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Abstract

Chronic Kidney Disease (CKD) is a progressive and irreversible disease whereby the kidneys' ability to function gradually diminishes until they no longer function at all, resulting in higher morbidity and lower quality of life (QOL). Diabetes Mellitus and Hypertension are the two main risk factors for CKD progression. In addition to this, the acceleration of renal deterioration and increased burden on renal disease can also result from delayed diagnosis, low patient awareness, and lack of effective monitoring of CKD.The goal of this study was to assess the clinical characteristics of CKD, risk factors for CKD prevalence and stage of CKD, and whether structured counseling for CKD patients has a positive effect on the quality of life for patients. Using a prospective observational research design, the CKD samples (N=196) in this study were recruited through questionnaires that provided information about demographic variables, BMI, primary insurance, risk factors for CKD, CKD stage, glomerular filtration rate (GFR), creatinine, diabetes, hypertension, and clinical presentations of CKD.CKD patients' quality of life was measured before and after the CKD patient received structured counseling. To determine the statistical significance of the results, descriptive statistics and chi-square goodness-of-fit tests were used. The results show that the majority of CKD patients in the study were male (60.20%) and presented the majority in the (43-52) year age range (31.12%), with the mean age for all the CKD patients being 51.84 ± 12.74. The patients in this study were primarily of normal BMI (60.71%) but were suffering from both diabetes and hypertension, which accounted for 75% of CKD cases reported in this study..

Keywords

Chronic Kidney Disease, Prevalence, Risk Factors, Hypertension, Diabetes Mellitus, Serum Creatinine, Glomerular Filtration Rate, Quality of Life

Introduction

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Kidney disease (CKD) is a chronic illness in which the kidneys can no longer filter the blood effectively due to kidney damage - either from pathology confirmed through imaging studies or renal biopsy, or from other types of abnormalities in urinary sediment, or from an increased albumin level in the urine unless the albumin level is lower than what would be considered "normal" (ACR). This condition will produce a progressive decline in kidney function, ultimately leading to the need for chronic renal replacement therapy (CRT) due to complete loss of kidney function.

The Kidney Disease Improving Global Outcomes (KDIGO) classification system for chronic kidney disease recommends indicating the specific cause for chronic kidney disease and classifying it into 6 stages based on the measured level of glomerular filtration rate (GFR); namely, stages G1 through G5 with stage G3 being further divided into G3a and G3b. In addition, using GFR as an indicator of chronic kidney disease, KDIGO recommends that 3 levels of albuminuria severity be incorporated into the classification for chronic kidney disease A1, A2, and A3 respectively. In staging chronic kidney disease, the clinician is required to measure the albumin-creatinine ratio (ACR mg/g or mg/mmol) in the morning "spot" urine sample for each stage.

The following provides an outline for each the 6 classifications of CKD; stages 1 through 5 (stages 3a and 3b are listed below):

•      G1: eGFR ≥ 90 mL/min/1.73m²* and evidence for CKD e.g. hematuria or proteinuria

•      G2: eGFR 60-89 mL/min/1.73m²*

•      G3a: eGFR 45-59 mL/min/1.73m²

Epidemiology

According to the US CDC / Million Americans Living with Chronic Kidney Disease at an estimate of ~15% of adults on average over the course of time. It's also worth noting approximately 90% of adults do not even know that they have CKD; additionally, 1 out of every 2 individuals whom are not utilizing dialysis and have a very low functioning renal system do not realize that they are afflicted with CKD [NCVI, 2013]. Furthermore, the principal causes for development of CKD amongst adults include diabetic and hypertensive related disorders; furthermore the CDC states that approximately one-third of adults that are diabetic will develop CKD while one-fifth of those whom are hypertensive will develop CKD. In accordance with current CDC statistics, CKD appears to be significantly more prevalent in the greater than or equal to 65 age category (38%) than in the 45 to 64 (13%) or in the 18-44 (7%). Furthermore, CKD occurs slightly more commonly in women (15%) than in their male counterparts (12%); additionally, African American individuals are 3x more likely to develop End Stage Renal Disease (ESRD) when compared to their Caucasian counterparts [NCVI, 2013].

Etiology

Although causes for CKD differ around the world, the most frequently reported primary diseases leading to CKD and eventually to ESRD are: [StatPearls, 2016]

•      Diabetes Mellitus Type 2 (30%-50%)

•      Diabetes Mellitus Type 1 (3.9%)

•      Hypertension (27.2%)

•      Primary Glomerulonephritis (8.2%)

•      Chronic Tubulointerstitial Nephritis (3.6%)

•      Inherited/Cystic Disorders (3.1%)

•      Secondary Glomerulonephritis/Vasculitis (2.1%)

•      Plasma Cell Dyscrasias/Neoplasms (2.1%)

•      Sickle Cell Nephropathy which accounts for less than 1% among ESRD patients in America. For additional information and associated publications, please refer to StatPearls’ associated publication titled “Sickle Cell Disease and its Impact on ESRD”.

