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 …show more content…
diabetic patients about the importance of carefully monitoring and controlling blood glucose levels. In some cases, the damage to the kidneys can be reversed to a non-symptomatic level. As kidney function deteriorates, there may be less insulin or oral hypoglycemic drugs needed. That is because insulin is metabolized and excreted by the kidneys, and as kidney function deteriorates, insulin is available in the bloodstream for a prolonged time. Cigarette smoking and uncontrolled hypertension can increase the rate of progression of diabetic nephropathy. Evidenced based practice of nursing interventions to prevent and treat glomerulosclerosis of will be discussed.
Glomerulonephritis and Glomerulosclerosis of Kidneys and Nursing Considerations
Glomerulonephritis is the inflammation of the glomerular structure found in the kidney. Although the manifestations of these disorders fall into five categories, many of the symptoms can represent more than one glomerular disorder not always easily defined in laboratory tests and biopsies. It is important for today’s nurse to be aware of these diseases in order to help diagnose, implement interventions and treat glomerulonephritis and glomerulosclerosis.
There are many different mechanisms that may cause glomerular injuries that can eventually result in a less than functional kidney. First, there needs to be defined location and function of the glomeruli. Humans have a pair of bean-shaped organs that are located on either side of the vertebral column on the outside and back of the peritoneal cavity. The right kidney is normally larger than the left. Each kidney is divided in to lobes which together contain approximately one million nephron units, and each nephron contains one glomerulus (D 'Agati, Kaskel, & Falk, 2011, p. 2). The glomerulus of the kidney is where high-pressure capillary filtration of blood happens within the kidney and represents the first step in generation of urine (Grossman & Mattson-Porth, 2014, p. 999). Within the glomerulus, unfiltered blood enters though afferent arterioles into a node called a Bowman capsule and out through efferent arterioles.
Within the Bowman capsule, fluid and particles are filtered from the blood through the capillary membrane called a slit diaphragm made of nephrin, into the Bowman space (D 'Agati, Kaskel, & Falk, 2011, pp.
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 …show more content…
syndrome
2. Rapidly progressive glomerulonephritis
3. Nephrotic syndrome
4. Asymptomatic disorders of urinary sediment
5. Chronic glomerulonephritis (Grossman & Mattson-Porth, 2014, p. 1100)
Of these, the general terms glomerulonephritis and glomerulosclerosis cover those categories. Divisions used in broadly classifying glomerular diseases is grouping by proliferative and nonproliferative. Proliferative is characterized by an increase of cells and antibodies found in the glomerulus (Nasr, et al., 2009, p. 2061). Proliferative glomerulonephritis can be further classified in five categories: Nephritic syndrome; Berger’s disease also known as IgA nephropathy; Post-infectious glomerulonephritis; Membranoproliferative (MPGN); and Rapidly progressive glomerulonephritis (Couser, Glomerulonephritis, 1999, p. 1509). Nonproliferative can be simple explained the opposite on proliferative as the number of cells do not change. Classifications of nonproliferative include: Nephrotic syndrome; Minimal change disease; Focal segmental glomerulosclerosis (FSGS); Membranous glomerulonephritis; and thin basement membrane disease.
Nephrotic and nephritic syndromes may sometimes present at the same time in the same glomerular disease. Nephritic syndrome is characterized a decrease in urine, blood in the urine and hypertension. Inflammation damages to the capillary walls and the closing of the lumen decreases the function of the kidney resulting in hypertension and edema (Grossman & Mattson-Porth, 2014, p. 1100).
Glomerulonephritis is an applied term to cover several of the proliferative diseases that are characterized by the inflammation of the glomeruli in the kidney and is the third most common cause of end-stage renal disease, diabetes and hypertension are first and second respectively (Couser, Glomerulonephritis, 1999, p. 1509). Most of the time glomerulonephritis has an acute presentation of hematuria (blood in urine), proteinuria (protein in urine), fluid retention, hypertension and in most instances an overall diminished renal function (Couser, Glomerulonephritis, pp. 1510-1511). When glomerulonephritis is suspected, it is important to know the type and severity of the inflammation to determine the therapy used and the potential to reverse damage. After testing the urine and obtaining the patient’s history, blood is tested to check for antibodies and other serological markers that are typically formed in response to various infections.
