Disease Pathophysiology and Concept Map

Running head: DISEASE PATHOPHYSIOLOGY AND CONCEPT MAP
DISEASE PATHOPHYSIOLOGY AND CONCEPT MAP
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1DISEASE PATHOPHYSIOLOGY AND CONCEPT MAP
Figure 1: Concept of Risk Factors, Pathophysiology, Clinical Manifestations and
Treatment for Steve

2DISEASE PATHOPHYSIOLOGY AND CONCEPT MAP
Risk factors and Pathophysiology
It has been evidenced that chronic conditions like type 2 diabetes mellitus (T2DM) and
hypertension are some of the strongest risk factors of chronic kidney disease (Webster, Nagler,
Morton & Masson, 2017).
Insulin resistance due to T2DM results in increased circulating levels of glucose in the
blood coupled by the activation of gluconeogenetic mechanisms resulting circulating levels of
fatty acids in the blood further results increased adipose tissue accumulation and oxidative
stress. Diabetes-associated oxidative stress occurs primarily due to oxidation of the accumulated
adipose tissues resulting in production of advanced glycation end products (AGEs) (Thomas,
Cooper & Zimmet, 2016). High blood glucose levels result in over expression of the glucose
transporter I (GLUT I) within the mesanglial cells of the kidney resulting in glycation within the
nephrons and associated symptoms of glomeruloschlerosis. Nodular glomeruloschlerosis is
accompanied by a gradual thickening of the glomerular basement membrane and increase in the
width of the podocytes’ slit membranes (Gharbi et al., 2016). The thickening is associated with
afferent arteriole dilation and efferent arteriole constriction followed by gradual hypofiltration of
the capillaries within the nephron resulting in decreased rate of glomerular filtration, gradual loss
of renal function, anuria and accumulation of nitrogenous wastes characteristic in chronic kidney
disease (Sulaiman, 2019). Additionally, the thickening of the basement membrane has been
associated with increased matrix in the mesanglia, its invasion within the capillaries of the
glomerulus resulting in formation of Kimmelstiel-Wilson nodules which completely decreases
filtration and causes chronic kidney disease (CKD) via consuming the glomerulus (Miranda-
Díaz, Pazarín-Villaseñor, Yanowsky-Escatell & Andrade-Sierra, 2016) (See Figure 1).