Pathophysiology:

 

 

 

 

Clinical Manifestations:

Individuals may not experience signs or symptoms until the later stages of CKD (stages 4 and 5). The following are frequently cited signs and symptoms at this phase of CKD:

- Nausea

- Vomiting

- Loss of appetite (anorexia)

- Fatigue/weakness

- Difficulty sleeping (insomnia)

- Oliguria

- Decreased mental sharpness (cognitive impairment)

- Muscle spasms/cramps

- Swelling of feet and ankles (peripheral edema)

- Itching/itchy skin (pruritus)

- Chest pain from uremic pericarditis (inflammation of the lining around the heart)

- Shortness of breath from fluid accumulation in the lungs (pulmonary edema)

- High blood pressure ( hypertension)

In terms of examining the body for the patient’s clinical signs, the physical examination may not add valuable information; however, some examples of the physical signs the health-care provider may observe during examination include:

- Colour changes in skin (skin pigmentation changes)

- Scratch marks ( abrasions) from pruritus ( itching)

- Presence of a pericardial friction rub (means there is rubbing/ irritation on the lining surrounding the heart) from uremic pericarditis.

- Uremic frost where high blood urea nitrogen ( BUN) levels cause the urea in sweat to crystallize into fine, white powder form on the skin.

- Hyperreflexia (increased reflexes) and/or tremors ( muscle twitching)

- Hypertensive fundal changes, indicating a chronic process.

Factor's risk that lead to chronic kidney disease progression

The CKD non-modifiable risk factors include being older, male, and belonging to a non-white ethnic group, including black American, Afro-Caribbean, Hispanic, and Asian (South Asians and Pacific Asian).

Poor genetic determinants for renal disease progression have also been identified in people with renal diseases. A population-based cohort study found that single nucleotide polymorphisms in the TCF7L2 and MTHFS genes are associated with diabetic nephropathy and CKD progression. This same study provided evidence for the existence of polymorphisms in the genes responsible for renal scarring as well as for the RAAS, and the influence of these polymorphisms on CKD progression.

The CKD modifiable risk factors consist of hypertension, proteinuria, and metabolic conditions. Systemic hypertension represents a major cause of ESRD worldwide and is the second most common cause in the United States after diabetes. The transmission of systemic hypertension to the glomerular capillaries is thought to contribute to the glomerular hypertension that leads to the progressive development of glomerulosclerosis. Nighttime and 24-hour BP measurements (e.g., ABPM) correlate more closely with CKD progression than do standard BP measurements. In particular, systolic BP has been shown to be the main predictor of CKD progression and is associated with the complications of CKD.

Diagnosis

Current theoretical diagnostic indicators by which to assess CKD from a clinical perspective include; serum creatinine, glomerular filtration rate, and proteinuria. The serum creatinine infers change from the volume of creatine (by product of muscle metabolism), through its relationship to how much is excreted from our body, therefore make it a primary parameter for diagnosing CKD. However, creatinine has an overwhelming number of measurement errors associated with it, (due to interference from numerous physical and biochemical factors, poor specificity and wide variation). Also, creatinine is not a disease specific marker of CKD and is impacted by such markers as muscle mass, muscle composition, protein intake in one's diet, medication taken in diet, etc., therefore also causing imprecision in determining one's GFR. In addition, creatinine does not correlate with the presence of co-morbidities [46]. Furthermore, the association of muscle mass to creatinine can lead to the same creatinine values for patients with different GFRs and results in CKD diagnosis being falsely positive. Also, about half of GFR must be lost before creatinine level from a lab test is abnormal and; this is when 3rd stage of CKD is diagnosed. Due to the inverse relation of GFR to creatinine, any large reduction in a person's GFR will only lead to small increases in the level of serum from the laboratory (due to creatinine); therefore, because the amount of time between CKD diagnosis and creatinine test and the treatment of CKD will be substantial, if a person has only renal function loss but has no effect yet on creatinine they may be considered to have a normal creatinine level, despite the continued sodal incidence of deterioration of the kidney's ability to function.

Management of cardiovascular disease risk

The incidence and prevalence of cardiovascular disease (CVD) are greater in patients with chronic kidney disease (CKD) than in patients without CKD. In a Medicare 5% sample of 175,840 adults aged 66 years and over with CKD, the percentage with CVD was significantly higher than for those without CKD; for example, 65% of patients with CKD versus 32% of patients without CKD had at least one type of CVD [63]. In addition, having a diagnosis of CKD is associated with lower cardiovascular outcomes. In the same study, for people with CKD and coronary artery disease, the survival rate at 2 years was lower (77% vs. 87%) than for people without CKD; the same is true for those with acute myocardial infarction (69% vs. 82%), heart failure (65% vs. 76%), atrial fibrillation (70% vs. 83%), and cerebrovascular accident/transient ischemic attack (73% vs. 83%) [63], all of which demonstrate the increased CVD risk in individuals with CKD.