Berger’s disease also known as IgA nephropathy is the most common type of glomerulonephritis worldwide, characterized by the presence of glomerular IgA immune deposits (Couser, Glomerulonephritis, 1999, p. 1512). It is more common in developed countries, has a peak age group between 15-30, more likely to affect men than women and Asians more than any other group (Grossman & Mattson-Porth, 2014, p. 1103). According to Couser, the common signs and symptoms are abrupt onsets of hematuria, sometimes flank pain is present, usually occurs 24-48 hours after a upper respiratory of gastrointestinal viral infection lasting 6-8 days (Glomerulonephritis, 1999). In children, acute glomerulonephritis signs are periorbital oedema, dark and cloudy urine, paleness, lethargy and in later stages urine output decreases and vomiting is not uncommon (Tan, 1994, p. 175). Another form of IgA nephropathy is Henoch-Schonlein purpura that typically affects children, signs of a rash of small bruises on the buttocks and lower legs and accompanied with abdominal pain due to bowel angina, usually with bloody diarrhea (Ballinger, 2003, p. 591). Currently there is no diagnostic laboratory tests for Berger’s disease, though biopsy samples can show the IgA deposits using immunofluorescence microscopy (Grossman & Mattson-Porth).
Common disorders that are associated with Berger’s include lupus nephritis, hepatic cirrhosis, coeliac disease and HIV nephropathy (Couser, Mediation of Immune Glomerular Injury, 1990, p. 20). Treatment is focused on treating the symptoms. Use of immunosuppressive drugs, steroids and platelet inhibitors have not displayed a reliable value (Ballinger, 2003, p. 593). Good blood pressure control and use of Ace inhibitors does show a decrease in protein excretion (Couser, Glomerulonephritis, 1999, p. 1512)
Next, post-infectious glomerulonephritis usually can occur after any infection. The most common inflammatory cause is streptococci bacterium (Grossman & Mattson-Porth, 2014, p. 1100). The streptococci antigens may concentrate in the glomerulus and activate the autoimmune inflammatory response leading to a decreased glomerular filtration (Tan, 1994, p. 175). Typically it follows 1-4 weeks after a pharyngeal infection such as strep throat, symptoms include malaise, low fever, nausea, slightly increased blood pressure and smoky-brown urine due to large amounts of blood in the urine (Couser, Glomerulonephritis, 1999, p. 1511).
Blood tests are usually confirm the poststreptococcal infection with findings of elevated antisteptococcal antibodies and a decline of serum concentration of cryoglobulin and C3 (Grossman & Mattson-Porth, 2014, p. 1100). Renal biopsy is usually not indicated unless the glomerulonephritis develops into oliguria (urine output between 100- 400 ml/day) signifying acute renal failure (Couser, Glomerulonephritis, 1999, p. 1511). Treatments include antibiotics to eliminate the infection, supportive therapy with antihypertensives and diuretics to control blood pressure and fluid retention (Couser).
Membranoproliferative glomerulonephritis is categorized as both an increase of the cells in the glomerulus and alteration of the glomerular basement membrane (Couser, Mediation of Immune Glomerular Injury, 1990, p. 14). Two types are identified. Type 1 is caused by chronic or recurring infections such as systemic lupus erythematosus, hepatitis B and hepatitis C leading to inflammation and the increase of inflammatory cells in the blood stream (Couser, Glomerulonephritis, 1999, p. 1514). Type II is also call Dense Deposit Disease, cause by an excessive activation of cryoglobulins and autoantibodies in high concentration causing inflammation in to the glomerulus. Treatment options have included steroids, antivirals and cytotoxic medication which have no consistent success (Couser). Cytotoxic medications such as chemotherapy and radiotherapy can cause further damage to the kidneys.
Rapidly progressive glomerulonephritis such that of Goodpasture syndrome is characterized with a progressive and rapid deterioration of kidney function, causing severe glomerular injury and has no specific causes (Grossman & Mattson-Porth, 2014, p. 1101). Rapidly progressive glomerulonephritis is a medical emergency and success is dependent on how quickly the antibody containing plasma is removed though plasmapheresis and use of immunosuppressive medication to slow production of antibodies (Couser, Glomerulonephritis, 1999, p. 1513).
