Pathophysiological Basis of Chronic Kidney Disease – Medical Science Assignment Help

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Pathophysiological Basis of Chronic Kidney Disease

Q1. What is the pathophysiological basis of chronic kidney disease in a patient with poorly controlled long-standing diabetes mellitus?
The precise pathway from diabetes to diabetic nephropathy is not known (Filippone et al., 2014) but below is a summary of what is known.
Initial causes of diabetes; one or more of the following lead to an excess of glucose in the blood (hyperglycemia).

• Genetic factors
• Metabolic problems, particularly in availability (type I diabetes) and efficacy (type II diabetes) of insulin in assisting regulation and storage of blood glucose
• Environmental factors – such as excess sugar and salt in diet, and insufficient exercise (type II)

Chronic hyperglycemia triggers insulin resistance.

• This leads to downregulation of insulin response, requiring more production of insulin by beta cells in the pancreas.
• Beta cells are overworked and, over time, damaged or lost (Marlon, 2013).
• Again, the precise pathogenesis of diabetes from the interrelation of beta cell dysfunction and insulin resistance is somewhat undefined (Marlon, 2013).

Leads to more hyperglycemia (Marlon, 2013).

Persistent hyperglycemia causes:

• Toxic diabetic metabolism (more glucose available so increased use of glucose for energy, producing reactive oxygen species (ROS) and in turn protein kinase-C (PKC), which promotes, among other issues, more use of glucose for energy, so the process becomes cyclic.
• Endothelial dysfunction – vessel walls become more permeable, allowing through inflammatory cells (monocytes) and low density lipoproteins (LDL) which ultimately form plaque and atherothrombosis, a form of atherosclerosis, which leads to hypertension (Health Direct, n.d.).
• Vascular inflammation, triggered by monocytes that leak through damaged endothelium (Hasudungan, 2016).
• Diabetes also increases risk of kidney disease indirectly as atherosclerosis can lead to hypertension – a complication that increases the risk of heart disease which is another common cause of kidney disease (Akram, 2022).

These factors lead to various microvascular and macrovascular complications, in the eyes, nervous system, kidneys and heart, to name a few sites.

• Damage to the kidneys is microvascular, in the small blood vessels of the glomerulus and the juxtaglomerular apparatus (Akram, 2022). This is called diabetic nephropathy (DN, or diabetic kidney disease) and is the leading cause of end-stage renal disease (ESRD) in the Western world (Giunti et al. 2006).
• Endothelial damage in the kidneys is called glomerulosclerosis (Akram, 2022) related to impaired auto-regulation of intraglomerular capillary pressure, leading to excessive stretching of the elastic endothelium (Giunti et al., 2006).
• Glomerulosclerosis, like the similar but more general blood vessel complication of atherosclerosis, creates lesions and hardening of endothelium through the buildup of connective tissue related to the triggering of an inflammation cascade (Jardine & Fellstrøm, 2009).
• This particularly affects the mesangial cells of the glomerulus and the juxtaglomerular apparatus, the glomerular basement membrane, and the foot
• processes that form part of the glomerular filter (Craft et al., 2010).
• Many of these factors lead to a decrease in the glomerular filtration rate (GFR) leading to more hypertension, more toxins in blood, and greater renal damage and dysfunction.
• Once kidney function deteriorates below 30% (or stage 4 or above), dialysis or kidney transplant may be necessary (Craft et al., 2010).

Q2. Based on the clinical picture and laboratory investigations provided, what stage of chronic kidney disease this patient is in and what will be the main management approachat this stage?

The aim of diabetes management generally is to maintain glycemia at 4 to 6 mmol/g (Diabetes Australia, n.d.).
For this case, the above table (Akram, 2022) shows that a GFR of 30 to 44 indicates stage 3b CKD. The management of this patient is guided by stage, and the severity of albuminuria (for which testing is still needed).

If urine ACR is below 35 mg/mmol (constituting ‘microalbuminuria’, at worst) a stage 3 CKD patient requires monitoring every 3 to 6 months for changes in GFR and albuminuria, as well as other cardiovascular risk factors such as blood pressure, blood lipids and blood glucose. Ideally they would also avoid smoking, weight gain, excess dietary salt, and alcohol. If urine ACR is above 35 mg/mmol (‘macroalbuminuria’), together with their GFR of 32, the patient is at similar risk to someone with stage 5 kidney disease and should have all key symptoms and CV risk factors monitored every 1 to 3 months. Preparations should also be made for either dialysis or kidney transplant, and for making end-of-life decisions.

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