Thus, a key component of managing CKD is decreasing cardiovascular risk. For patients aged 50 years or older with CKD, it has been recommended that they be treated with low-to-moderate-dose statins regardless of low-density lipoprotein (LDL) cholesterol level [64][65][66]. Smoking cessation is also an important consideration [67][68]. Both the Eighth Joint National Committee (JNC 8) and Kidney Disease: Improving Global Outcomes (KDIGO) recommend that the systolic and diastolic blood pressure of adults with CKD be <140 mmHg and <90 mmHg, respectively, based on expert opinion [67][69]. The KDIGO guideline also recommends that patients.

Dietary Management:

The idea of using dietary management to stop CKD from becoming worse is highly debated due to the vast number of trials that do not have clear and conclusive results regarding this approach [102-104]. The MDRD study showed insignificant or conflicting results when comparing the two different levels of protein restriction (2 types of low-protein diet) for 840 patients enrolled in this study. While there was an indication of a low-protein diet leading to a slower decline in GFR after the first 4 months of beginning the low-protein diet compared to the regular-protein intake diet (used in the study), there was no evidence of a very low-protein diet leading to a slower decline in GFR compared to a low-protein diet. Patients who developed proteinuria (>3 gm urine protein/day) did show some benefit by being on a low-protein diet (but this group of patients was not large enough to provide a conclusion) [102]. Some smaller trials do suggest that there may be some benefit from protein restriction in preventing CKD progression/ESKD [105-107]. The KDIGO Guidelines recommend that patients with CKD Stage G4-G5 reduce their protein intake to less than 0.8 gm/kg of body weight/day (after adequate nutrition education) and that other adult patients with CKD who are at risk for CKD progression reduce their protein intake to less than 1.3 gm/kg of body weight/day [67]. The potential benefits associated with dietary protein restriction are often weighed against the potential side effects associated with malnutrition and/or protein-wasting syndrome seen as a result of implementing a protein-restricted diet [67][102][103][108]. Decreasing dietary acid load (ie, increasing intake of fruits and vegetables and decreasing intake of animal-based foods such as meat, eggs, and cheese) may also reduce the risk of kidney injury.

Study site:

Kosuru Kidney and Skin hospital at Narasaraopet.

Study design:

A hospital-based prospective Observational study.

Study period:

The study was conducted for a period of 6 months.

Sample size:

Based on N- Masters formula considering a 95% confidence level, 5% margin of error and the minimum required sample size for our study is 196.

Materials:

      • Informed consent form
      • Data collection form
      • Questionnaire form
      • Counselling aids- Patient information leaflet

Study criteria:

The study will be carried out by considering the following criteria:

Inclusion criteria:

  1. Male and female patients above 18 years to 85 years age.
  2. CKD patients.
  3. Cooperative patient.

Exclusion criteria:

  1. Patients who are less than 18 years and greater than 85 years of age.
  2. Pregnant women.
  3. Lactating women.
  4. Non-cooperative patient.

Ethical approval:

This study was approved by the Institutional Ethics Committee of Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopeta.

IEC-NIPS/PPP/2025-26/006

 Study procedure:

The purpose of this study was to determine the number of individuals diagnosed with chronic kidney disease who come to the nephrology department. To determine this, all patients with CKD were assessed for their prevalence, risk factors, and how long they have had CKD by looking at their creatinine levels and glomerular filtration rates. To be eligible for inclusion in the study, patients had to meet all study inclusion criteria. To collect information on the participants, a specific data collection sheet will be created.

Demographic information includes name, age, sex, height, weight, and clinical data will include chief complaint(s), date of symptom onset, previous medical history, medications taken, laboratory investigations performed, diagnosis(es) made, and overall status of the subject. Clinical data will be obtained from medical record review and/or by interviewing the participant.

RESULTS

1.Distribution based on age:

 

AGE (Years)

NO.OF PATIENTS

PERCENTAGE (%)

23-32

14

7.14

33-42

30

15.31

43-52

61

31.12

53-62

49

25.00

63-72

33

16.84

73-82

8

4.08

83-92

1

0.51

Grand Total

196

100.00

 

2.Distribution based on gender:

 

GENDER

NO.OF PATIENTS

PERCENTAGE %

FEMALE

78

39.80

MALE

118

60.20

Grand Total

196

100.00

 

3.Distribution based on BMI:

 

BMI

NO.OF PATIENTS

PERCENTAGE %

NORMAL

119

60.71

OBESE

4

2.04

OBESE CLASS I

7

3.57

OBESE CLASS III

3

1.53

OVER WEIGHT

50

25.51

UNDER WEIGHT

13

6.63

Grand Total

196

100.00

 