Switching to nonproliferating glomerulonephritis, there are at least four different diseases that result in nephrotic syndrome. Nephrotic syndrome is characterized by the signs of edema in a patient that has a decreased amount of protein in the blood, but increased in the urine and increased lipid levels in the blood. Inflammation of the cells surrounding the glomerulus increases the permeability of the visceral epithelial layer resulting in an increase amount of excreted protein (Grossman & Mattson-Porth, 2014, p. 1101). This impacts other body systems; the liver is unable to compensate to produce enough protein albumin. The decrease of protein in the blood decreases the ability or the oncotic pressure to pull water into the bloodstream and decrease of circulating blood causes the adrenal gland to secrete aldosterone increasing water and sodium retention, resulting in edema, especially in the lower extremities. Pulmonary edema, pleural effusions and diaphragmatic compromise due to ascites are also problems related to nephrotic syndrome (Grossman & Mattson-Porth).
Minimal-change disease is commonly found in children and as the name indicates there is a slight change of destruction of the epithelial cells. It usually does not evolve to renal failure, but it can cause susceptibility to infection to gram-positives, hyperlipidemia, protein malnutrition and thromboembolic disease (Grossman & Mattson-Porth, 2014, p. 1102).
Membranous glomerulonephritis is largely idiopathic but is associated with many secondary diseases such as cancers of the bowel and lungs, hepatitis B, systemic lupus erythematosus, malaria, diabetes mellitus and drugs to include penicillin (Wasserstein, 1997, pp. 664-665). The clinical presentations are heavy amount of protein in the urine, hypertension, and abnormally high levels of nitrogen-containing compounds otherwise known as azotemia (Wasserstein, p. 677). “Membranous glomerulonephritis is the most common cause of primary nephrosis in adults” (Grossman & Mattson-Porth, 2014, p. 1102). Treatments are controversial, Wasserstein writes that “overly aggressive diuresis” can lead to azotemia or peripheral edema (Membranous Glomerulonephritis, p. 667). Many go on to death due renal vein thrombosis and other complications of hypercoagulation. In rare cases there has been a familial trait passed down through females (Bockenhauer, et al., 2008, p. 14).
Another of the diseases is focal segmental glomerulosclerosis, it is the most common primary glomerular disorder to cause end-stage renal disease in the United States, 20% for children and 40% of adult cases (D 'Agati, Kaskel, & Falk, 2011, p. 2398). Males are more likely than females to be susceptible, African Americans are at more risk and a hereditary connection has been linked due to living related donor kidneys have an increased probability for recurrence for focal segmental glomerulosclerosis (Bolton & Abdel- Rahman, 2001, p. 11). Data has also suggested that obesity and obesity-related metabolic problems such as diabetes mellitus and hyperlipidemia, are associated with a chronic, low-grade inflammation that may affect the kidneys (Ma & Fogo, 2007, p. 391).
Focal segmental glomerulosclerosis is separated from the other disorders by progressive glomerular scarring. Glomerulosclerosis begins only involving a small amount of the glomeruli. With progression, glomerulosclerosis becomes more widespread. Often it is idiopathic in 80% of primary cases, once considered as s single disease, it is now viewed that focal segmental glomerulosclerosis as a group of clinical-pathogic syndromes that share a common glomerular lesion (D 'Agati, Kaskel, & Falk, pp. 2400-2401). It has been theorized that may be related to lowered oxygen levels available in the blood as in sickle cell disease, human immunodeficiency virus (HIV), as a secondary result of a glomerulonephritis disease, or intravenous drug use such as heroin and methamphetamines (Grossman & Mattson-Porth, 2014, p. 1102).
