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Laboratory Analysis

Discuss about the Chronic Kidney Disease for Laboratory Analysis.

This is a case of patient X, an African female who is 53-years old, with a history of diabetes type 2 (16 years now), hyperlipidaemia and high blood pressure. Also reported is a smoking history (34 years now). She enjoys three to four mixed drinks every day and occasionally, she takes wine at dinner. Patient X presents in the medical clinic complaining of dyspnoea, pruritus and bipedal pitting oedema. Her blood pressure is 166/93 mmHg while her heart rate is 95 beats per minute (both the rate and the rhythm are regular). Her respiration is 27 breaths per minute and, at room temperature, her oxygen saturation is 94. When asked about physical activity, she says she bowls at times. Of important note is that her father passed on at the age of 58, of a heart attack. He was overweight. She is 5’3” tall and she weighs 202 pounds; her BMI is 35.7. The review of systems and the remainder of the past medical and surgical history is unremarkable. A blood sample is taken. It is sent to the laboratory for analysis. An abnormal finding is revealed as shown in the table below:

Laboratory Analysis

Test

Patient X’s Results

Target Range

Haemoglobin (g/dL)

7.9

11.5-12.5

Creatinine (mg/dL)

2.3

0.7-1.3

GFR (mL/min/1.72 m2)

4

90-120

Albumin (g/dL)

3.2

≥4.0

HbA1c (%)

9.0

<7.0

LDL (mg/dL)

145

<100

HDL (mg/dL)

45

>40

Random Glucose (mg/dL)

187

<140

Ratio of albumin to creatinine (mg/g)

281

<30.5

Calcium (mg/dL)

9.1

8.5-9.6

Phosphorus (mg/dL)

3.3

2.8-4.7

Parathyroid hormone (pg/mL)

78

35.5-70.5

Kumar et al. (2009) posit that chronic renal failure is a changeless impairment in kidney function that definitively evolves over a long period of time; years. According to Agodoa (2017), at first, it manifests only as a biochemical abnormality while in the long run, loss of the excretory, endocrine and metabolic functions of the organ result in the clinical signs and symptoms of kidney failure, all which are collectively referred to as uraemia. Chronic kidney disease is called to end-stage kidney disease (ESKD) when loss of life is likely in case kidney replacement therapy is not sought (Kumar et al. 2009). According to Lewis (2017), the economic and social consequences of CKD are noticeable. The incidence of CKD is significantly higher in particular countries. Bomback and Bakris (2011) argue that it is perhaps due to the differences in racial and regional incidences of the disease pattern coupled with the difference in the practice of medicine across the globe. For instance, in the United States of America, the incidence rate per a million people is over 350 persons, most of which are patients with an underlying diagnosis of diabetes mellitus (Shaw & Cummings 2012).

Causes of Chronic Renal Failure

There are many causes of chronic renal failure. The most common is diabetes mellitus, tied in large geographical and racial differences as Shaw and Cummings (2012) note. According to Colledge et al. (2010), diabetes mellitus accounts for 20-40% of CKD cases. Systemic inflammatory conditions such as vasculitis and systemic lupus erythematosus (SLE) are the reason for 5-10% of the cases while interstitial disease justifies 20-30% of CKD. Also, glomerular diseases including igA nephropathy is responsible for a good number of cases. Berbari and Mancia (2010) report that hypertension is the explanation for 5-20% of CKD cases. Field, Pollock and Harris (2010) elucidate that renal artery stenosis, if not managed early enough, it may lead to chronic renal failure. Moreover, inherited or congenital diseases such as Alport’s syndrome and polycystic kidney disease also result in the development of CKD. They are the reason for 5% of cases (Himmelfarb & Sayegh 2010). Nevertheless, as Nitta (2015) argues, the elemental diagnosis of this condition is not always instituted, especially among several the aged patients with moderate GFR reductions. The organs of many of the patients who are diagnosed with the disease late are bilaterally small in size (Kumar et al. 2009).