4.Distribution based on risk factors:

 

 

 

RISK FACTORS

NO OF PATIENTS

PERCENTAGE %

CELLULITIS

2

1.02

DM

46

23.47

DM,ALD

1

0.51

DM,ASTHMA

2

1.02

DM,CELLULITIS

1

0.51

DM,COPD

1

0.51

DM,RENAL CALCULI

3

1.53

DM,SMOKING

2

1.02

DM,UTI

12

6.12

HTN

30

15.31

HTN,ALCOHOLIC

4

2.04

HTN,CELLULITIS

2

1.02

HTN,DM

58

29.59

HTN,DM,COPD

1

0.51

HTN,DM,RENAL CALCULI

2

1.02

HTN,DM,SMOKING,ALCOHOLIC

7

3.57

HTN,DM,UTI

2

1.02

HTN,POISONING

1

0.51

HTN,RENAL CALCULI

1

0.51

HTN,UTI

5

2.55

NIL

1

0.51

SEIZURES

1

0.51

SMOKING

2

1.02

SMOKING,ALCOHOLIC

9

4.59

Grand Total

196

100.00

 

5. Distribution based on CKD stages:

 

STAGES

NO OF PATIENTS

PERCENTAGE %

1

13

6.63

2

23

11.73

4

53

27.04

5

62

31.63

3A

17

8.67

3B

28

14.29

Grand Total

196

100.00

 

6. Distribution of diabetes among CKD patients:

 

DIABETES

NO OF PATIENTS

PERCENTAGE %

CONTROLLED

20

10.20

NIL

57

29.08

UNCONTROLLED

119

60.71

Grand Total

196

100.00

 

7. Distribution of hypertension among CKD patients:

 

HYPERTENSION

NO OF PATIENTS

PERCENTAGE %

CONTROLLED

25

12.76

NIL

83

42.35

UNCONTROLLED

88

44.90

Grand Total

196

100.00

 

8. Distribution based on GFR:

 

GFR

NO OF PATIENTS

PERCENTAGE %

3-13

47

23.98

13-23

35

17.86

23-33

38

19.39

33-43

17

8.67

43-53

21

10.71

53-63

3

1.53

63-73

6

3.06

73-83

16

8.16

83-93

13

6.63

Grand Total

196

100.00

 

9. Distribution based on serum creatinine:

 

Sr. CREATININE (mg/dl)

NO.OF PATIENTS

PERCENTAGE (%)

0.5-5.5

154

78.57

5.5-10.5

36

18.37

10.5-15.5

6

3.06

Grand Total

196

100.00

 

10. Distribution based on signs and symptoms:

 

SIGNS AND SYMPTOMS

NO.OF PATIENTS

PERCENTAGE (%)

ANURIA

1

0.51

GLYCOSURIA

9

4.59

HEMATURIA

13

6.63

HEMATURIA,ALBUMINURIA

2

1.02

HEMATURIA,ANURIA

2

1.02

HEMATURIA,GLYCOSURIA

6

3.06

HEMATURIA,OLIGURIA

18

9.18

HEMATURIA,PYURIA

2

1.02

NAUSEA,EDEMA

7

3.57

NAUSEA,FATIGUE,FEVER

34

17.35

OLIGURIA

32

16.3

OLIGURIA,ANURIA

1

0.51

OLIGURIA,EDEMA

24

12.24

OLIGURIA,FACIAL PUFFINESS

1

0.51

OLIGURIA,GLYCOSURIA

1

0.51

OLIGURIA,NAUSEA

7

3.57

OLIGURIA,NAUSEA,FEVER

2

1.02

OLIGURIA,PYURIA

9

4.59

PEDAL EDEMA

2

1.02

PROTEINURIA,ALBUMINURIA

13

6.63

PYURIA

10

5.10

Grand Total

196

100.00

 

11. QOL scale before counselling:

 

SCORE

NO OF PATIENTS

PERCENTAGE %

FAIR

50

25.51

GOOD

18

9.18

POOR

85

43.37

VERY POOR

43

21.94

Grand Total

196

100.00

 

12. QOL scale after counselling:

 

SCORE

NO OF PATIENTS

PERCENTAGE %

EXCELLENT

22

11.22

FAIR

75

38.27

GOOD

70

35.71

POOR

27

13.78

VERY POOR

2

1.02

Grand Total

196

100.00

 

DISCUSSION

In this study, we evaluated 196 patients with a diagnosis of chronic kidney disease (CKD) to evaluate the demographic characteristics of the patients, identify symptoms and patterns of CKD, provide information on risk factors associated with CKD, evaluate the effect of counselling on patients' quality of life (QOL) and describe how CKD is distributed geographically, progresses and is treated. The results of this study provide valuable information on how CKD is distributed, its clinical profile, progression and management outcomes.