Diagnosing focal segmental glomerulosclerosis is much like the other glomeruli diseases in that proteinuria and albuminuria are discovered. Which can lead to a biopsy to confirm a diagnosis, even then potential secondary causes need to be ruled out and treated before presuming primary focal segmental glomerulosclerosis (D 'Agati, Kaskel, & Falk, 2011, p. 2409). Other related symptoms are: foamy urine caused by large amounts of protein; low serum albumin due to loss of protein; weight gain caused by fluid retention; edema (swollen ankles, feet, hands, face or abdomen); and high blood pressure (often seen with primary FSGS) (Bolton & Abdel- Rahman, 2001, p. 11)
Treatment usually involves use of angiotensin-converting-enzyme (ACE) inhibitors that lower glomerular pressures and a sodium restriction and low protein diet as initial therapy (Fogo, 2006, p. 290). Fogo has even explored using higher doses of ACE inhibitors it lab rats that showed a possibility to reduce sclerosis, but not completely to pre disease form. Glucocorticoids have shown no improvement of focal segmental glomerulosclerosis (D 'Agati, Kaskel, & Falk). Changing some environmental factors have shown to slow and stop sclerosis. These include smoking cessation, avoiding exposure to certain hydrocarbons and chemicals, increasing activity, decreasing weight, controlled hypertension and diabetes type II (Bolton & Abdel- Rahman, 2001, p. 12).
The final element to be addressed is that of diabetic glomerulosclerosis which can progress to kidney nephropathy. It is a major cause of kidney disease and mover prevalent African Americans, Asians and Naive Americans than whites (Grossman & Mattson-Porth, 2014, p. 1104). Other risk factors of diabetic glomerulosclerosis is genetic susceptibility and having prolong untreated hyperglycemia and hypertension, smoking, and having a high protein or fat diet (Gross, de Azevedo, Silveiro, & Canani, 2005, p. 166). Higher health care costs are associated with the progression of nephropathy. Not only due to the cost of medication, but albuminuria increases risk of cardiovascular disease, heart failure, and retinopathy (Nichols, Vupputuri, & Lau, 2011, p. 2374). Diabetes causes unique alterations in the kidney structure to include glomerular lesions, microaneurysms, extreme mesangial cell layer expansion and sclerosis, and tubular and interstitial changes (Gross, de Azevedo, Silveiro, & Canani, 2005, p. 166). The clinical manifestations of diabetic glomerulosclerosis mirror those of diabetes such as microalbuminuria which can be a predictor of diabetic nephropathies in the future (Grossman & Mattson-Porth, 2014, p. 1104). Treatments include controlling hyperglycemia, hypertension and use of ACE inhibitors and smoking cessation to reduce progression of diabetic renal disease.
Nursing interventions for glomerulonephritis start with a history, it may be obtained to focus on any recent infections or immunologic disorders such as SLE, also get a subjective report from the patient on any signs and symptoms they may have had. Monitor cardiac, serum and urine labs focusing on abnormals such as an increase of creatinine and blood urea nitrogen (BUN) levels and decrease of glomerular filtration rate (GFR) in blood and increases of microalbuminuria and proteins in blood. Do a physical nursing examination looking for signs of edema, hypertension, and hypervolemia. Assess for any pain that maybe related to edema of the kidney. Finally an assessment of any knowledge deficient that lead to ineffective health maintenance, the nurse should educate the patient how important to take medications as prescribed, offer smoking cessation programs and teaching or give a referral to a dietician to explain changes in diet, especially to lower fat intake. (Ackley & Ladwig, 2008, pp. 413-418 ,604-605) .
In conclusion, glomerulonephritis is an inflammatory progression that involves the glomerular part of the kidney, most likely caused by an immune reaction. There are many different types of glomerular disorders that cause glomerulonephritis and glomerulosclerosis. Many of the same symptoms can be associated with multiple glomerular disorders, in fact it is possible that a patient may be experiencing more than one disorder at the same time. Common controllable factors include treating infections in a timely manner, controlling high blood pressures, hyperglycemia and high cholesterol and by encouraging smoking cessation.
References
Ackley, B. J., & Ladwig, G. B. (2008). Nusing Diagnosis Handbook: An Evidenced- Bases Guide to Planning Care (8th ed.). Philadelphia: Mosby.
Ballinger, S. M. (2003, September). Henoch–Schonlein purpura. Current Opinion in Rheumatology, 15(5), 591-594.
Bockenhauer, D., Debiec, H., Sebire, N., Barratt, M., Warwicker, P., Ronco, P., & Kleta, R. (2008). Familial Membranous Nephropathy:. Nephron. Clinical Practice, 108(1), 10-15.