Chronic renal failure always presents as an elevated blood creatinine and urea found in the routine analysis of a patient’s serum. This usual rise in blood urea and creatinine is often accompanied by proteinuria, hypertension and anaemia. Many of the patients with the gradually progressive disease never exhibit associated symptoms until their GFR is very low (Colledge et al. 2010). Excessive urination at night (nocturia) is an early symptom of CKD, often as a result of a rise in each nephron’s osmotic load and loss of ability to concentrate urine. Thenceforth, in every body system, new symptoms such as fatigue or breathlessness develop.  And, in end-stage renal disease, there may be pruritus, nausea, vomiting and anorexia (Kimmel & Rosenberg 2015). Later, as a result of metabolic acidosis, hiccups, fits, twitching, drowsiness and comma ensue.

Basing an argument on the results indicated by patient X’s blood serum analysis, with profound macroalbuminuria and a low GFR, a diagnosis of stage 3 disease is made. Marked elevation of the HbA1c and rise in the levels of blood glucose substantiate the diagnosis. With a haemoglobin level of 8.6 g/dL, it suffices to say that patient X is also experiencing anaemia. Also noted are initial features of bone disease and disorder in mineral metabolism. Patient X is risking developing a cardiovascular condition because of the longstanding history of diabetes mellitus, hyperlipidaemia, high blood pressure and tobacco use. All of them are evidently uncontrolled.

Complications of Chronic Renal Failure

Floege, Johnson and Feehally (2010) note that anaemia is a very common complication, usually correlating with the severity of renal disease. According to Floege, Johnson and Feehally (2010), anaemia contributes to several non-specific signs and symptoms of CKD. The mechanisms linked to this are relative erythropoietin deficiency and reduced red cell lifespan. Reduced erythropoiesis as a result of toxic uremic effects on the precursor cells in the bone marrow is another mechanism implicated for anaemia. Again, in CKD, there is increased blood loss due to poor platelet function and capillary fragility and also, reduced dietary intake, absorption and utilization of iron (Colledge et al. 2010).

Fluid and electrolyte imbalance is another complication which renal patients encounter as their disease progresses. Himmelfarb and Sayegh (2010) posit that in advance CKD, fluid retention is very common while Field, Pollock and Harris (2010) note that renal artery stenosis is greatly linked to disproportional fluid retention in milder cases of CKD, which oftentimes result in occasional pulmonary oedema. According to Cummings and Klahr (1985) limiting the intake of sodium is a good practice for instance 100mmol/day. Slaughter (2007) suggests sodium has an effect on both blood pressure and fluid balance thus, loop diuretics are regularly requisite. But, other patients suffering from ‘salt wasting’ syndrome oftentimes require a high water and salt intake to avoid diminution of fluid. Time after time, this occurs in patients with obstructive uropathy, renal cystic disease, other tubulo-interstitial diseases and also those with reflux nephropathy (Slaughter 2007). Colledge et al. (2010) suggest that in the eventuality hyperkalaemia develops, a review of drug therapy should be done (avoid potassium sparing diuretics, ARBs and ACE inhibitors). Calcium resonium therapy and correcting acidosis is helpful. But, limiting potassium intake is necessary in late CKD (Drukker, Parsons & Maher 1979).

Furthermore, Slaughter (2007) points that cardiovascular events and dyslipidaemia are some of the complications which renal patients develop. Slaughter (2007) argues that independently, CKD is a peril for cardiovascular conditions while Berbari and Mancia (2010) suggest that atherosclerosis is a common factor, more often than not heightened by hypertension. Again, medial vascular calcification in association with vascular occlusion and rigidity develops, often accelerated by increased levels of phosphate in plasma (Colledge et al. 2010). In end-stage vascular disease, the development of left ventricular hypertrophy is frequent and often accounts for the several presumed arrhythmic demises in this group (Slaughter 2007). In inadequately or untreated end-stage kidney disease, pericarditis is a common complication. Often it leads to pericardial tamponade and later constrictive pericarditis (Berbari & Mancia 2010) Moreover, in patients with proteinuria that is significant, hypercholesterolemia is near universal (Floege, Johnson & Feehally 2010). Elevated levels of triglycerides are also a common complication in patients with CKD, HMG CoA reductase inhibitors achieve substantial reductions in lipids in CKD. In addition to their cardioprotective effect, there is some evidence that control of dyslipidaemia with statins slows the rate of progression of renal disease (National Collaboration Centre for Chronic Conditions, 2008).

