Thanks to the scientific research of the last decades in healthcare, it has been possible to make changes related to the study of kidneys and chronic renal diseases and complications. In the UK, renal diseases consume more than 2% of the national budget, and the figure is likely to increase significantly due to rising cases fueled by the enormous aging population (1). The National Kidney Foundation established simple characterization based on calculating estimated glomerular filtration rather than the traditional creatinine concentration level. The recent NICE guidelines and renal disorders studies show that 30-50% of the patients who progress to chronic kidney disease die prematurely from cardiovascular disease rather than progression to end-stage renal failure (20, 21). Proper kidney disease staging allows for improved patient management by alerting the clinicians and dictating the treatment regime. Also, CKD guidelines outline the process of patient referral from primary care to nephrology services.
Identification and Monitoring DKD
According to a report by Katherine et al. (2014), the active spread of diabetes mellitus and the increase in morbidity may be associated with the occurrence of type 2 diabetes. Diabetic Kidney Disease (DKD) is the major factor with more than 50% of the end-stage renal cases in the developed world compared to the low cases in developing world. In addition, the cost of care is high, especially among the old group (1, 21). Significant areas of concern in DKD are identification, monitoring, managing dyslipidemia, hypertension, using renin-angiotensin-aldosterone system blockade, glycemic measurement, hypoglycemia drug therapies, general nutrition and care in advanced stages, child and adolescent care, and multidisciplinary approaches.
Identification and monitoring of DKD depend on kidney function assessment and estimated GFR (eGFR), which is approximately <60ml/min.1.73 m2, kidney damage, estimation of albuminuria, which should have more than 30mg/g creatinine. In addition, the utilization of routine laboratory measurements facilitates earlier recognition of DKD and forms the basis of clinical staging. As a result, it is essential to understand the precision and the challenges associated with the tests for appropriate utilization in clinical care (19, 21). For instance, Egfr has limitations such as lower P30 performances with 90% chances of falling between the 30% of the measured GFR. Also, the characteristics and the existing estimation equations make it significantly less precise at higher GFR, which is a concern during the early course of DKD, which is associated with the elevated levels of GFR (1). Similarly, hyperfiltration is a sign of increased intra-glomerular capillary pressure leading to experimental nephropathy in mouse models. Therefore, reduction in the GFR pressure forms the basis of the clinical trials.
Use of Albuminuria as a test parameter to detect presence of DKD have specific limitations. It is crucial in predicting the prognosis and monitoring the response of the DKD patients to therapy. However, despite its scientific strength, there are considerable limitations, such as poor coverage because a smaller proportion of people with DKD and lower egfr have elevated levels of albuminuria. Spires et al. claim: “In the United Kingdom Prospective Diabetes Study (UKPDS), approximately 51% of patients who have creatinine clearance of <60ml/mi/1.73m2 always test positive for albuminuria” (19). Based on other tests, a decrease in GFR levels was revealed, which demonstrated that it was slightly slower in those patients who were diagnosed with type 2 diabetes and low albuminuria. In patients with suppressed GFR, low or no albuminuria significantly increases the likelihood of progress to CKD. Work by NKF KDOQI on diabetes and CKD concluded that the detection of retinopathy in patients with albuminuria less than 300 mg/g creatinine suggests development of DKD (22, 23). The recent meta-analysis supported these results and recommendations by the NKF KDOQI studies on diabetes and CKD guidelines which are relevant for the diabetic patients with low detection of albuminuria, approximately <60ML/MIN/1.73 m2.
Albuminuria may be elevated due to episodic hyperglycemia, elevated blood pressure, high protein diet, UTI, fever, congestive heart failures, and exercise. On the contrary, sustained normalization of an initially high level albuminuria from 30-300 mg/g creatinine rage to normal have a three times occurrence likeness in diabetic patients with hemoglobin levels of less than 8%, systolic pressure <115mmHg, and serum lipid of target cholesterol at <198mg/Dl and triglycerides <145mg/Dl less than those with lower levels that do not meet the threshold levels a critical method that helps to mitigate the albuminuria limitations is to standardize urine collection by linking the data to the patient’s clinical situation and the number of follow up samples (20). ADA, NKF, and the National Kidney Disease Education Program (NKDEP) seconds the recommendations of measuring albuminuria at more than one-time point where there will be elevation between 3- to 6- month period for proper diagnosis abnormal albuminuria (10). In the UKPDS report, there was a reduction in both albuminuria and kidney disease occurrences in the intensive arm of the patients who are newly diagnosed and two-fold increase in serum creatinine.