Bolton, W. K., & Abdel- Rahman, E. (2001, May). Pathogenesis of Focal Glomerulosclerosis. Nephron, 88(1), 6-13. Retrieved from http://search.proquest.com/docview/274270740?accountid=12085
Britt MD, L., Peitzman MD, A., Barie MD, P., & Jurkovich MD, G. (2012). Acute Care Surgery. Philadephia: Lippincott Williams and Wilkins.
Couser, W. G. (1990, July 1). Mediation of Immune Glomerular Injury. Journal of the American Society of Nephrology, 1(1), 13-29.
Couser, W. G. (1999, May 1). Glomerulonephritis. Lancet, 353(9163), 1509-1515.
D 'Agati, V. D., Kaskel, F. J., & Falk, R. J. (2011). Medical progress: Focal segmental glomerulosclerosis. The New England Journal of Medicine, 365(25), 2398-2411. Retrieved from http://search.proquest.com/docview/912723590?accountid=12085
Fogo, A.
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),
664-674.
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 …show more content…
diabetic patients about the importance of carefully monitoring and controlling blood glucose levels. In some cases, the damage to the kidneys can be reversed to a non-symptomatic level. As kidney function deteriorates, there may be less insulin or oral hypoglycemic drugs needed. That is because insulin is metabolized and excreted by the kidneys, and as kidney function deteriorates, insulin is available in the bloodstream for a prolonged time. Cigarette smoking and uncontrolled hypertension can increase the rate of progression of diabetic nephropathy. Evidenced based practice of nursing interventions to prevent and treat glomerulosclerosis of will be discussed.
Glomerulonephritis and Glomerulosclerosis of Kidneys and Nursing Considerations
Glomerulonephritis is the inflammation of the glomerular structure found in the kidney. Although the manifestations of these disorders fall into five categories, many of the symptoms can represent more than one glomerular disorder not always easily defined in laboratory tests and biopsies. It is important for today’s nurse to be aware of these diseases in order to help diagnose, implement interventions and treat glomerulonephritis and glomerulosclerosis.
There are many different mechanisms that may cause glomerular injuries that can eventually result in a less than functional kidney. First, there needs to be defined location and function of the glomeruli. Humans have a pair of bean-shaped organs that are located on either side of the vertebral column on the outside and back of the peritoneal cavity. The right kidney is normally larger than the left. Each kidney is divided in to lobes which together contain approximately one million nephron units, and each nephron contains one glomerulus (D 'Agati, Kaskel, & Falk, 2011, p. 2). The glomerulus of the kidney is where high-pressure capillary filtration of blood happens within the kidney and represents the first step in generation of urine (Grossman & Mattson-Porth, 2014, p. 999). Within the glomerulus, unfiltered blood enters though afferent arterioles into a node called a Bowman capsule and out through efferent arterioles.
Within the Bowman capsule, fluid and particles are filtered from the blood through the capillary membrane called a slit diaphragm made of nephrin, into the Bowman space (D 'Agati, Kaskel, & Falk, 2011, pp.
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 …show more content…
syndrome
2. Rapidly progressive glomerulonephritis
3. Nephrotic syndrome
4. Asymptomatic disorders of urinary sediment
5. Chronic glomerulonephritis (Grossman & Mattson-Porth, 2014, p. 1100)
Of these, the general terms glomerulonephritis and glomerulosclerosis cover those categories. Divisions used in broadly classifying glomerular diseases is grouping by proliferative and nonproliferative. Proliferative is characterized by an increase of cells and antibodies found in the glomerulus (Nasr, et al., 2009, p. 2061). Proliferative glomerulonephritis can be further classified in five categories: Nephritic syndrome; Berger’s disease also known as IgA nephropathy; Post-infectious glomerulonephritis; Membranoproliferative (MPGN); and Rapidly progressive glomerulonephritis (Couser, Glomerulonephritis, 1999, p. 1509). Nonproliferative can be simple explained the opposite on proliferative as the number of cells do not change. Classifications of nonproliferative include: Nephrotic syndrome; Minimal change disease; Focal segmental glomerulosclerosis (FSGS); Membranous glomerulonephritis; and thin basement membrane disease.
Nephrotic and nephritic syndromes may sometimes present at the same time in the same glomerular disease. Nephritic syndrome is characterized a decrease in urine, blood in the urine and hypertension. Inflammation damages to the capillary walls and the closing of the lumen decreases the function of the kidney resulting in hypertension and edema (Grossman & Mattson-Porth, 2014, p. 1100).