Anaemia

Additionally, renal osteodystrophy is a metabolic disease of the bone which accompanies chronic renal failure. It consists of osteitis fibrosa (hyperparathyroid bone disease), osteomalacia, osteosclerosis and osteoporosis. Osteomalacia comes as a result of loss of an enzyme; kidney 1-alpha hydroxylase, thus there is failure of conversion of vitamin D (cholecalciferal) to 1,25-dihydrocholecalciferol- its active metabolite. This consequently results in diminished absorption of calcium in the intestines. In turn, this results in hypocalcaemia and substantive reduction of the process of osteoid bone calcification (Agodoa 2017). According to Agodoa (2007), the low calcium in plasma stimulates parathyroid glands. These glands are also stimulated by elevated levels of plasma phosphate, concomitant upon reduced excretion of phosphate ions in the kidneys and very poor clearing of phosphate ions by haemodialysis. In the sheer absence of elevated levels of phosphate in plasma, secondary hyperparathyroidism results in osteitis fibrosa. In other patients, autonomous or tertiary hyperparathyroidism occurs, leading to hypercalcaemia.

The list of these complications is long. Other complications of chronic kidney disease include impairment of humoral and cellular immunity, usually evidenced by marked susceptibility to infection (Colledge et al. 2010). There is also increased tendency to bleed in CKD, manifested as mucosal bleeds and cutaneous ecchymosis. There is impairment of the platelet function and thus prolongation of the bleeding time (Colledge et al. 2010). Again, as Colledge et al. (2010) suggest, renal patients may suffer from generalised myopathy as a result of hyperparathyroidism, vitamin D deficiency, poor nutrition and electrolyte metabolism disorders (Kumar 2009). Muscle cramps are a common feature. At a later stage in the progression of CKD, neuropathy may appear but often resolves or improves with the establishment of dialysis (Drukker, Parsons & Maher 1979). Paraesthesia may be due to sensory neuropathy while motor neuropathy often manifests with foot drop (Colledge et al. 2010). According to Colledge et al. (2010), a number of hormonal abnormalities may be present including loss of libido in both sexes and even loss of sexual function, all which are associated with hyperprolactinaemia. There is also reduced appetite and significant insulin resistance (Colledge et al. 2010). At lower GFR, quite common are several gastrointestinal manifestations including nausea, vomiting, anorexia and peptic ulcer disease. Lastly, depression is also a common complication in the patients approaching or on renal replacement therapy (Colledge et al. 2010).

El Nahas and Levin (2010) posit that many patients with chronic renal failure, stages 1-3 never develop end stage kidney failure. To manage CKD, blood pressure control is fundamental, with 130/80 mmHg as the maximum target.  This in diabetes mellitus and among those with an elevated ACR or PCR is reduced to 125/75 mmHg (Colledge et al. 2010). The use of Angiotensin Receptor Blockers (ARBs) or ACE inhibitors in those patients with proteinuria is another added-on form of management. Lipid management and lifestyle advice regarding among other things smoking, weight, diet and exercise is part of the management process (El Nahas & Levin 2010). Another appropriate component of the management process is referral to a nephrologist. This is especially for the category patients with potentially underlying disease conditions or those who are likely to progress to end-stage renal disease including, young patients, patients with more severe kidney damage and those with deteriorating renal function (Colledge et al. 2010). If the disease progresses slowly or in stable disease state annual monitoring is recommended.  Severe proteinuria is proposed as the threshold for referral however, the interpretation of this should be with reference to comorbidity, age and other factors. Inflammatory nephritis is marked by haematuria (Colledge et al. 2010). Management of CKD is aimed at retarding its progression.

Fluid and Electrolyte Imbalance

Patient X goes to classes for diabetes mellitus to learn about self-management. These classes are conducted by a nurse who works hand in hand with a dietitian. Recalling her daily dieting, she demonstrates a high protein dietary intake. She also demonstrates difficulty complying with the necessary plan of low carbohydrates that aims to bring her levels of blood glucose under control. In a period, close to seven months, patient X lost and recovered back 12 pounds. Generally, she does not take breakfast but often has salads for lunch. Most days, it is typical for her to stop at a fast food restaurant. Due to worsening loss of energy and fatigue, she often orders delivery for dinner. She lives alone and she never enjoys cooking at all. She also lays claim that her sleeping pattern has significantly changed. Frequently, she wakes up most nights to eat. The management goals for her include among other things management of her glucose levels, blood pressure regulation, education on smoking cessation and lowering her intake of protein.