The distribution of patients by age was as follows; 31.12% of patients belonged to the age group of 43-52 years, and 25.00% to the age group of 53-62 years. The mean age of patients was 51.84 ± 12.74 years. The majority of CKD patients are in the middle age range, presumably due to the impact of risk factors, such as diabetes and hypertension, lifestyle issues (e.g., lack of exercise), occupational stress, and delay in diagnosis. CKD generally follows a progressive course, and therefore, metabolic abnormalities that begin in childhood or early adulthood may be evidenced by changes in kidney function in middle-aged adults. With an overall statistically-significant difference (p < 0.001), the prevalence rate of CKD increases as age increases and is not evenly distributed by age.

On average, there were more males (60.20%) than females (39.80%) with a diagnosis of CKD. A number of reasons have been postulated for this difference in the male-female CKD ratio. For example, the rate of smoking, alcohol consumption, occupational stress and inadequate health seeking behaviour is significantly higher among males than among females. The presence of oestrogen in women's bodies until the time of menopause may also protect the kidneys of females from early damage and/or enhance their ability to obtain medical attention. In many societies, male and female gender roles will influence the pattern of hospital attendance.

CONCLUSION

The current research indicates that chronic kidney disease (CKD) primarily affects individuals in their middle years of life and occurs more often among men than women. In this study, it is obvious that diabetes mellitus and hypertension—alone or in combination—are the main contributing risk factors for the onset and worsening of CKD. Many patients in this study were diagnosed with advanced-stage CKD (stages 4 and/or 5), which means that CKD was not diagnosed in a timely manner; many patients had their CKD diagnosed late due to inadequate monitoring of their progression and/or lack of control over their other medical conditions.

In addition, this study showed that most of the patients who were studied had a low level of glomerular filtration rate (GFR), including a range of serum creatinine levels that indicated significant kidney damage at the time of diagnosis and treatment. Clinical findings such as oliguria, nausea, tiredness, and swelling from edema were common among the study participants and demonstrated that advanced kidneys affect all body systems.

Finally, the research revealed that most study subjects had a low initial quality of life (QOL) as a result of their CKD diagnosis and treatment. However, following counselling by their clinical pharmacist, there was considerable improvement in the patients’ quality of life (with a significant number of patients moving into fair and good quality of life categories). This illustrates the important role that clinical pharmacists play in patient counselling to help improve patient education, encourage patients to take and continue to take their medications, make patients aware of the potential effect of lifestyle choices on their health, and improve a patient’s overall quality of life.

In conclusion, patients at increased risk for developing CKD should be screened for CKD early, have their diabetes and blood pressure tightly controlled, and have their CKD regularly monitored.

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  5. Vidt DG. Telmisartan, ramipril, or both in patients at high risk for vascular events.

Curr Hypertens Rep. 2008;10(5):343–4.

  1. Moorhead JF, Chan MK, El-Nahas M, Varghese Z. Lipid nephrotoxicity in chronic progressive glomerular and tubulo-interstitial disease. Lancet. 1982;2(8311):1309–11.
  2. Johnson RJ, Nakagawa T, Jalal D, Sánchez-Lozada LG, Kang DH, Ritz E. Uric acid and chronic kidney disease: which is chasing which? Nephrol Dial Transplant. 2013;28(9):2221–8.
  3. Cheung AK, Chang TI, Cushman WC, Furth SL, Hou FF, Ix JH, et al. Executive summary of the KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int. 2021;99(3):559–69.
  4. Bundy JD, Chen J, Yang W, Budoff M, Go AS, Grunwald JE, et al.; CRIC Study Investigators. Risk factors for progression of coronary artery calcification in patients with chronic kidney disease: the CRIC study. Atherosclerosis. 2018;271:53–60.
  5. Aeddula NR, Cheungpasitporn W, Thongprayoon C, Pathireddy S. Epicardial adipose tissue and renal disease. J Clin Med. 2019;8(3):302.
  6. Schrauben SJ, Jepson C, Hsu JY, Wilson FP, Zhang X, Lash JP, et al. Insulin resistance and chronic kidney disease progression, cardiovascular events, and death: findings from the Chronic Renal Insufficiency Cohort study. BMC Nephrol. 2019;20(1):60.
  7. Davies R. The metabolomic quest for a biomarker in chronic kidney disease. Clin Kidney J. 2018;11(3):297–9.
  8. Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G. Clinical practice guidelines for chronic kidney disease in adults: part II. Glomerular filtration rate, proteinuria, and other markers.
  9. Delanaye P, Cavalier E, Pottel H. Serum creatinine: not so simple! Nephron.

2017;136(4):302–8.

