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Type 2 diabetes is a multifactorial disease that can lead to damage to function.l activity of several organs such as eye, kidney, and heart. The case study indicates that a middle-aged woman (58 years old) came with a complaint of a pinning sensation in her upper extremities to GP and based on diagnosis, GP suggested tests which reveal that creatinine level is higher and glomerular filtration rate is lower. Therefore GP suggested a nephrologist as diabetic kidney disease (DKD) has been identified.
Question 1: Pathophysiology of diabetic nephropathy
Diabetic kidney disease (DKD) is a hemodynamic and inflammatory process that declines glomerular filtration rate (GFR). The pathophysiology includes various pathways that can contribute in DKD. As mentioned by DeFronzo et al. (2021), reduced GFR occurs due to messangial expansion, glomeruloscelerosis, podocyte abnormalities, tubular atrophy. As opined by Sagoo & Gnudi (2018), oxidative stress is another factor which responsible for progressive chronic diabetic nephropathy. An increased glucose level blood sugar in type 2 diabetic patients alters the hexamine and aldose reductase pathway. Additionally, protein glycosylation increases which in turn increases AGEs. Therefore, extracellular matrix alters along with albumin concentration.Therefore, advanced glycation end product (AGE) receptors are activated which stimulates in production of inflammatory cytokines and growth factors. This contributes to glomerulosclerosis and reduces GFR. In case of Jennifer it may be a reason for DKD.
The above figure indicates the overall possible pathophysiology behind the development of diabetic chronic kidney disease Jennifer. Polyol flux increases which diminish the NADPH and glutathione. Therefore oxidative stress on kidneys increases. Similarly, mitochondrial flux and superoxide production in cases with prolonged high blood glucose levels that also responsible for oxidative stress. Therefore, damage to protein and DNA occurs which sequentially increases podocyte loss and damage which is responsible for regulating glomerular filtration rate. Hence, GFR is reduced along with increased protein albuminuria in patients with prolonged high glucose levels. As mentioned by Rabbani & Thornalley (2018), AGEs such as hydroimidazolones, glucosepane and N-carboxymethyl lysine increase dicarbonyl stress which causes renal cell dysfunction.Hence, inflammatory signalling from dicarbonyl stress causes a decrease in glyoxalase which increases proteolysis.
The above figure indicates the glyoxalase system and overexpression of glyoxalase lead to diabetic nephropathy. As observed by Sulaiman (2019), with type 2 diabetes chances of reduced GFR and microalbuminuria are about 15% and 38% respectively; afterwards, microalbuminuria converts to macroalbuminuria which indicates the progress of diabetic nephropathy. Hence, continuous follow is required to perfect the progression and complications of type 2 diabetes to prevent the occurrence of diabetic kidney disease. Self-care and patient education regarding taking care of patients are intervention strategies that can be considered by health professionals to reduce the consequences of extended type 2-diabetes (Gov, 2022). However, in this case, Jennifer has already developed chronic kidney disease due to ignorance of her own diabetic complications.
It can be discussed as diabetic nephropathy is a multifactorial pathway led by higher concentrations of glucose in the bloodstream and the case of Jennifer, oxidative stress and proteolysis led to the development of higher protein concentration in urine as well as urea and creatinine levels.
Question 2: Stage of chronic kidney diseases prevalent in Jennifer
As per test results ordered by GP for Jennifer shows a glomerular filtration rate of 32 mL/min/1.73m2. As mentioned by Sulaiman (2019), the glomerular filtration rate ranges from 30 to 44 mL/min categorized under stage 3B chronic kidney disease. Henceforth, Jennifer’s chronic condition can be categorized under moderate stage 3B CKD based on laboratory investigation.
The main management approaches required for Jennifer are dietary management and self-management. As per the views of Nguyen et al., (2019), self-management of moderate level CKD potentially slows down the progress of moderate level CKD to end-stage chronic kidney disease. Verbal persuasion, self-appraisal and evidence-based practice can be considered as management approaches for Jennifer which will enlighten Jennifer about the importance of self-management at this stage (DeLaune et al., 2019). As per NMBA standards, nurses are registered, and nurses are in charge of the development of intervention plans to ensure patient safety and achieve better health outcomes (Nursingmidwiferyboard, 2022). Therefore, for Jennifer Nurses can consider a health intervention plan such as patient education and dietary management which can control blood sugar as well as protein level in blood. Additionally, nurses can provide education for self-management which will reduce complications of stage 3B.
It can be concluded that as per laboratory investigation Jennifer’s GFR is 32 mL/min and has a higher level of protein in the urine. Additionally, the absence of any bacteria has been found which led to GP ‘to suggest nephrologists as chronic kidney disease (stage 3B) has been identified. The probable pathway for the development of chronic kidney disease in the presence of diabetes has been mentioned which includes oxidative stress and others. As per laboratory investigation, it has been found that Jennifer has stage 3B kidney disease which can be managed with self-education and dietary management intervention process.
Gov, (2022), Australian National Diabetes Audit (ANDA), retrieved on 4th September 2022 https://www1.health.gov.au/internet/main/publishing.nsf/Content/publications-Diabetes
Nursingmidwiferyboard, (2022), Midwife standards for practice, retrieved on 4th September 2022 retrieved from: https://www.nursingmidwiferyboard.gov.au/Codes-Guidelines-Statements/Professional-standards.aspx
DeLaune, S. C., McTier, L., Tollefson, J., Lawrence, J., & Ladner, P. K. (2019).Fundamentals of Nursing: Australia & NZ Edition 2e. Cengage AU.
DeFronzo, R. A., Reeves, W. B., & Awad, A. S. (2021). Pathophysiology of diabetic kidney disease: impact of SGLT2 inhibitors.Nature Reviews Nephrology,17(5), 319-334. https://doi.org/10.1038/s41581-021-00393-8
Nguyen, N. T., Douglas, C., & Bonner, A. (2019). Effectiveness of self?management programme in people with chronic kidney disease: A pragmatic randomized controlled trial.Journal of advanced nursing,75(3), 652-664. https://doi.org/10.1111/jan.13924
Rabbani, N., & Thornalley, P. J. (2018). Advanced glycation end products in the pathogenesis of chronic kidney disease.Kidney international,93(4), 803-813. https://doi.org/10.1016/j.kint.2017.11.034
Sagoo, M. K., & Gnudi, L. (2018). Diabetic nephropathy: is there a role for oxidative stress?.Free Radical Biology and Medicine,116, 50-63. https://doi.org/10.1016/j.freeradbiomed.2017.12.040
Sulaiman, M. K. (2019). Diabetic nephropathy: recent advances in pathophysiology and challenges in dietary management.Diabetology & metabolic syndrome,11(1), 1-5. https://doi.org/10.1186/s13098-019-0403-4