A plan on how she takes her meals is created for patient X which aims at weight loss. It is a composition of low carbohydrate and significantly low protein content to avoid any more damage of her kidneys. The planning of her meals is thoroughly simplified to incorporate quickly made homemade meals or low fat content recipes. She is given particular emphasis on the avoidance of foods that are high protein rich. She is also encouraged to take meals regularly, breakfast included.

Education on anaemia has already done. Further explanation which regards the need for further testing to find out if an agent which stimulates erythropoiesis is necessary or if iron supplementation is needed. In order to avert injury associated with cardiovascular disease, in conjunction with a diet rich in low fat content, she is prescribed for a statin to lower the lipid levels in her. In addition, due to the parathyroid hormone level elevation, vitamin D supplementation is given to her.

First and foremost, there is a greater need for a little physical activity. It is integral particularly for patient X as it would help her cut weight, management of hypertension and stress control. Patient X should be reassured to put on a measuring device and make an attempt to walk more than eight thousand steps every other day. She should be encouraged to begin slowly by slowly as she gradually increases her physical activity.

Cardiovascular Events and Dyslipidemia

Secondly, taking medicine faithfully is a vital part of the management plan of patient X.  For her other comorbidities including diabetes, cardiovascular disease, high blood pressure and anaemia, medications have been prescribed for her. For the medications to manage diabetes, instructions should include the explanation of the fundamental reasons for adequately keeping glucose levels under control. This is because patient X’s history vividly shows a total lack of control of the same. So, adherence to medication already prescribed is key. Patient X’s education includes among others instructions insulin therapy. The nurse must also discuss the mode of action of the drugs given, the dosage of each drug, the side effects and the need for any additional drug prescribed. The patient must also be apprised to properly observe her pressure while at home and asked to inform her personal primary care provider in case of an encounter with any highs or lows in the reading.

Lastly, patient X must be encouraged to conduct self-monitoring of the blood glucose levels and also to maintain regular check-ups with her personal primary care provider. She should follow up with her nephrologist, with the aim of further impeding the progression of renal disease.  Currently, patient X can maintain the functions of her kidneys. But, if she goes on with the present discourse, the progression of her current renal state into end-stage kidney disease is sadly likely to be inevitably.

Conclusions

The rate at which renal function becomes worse changes between patients even though the deterioration rate is fairly perpetual for a specific individual (Molzahn & Butera 2006). A GFR plot offers a prediction of when dialysis would be required. It also proffers a detection of any unexpected worsening of renal disease. According to Colledge et al. (2010), it is also used in monitoring success rates of novel interventions. Control of the patient’s blood pressure decelerates decline of kidney function in CKD independent of the used agent. The threshold to this effect has not been found yet and the punchline is that reduction of any level of blood pressure is quite beneficial. Achievement of various target blood pressure levels requires multiple drugs often limited by non-compliance or toxicity. As Thomas (2014) notes, the high incidence of heart failure, ventricular hypertrophy and occlusive vascular disease in patients with longstanding kidney disease also proffers a justification of vigorous efforts to lower blood pressure.

Kopple, Massry and Kalantar (2013) see a rather vivid relation between the rate at which kidney disease progresses and proteinuria thus, their view is that, cutting down proteinuria lowers renal risk. ARBs and ACE inhibitors are largely effective at reducing proteinuria thus lead to retardation of the progression of renal disease compared to other therapies that bring down blood pressure to a more or less the same degree, even though their effect on glomerular perfusion pressure usually causes an immediate reduction in GFR at the initiation of therapy. Cardiovascular events are also reduced by the ACE inhibitors and all result in mortality in patients with CKD. ACE inhibitors together with ARBs should be the best option for the patients with overt or incipient diabetic nephropathy, if well tolerated, independently of hypertension.

Renal Osteodystrophy

Lastly, lifestyle and dietary interventions ought to be implemented. Restriction of dietary protein can retard progression of renal disease even though diets that are rich in low protein diet are tough to adhere to and they carry along malnutrition risk (Kopple, Massry & Kalantar 2013). However controversial this may seem like, for a large number of patients who live in areas with access to renal replacement therapy, severely restricting protein intake is not at all recommended. Advice on dietary intake should be aimed at prevention of excessive protein consumption and, when approaching end stage renal disease, an adequate caloric intake should be the target for prevention of malnutrition ((Kopple, Massry & Kalantar 2013). Again, smoking cessation also slows the decline in renal function. Physical activity and weight loss retards the progression of renal disease by reducing proteinuria.

