Management of Diabetic Nephropathy





Management of Diabetic Nephropathy

Diabetes mellitus is a highly convoluted disease that possesses an overall implication on the body of the host it affects. Usually, the main identification of the disease comprises the ineffectual or insufficient supply of insulin within the infected person. Accordingly, insulin assumes a very significant responsibility within the human body. Normally, the natural enzyme concentrates on the alteration of blood glucose in order to create energy. This energy is then accessible for various body processes via the mitochondria of the cells. Based on this assertion, it is apparent that the right rate of insulin is highly important for routine and healthy bodily function. However, a deficiency in the rate of this chemical leaves the body at risk of acquiring diabetes. Insufficient insulin within the body leads to hyperglycemia. If this condition does not undergo effective management, then it will lead to the destruction of a range of vital organs such as the kidney and even may lead to complications within the nervous system.

The most common variants of diabetes constitute Type 1 Diabetes and Type 2 Diabetes. Type 1 Diabetes usually affects persons who are 30 years and below. This type of diabetes influences the body’s immune system to go against the beta cells located within the pancreas. Attacking the beta cells is detrimental to the host’s blood sugar level since these cells are responsible for the secretion of insulin, which is responsible for the control of the blood sugar level. Because of this, it is evident that Type 1 Diabetes hinders the production of insulin. The other variant, Type 2 Diabetes arises from the resistance of insulin by the host’s immune system. Usually, this condition arises when the cells are unable to utilize insulin appropriately. Both Diabetes mellitus types are risky to a person’s health. However, without adequate intervention, persons enduring both types often acquire Diabetic Nephropathy. Diabetic Nephropathy is a progressive kidney illness resulting from malfunction within the kidney glomeruli. The implications of this disease require effective management of the patient via the use of hemodialysis.


Also described as Kimmelstiel-Wilson syndrome or Nodular Diabetic Glomerulosclerosis, diabetic nephropathy arises from the occurrence of angiopathy within the blood capillaries located within the kidney glomeruli. The disease is preeminent within patients suffering from both alternatives of diabetes mellitus for 15 years. However, the most possible indication of diabetic nephropathy is regular within patients suffering from Type 1 diabetes mellitus for nearly five years. Usually, clinical nephropathy materializes from 15 to 25 years after identification of the illness and poses an effect on over 25 percent of patients who fall under the 30-year age group. Diabetic nephropathy is the principal basis of sudden death among young persons suffering from the disease. Normally, diabetic patients aged 50 to 70 years old face premature death due to the effect of diabetic nephropathy. Currently, this disease affects 7 percent of the existing population residing in the United States.

Diabetic nephropathy is the principal reason for the occurrence of Chronic Kidney disease among patients beginning Renal Replacement Therapy (RRT). Typically, the illness possesses associations with enhanced cardiovascular mortality. Furthermore, the definition of diabetic nephropathy occurs through the evidence of proteinuria. This stage of the disease also gains reference as explicit or clinical nephropathy or macroalbuminuria. Seminal studies conducted in Europe in the 1980s illustrated that diminutive quantities of albumin within the subjects’ urine were responsible for the later progression of proteinuria in patients suffering from both types of diabetes (Parving et al 870). Furthermore, Gross et al (164) asserts that the occurrence of this incidence within patients suffering from type 1 diabetes was 12.6 percent in the last 7 years according to findings by the European Diabetes Prospective Communications Study Group (EURODIAB). In the United Kingdom, diabetic nephropathy among patients with type 2 diabetes was 2 percent every year (Gross et al 164).

Diabetic nephropathy is exceedingly common among other racial groups aside from Caucasians. Accordingly, the illness is more common in Asians, Native Americans and African Americans (Gross et al 164). The disease develops progressively among 5 to 10 percent of persons suffering from Diabetes mellitus Type 2 (Parving et al 870). Approximately, Parving et. al (870) states that diabetic nephropathy is progressive in 40 percent of most patients having type 2 diabetes. In addition, the disease is responsible for the occurrence of End-Stage Renal Disease (ESRD) in the United States, Europe and Japan, based on its prevalence in 25 to over 35 percent of the renal failure cases. Furthermore, a study performed on patients engaging in RRT indicated that the occurrence of diabetic nephropathy increased twice its current rate between 1991 and 2001. Currently, the increasing rate of the ailment has started decreasing. This is because of the adoption of a range of interventions in clinical settings and hospitals that contribute to early identification and countermeasure of diabetic nephropathy.

