Pathophysiology of Obesity and Diabetic Kidney Disease

This presentation delves into the pathophysiology of obesity and its connection to diabetic kidney disease. It discusses the risk factors, clinical manifestations, diagnostic tests, and treatment options for this condition. The presentation also highlights the importance of continuous glucose monitoring systems and non-pharmacological treatments in managing the disease. References to relevant studies and research are provided throughout the presentation.

Clinical manifestation
Diagnostic tests
Glomerular injury
Worsening fatigue
Extremely itchy
skin
Metabolic
acidosis
Glycoprotein Cytokine
Assessment of
fluid
intake
Use in-text
referencing
750 words for
the
explanation
Angiotensin II
Receptor
Blockers
(Arbs)
Generalized Edema and
Fluid and Sodium
retention
Reduced Kidney
Function
Diuretic
Glomerular
Hyperfiltration
Biopsy
Treatment
Low Protein Diet
AetiologyObesity
Damage to
Nephrons
Rapid or Inter Mediate Acting Insulin
Secretion of
Erythropoietin
Type 2
Diabetes
Mellitus
Continuous
Glucose
Monitoring
System
Hypertension
Renal
failure
Chronic
Diabetic Kidney
Disease (Diabetic
Nephropathy
Hyperkalaemia
Pathophysiolog
y
Diabetes

• Steve McManus, and obese man with pitting oedema, is diagnosed with chronic kidney disease due to diffuse nephron loss. Chronic kidney disease (CKD) is a long-standing
disease which causes damage where kidneys fails to filter waste fluid from blood (Webster, Nagler, Morton & Masson, (2017)). However, loss of nephron is counterbalanced by adaptive
increase in secretory rate of Potassium ion (K+) in remaining nephrons (Palmer, (2015).). In accordance with case scenario it can be articulated that patient is at risk of diabetic kidney
disease that is diabetic nephropathy. Obesity is a risk factor which in turn results in stroke, hart disease, breathing problems, sleep apnea, type 2 diabetes, asthma, etc.
• Risk factors for the patient comprise hypertension, type 2 diabetes mellitus and obesity. As per the view Day & TROUPIN, (2018), increase in obesity is major developing risk factor for
CKD because it comprises cause of hypertension and Diabetes. Diabetes occur when the blood sugar level of body is high. Excessive glucose in blood causes damage to filters of kidneys.
The pathophysiology for type 2 diabetes is characterized as peripheral insulin resistance, hepatic glucose production, declining Beta cell function, etc. On the other hand, high blood
pressure cause damage to blood vessels in kidneys due to which kidneys become unable to remove extra fluid and waste from body (Causes of Chronic Kidney Disease, 2019).
• From the electrocardiogram (ECG) of patient, helps in identifying that the patient has hyperkalaemia and metabolic acidosis. As per observation, it can be said that potassium and acid
excretion are the common reasons behind hyperkalaemia and metabolic acidosis. Metabolic acidosis leads to decreased renal exertion of ammonium and resorption od bicarb. According to
Gnudi, Coward & Long, (2016), chronic hyperglycaemias is a primary cause of diabetic nephropathy. In this transmembrane glucose transporters (GLUT) receptors stop facilitation of
intracellular glucose transport in kidneys. This occurs due to activation of mechanism like direct effect of hyperglycaemia, secretion of cytokine, advanced glycosylation of end products
and glomerular hyperfiltration.
• In accordance with patient condition that is swollen legs is evident to activation of glomerular hyperfiltration has been found out which is mediated via dilation the afferent arteriole
which causes rise in Glomerular filtration rate (GFR). As per Toth-Manikowski & Atta, 2015, Glomeruli are tiny filters in kidneys which filters waste from the blood. Hyperfiltration can be
recorded as GFR ≥150 mL/min/1.73 m 2. GFR activation leads to generalized edema which is reflected in swelling, and occurs due to water retention because of loss GFR which leads to
fluid and sodium retention. Focal segment glomerulosclerosis is a kidney disease which in turn results in glomerulosclerosis. If this is untreated then it leads to kidney failure and in turn
also results in biopsy. However, worsening fatigue denotes Anaemia which occurs due to activation of glycoprotein cytokine which causes secretion of Erythropoietin (EPO) from
kidneys. Lim, 2014, stated that elevations in vascular endothelial growth factor (VEGF) is a growth factor for profibrotic proteins and beta (TFG-β) which causes damage to nephrons at
different levels. Further, activation of hyperkalemia impacts ability of kidneys to secret potassium in urine which in case of Steve McManus is because of uncontrolled type 2 diabetes
mellitus which diminish capacity of kidneys to excrete potassium into urine. Thus, severity of GFR mechanism leads to Glomerulonephritis which causes Glomerular injury which causes
chronic kidney diseases. According to Rossignol, 2015, Glomerulonephritis leads to high blood pressure because of reduced kidney function and influence ability of kidney to handle
sodium which causes chronic diabetic kidney disease (diabetic nephropathy). This stage of illness leads to long term kidney disease and end stage renal diseases.
• According to Gallagher & LeRoith, (2015)., risk of diabetes mellitus increases by increase in obesity and therefore Diabetic nephropathy is most significant complication of type ii diabetes
mellitus which leads to end stage kidney diseases. For Steve McManus, dialysis is an effective treatment in order to effectively treat chronic kidney disease. Dialysis helps in filtering and
removing waste products from the body. Dialysis helps in performing the functions of kidney at the time of chronic kidney failure. It helps in treating excess waste and fluid from the body.
• However, non-pharmacological treatment continuously measuring glucose levels by Continuous Glucose Monitoring Systems (CGMS) can aid the nurse in detecting downward and
upward trend in glucose. As per the views of Ahmad, 2015, it is important to note amount of fluid intake in case of Steve McManus will aid in stabilizing fluid volume, weight an d signs of
edema. In addition, nurse will assess appetite of Steve McManus to ensure low protein diet to decrease waste products from blood. Terami, 2014, articulated that restricting protein diet
helps in managing progression of kidney disease because protein intake affects renal hemodynamic by raising GFR.

