Key obesity

Hypertension Type 2 diabetes mellitus

ACE
Risk Factors
inhibitors
Decrease blood flow to kidneys Excess blood glucose level
Aetiology due to narrowing of lumen.

Glycation of basement
Pathophysiology Renin release from kidneys -> membrane in efferent
RAAS activation -> further arteriole of kidneys
Clinical increase in Blood pressure.
manifestations
Stiffen efferent arteriole ->
Decrease blood flow to kidneys
Diagnostic tests decrease blood flow out of Insulin
-> ischaemic injury to
kidneys
glomerular capillaries
Treatment
Release of growth factors by Increased pressure in
infiltrated White blood cells. glomerulus -> hyperfiltration
Weight loss Elevation of legs

Increased glomerular
permeability Pitting oedema in
lower extremities Swollen legs

urinalysis Increased filtration of proteins

Sodium restriction Diuretic
and macromolecules medications
in diet
Increased hydrostatic pressure
Use of
moisturiser Decrease in the number of nephrons

Adaptive hyperfiltration
Fluid and sodium retention
Metabolic panel Later in course Avoid NSAID’S
Worsening fatigue Itchy skin
Nephrotoxic inflammation
Sodium
Electrolyte bicarbonate
Decrease in Glomerular filtration rate panel
Body is unable to excrete urea, hyperkalaemia
haemodialysis
nitrogenous waste
Decrease in urine output Decreased secretion of Metabolic acidosis
potassium and acid.
 Obesity can lead to insulin resistance which acts as a major factor in the development of hypertension and type 2 diabetes mellitus (Patel et al., 2016). Chronic hypertension can lead to the

thickening of the afferent arteriole that leads to the glomerulus. This results in inadequate blood flow to the kidneys due to the decrease in the size of lumen. Renin is released by the kidneys in

response to the decreased amount of the blood flow, release of renin activates the Renin Angiotensin Aldosterone System (RAAS) which leads to further increase in the Blood pressure. Overtime,

this decrease in blood flow leads to ischaemic injury within the glomerular capillaries, which can cause the filtration of White blood cells that release growth factors in the surrounding tissues.

Thus, leading to increased permeability of glomerulus (Bidani, Griffin & Epstein, 2012). On the other hand, increased blood glucose levels cause glycation in efferent arteriole of glomerulus. This

leads to decrease in blood flow from the kidneys which tends to increase the pressure in the glomerular capillaries and thus, leading to hyperfiltration from the capillaries. Overtime, hyperfiltration

can also increase the permeability of glomerulus (AK, 2014).

This increased permeability can lead to the filtration of various macromolecules such as proteins thus, causing a decrease in the number of nephrons. Due to loss of nephrons, the nephrons

left adapt to these haemodynamic changes by increasing their function leading to adaptive hyperfiltration. Overtime, hyperfiltration can lead to nephrotoxic inflammation which decrease the

Glomerular Filtration Rate (GFR) and ultimately decreasing the urine output (Solini & Ferrannini, 2011).

There are five stages of the chronic kidney disease depending on the amount of the GFR produced by the kidney. Clinical manifestations become evident when the disorder is in stage 4 or 5

and the GFR goes below than 30 mL/min (Solini & Ferrannini, 2011). In the given scenario, Steve is experiencing pitting oedema in his lower extremities and his legs are swollen, this happens as

there is a significant decrease in the GFR production which leads to water retention and thus, there is an increase in the levels of sodium and fluid in the body. This excess amount of sodium tends

to attract fluid towards it and then leaks the fluid into the cardiovascular spaces, causing pitting oedema and swelling of the legs (Khan et al., 2016). Steve’s blood tests also show increased amount

of potassium and acid in his blood, this is due to the decrease in the urine output from the kidneys. Kidneys are no longer able to excrete electrolytes such as potassium ions and hydrogen ions in

normal amount thus, leading to hyperkalaemia and metabolic acidosis. Urea and other nitrogenous components which are generally the major components excreted by urine are also left behind in

