics distinguish their presentations. Major disease symptoms include proteinuria and hematuria, nephritic or nephritic syndrome or both, and prolonged or acute renal failure[Nam04]. Nephritic Syndrome The disease is present in patients with bloody urine, or hematuria, and low levels of urine accompanied by hypertension[Nam04]. This disease is linked to damaged glomerulus lining cells owing to the destruction of epithelial barrier. Consequently, the patient’s urine is bloody while compensating alterations may lower renal perfusion thus little or no urine production. Nephritic syndrome is evident in patients with high cellular levels in the glomerulus resulting in bloody urine, hypertension, and the lessened production of urine. Under severe conditions, nephritic syndrome causes end-stage renal failure. The major causes include rapidly progressive glomerulonephritis, post-infectious glomerulonephritis, and membranoproliferative glomerulonephritis. Nephrotic Syndrome Major signs include edema in patients. Edema results from high urine protein or proteinuria with low blood protein and high fat levels in the blood. Edema accounts for elevated protein permeability in the cells around the glomerulus, hence more proteins excreted (Namnalwar & Vijayakumar, 2004). Conversely, High protein excretion disables the liver’s capacity to compensate, thus very little protein, mostly albumin, is left in the blood. Nephrotic syndrome arise from minimal change disease, focal segmental, membrane glomerulonephritis, and glomerulosclerosis. These conditions represent the non-proliferative glomerulonephritis. Acute and Chronic Glomerulonephritis Acute Glomerulonephritis According to Ronco, Bellomo, & Kellum [Ron09], acute glomerulonephritis develops swiftly with the evident onset of casts of proteinuria, red blood cells, and hematuria. Clinically, acute GN signs and symptoms include azotemia or lessened rate of glomerular filtration, edema, renal salt, and hypertension. The patient also demonstrates water retention. These symptoms confirm that the presence of an immunologic mechanism causes glomerular structures’ inflammation causing damage[Ron09]. Damaged organs in acute GN include basement membrane, capillary endothelium, and mesangium. Since no particular therapy has been associated with the disease, support is the most crucial treatment. Pathophysiology The damages on the glomerular tissues are in the form of lesions caused by glomerular complexes or deposition and this may cause 50% kidney enlargement. Acute GN results in structural changes such as elevated cell levels in the glomerular tuft either as endocapillary or extracapillary[Pon09]. Functional changes include intravascular volume expansion in response to water retention, low GFR and avid distal nephron. In addition to structural and functional changes, acute GN causes poststreptococcal glomerulonephritis owing to streptococcal infections. Causes The etiological factors responsible for acute GN are classified as infectious or non-infectious[Nam04]. The infectious causes are caused by Streptococcus species, while non-infectious causes are subdivided into primary renal disease, other agents, and systemic disease. The systemic diseases comprise of vasculities, systemic lupus, hypersensitivity disease, Henoch-schonlein purpura, and cryoglobulinemia. The key renal diseases responsible for acute GN are Berger disease, idiopathic glomerulonephritis, and membranoproliferative glomerulonephritis. Finally, other causes include serum sickness, diphtheria-pertussis-tetanus, and irradiation Wilms tumor. Progression Upon occurrence, acute GN has mostly proceeded to chronic GN although it is possible to have some people healed. Initially, patients experience persistent proteinuria and microscopic haematuria for up to one year. With time, urinary disorders disappear while hypertension and renal function stabilizes. For nonstreptococcal post infections GN, the causative agents, has to be identified and managed, while the outcomes may vary from full recovery to kidney failure depending on disease cause. Treatment Based on the cause of the acute GN, treatment varies from making simple lifestyle adjustments to medication or a kidney transplant[Nam04]. Lifestyle changes include lessened salt intakes, periodic monitoring of individual blood pressure, prolonged urinary abnormalities monitoring, and protein restriction. Medications include antibiotics, immunosuppressant, and angiotensin converting enzyme inhibitors. Patients should be educated on the need to take adhere to these treatment measures. Chronic Glomerulonephritis Chronic glomerulonephritis almost always result from acute glomerulonephritis. Irreversible progressive glomerular and tubulointerstitial fibrosis are the most common conditions in prolonged glomerulonephritis. The ultimate result is lessened GFR and uremic toxin reduction. Advancement of prolonged glomerulonephritis results in chronic kidney disease (CKD), cardiovascular disease, or end-stage renal disease (ESRD). CKD is classified according to evidence of kidney damage, characterized by structural abnormalities or abnormal outcomes of urinalysis, and A GFR of not more than 60mL/min for more than three years. Pathophysiology Lessened GFR causes hyperfiltration and hypertrophy in the remaining nephrons while causing glomerular hypertension onset.[Pon09] The changes occur in response to reduced GFR thus attempting to improve GFR while lessening nephron loss outcomes. Either way, these alterations result in ultimate unfavorable situations such as glomerulosclerosis. Between stage 1 and 3, GFR decreases substantially and causes an increment in serum creatinine levels, and azotemia raises blood urea and serum creatinine levels where the GFR decreases lower than 60-70 mL/min. As GFR reduces, erythropoietin causes anemia, minimized vitamin D production, lowered acid, salt, potassium, and water excretion, and dysfunctional platelets. Progression The progression patterns of chronic glomerulonephritis vary from a rapidly gentle course to include progressive glomerulonephritis, membrane nephropathy, membranoproliferative glomerulonephritis, Iga nephropathy, and poststreptococcal glomerulonephritis[Ron09]. Patient education Dietary education is crucial in CKD patients’ disease management. The patient has to adhere to dietary restriction of 2 g of potassium and sodium, and protein intakes of 40-60 g. Patients also need ESRD therapy such as peritoneal dialysis, hemodialysis, and renal transplantation. Additionally, hemodialysis patients require education on how to perform it at home or at the health center 3 to 4 times each day. For CKD patients willing to get pregnant, physician’s advice is essential given the risks of high maternal morbidity and low fetal viability. Bibliography Namnalwar, B. R., & Vijayakumar, M. (2004). Principles and Practice of Pediatric Nephrology. United States: Jaypee Brothers Publishers. Ponticelli, C., & Glassock, R. (2009). Treatment of primary glomerulonephritis. New York: Oxford University Press. Ronco, C., Bellomo, R., & Kellum, J. (2009). Critical care nephrology. Philadelphia: Elsevier. Read More