  1. Waikar SS, Bonventre JV. Creatinine kinetics and the definition of acute kidney injury. J Am Soc Nephrol. 2009;20(3):672–9.
  2. Lopez-Giacoman S, Madero M. Biomarkers in chronic kidney disease, from kidney function to kidney damage. World J Nephrol. 2015;4(1):57–73.
  3. Nordin F, Shaharir SS, Abdul Wahab A, Mustafar R, Abdul Gafor AH, Mohamed Said MS, et al. Serum and urine interleukin-17A levels as biomarkers of disease activity in systemic lupus erythematosus. Int J Rheum Dis. 2019.
  4. Curhan GC. Cystatin C: a marker of renal function or something more? Clin Chem. 2005.
  5. Benoit SW, Ciccia EA, Devarajan P. Cystatin C as a biomarker of chronic kidney disease: latest developments. Expert Rev Mol Diagn. 2020.
  6. Tonelli M, Dickinson JA. Early detection of CKD: implications for low-income, middle-income, and high-income countries. J Am Soc Nephrol. 2020.
  7. Liu KZ, Tian G, Ko ACT, Geissler M, Brassard D, Veres T. Detection of renal biomarkers in chronic kidney disease using microfluidics: progress, challenges and opportunities. Biomed Microdevices. 2020.
  8. Bello AK, Nwankwo E, El Nahas AM. Prevention of chronic kidney disease: a global challenge. Kidney Int Suppl. 2005.
  9. Delanaye P, Rule AD. Assessing kidney function. In: Chronic renal disease. 2015.
  10. Lai S, Mazzaferro S, Muscaritoli M, Mastroluca D, Testorio M, Perrotta A, et al. Prebiotic therapy with inulin associated with low protein diet in chronic kidney disease patients: evaluation of nutritional, cardiovascular and psychocognitive parameters. Toxins (Basel). 2020.
  11. Lopez-Giacoman S. Biomarkers in chronic kidney disease, from kidney function to kidney damage. World J Nephrol. 2015.
  12. Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G. Clinical practice guidelines for chronic kidney disease in adults: part II. Glomerular filtration rate, proteinuria, and other markers. Am Fam Physician. 2004.
  13. Shah BV, Patel ZM. Role of low protein diet in management of different stages of chronic kidney disease: practical aspects. BMC Nephrol. 2016.
  14. Wang M, Chou J, Chang Y, Lau WL, Reddy U, Rhee CM, et al. The role of low protein diet in ameliorating proteinuria and deferring dialysis initiation: what is old and what is new. Panminerva Med. 2017.
  15. US Renal Data System. 2018 USRDS annual data report: epidemiology of kidney disease in the United States. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2018.
  16. Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. KDIGO clinical practice guideline for lipid management in chronic kidney disease. Kidney Int Suppl. 2013;3(3):259–305.
  17. Tonelli M, Wanner C; Kidney Disease: Improving Global Outcomes Lipid Guideline Development Work Group Members. Lipid management in chronic kidney disease: synopsis of the KDIGO 2013 clinical practice guideline. Ann Intern Med. 2014;160(3):182.
  18. Anderson TJ, Grégoire J, Pearson GJ, et al. 2016 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in the adult. Can J Cardiol. 2016;32(11):1263–1282.
  19. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1–150.
  20. Ricardo AC, Anderson CA, Yang W, et al.; CRIC Study Investigators. Healthy lifestyle and risk of kidney disease progression, atherosclerotic events, and death in CKD: findings from the CRIC study. Am J Kidney Dis. 2015;65(3):412–424.
  21. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507–520
  22. Wright JT Jr, Williamson JD, Whelton PK, et al.; SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103–2116.
  23. Zhang WR, Craven TE, Malhotra R, et al.; SPRINT Research Group. Kidney damage biomarkers and incident chronic kidney disease during blood pressure reduction: a case-control study. Ann Intern Med. 2018;169(9):610–618.