CKD diseases are classified based on the estimated GFR and the level of albuminuria or proteinuria, which are the risk factors used to stratify patients. Therefore, the patients are classified as G1-G5 based on the estimated GFR and A1-AAA3 based on albumin: creatinine ratio. These classifications are the guidelines that assist the clinicians to have a proper timing and determine the need for nephrologist referral. When identifying high-risk patients, it is necessary to make a referral. In the first and second stages, people have increased S(Cr) content, urea nitrogen in the blood, and albuminuria. (1). In stage 3, with GFR2. of 30-59 ml.min/1.73 m2, A,25-dihydroxycholecalciferol (calcitriol) deficiency tends to occur alongside the elevation of parathyroid hormonal circulation level and changes in blood pressure. Erythropoietin deficiency occurs in CKD stage 3b, which manifests as normocytic anemia (7, 25). In CKD stage 4 with GFR levels of 25-29 ml/min/1.73m2, deviations become more pronounced, and in addition, the cases of cardiovascular problems, hospitalizations, and death increase. (13, 10). At this later stage, diagnosis of the CKD patient indicates presence of metabolic acidosis due to higher retention of nitrogenous wastes, which is a major factor in the secondary deficits in secretion of proton by the renal tubular and hormonal imbalance, which impairs homeostasis.
Patients in the fifth stage do not have uremia, which occurs because of stagnation of fluids, acids, electrolytes, metabolic products, and uremic toxins. At this stage, the patients have an estimated GFR of <15ml/min/1.73m2, and the onset of uremia varies between patients. Those uremic experience episodes of nausea, vomiting, pruritus, weight loss, and constant complaints of sororities manifesting through chest pains, lack of sleep, malaise, and inability to concentrate. Upon physical examination, these patients present classic symptoms, including asterixis, clonus, and neurocognitive disease (2). The potassium metabolism becomes adequately compensated until the end-stage CKD, but diabetic patients are more likely to develop hyperkalemia at stage 3 (14, 24). Indications of initiating end-stage renal disease therapy with hyperkalemia resistance to medical treatment, metabolic acidosis, congestive heart failure, uncontrolled hypertension, pericarditis, neuropathy, encephalopathy, and uremic coagulopathy.
Identifying the causes of CKD is included in the KDIGO guidelines, with the basis of the presence or absence of diabetes, autoimmune deficiencies, high blood pressure, and HIV infection. Moreover, the causes include anomalies of the glomeruli, various congenital diseases of the vascular, cystic, and gastrointestinal groups, which are located near the anomalies, which makes it possible to diagnose and prescribe the necessary treatment (4, 23). The diagnosis of nephrotic syndrome presupposes the presence of inflammatory and non-inflammatory glomerular disease, which provokes diabetes mellitus and can periodically cause the appearance of systemic lupus erythematosus, dysproteinemia, infections generated by viruses, and malignant formations. (10). In some patients, nephrotic syndrome and idiopathic kidney diseases may be detected, including membranous nephropathy, focal segmental glomerulosclerosis, and changes provoked by the disease. (11).
The presence of signs such as dysmorphic erythrocytes, chronic edema, hypertension, sub-nephrotic proteinuria, and low GFR indicates the presence of inflammatory glomerulonephritis. A nephropathy, lupus nephritis, membranoproliferative glomerulonephritis, Good pastures disease, vasculitis, and other renal complications (5). In patients with CKD in which protein secretion in the urine does not reach 3 g per day, hypertensive nephrosclerosis, various diseases of the renal vessels, chronic nephritis, and analgesic nephropathy are observed. Thanks to a kidney biopsy, it becomes possible to determine the diagnosis of these patients (6). Furthermore, based on the data obtained from an ultrasound examination of the kidneys, it becomes possible to diagnose CKD at an early stage since ultrasound will help in a short time to detect an increased level of intestinal fibrosis (9). Ultrasound examination is performed noninvasively and is quite budgetary, which makes it a leader in choosing it as a diagnostic tool for the detection of CKD. It also includes determining the size of the kidneys, searching for cysts, vascular anomalies, both in primary and transplanted kidneys.
