Renal Case Study

Glomerulonephritis

Glomerulonephritis is a group of conditions which damage the glomeruli in the kidney. The glomeruli filter blood and help to remove excess fluids from the body in the body. Glomerulonephritis is characterized by inflammation of the glomeruli. When the glomeruli are damaged, the kidneys will stop functioning properly, and this condition can proceed with kidney failure. Glomerulonephritis is a severe condition that can be lethal, and hence it demands immediate care (Davin et al. 2014). It can occur suddenly thus referred to as acute, or it can occur after a long time hence referred to as chronic glomerulonephritis. The cause of glomerular nephritis depends on when the condition is acute or chronic. Acute glomerulonephritis can be a response to an infection in the body such as an abscessed tooth or strep throat. It can also result from the immune system reacting to an infection. Conversely, chronic glomerulonephritis develops after several years with very few or no symptoms. It can result in irreversible kidney damage which ultimately leads to kidney failure (Davin et al. 2014). The purpose of this paper is to discuss pathophysiology and manifestations of glomerulonephritis as well as comparing and contrasting nephritic syndrome and nephrotic syndrome.     

Pathophysiology

  Glomerular lesions are caused by situ formation of immune complexes or glomerular deposition. The size of the kidney may increase up to 50% on gross appearance. The histopathologic changes associated with this condition include infiltration with polymorphonucleocytes and swelling of the glomerular. Immunofluorescence can be used to detect deposition of immunoglobulins and complement. The exact triggers of these immune complexes are unclear; however, derivatives of streptococcal proteins have been reported trigger the immune complexes. Streptococcal neuraminidase may alter the immunoglobulin G of the host. When this immunoglobulin complex is formed, they collect in the glomeruli (Davin et al. 2014). 

Structural and Functional Changes

Glomerulonephritis is characterized by both functional and structural changes of the glomeruli. For instance, glomerulonephritis leads to cellular proliferation which leads to increased cells in the glomerular because of the proliferation of epithelial, mesangial, and endothelial cells. This replication of cells may be endocapillary or extracapillary. In endocapillary proliferation, propagation occurs inside the confines of the glomerular capillary tufts while in extracapillary proliferation, the proliferation of epithelial cells results in the development of loops.  The presence of monocytes and neutrophils within the glomerular indicates leukocyte proliferation which usually accompanies cellular proliferation. The basement membrane of the glomerular manifests as thickening of the capillary walls under a light microscope (Davin et al. 2014).      

     The functional changes associated with glomerulonephritis include active urine sediment with Red Blood Cells (RBC) and RBC casts, hematuria, proteinuria, and reduction in glomerular rate (GFR). The decrease of GFR and water retention and avid distal nephron salt lead to increase of the intravascular volume, systemic hypertension, frequently, and edema (Davin et al. 2014). 

Manifestations

The clinical manifestations of glomerulonephritis depend on whether an individual has acute or chronic glomerulonephritis and the cause of infection. The initial signs that something is wrong may be detected from routine urinalysis and signs associated with this condition. The signs and symptoms related to glomerulonephritis include: 

•   Fluid retention (edema) characterized by swelling in the feet, hands, face, and abdomen. 
•   High blood pressure (hypertension)
•   Foamy urine characterized by excess protein (proteinuria)
•   Hematuria which is associated with pink urine from red blood cells. 

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In chronic glomerulonephritis, the patient may develop kidney failure which is characterized by the following symptoms: muscle cramps at night, dry, itchy skin, insomnia, nausea and vomiting, lack of appetite and fatigue.  

Nephrotic Syndrome and Nephritic Syndrome

Nephrotic syndrome is a kidney condition which causes the body to release too much protein in the urine. This disorder usually results from damage of clusters of small blood vessels in the kidney which filter excess waste from the blood. On the other hand, the nephritic syndrome is a kidney disorder characterized by inflammation of the glomeruli and renal dysfunction (Meyrier & Niaudet, 2018). 

Pathophysiology

In nephrotic syndrome, the glomerular structural syndrome which may lead to proteinuria are damage to the basement membrane of the glomerular and the endothelial surface. These mechanisms may be seen in nephrotic syndrome. With chronic injury albuminuria is likely to take place may take place. Increased permeability of the glomerular leads to albuminuria and eventually hypoalbuminemia which causes greater transcapillary of water leading to the development of edema (Meyrier & Niaudet, 2018).  

     The nephritic syndrome causes inflammation of the kidneys and infiltration with polymorphonucleocytes. Nephritic syndrome cause functional and structural changes. The structural modifications involve proliferation leading to an increase in the number of cells in the glomerular tuft. Function changes associated with nephritic syndrome include a reduction in glomerular filtration rate, hematuria, and proteinuria. Decreased glomerular filtrate rate leads to edema and expansion of intravascular volume (Rashid, 2018).

Comparing and Contrasting Nephrotic Syndrome and Nephritic Syndrome