Diabetic nephropathy also leads to renal disease. This is evident in approximately 43 percent of the ESRD incident cases in the United States (Cotovio, Rocha and Rodrigues 1). This depicts the United States as one of the countries with the highest number of ESRD cases globally. Accordingly, there is significant variability of ESRD cases internationally based on the disparities arising from economic viability and infrastructure. Additionally, the cost for availing treatment for patients with diabetic nephropathy, in terms of ESRD, was over US$ 15.6 billion in 1997. Furthermore, the costs of treating the disease have increased from that particular period. Treatment based specifically for ESRD patients as an effect of diabetic nephropathy is significantly expensive in comparison to persons suffering from renal failure arising from other cases. Usually, the expenditures for diabetic patients undergoing hemodialysis are greater than the costs incurred by patients undergoing dialysis for glomerulonephritis and hypertension.

In comparison to persons who do not suffer from diabetes, the results for diabetic patients are considerably worse, especially for those who acquire ESRD from diabetic nephropathy. This is because of the incidence of contributing factors that contribute to the diminishing health of the respective patient. The most common of these factors comprise cerebrovascular and cardiac diseases. These diseases contribute sufficiently to greater rates of mortality and morbidity. Furthermore, because of diabetes, patients suffering from ESRD gain hospital admission at higher frequency. However, the admission rate is lower for patients ailing from renal failure originating from other derivatives. Additionally, regardless of the enhancement in intervention for diabetic patients, the survival rates in 5 years for patients with diabetes are low especially for persons on hemodialysis and peritoneal dialysis (Nand, Aggarwal and Sharma 83). Furthermore, nearly 40 percent of the deaths arising from ESRD are usually among persons suffering from long-term diabetes (Gross et al 165). This illustrates the effect of diabetic nephropathy in higher mortality rates among diabetic patients.


The term, diabetes, relates to the unusual amplification in the production of urine, defined as polyuria. When the degree of blood glucose increases above the capacity of the kidney to retake it in from the renal ultrafiltrate, the fluid retains diluted glucose. This is a negative implication for the kidney. This is because the diluted glucose influences an increase in osmotic pressure of the fluid, which causes the expulsion of a greater amount of water. This leads to a considerable increase in the volume of urine excreted from the human body. Accordingly, the augmented volume attenuates the sodium chloride that is present within the urine. This process, in turn, signals the macula densa to discharge a greater amount of renin, which leads to vasoconstriction. Vasoconstriction is a survival means that involves the retention of water through the passage of a limited amount of blood via the kidneys. Consequently, since the filtrated blood nurtures the kidney exclusively, vasoconstriction also condenses the nutrients provided to the kidney. This leads to infarction of the tissues and restriction of the renal function.

After a person acquires diabetes, operational changes take place within the renal system. These changes symbolize the progression of diabetic nephropathy. This includes the facilitation of hypertrophy in the kidneys and the increase in blood flow in the renal system and rates of glomerular filtration. After this process occurs, a subsequent stage takes place. This stage is usually asymptomatic and may influence the affected person to deny any considerations of diabetes. Understated morphological alterations take place within this stage. These alterations comprise the coagulation of the glomerular tissue. In addition, the earliest proof of diabetic nephropathy involves macroalbuminuria (American Diabetes Association 79). The manifestation of this component in urine is comparatively low. Regardless, this does not mean that it is normal. Atypical degrees of albumin (>20 µg/min) portray the progression of embryonic nephropathy (Gross et al 164-165).

At this point, it is possible to identify glomerular injury within samples arising from renal biopsy. The observed morphological modifications are invariable and expected in individuals with type 1 diabetes. However, the outcomes in patients with type 2 diabetes illustrate the variability of these results. Samples collected from type 2 patients can also be normal. This is because they may possess changes that are similar to those experienced by patients with type 1 diabetes (Gross et al 166). Furthermore, these samples may illustrate similar glomerular injury patterns related to diabetic nephropathy. The nephropathological genetic varieties among patients with type 2 diabetes are able to depict the disparities evident in mechanisms of renal pathophysiology as well as rejoinders from these patient groups. Consequently, the levels of protein in urine prolong their increase based on an associated increase of blood pressure. This is because of the presence and recognition of macroalbuminuria. The result of this incidence involves overt nephropathy which undergoes characterization by consistent albuminuria (>200µg/min) (Gross et al 166).