Treatment of CKD
Prevention is the primary care and management of CKD, but it is difficult to achieve in patients who already have the disease. The guiding principle is to reduce CKD progression to avoid further harm and avoidance of treatment, medications, or procedures that are known to worsen the situation. The main predisposing factors of AKI include aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, and other drugs toxic to the kidneys, and therefore their use is unacceptable. A sharp deterioration in kidney function may be caused by iodized radiocontrast, which may subsequently lead to the need for dialysis (8). However, the therapies above are necessary when the prior assessment of the risks of renal injury, the volume of expansion is pre-determined, and the use of low-osmolar contrast and N-acetyl cysteine administration is also controversial. Another principle forces to recognize the treatment of the causes of AKI that were caused by an actual injury (7, 27). It is necessary to consider several other factors that harm the functioning of the kidneys in patients with various kidney diseases. This necessity comes from the fact that these factors can lead to exhaustion and the inability to adapt to the changes that were caused by the current treatment.
Specific Mediation for the Patient
Based on the etiology of CKD patients, the severity of their current condition, the presence of other diseases, and the risk of CVD, it is crucial to quickly recognize the disease and build an individual approach to clinical recommendations and actions. First, a drug adjustment is required because there is evidence of compromised kidney functions based on the GFR ranges, which can drastically change the pharmacokinetics of the current medication (17). Second, it is essential to manage hypertension regardless of the causes of CKD because it slows the progression of CKD. Studies show that patients with uncontrolled blood pressure are ten times more likely to progress ESRD than patients with systolic blood pressure control below 130 mmHg. (16). To control the blood pressure, the patient will receive an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) because there is no contraindication to their use. Zheng et al. said: “Combining ACEI and ARBs in the patient confer added renal protection and reduce cardiovascular events” (27).
All treatments are effective, only if the patient follows the prescription. As a result, it is important to empower the patient to finish their medication. It is also necessary to advise the patient to consider dietary protein restriction, use sodium-glucose cotransporter two inhibitors, use therapies targeting uric acids, use vitamin D supplements, and serum phosphate, which increases the response to the primary treatments. Dietary protein restriction slows CKD progression because high protein intake is associated with the increased incidence of cardiovascular events, CKD progression, and mortality in CKD patients. In addition, growing fruit and vegetable intake may improve blood pressure and LDL cholesterol (15). Studies show that glucose-lowering drugs have beneficial effects on diabetic nephropathy and cardiovascular outcomes above glucose control. For instance, cotransporter two inhibitors and sodium-glucose lower blood pressure improve weight and albuminuria (18). The patient will always be advised to wear the shoe, wash the feet daily, and dry well with an emollient on the feet if necessary (13, 19, 25). However, the oil is not for use between the toes. Besides, the patient should cut toenails straight across and never down the sides of the nails. These self-care routines will help improve the patient’s condition because they will increase the drug metabolism and prevent sepsis at the injury site.
The patient has a moderate risk because of impaired peripheral sensation and structural foot deformity. The patient will be referred by the general practitioner (GP) to the podiatrist, in the hospital, for an annual review. At the hospital, the patient will remain under the clinical supervision of the GP and podiatrist. The podiatrist will conduct the foot protection team or foot care service to review each high-risk foot annually if ulceration is present. If the injury is severe, the case will be referred to the multidisciplinary foot care service within 24 hours or the next working day for review. If there are problems with shoes, it is necessary to refer the patient to an orthopedist in order for them to give recommendations on wearing correct shoes, as well as additional means, such as orthoses. In addition, it is essential to refer the patient to the orthopedic or vascular department in the presence of foot pathologies, corns, injuries, and nail diseases. Anything that may bother the patient in these areas can be clarified with a local orthopedist.
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