the body due to decreased urine production. Increased amount of urea in the bloodstream is the major cause behind Steve’s worsening fatigue and itchy skin (Wang et al., 2017).
 Electrolyte panel is a blood test used to measure levels of different electrolytes such as potassium, sodium ions and acid in the blood therefore, it is helpful in diagnosing hyperkalaemia

and metabolic acidosis. Whereas, metabolic panel is also type of blood test that is used to measure kidney function by measuring the amount of urea and nitrogenous waste in the blood stream

thus, diagnosing uraemia. Furthermore, there are traces of macromolecules such as proteins in urine during chronic kidney disease which can be easily detected through urinalysis therefore, it

can be used to diagnose proteinuria or haematuria (Gounden & Jialal, 2019).

Treatment of chronic kidney disease consists of managing its signs, symptoms and factors affecting the disease. NSAID’s can increase the levels of potassium in the blood thus, stopping

their use can help in managing hyperkalaemia. Whereas, the use of insulin and sodium bicarbonate which acts as a base can neutralize the effects of acid thus, treating metabolic acidosis.

Oedema can be managed by decreasing the amount of sodium in the body which can be managed by restricting sodium in the diet and use of diuretics such as frusemide that can help in

elimination of sodium through urine. Elevation of legs help to take fluid out of the cardiovascular spaces thus, treating oedema and swollen legs. Uraemia can only be managed using

haemodialysis that helps in excreting the urea out of the blood thus, managing itchy skin and fatigue. Use of medications such as ACE inhibitors and insulin in collaboration with weight loss

can assist in managing hypertension and diabetes (Lederer & Klein, 2012).

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 Reference list
AK, L. (2014). Diabetic nephropathy - complications and treatment. International Journal of Nephrology and Renovascular Disease, 2014(default), 361-381.

Bidani, Anil K., MD, FASN, Griffin, Karen A., MD, FACP, FASN, & Epstein, Murray, MD, FACP, FASN. (2012). Hypertension and chronic kidney disease progression: Why the suboptimal

outcomes? American Journal of Medicine, the, 125(11), 1057-1062. doi:10.1016/j.amjmed.2012.04.00

Chen, W., MD, & Abramowitz, Matthew K., MD, MS. (2014). Treatment of metabolic acidosis in patients with CKD. American Journal of Kidney Diseases, 63(2), 311-317.

doi:10.1053/j.ajkd.2013.06.017

Gounden, V. and Jialal, I. (2019). Renal Function Tests.

Khan, Y. H., Sarriff, A., Adnan, A. S., Khan, A. H., & Mallhi, T. H. (2016). Chronic kidney disease, fluid overload and diuretics: A complicated triangle. Plos One, 11(7), e0159335-e0159335.

doi:10.1371/journal.pone.0159335

Lederer, E. D., & Klein, J. B. (2012). New treatments for CKD - new insights into pathogenesis. Journal of the American Society of Nephrology, 23(10), 1601-1603. doi:10.1681/ASN.2012080842

Patel, S. A., Ali, M. K., Alam, D., Yan, L. L., Levitt, N. S., Bernabe-Ortiz, A., . . . Prabhakaran, D. (2016). Obesity and its relation with diabetes and hypertension. Global Heart (Formerly CVD

Prevention and Control), 11(1), 71- 79.e4. doi:10.1016/j.gheart.2016.01.003

Solini, A., & Ferrannini, E. (2011). Pathophysiology, prevention and management of chronic kidney disease in the hypertensive patient with diabetes mellitus. The Journal of Clinical

Hypertension, 13(4), 252-257. doi:10.1111/j.1751-7176.2011.00446.x

Wang, X., Shen, B., Zhuang, X., Wang, X., & Weng, W. (2017). Investigating factors associated with depressive symptoms of chronic kidney diseases in china with type 2 diabetes. Journal of

Diabetes Research, 2017, 1769897- 7. doi:10.1155/2017/1769897

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