Chronic Kidney Disease
Pathophysiology and Clinical Manifestations
Annie’s chronic kidney disease may have occurred as a result of the complication of Type 2 diabetes mellitus and hypertension, diagnosed when she was 60. The two conditions have been associated with causing chronic kidney disease (Vassalotti et al., 2016).
Annie complained of nocturia on assessment. This occurred because of Chronic Kidney Disease as a result of the inability to elaborate concentrated urine that has low solute content at night. However, under normal circumstances, the amount of solute in urine plays a major role in determining the flow rate and volume of urine (Patel et al., 2016). In addition, the response to vasopressin and the osmolality of the medullary interstitium also plays a part in determining the volume and flow rate of urine. Furthermore, there is a low excretion of potassium, chloride, and sodium at night as compared to the high rate of their excretion during the day. Also, the level of vasopressin in plasma is usually higher during the night than during the day. As a result, most of our solute load (electrolytes) are excreted during waking hours while we produce concentrated urine (that is also acidic) during the night. As can be seen the main cause of nocturia in Chronic Kidney Disease is because of the increase in excretion of solutes.
Annie also complained of itching of the skin because of the accumulation of urea in the body (uremic pruritus). In this case, there have been specific abnormalities to uremia which have led to the activation of itch fibers which includes, structural changes of the skin associated with dehydration, and significant changes that take place with hyperparathyroidism related to metabolic bone disease (Mettang, 2016) . Additionally, itching occurs because of changes in nociceptive sensory pathway.
In chronic kidney disease, erythropoietin production by the kidney decreases, causing profound anemia this is manifested when the patient complains of being tired (Bonomini, Del Vecchio, Sirolli, & Locatelli, 2016). Also, the patient’s hemoglobin is decreasing as observed by the nurse. The consequences of decreasing renal function are manifested by the stages which range from decreased renal reserve to renal insufficiency then to renal failure and finally ESRD. Retention of sodium and water causes edema (patient complains of puffiness), hypertension with a blood pressure of 155/97 mmHg as observed by the nurse (Piccoli et al., 2016). Decreased GFR causes stimulation of the renin-angiotensin axis and increases aldosterone secretion, which raises Blood Pressure as observed by the nurse (Raghavan, & Holley, 2016).
Classification of CKD
| Stage | GFR, mL/min per 1.73 m2 |
| 0 | > 90 (with risk factors for CKD) |
| 1 | ≥ 90 (with demonstrated kidney damage) |
| 2 | 60–89 |
| 3 | 30–59 |
| 4 | 15–29 |
| 5 | < 15 |
Chronic renal failure involves the process which leads to an irreversible reduction in nephron number and typically corresponds to CKD stages 3–5 (Rocco et al., 2016). The fifth stage often reflects end-stage renal disease (ESRD). The patient had a GFR of 31 mL/min per 1.73 m2, creatinine 153 umol/L, Na+ 141 mmol/L, K+ 4.7 mmol/L, and Urea 7.6 mmol/L. Therefore CKD was at the third stage.
Management
The goal of management is based on the conservation of renal function as long as possible. Diagnosis and treatment of reversible causes of renal failure such as control Diabetes Mellitus and hypertension are crucial and entails low-protein diet supplemented with essential amino acids to minimize uremic toxicity and to prevent wasting and malnutrition. Treatment of associated conditions is often done to improve renal dynamics (Havas, Bonner, & Douglas, 2016). For instance, for anemia, erythropoiesis-stimulating agents are given. In Acidosis replacement of bicarbonate stores by administration of sodium bicarbonate. The restriction of dietary potassium usually manages hyperkalemia; administration of cation exchange resin. Additionally, Phosphate retention is controlled by a decrease in dietary phosphorus (chicken, milk, legumes, carbonated beverages); administration of phosphate-binding agents (bind phosphorus in the intestinal tract). Finally, Maintenance dialysis or kidney transplant when symptoms can no longer be controlled with conservative management.
To slow theProgression of CKD, Exclude and treat any reversible causes (such as obstruction) specifically in elderly patients. Assessing the rate of progression by calculating the rate of fall of GFR (mL/min/1.73 m2/year). Optimize Blood Pressure control to be less than 130/80 mmHg; lower in diabetic nephropathy. Start with Angiotensin Converting Enzyme Inhibitors s or Angiotensin Receptor Blockers in proteinuric and diabetic nephropathies (with proteinuria). Close monitoring of any change in serum creatinine/GFR is very crucial. Stop ACEI or ARB if the GFR reduces by more than 25% at 1 – 4 wks after initiation or change of regimen. In nonproteinuric, nondiabetic CKD, calcium antagonist plus diuretic are an alternative antihypertensive treatment. Prevent acute decline of GFR precipitated by intercurrent illnesses. Volume depletion, use of NSAIDs, aminoglycosides, and contrast agents in diagnostic imaging.
Nursing Management
Nursing Assessment is done to obtain a history of chronic disorders. It also assesses the degree of renal impairment and involvement of other body systems by obtaining a review of systems and reviewing laboratory results (Textor & Mailloux, 2016). Additionally, it is done by performing a thorough physical exam, including vital signs, cardiovascular, pulmonary, gastrointestinal, neurologic, dermatologic, and musculoskeletal systems.