Reference list
• Ahmad, J. (2015). Management of diabetic nephropathy: recent progress and future perspective. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 9(4).
343-358.
• Gallagher, H., & Suckling, R. J. (2016). Diabetic nephropathy: where are we on the journey from pathophysiology to treatment? Diabetes, Obesity and
Metabolism. 18(7). 641-647.
• Lim, A. K. (2014). Diabetic nephropathy–complications and treatment. International journal of nephrology and renovascular disease. 7. 361.
• Mulay, S. R., & Anders, H. J. (2017). Crystal nephropathies: mechanisms of crystal-induced kidney injury. Nature Reviews Nephrology. 13(4). 226.
• Papadopoulou, E., Varouktsi, A., Lazaridis, A., Boutari, C., & Doumas, M. (2015). Erectile dysfunction in chronic kidney disease: From pathophysiology to
management. World journal of nephrology. 4(3). 379.
• Porrini, E., Ruggenenti, P., Mogensen, C. E., Barlovic, D. P., Praga, M., Cruzado, J. M., ... & ERA-EDTA Diabesity Working Group. (2015). Non-proteinuric pathways in loss
of renal function in patients with type 2 diabetes. The Lancet Diabetes & Endocrinology. 3(5). 382-391.
• Rossignol, P., Massy, Z. A., Azizi, M., Bakris, G., Ritz, E., Covic, A., ... & Mallamaci, F. (2015). The double challenge of resistant hypertension and chronic kidney
disease. The Lancet. 386(10003). 1588-1598.
• Terami, N., Ogawa, D., Tachibana, H., Hatanaka, T., Wada, J., Nakatsuka, A., ... & Takei, K. (2014). Long-term treatment with the sodium glucose cotransporter 2
inhibitor, dapagliflozin, ameliorates glucose homeostasis and diabetic nephropathy in db/db mice. PloS one. 9(6). e100777.
• Toth-Manikowski, S., & Atta, M. G. (2015). Diabetic kidney disease: pathophysiology and therapeutic targets. Journal of diabetes research. 2015.
• Regulation of potassium homeostasis. Clinical Journal of the American Society of Nephrology, 10(6), 1050-1060.
• Gallagher, E. J., & LeRoith, D. (2015). Obesity and diabetes: the increased risk of cancer and cancer-related mortality. Physiological reviews, 95(3), 727-748.
• Gnudi, L., Coward, R. J., & Long, D. A. (2016). Diabetic nephropathy: perspective on novel molecular mechanisms. Trends in Endocrinology & Metabolism, 27(11), 820-
830.
• Day, W., & TROUPIN, B. (2018). U.S. Patent Application No. 10/058,532.
• Webster, A. C., Nagler, E. V., Morton, R. L., & Masson, P. (2017). Chronic kidney disease. The lancet, 389(10075), 1238-1252.
• Online
• Causes of Chronic Kidney Disease. (2019). [Online]. Available through: <
https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-ckd/causes >.