The pathology of diabetic nephropathy arises from the interaction between the metabolic and the hemodynamic conduits present within the microcirculation of the renal system (Dronavalli, Duka and Bakris 444). Hemodynamic factors are largely responsible for the origination of diabetic nephropathy. This is because they comprise biological changes within the kidney and the renal system. Accordingly, hemodynamic alterations comprise activities such as hypertrophy in kidneys and amplifications in the blood flow of the renal system (Dronavalli, Duka and Bakris 445). These changes usually take place after the acquisition of diabetes and contribute exceedingly to diabetic nephropathy. Furthermore, the application of stress on the mesangial and endothelial cells that form the glomerulus enhances growth factors, extracellular matrices and cytokines such as TGF-b (Dronavalli, Duka and Bakris 445-446). 

With respect to metabolic factors, the diabetic state of hyperglycemia gains consideration as the hallmark for the origin of diabetic nephropathy (Dronavalli, Duka and Bakris 444). This occurs via a range of metabolic procedures that are dependent on glucose. Additionally, high concentrations of glucose are also capable of causing toxicity within the cells. This may lead to modifications in the growth of cells and the expressions in proteins and genes as well as an increase in extracellular population and construction of growth factors. Glucose applies pathogenic implications on kidneys. The glucose level leads to the creation of metabolic products such as glycation derivatives and oxidants. These glycation products accumulate within the renal system and may destroy the cells by altering the extracellular and cellular proteins. Accumulation of these products may also activate unusual cell functions by conjoining to related receptors (Dronavalli, Duka and Bakris 446).

Consistent glucose-reliant launch of signaling conduits is also evident in the development of diabetic nephropathy. This involves other glucose-end products such as phospholipids and kinases. Accordingly, the functions of the enzyme, Protein Kinase C, increase within the glomerulus, specifically within diabetic tissues (Dronavalli, Duka and Bakris 446). Additionally, hyperglycemia also expresses involvement in excess release of Protein Kinase C through augmented degrees of Diaglycerol (Dronavalli, Duka and Bakris 446). The enzyme, on its own, leads to microvascular damage, which is responsible for the facilitation of diabetic nephropathy. Furthermore, Protein Kinase C is also responsible for modified blood flow in the renal system, vascular absorbance and enhanced growth factor. It is also responsible for the increased production of intracellular matrices within the kidneys of diabetic patients (Dronavalli, Duka and Bakris 446).    

Still on metabolic factors, Angiotensin II is also responsible for the progression of diabetic nephropathy among diabetic patients. However, it is unclear whether the conduits triggered by this vasoactive hormone undergo modification during diabetes or if the function undergoes enhancement due to the occurrence of hyperglycemia (Dronavalli, Duka and Bakris 448). Angiotensin II also influences the incidence of hemodynamic deviations within the kidney. These alterations comprise activities such as the increase of intraglomerular pressure, enhanced accumulation of extracellular population, triggering of growth factors in the connective tissue (Dronavalli, Duka and Bakris 448). The vasoactive hormone may also influence production of growth factors through the platelet, activation of the macrophages as well as stimulation of cytokines, which may lead to alteration of production of growth factors (Dronavalli, Duka and Bakris 448).  

Cytokines are also metabolic factors responsible for the development of diabetic nephropathy. An example of the respective cytokine is the TGF-b (Dronavalli, Duka and Bakris 447). As a prosclerotic cytokine, TGF-b undergoes stimulation from Angiotensin II, glycation products and glucose. The cytokine is a major factor in developing diabetic nephropathy. Additionally, it is also a chief mediator in the interplay between hemodynamic and metabolic factors (Dronavalli, Duka and Bakris 447). These factors accumulate extracellular matrices within the kidney. Furthermore, there are other factors responsible for the progression of diabetic nephropathy. One factor is proteinuria. Proteinuria quickens diabetic nephropathy. This is because of the effect arising from tubular cells being exposed to highly concentrated solutions of filtered proteins and expansion factors (Dronavalli, Duka and Bakris 448).                                                      

Care and Management of Diabetic Nephropathic Patients

The objective for providing care and management for patients with diabetic nephropathy focuses on enabling them to stabilize the challenge arising from the complications of using hemodialysis in glucose control. Normally, diabetic patients are difficult to manage based on their predisposition to ESRD due to diabetic nephropathy. Furthermore, it is also difficult to handle such patients based on the effect of hemodialysis on production, clearance and sensitivity of insulin (Shrishrimal, Hart and Michota 649). In general, offering quality care and management to diabetic nephropathy patients also focuses on the provision of a suitable method that is ardent enough for slowing the progression of diabetic nephropathy. This involves the use of hemodialysis in treatment and maintenance of the patient’s glucose level, the implications of utilizing hemodialysis and its effect on the psychosocial and familial condition of the patient.