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  14. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604–12. Erratum in: Ann Intern Med. 2011;155(6):408.
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  16. Inker LA, Schmid CH, Tighiouart H, Eckfeldt JH, Feldman HI, Greene T, et al. Estimating glomerular filtration rate from serum creatinine and cystatin C. N Engl J Med. 2012;367(1):20–9. Erratum in: N Engl J Med. 2012;367(7):681; 2012;367(20):2060.
  17. Braveman P, Parker Dominguez T. Abandon “race.” Focus on racism. Front Public Health. 2021;9:689462.
  18. Inker LA, Tighiouart H, Adingwupu OM, Shlipak MG, Doria A, Estrella MM, et al. CKD-EPI and EKFC GFR estimating equations: performance and other considerations for selecting equations for implementation in adults. J Am Soc Nephrol. 2023;34(12):1953–64.
  19. Iseki K, Ikemiya Y, Iseki C, Takishita S. Proteinuria and the risk of developing end-stage renal disease. Kidney Int. 2003;63(4):1468–74.
  20. Remuzzi G, Bertani T. Pathophysiology of progressive nephropathies. N Engl J Med. 1998;339(20):1448–56.
  21. Freedman BI, Limou S, Ma L, Kopp JB. APOL1-associated nephropathy: a key contributor to racial disparities in CKD. Am J Kidney Dis. 2018;72(5 Suppl 1):S8– 16.
  22. Palsson R, Waikar SS. Renal functional reserve revisited. Adv Chronic Kidney Dis. 2018;25(3):e1–8.
  23. Johnson RJ, Wesseling C, Newman LS. Chronic kidney disease of unknown cause in agricultural communities. N Engl J Med. 2019;380(19):1843–52.
  24. Jha V, Garcia-Garcia G, Iseki K, Li Z, Naicker S, Plattner B, et al. Chronic kidney disease: global dimension and perspectives. Lancet. 2013;382(9888):260–72. Erratum in: Lancet. 2013;382(9901):208.
  25. Hannan M, Ansari S, Meza N, Anderson AH, Srivastava A, Waikar S, et al. Risk factors for CKD progression: overview of findings from the CRIC study. Clin J Am Soc Nephrol. 2021;16(4):648–59.
  26. Levey AS, Eckardt KU, Dorman NM, et al. Nomenclature for kidney function and disease: report of a Kidney Disease: Improving Global Outcomes (KDIGO) Consensus Conference. Kidney Int. 2020;97(6):1117–29.
  27. Navaneethan SD, Zoungas S, Caramori ML, et al. Diabetes management in chronic kidney disease: synopsis of the 2020 KDIGO clinical practice guideline. Ann Intern Med. 2020;173(9):W27–8.
  28. Schrauben SJ, Chen HY, Lin E, et al. Hospitalizations among adults with chronic kidney disease in the United States: a cohort study. PLoS Med. 2020;17(12):e1003470.
  29. Vart P, Powe NR, McCulloch CE, et al. National trends in the prevalence of chronic kidney disease among racial/ethnic and socioeconomic status groups, 1988–2016. JAMA Netw Open. 2020;3(7):e207932.
  30. Webster AC, Nagler EV, Morton RL, Masson P. Chronic kidney disease. Lancet.

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  1. Luttropp K, Lindholm B, Carrero JJ, Glorieux G, Schepers E, Vanholder R, et al. Genetics/genomics in chronic kidney disease—towards personalized medicine? Semin Dial. 2009;22(4):417–22.
  2. Levey AS, Coresh J. Chronic kidney disease. Lancet. 2012;379(9811):165–80.
  3. Hostetter TH. Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation. J Am Soc Nephrol. 2001;12(6):1315–25.
  4. Jamerson K, Weber MA, Bakris GL, Dahlöf B, Pitt B, Shi V, et al.; ACCOMPLISH Trial Investigators. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med. 2008;359(23):2417–28.
  5. Vidt DG. Telmisartan, ramipril, or both in patients at high risk for vascular events.

Curr Hypertens Rep. 2008;10(5):343–4.

  1. Moorhead JF, Chan MK, El-Nahas M, Varghese Z. Lipid nephrotoxicity in chronic progressive glomerular and tubulo-interstitial disease. Lancet. 1982;2(8311):1309–11.
  2. Johnson RJ, Nakagawa T, Jalal D, Sánchez-Lozada LG, Kang DH, Ritz E. Uric acid and chronic kidney disease: which is chasing which? Nephrol Dial Transplant. 2013;28(9):2221–8.
  3. Cheung AK, Chang TI, Cushman WC, Furth SL, Hou FF, Ix JH, et al. Executive summary of the KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int. 2021;99(3):559–69.
  4. Bundy JD, Chen J, Yang W, Budoff M, Go AS, Grunwald JE, et al.; CRIC Study Investigators. Risk factors for progression of coronary artery calcification in patients with chronic kidney disease: the CRIC study. Atherosclerosis. 2018;271:53–60.
  5. Aeddula NR, Cheungpasitporn W, Thongprayoon C, Pathireddy S. Epicardial adipose tissue and renal disease. J Clin Med. 2019;8(3):302.
  6. Schrauben SJ, Jepson C, Hsu JY, Wilson FP, Zhang X, Lash JP, et al. Insulin resistance and chronic kidney disease progression, cardiovascular events, and death: findings from the Chronic Renal Insufficiency Cohort study. BMC Nephrol. 2019;20(1):60.
  7. Davies R. The metabolomic quest for a biomarker in chronic kidney disease. Clin Kidney J. 2018;11(3):297–9.
  8. Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G. Clinical practice guidelines for chronic kidney disease in adults: part II. Glomerular filtration rate, proteinuria, and other markers.
  9. Delanaye P, Cavalier E, Pottel H. Serum creatinine: not so simple! Nephron.

2017;136(4):302–8.