References

Agodoa, L. (2017). Chronic kidney disease in disadvantaged populations. Academic Press Inc.

Berbari, A. E., & Mancia, G. (2010). Cardiorenal syndrome: mechanisms, risk, and treatment. Milan, Springer.

Bomback, A. S., & Bakris, G. L. (2011). Chronic kidney disease (CKD) and hypertension essentials. Sudbury, Mass, Physicians’ Press/Jones & Bartlett Learning.

Colledge, N. R., Walker, B. R., Ralston, S., Britton, R., & Davidsons, S. (2010). Davidson’s principles and practice of medicine. Edinburgh, Churchill Livingstone Elsevier.

Cummings, N. B., & Klahr, S. (1985).  Chronic Renal Disease: Causes, Complication, and Treatment. Boston, MA, Springer US. [online]. ‘Available at’ https://public.eblib.comm/choice/publicfullrecord.aspx?p=3083581.

Drukker, W., Parsons, F. M., & Maher, J. F. (1979).  Replacement of Renal Function by Dialysis. Dordrecht, Springer Netherlands. [online]. ‘Available at’ https://public.eblib.com/choice/publicfullrecord.aspx?p=3108415.

El Nahas, A. M., & Levin, A. (2010). Chronic kidney disease: a practical guide to understanding and management. Oxford, Oxford University Press.

Field, M. J., Pollock, C. A., & Harris, D. C. (2010). The Renal System. Churchill Livingstone, Sydney.

Floege, J., Johnson, R. J., & Feehally, J. (2010). Comprehensive clinical nephrology. Philadelphia, PA, Saunders/ Elsevier. [online]. ‘Available at’ https://www.clinicalkey.com/dura/browse/bookChapter/3-s2.0-C20090465395.

Himmelfarb, J., & Sayegh, M. H. (2010). Chronic kidney Disease, Dialysis, and Transplantation E-Book: A Companion to Brenner and Rector’s The Kidney. [online]. ‘Available at’ https://nls.Idls.org.uk?welcome.html?ark:/81055/vdc_100052715655.ox000001.

Kimmel, P. L., & Rosenberg, M. E. (2015). Chronic renal disease. [online]. ‘Available at’ https://search.ebscohost.com/login.aspx?direc=true&scope=site&db=nlebk&db=nlabk&AN=565103.

Kopple, J. D., Massry, S. G., & Kalantar- Zadeh, K. (2013). Nutritional management of renal disease. London, Academic Press. [online]. ‘Available at’ https://www.sciencedirect.com/science/book/9780123919342.

Kumar, V., Abbas, A. K., Fausto, N., & Aster, J. C. (2009). Robbins & Contran Pathologic Basics of Disease E-Book. [online]. ‘Available at’ https://nls.IdlS.org.uk/welcome.html?ark:/81055/vdc_100052715614.0x000001.

Lewis, R. (2012). Understanding chronic kidney disease: a guide for the non-specialist. Keswick, M and K Update. [online]. ‘Available at’ https://site.ebrary.com/id/10608735.

Molzahn, A. E., & Butera, E. (2006). ANNA Contemporary Nephrology Nursing: Principles and Practice. Janetti Inc., New Jersey.

NATIONAL COLLABORATION CENTRE FOR CHRONIC CONDITIONS (GREAT BRITAIN). (2008). Chronic kidney disease national clinical guideline for early identification and management in adults in primary and secondary care. London, Royal College of Physicians. [online]. ‘Available at’ https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=nicecg73.

Nitta, K. (2015). Chronic kidney diseases: recent advances in clinical and basic research. [online]. ‘Available at’ https://search.ebscohost.com/login.aspx?direct=true&scope=site&db=nlebk&db=nlabk&AN=1002058.

Shaw, K. M., & Cummings, M. H. (2012). Diabetes Chronic Complications. Hoboken, Wiley.

Slaughter, M. S. (2007). Cardiac surgery in chronic renal failure. Malden, Mass, Blackwell Futura. [online]. ‘Available at’ https://site.elibrary.com/id/10240378.

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