Some of the nursing diagnoses for the patient include; Excess fluid volume related to the disease process, Imbalanced nutrition: Less than body requirements related to anorexia, nausea, vomiting, and restricted diet. Impaired skin integrity related to changes in oil and sweat glands as well as uremic frost. Constipation related to fluid restriction and ingestion of phosphate-binding agents. Risk for injury while ambulating related to potential fractures and muscle cramps due to calcium deficiency. Ineffective therapeutic regimen management related to restrictions imposed by CRF and its treatment
Achieving Fluid and Electrolyte Balance is done throughmonitoring for signs and symptoms of hypovolemia or hypervolemia because regulating the capacity of kidneys is inadequate (Arnold et al., 2016).Monitoring urinary output and urine specific gravity; measure and record intake and output including urine, gastric suction, stools, wound drainage, perspiration (estimate), and monitoring serum and urine electrolyte concentrations
Maintaining Adequate Nutrition is achieved in collaboration with a dietitian, regulate protein intake according to impaired renal function because metabolites that accumulate in blood derive almost entirely from protein catabolism.Protein should be of high biologic value-rich in essential amino acids (dairy products, eggs, meat) – so that the patient does not rely on tissue catabolism for essential amino acids.A low-protein diet may be supplemented with essential amino acids and vitamins (Zelnick et al., 2017). As renal function declines, protein intake may be restricted proportionately.Protein will be increased if the patient is on dialysis to allow for the loss of amino acids occurring during dialysis. Provide high-carbohydrate feedings because carbohydrates have greater protein-sparing power and provide additional calories.Weigh the patient daily.Monitor BUN, creatinine, elect, albumin, pre-albumin, total protein, and transferrin.Food and fluids that contain large amounts of sodium, potassium, and phosphorus may need to be restricted.
To prevent constipation, be aware that phosphate binders cause constipation that cannot be managed with usual interventions.Encourage a high-fiber diet, bearing in mind the potassium content of some fruits and vegetables (Whittaker et al., 2018). Commercial fiber supplements may be prescribed.Use stool softeners as prescribed.Avoid laxatives and cathartics that cause electrolyte toxicities (compounds containing magnesium or phosphorus).Increase activity as tolerated.
Reference
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Bonomini, M., Del Vecchio, L., Sirolli, V., & Locatelli, F. (2016). New treatment approaches for the anemia of CKD. American Journal of Kidney Diseases, 67(1), 133-142.
Havas, K., Bonner, A., & Douglas, C. (2016). Self‐management support for people with chronic kidney disease: Patient perspectives. Journal of renal care, 42(1), 7-14.
Mettang, T. (2016). Uremic itch management. In Itch-Management in Clinical Practice (Vol. 50, pp. 133-141). Karger Publishers.
Patel, M., Vellanki, K., Leehey, D. J., Bansal, V. K., Brubaker, L., Flanigan, R., … & Kramer, H. (2016). Urinary incontinence and diuretic avoidance among adults with chronic kidney disease. International urology and nephrology, 48(8), 1321-1326.
Piccoli, G. B., Cabiddu, G., Attini, R., Parisi, S., Fassio, F., Loi, V., … & Todros, T. (2016). Hypertension in CKD pregnancy: a question of cause and effect (cause or effect? This Is the question). Current hypertension reports, 18(5), 35.
Raghavan, D., & Holley, J. L. (2016). Conservative care of the elderly CKD patient: A practical guide. Advances in chronic kidney disease, 23(1), 51-56.
Rocco, M. V., Chapman, A., Chertow, G. M., Cohen, D., Chen, J., Cutler, J. A., … & Killeen, A. A. (2016). Chronic Kidney Disease Classification in Systolic Blood Pressure Intervention Trial: Comparison Using Modification of Diet in Renal Disease and CKD-Epidemiology Collaboration Definitions. American journal of Nephrology, 44(2), 130-140.
Textor, S., & Mailloux, L. U. (2016). Clinical manifestations and diagnosis of chronic kidney disease resulting from atherosclerotic renal artery stenosis. UpToDate:[Online]. Available.
Vassalotti, J. A., Centor, R., Turner, B. J., Greer, R. C., Choi, M., Sequist, T. D., & National Kidney Foundation Kidney Disease Outcomes Quality Initiative. (2016). A practical approach to the detection and management of chronic kidney disease for the primary care clinician. The American journal of medicine, 129(2), 153-162.
Whittaker, C. F., Miklich, M. A., Patel, R. S., & Fink, J. C. (2018). Medication safety principles and practice in CKD. Clinical Journal of the American Society of Nephrology, 13(11), 1738-1746.
Zelnick, L. R., Weiss, N. S., Kestenbaum, B. R., Robinson-Cohen, C., Heagerty, P. J., Tuttle, K., … & de Boer, I. H. (2017). Diabetes and CKD in the United States population, 2009–2014. Clinical Journal of the American Society of Nephrology, 12(12), 1984-1990.