Glomerulonephritis is an applied term to cover several of the proliferative diseases that are characterized by the inflammation of the glomeruli in the kidney and is the third most common cause of end-stage renal disease, diabetes and hypertension are first and second respectively (Couser, Glomerulonephritis, 1999, p. 1509). Most of the time glomerulonephritis has an acute presentation of hematuria (blood in urine), proteinuria (protein in urine), fluid retention, hypertension and in most instances an overall diminished renal function (Couser, Glomerulonephritis, pp. 1510-1511). When glomerulonephritis is suspected, it is important to know the type and severity of the inflammation to determine the therapy used and the potential to reverse damage. After testing the urine and obtaining the patient’s history, blood is tested to check for antibodies and other serological markers that are typically formed in response to various infections.
Berger’s disease also known as IgA nephropathy is the most common type of glomerulonephritis worldwide, characterized by the presence of glomerular IgA immune deposits (Couser, Glomerulonephritis, 1999, p. 1512). It is more common in developed countries, has a peak age group between 15-30, more likely to affect men than women and Asians more than any other group (Grossman & Mattson-Porth, 2014, p. 1103). According to Couser, the common signs and symptoms are abrupt onsets of hematuria, sometimes flank pain is present, usually occurs 24-48 hours after a upper respiratory of gastrointestinal viral infection lasting 6-8 days (Glomerulonephritis, 1999). In children, acute glomerulonephritis signs are periorbital oedema, dark and cloudy urine, paleness, lethargy and in later stages urine output decreases and vomiting is not uncommon (Tan, 1994, p. 175). Another form of IgA nephropathy is Henoch-Schonlein purpura that typically affects children, signs of a rash of small bruises on the buttocks and lower legs and accompanied with abdominal pain due to bowel angina, usually with bloody diarrhea (Ballinger, 2003, p. 591). Currently there is no diagnostic laboratory tests for Berger’s disease, though biopsy samples can show the IgA deposits using immunofluorescence microscopy (Grossman & Mattson-Porth).
Common disorders that are associated with Berger’s include lupus nephritis, hepatic cirrhosis, coeliac disease and HIV nephropathy (Couser, Mediation of Immune Glomerular Injury, 1990, p. 20). Treatment is focused on treating the symptoms. Use of immunosuppressive drugs, steroids and platelet inhibitors have not displayed a reliable value (Ballinger, 2003, p. 593). Good blood pressure control and use of Ace inhibitors does show a decrease in protein excretion (Couser, Glomerulonephritis, 1999, p. 1512)
Next, post-infectious glomerulonephritis usually can occur after any infection. The most common inflammatory cause is streptococci bacterium (Grossman & Mattson-Porth, 2014, p. 1100). The streptococci antigens may concentrate in the glomerulus and activate the autoimmune inflammatory response leading to a decreased glomerular filtration (Tan, 1994, p. 175). Typically it follows 1-4 weeks after a pharyngeal infection such as strep throat, symptoms include malaise, low fever, nausea, slightly increased blood pressure and smoky-brown urine due to large amounts of blood in the urine (Couser, Glomerulonephritis, 1999, p. 1511).
Blood tests are usually confirm the poststreptococcal infection with findings of elevated antisteptococcal antibodies and a decline of serum concentration of cryoglobulin and C3 (Grossman & Mattson-Porth, 2014, p. 1100). Renal biopsy is usually not indicated unless the glomerulonephritis develops into oliguria (urine output between 100- 400 ml/day) signifying acute renal failure (Couser, Glomerulonephritis, 1999, p. 1511). Treatments include antibiotics to eliminate the infection, supportive therapy with antihypertensives and diuretics to control blood pressure and fluid retention (Couser).
Membranoproliferative glomerulonephritis is categorized as both an increase of the cells in the glomerulus and alteration of the glomerular basement membrane (Couser, Mediation of Immune Glomerular Injury, 1990, p. 14). Two types are identified. Type 1 is caused by chronic or recurring infections such as systemic lupus erythematosus, hepatitis B and hepatitis C leading to inflammation and the increase of inflammatory cells in the blood stream (Couser, Glomerulonephritis, 1999, p. 1514). Type II is also call Dense Deposit Disease, cause by an excessive activation of cryoglobulins and autoantibodies in high concentration causing inflammation in to the glomerulus. Treatment options have included steroids, antivirals and cytotoxic medication which have no consistent success (Couser). Cytotoxic medications such as chemotherapy and radiotherapy can cause further damage to the kidneys.