Hemodialysis for Patients with Diabetic Nephropathy

For most patients with diabetic nephropathy, hemodialysis is the most considered treatment. Most of the dialysis patients rely significantly on hemodialysis than other forms of dialysis mechanisms (Nand, Aggarwal and Sharma 83). Regardless of the popularity of this technique among diabetic patients, hemodialysis possesses one of the worst survival rates for diabetic patients globally. This is in comparison with other dialysis methods for diabetic patients such as peritoneal dialysis and Continuous Ambulatory Peritoneal Dialysis (CAPD). Nonetheless, the provision of this treatment requires the consideration of individual versus rehabilitation basis. Personally, it is important for me to compare hemodialysis as a viable treatment with other treatment modalities such as CAPD and peritoneal dialysis. This is because the patient requires an effective hemodialysis that possesses more benefits than the proposed modalities.

Indeed, the use of hemodialysis versus the other modalities should focus more on the individual patient rather than the rehabilitation or the survival data for the technique. This is because the survival information and rehabilitation aspects for these therapies are similar even though the survival tempo of a modality such as CAPD reduces drastically as time passes. Therefore, I support the use of hemodialysis treatment, based on its affinity towards the health of the individual rather than the implications it possess on the medical centers. In contrast, the selected modality is dismal in terms of survival and rehabilitation in healthcare centers. Regardless, most physicians advocate for the use of this therapeutic intervention especially for patients suffering from extreme cases of diabetes or other related diseases. Furthermore, the use of maintenance of hemodialysis is important for my patient based on the positive implications it possesses on diabetic nephropathy such as enhanced control of blood pressure and glucose levels.

Using Hemodialysis in Treatment and Maintenance of the Patient’s Glucose Level

The range of glucose levels in the patient’s body possess an implication on the progression and slowing of diabetic nephropathy among diabetic patients. As mentioned, high concentrations of glucose are capable of poisoning the cells and altering their functions. Accordingly, high levels of glucose may lead to the production of oxidants and Advanced Glycation Ends (AGEs) that further the development of diabetic nephropathy. It is important to note these crucial factors in order to determine the effectiveness of hemodialysis in treating the patient as a nurse within the satellite unit. Since diabetic patients often have ESRD because of diabetic nephropathy, it is important to consider the implications of this resultant ailment on glucose levels. ESRD considerably modifies glycemic control (Shrishrimal, Hart and Michota 649). This effect by ESRD as well as the hemodialysis treatment can pose dangerous implications on the patient. This is because of the effect of the treatment and ESRD on the extensive fluctuation of glucose levels.

The lack of control of glucose levels put the patient at risk of acquiring hypoglycemia. Hemodialysis is capable of complicating glycemic control based on its effect on clearance, tangential tissue sensitivity and production of insulin. A number of factors may enhance the resistance of insulin by the patient’s immune system in ESRD. This may lead to a dull capability of regulating peripheral use of glucose and suppression of hepatic gluconeogenesis (Shrishrimal, Hart and Michota 650). It is also significant to note the implication of insulin resistance in type 2 diabetic patients. If the patient has type 2 diabetes but lacks any kidney illness, then the resistance of insulin may lead to amplification of insulin discharge. This activity does not take place in ESRD due to simultaneous metabolic acidosis. Furthermore, hemodialysis will modify the secretion, opposition and clearance of insulin due to the periodic improvement of management of phosphates, uremia and acidosis (Shrishrimal, Hart and Michota 650).