  1. Waikar SS, Bonventre JV. Creatinine kinetics and the definition of acute kidney injury. J Am Soc Nephrol. 2009;20(3):672–9.
  2. Lopez-Giacoman S, Madero M. Biomarkers in chronic kidney disease, from kidney function to kidney damage. World J Nephrol. 2015;4(1):57–73.
  3. Nordin F, Shaharir SS, Abdul Wahab A, Mustafar R, Abdul Gafor AH, Mohamed Said MS, et al. Serum and urine interleukin-17A levels as biomarkers of disease activity in systemic lupus erythematosus. Int J Rheum Dis. 2019.
  4. Curhan GC. Cystatin C: a marker of renal function or something more? Clin Chem. 2005.
  5. Benoit SW, Ciccia EA, Devarajan P. Cystatin C as a biomarker of chronic kidney disease: latest developments. Expert Rev Mol Diagn. 2020.
  6. Tonelli M, Dickinson JA. Early detection of CKD: implications for low-income, middle-income, and high-income countries. J Am Soc Nephrol. 2020.
  7. Liu KZ, Tian G, Ko ACT, Geissler M, Brassard D, Veres T. Detection of renal biomarkers in chronic kidney disease using microfluidics: progress, challenges and opportunities. Biomed Microdevices. 2020.
  8. Bello AK, Nwankwo E, El Nahas AM. Prevention of chronic kidney disease: a global challenge. Kidney Int Suppl. 2005.
  9. Delanaye P, Rule AD. Assessing kidney function. In: Chronic renal disease. 2015.
  10. Lai S, Mazzaferro S, Muscaritoli M, Mastroluca D, Testorio M, Perrotta A, et al. Prebiotic therapy with inulin associated with low protein diet in chronic kidney disease patients: evaluation of nutritional, cardiovascular and psychocognitive parameters. Toxins (Basel). 2020.
  11. Lopez-Giacoman S. Biomarkers in chronic kidney disease, from kidney function to kidney damage. World J Nephrol. 2015.
  12. Johnson CA, Levey AS, Coresh J, Levin A, Lau J, Eknoyan G. Clinical practice guidelines for chronic kidney disease in adults: part II. Glomerular filtration rate, proteinuria, and other markers. Am Fam Physician. 2004.
  13. Shah BV, Patel ZM. Role of low protein diet in management of different stages of chronic kidney disease: practical aspects. BMC Nephrol. 2016.
  14. Wang M, Chou J, Chang Y, Lau WL, Reddy U, Rhee CM, et al. The role of low protein diet in ameliorating proteinuria and deferring dialysis initiation: what is old and what is new. Panminerva Med. 2017.
  15. US Renal Data System. 2018 USRDS annual data report: epidemiology of kidney disease in the United States. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2018.
  16. Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. KDIGO clinical practice guideline for lipid management in chronic kidney disease. Kidney Int Suppl. 2013;3(3):259–305.
  17. Tonelli M, Wanner C; Kidney Disease: Improving Global Outcomes Lipid Guideline Development Work Group Members. Lipid management in chronic kidney disease: synopsis of the KDIGO 2013 clinical practice guideline. Ann Intern Med. 2014;160(3):182.
  18. Anderson TJ, Grégoire J, Pearson GJ, et al. 2016 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in the adult. Can J Cardiol. 2016;32(11):1263–1282.
  19. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1–150.
  20. Ricardo AC, Anderson CA, Yang W, et al.; CRIC Study Investigators. Healthy lifestyle and risk of kidney disease progression, atherosclerotic events, and death in CKD: findings from the CRIC study. Am J Kidney Dis. 2015;65(3):412–424.
  21. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507–520
  22. Wright JT Jr, Williamson JD, Whelton PK, et al.; SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103–2116.
  23. Zhang WR, Craven TE, Malhotra R, et al.; SPRINT Research Group. Kidney damage biomarkers and incident chronic kidney disease during blood pressure reduction: a case-control study. Ann Intern Med. 2018;169(9):610–618.

Photo
Sonti Ashok
Corresponding author

Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Dr. G. Tejaswini
Co-author

Associate Professor, , Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Dr. J. N. Suresh kumar
Co-author

Principal, Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Manda Yesoda
Co-author

Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Puvvula Divya kaveri
Co-author

Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Mohammed Bibi Ameena
Co-author

Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Photo
Shaik Usama
Co-author

Narasaraopeta Institute of Pharmaceutical Sciences, Narasaraopet, Palnadu, Andhra Pradesh, India. 522601.

Dr. G. Tejaswini, Dr. J. N. Suresh kumar, Sonti Ashok, Manda Yesoda, Mohammed Bibi Ameena, Puvvula Divya kaveri, Shaik Usama, A Prospective Observational Study on Prevalence, Major Risk Factors and Patient Counselling for Chronic Kidney Disease, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 4, 4685-4698, https://doi.org/10.5281/zenodo.19871905

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