Rapidly progressive glomerulonephritis such that of Goodpasture syndrome is characterized with a progressive and rapid deterioration of kidney function, causing severe glomerular injury and has no specific causes (Grossman & Mattson-Porth, 2014, p. 1101). Rapidly progressive glomerulonephritis is a medical emergency and success is dependent on how quickly the antibody containing plasma is removed though plasmapheresis and use of immunosuppressive medication to slow production of antibodies (Couser, Glomerulonephritis, 1999, p. 1513).
Switching to nonproliferating glomerulonephritis, there are at least four different diseases that result in nephrotic syndrome. Nephrotic syndrome is characterized by the signs of edema in a patient that has a decreased amount of protein in the blood, but increased in the urine and increased lipid levels in the blood. Inflammation of the cells surrounding the glomerulus increases the permeability of the visceral epithelial layer resulting in an increase amount of excreted protein (Grossman & Mattson-Porth, 2014, p. 1101). This impacts other body systems; the liver is unable to compensate to produce enough protein albumin. The decrease of protein in the blood decreases the ability or the oncotic pressure to pull water into the bloodstream and decrease of circulating blood causes the adrenal gland to secrete aldosterone increasing water and sodium retention, resulting in edema, especially in the lower extremities. Pulmonary edema, pleural effusions and diaphragmatic compromise due to ascites are also problems related to nephrotic syndrome (Grossman & Mattson-Porth).
Minimal-change disease is commonly found in children and as the name indicates there is a slight change of destruction of the epithelial cells. It usually does not evolve to renal failure, but it can cause susceptibility to infection to gram-positives, hyperlipidemia, protein malnutrition and thromboembolic disease (Grossman & Mattson-Porth, 2014, p. 1102).
Membranous glomerulonephritis is largely idiopathic but is associated with many secondary diseases such as cancers of the bowel and lungs, hepatitis B, systemic lupus erythematosus, malaria, diabetes mellitus and drugs to include penicillin (Wasserstein, 1997, pp. 664-665). The clinical presentations are heavy amount of protein in the urine, hypertension, and abnormally high levels of nitrogen-containing compounds otherwise known as azotemia (Wasserstein, p. 677). “Membranous glomerulonephritis is the most common cause of primary nephrosis in adults” (Grossman & Mattson-Porth, 2014, p. 1102). Treatments are controversial, Wasserstein writes that “overly aggressive diuresis” can lead to azotemia or peripheral edema (Membranous Glomerulonephritis, p. 667). Many go on to death due renal vein thrombosis and other complications of hypercoagulation. In rare cases there has been a familial trait passed down through females (Bockenhauer, et al., 2008, p. 14).
Another of the diseases is focal segmental glomerulosclerosis, it is the most common primary glomerular disorder to cause end-stage renal disease in the United States, 20% for children and 40% of adult cases (D 'Agati, Kaskel, & Falk, 2011, p. 2398). Males are more likely than females to be susceptible, African Americans are at more risk and a hereditary connection has been linked due to living related donor kidneys have an increased probability for recurrence for focal segmental glomerulosclerosis (Bolton & Abdel- Rahman, 2001, p. 11). Data has also suggested that obesity and obesity-related metabolic problems such as diabetes mellitus and hyperlipidemia, are associated with a chronic, low-grade inflammation that may affect the kidneys (Ma & Fogo, 2007, p. 391).
Focal segmental glomerulosclerosis is separated from the other disorders by progressive glomerular scarring. Glomerulosclerosis begins only involving a small amount of the glomeruli. With progression, glomerulosclerosis becomes more widespread. Often it is idiopathic in 80% of primary cases, once considered as s single disease, it is now viewed that focal segmental glomerulosclerosis as a group of clinical-pathogic syndromes that share a common glomerular lesion (D 'Agati, Kaskel, & Falk, pp. 2400-2401). It has been theorized that may be related to lowered oxygen levels available in the blood as in sickle cell disease, human immunodeficiency virus (HIV), as a secondary result of a glomerulonephritis disease, or intravenous drug use such as heroin and methamphetamines (Grossman & Mattson-Porth, 2014, p. 1102).