Accordingly, glucose control for the patient’s hemodialysis also involves a study of the dialysate. This is because the concentration of dextrose within the dialysate is capable of affecting the control of glucose during the patient’s treatment. Usually, dialysates that possess lower concentrations of dextrose experience utilization. Furthermore, they are also connected to the occurrence of hypoglycemia. In contrast, dialysates with high concentrations of dextrose undergo utilization in peritoneal dialysis. The use of such levels of dextrose concentrations in peritoneal dialysis is for the intensification of ultrafiltration (Shrishrimal, Hart and Michota 650). However, this function is also capable of auguring hypoglycemia. Consequently, hemodialysis and ESRD wield opposing efforts on the production and metabolism of glucose in the patient’s immune system. For instance, it is possible to assert that the patient requires a greater amount of supplemental insulin if he possesses resistance of insulin. However, this is incorrect based on the effect diabetic nephropathy may possess on the patient in terms of ESRD.

Effect on the Patient’s Psychosocial and Familial Condition

Based on the effects hemodialysis possesses on the family as well as psychosocial state of the patient, it is important for me to derive positive interventions that will calm both parties. Foremost, I will focus on educating the patient and his family on the various features of diabetic nephropathy in simplicity. Accordingly, it will be significant for the patient and family to learn about the various modalities used in treating diabetes. This will enable them to understand my support for the hemodialysis treatment. Furthermore, I will also make the family aware of the strategies and practices that they can input in order to support the patient as he receives his treatment (Dunning 106). Accordingly, since the patient may possess a superiority complex based on his prolonged hospitalization, it will be important to involve him in decision-making, especially in matters concerning his treatment. According to Mertig (99), patients who are under admission for diabetes for a long time may require self-management of their disease and thus distinguish from newly admitted patients.

In conclusion, patients with both types of diabetes are at risk of gaining diabetic nephropathy. Even though the ailment affects patients with type 2 diabetes greater than type 1 patients, it is still important to factor in the prevalence of the illness in both patients. Furthermore, the pathogenesis of diabetic nephropathy illustrates its possible occurrence in type 1 patients as well. This is due to the prevalence of metabolic and hemodynamic factors within the body. Regardless of the extensive scope of diabetic nephropathy, it is apparent that certain modalities are capable of slowing its progression and similarly, counteracting diabetes generally. These modalities, which comprise CAPD, hemodialysis and periodontal dialysis, facilitate the treatment against the illness and other renal complications. In addition, it is also important to consider the utilization of positive nurse-patient relationships in order to assist the patient in recovering psychosomatically.

Works Cited

American Diabetes Association. “Nephropathy in Diabetes.” Diabetes Care. 27.1 (2004): 79-83. Web. 23 Aug. 2010.

Cotovio, P., A. Rocha & A. Rodrigues. “Peritoneal Dialysis in Diabetics: There is Room for More.” International Journal of Nephrology. 2011 (2011): 1-10. Web. 23 Aug. 2010.

Dronavalli, Suma, Irena Duka & George L. Bakris. “The Pathogenesis of Diabetic Nephropathy.” Nature Clinical Practice: Endocrinology & Metabolism. 4.8 (2008): 444-452. Web. 23 Aug. 2010.

Dunning, Trisha. Care of People with Diabetes: A Manual of Nursing Practice. Oxford: Wiley-Blackwell Pub, 2009. Print.

Gross, L. Jorge, Mirela J. De Azevedo, Sandra P. Silveiro, Luis Henrique Canani, Maria Luiza Caramori & Themis Zelmanovitz. “Diabetic Nephropathy: Diagnosis, Prevention, and Treatment.” Diabetes Care. 28.1 (2005): 164-176. Web. 23 Aug. 2010.

Mertig, G. Rita. The Nurse’s Guide to Teaching Diabetes Self-Management: What Nurses Need to Know. New York: Springer Pub, 2006. Print.

Nand, Nitya, H. K. Aggarwal & M. Sharma. “Renal Replacement Therapy in Diabetic Nephropathy: An Update.” Journal Indian Academy of Clinical Medicine. 3.1 (2002): 81-84.

Parving, Hans-Henrik, Hendrik Lenhert, Jens Brochner-Mortensen, Ramon Gomis, Steen Andersen & Peter Arner. “The Effect of Irbesartan on the Development of Diabetic Nephropathy in Patients with Type 2 Diabetes.” The New England Journal of Medicine. 345.12 (2001): 870-878. Web. 23 Aug. 2010.

Shrishrimal, Kumarpal, Peter Hart & Franklin Michota. “Managing Diabetes in Hemodialysis Patients: Observations and Recommendations.” Cleveland Journal of Medicine. 76.11 (2009): 649-655. Web. 23 Aug. 2010. 

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