Diagnosing focal segmental glomerulosclerosis is much like the other glomeruli diseases in that proteinuria and albuminuria are discovered. Which can lead to a biopsy to confirm a diagnosis, even then potential secondary causes need to be ruled out and treated before presuming primary focal segmental glomerulosclerosis (D 'Agati, Kaskel, & Falk, 2011, p. 2409). Other related symptoms are: foamy urine caused by large amounts of protein; low serum albumin due to loss of protein; weight gain caused by fluid retention; edema (swollen ankles, feet, hands, face or abdomen); and high blood pressure (often seen with primary FSGS) (Bolton & Abdel- Rahman, 2001, p. 11)
Treatment usually involves use of angiotensin-converting-enzyme (ACE) inhibitors that lower glomerular pressures and a sodium restriction and low protein diet as initial therapy (Fogo, 2006, p. 290). Fogo has even explored using higher doses of ACE inhibitors it lab rats that showed a possibility to reduce sclerosis, but not completely to pre disease form. Glucocorticoids have shown no improvement of focal segmental glomerulosclerosis (D 'Agati, Kaskel, & Falk). Changing some environmental factors have shown to slow and stop sclerosis. These include smoking cessation, avoiding exposure to certain hydrocarbons and chemicals, increasing activity, decreasing weight, controlled hypertension and diabetes type II (Bolton & Abdel- Rahman, 2001, p. 12).
The final element to be addressed is that of diabetic glomerulosclerosis which can progress to kidney nephropathy. It is a major cause of kidney disease and mover prevalent African Americans, Asians and Naive Americans than whites (Grossman & Mattson-Porth, 2014, p. 1104). Other risk factors of diabetic glomerulosclerosis is genetic susceptibility and having prolong untreated hyperglycemia and hypertension, smoking, and having a high protein or fat diet (Gross, de Azevedo, Silveiro, & Canani, 2005, p. 166). Higher health care costs are associated with the progression of nephropathy. Not only due to the cost of medication, but albuminuria increases risk of cardiovascular disease, heart failure, and retinopathy (Nichols, Vupputuri, & Lau, 2011, p. 2374). Diabetes causes unique alterations in the kidney structure to include glomerular lesions, microaneurysms, extreme mesangial cell layer expansion and sclerosis, and tubular and interstitial changes (Gross, de Azevedo, Silveiro, & Canani, 2005, p. 166). The clinical manifestations of diabetic glomerulosclerosis mirror those of diabetes such as microalbuminuria which can be a predictor of diabetic nephropathies in the future (Grossman & Mattson-Porth, 2014, p. 1104). Treatments include controlling hyperglycemia, hypertension and use of ACE inhibitors and smoking cessation to reduce progression of diabetic renal disease.
Nursing interventions for glomerulonephritis start with a history, it may be obtained to focus on any recent infections or immunologic disorders such as SLE, also get a subjective report from the patient on any signs and symptoms they may have had. Monitor cardiac, serum and urine labs focusing on abnormals such as an increase of creatinine and blood urea nitrogen (BUN) levels and decrease of glomerular filtration rate (GFR) in blood and increases of microalbuminuria and proteins in blood. Do a physical nursing examination looking for signs of edema, hypertension, and hypervolemia. Assess for any pain that maybe related to edema of the kidney. Finally an assessment of any knowledge deficient that lead to ineffective health maintenance, the nurse should educate the patient how important to take medications as prescribed, offer smoking cessation programs and teaching or give a referral to a dietician to explain changes in diet, especially to lower fat intake. (Ackley & Ladwig, 2008, pp. 413-418 ,604-605) .
In conclusion, glomerulonephritis is an inflammatory progression that involves the glomerular part of the kidney, most likely caused by an immune reaction. There are many different types of glomerular disorders that cause glomerulonephritis and glomerulosclerosis. Many of the same symptoms can be associated with multiple glomerular disorders, in fact it is possible that a patient may be experiencing more than one disorder at the same time. Common controllable factors include treating infections in a timely manner, controlling high blood pressures, hyperglycemia and high cholesterol and by encouraging smoking cessation.
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