ABSTRACT: Obesity and other renal disorders like high cholesterol

ABSTRACT: Chronic kidney disease(CKD) is one of the major life threatening condition characterized byprogressive and irreversible loss of renal function. Chronic kidney disease (CKD) is a precursor to end-stage renal disease (ESRD), which is associated with increased risk of morbidity and mortality. Over 10% of Indian population aresuffering with CKD. Risk factors of Chronic kidney disease (CKD) includes Age,Diabetes, Hypertension, Smoking, Alcohol, Obesity. There is a chance to stopthe progress of the disease by proper choice of Reno protective combinationsand should make patient to adhere to the medication for better outcomes.

 Key words: Chronic kidney disease, Riskfactors, ACE Inhibitors, ARB`s, Disease progression.  Introduction:-Thekidneys are bean-shaped paired organs and also it is like filtering sponge, themajor function of the kidney is complex filtration from capillaries to urinaryspaces. Normally, glomerular filtration rate (GFR) is about 125ml/minute. Itfilters for about 113 to 114 litres of blood to set 0.94 to 1.8 litres of urineper day 1.

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Kidney just acts as filters of the blood, it retainsthe useful components like proteins and drains the waste material from theblood. If kidneys get damaged then the proteins get leaked into urine, in laterstages kidney loses its ability to filter which is a slow process, if thiscondition exists for more than 3months then it is called as Chronic kidneydisease (CKD) 1.1.Chronickidney Disease (CKD) is the worldwide health problem, and is more prevalent inelderly population of Age above 60 years 2.it is age relateddisease and triggered by hypertension 3, diabetes, Obesity andother renal disorders like high cholesterol and poly cystic kidney disease.

For about 10%of the Indian population is suffering from chronic kidney diseases 4.Classification of CKD 4.1: -Chronickidney disease was classified based on the rate of glomerular filtration rateand they are of about five stages. The 5 stages of CKD, they are: – Stage 1:  GFR (>90 mL/min/1.73 m 2). Stage 2:  GFR (60-89 mL/min/1.73 m 2). Stage 3a:  GFR (45-59 mL/min/1.

73 m 2). Stage 3b: GFR (30-44 mL/min/1.73 m 2). Stage 4: GFR (15-29 mL/min/1.73 m 2). Stage 5: GFR <15 mL/min/1.

73 m 2 or dialysis. The diagnosis for the CKD may not be finalized only byreduced Glomerular filtration rate (GFR) at 1st or 2ndstage of CKD. There is a need of other few parameters which are the markers ofkidney damage. The parameters are:1)     Albuminuria (albumin excretion >30 mg/24 hror albumin: creatinine ratio >30 mg/g >3 mg/m.mol).2)     Urine sediment abnormalities.3)     Electrolyte and other abnormalities because ofthe tubular disorders.

4)    Histologic abnormalities.5)    Detection of Structuralabnormalities by imaging.6)     Kidney transplantation history, in such cases. RISK FACTORS:-OBESITY:-·       Though people do not havehistory of hypertension or diabetes, a study states that they are at three-foldrisk of developing CKD 5.

SMOKING:-·       In a retrospectivestudy,4142 participants of about 65yrs old with history of smoking. Therecreatinine level is raised about 0.3% than the normal. This study revealssmoking causes CKD 6·       Smoking is also the riskfactor for urinary stone formation 7 it eventually leads to CKD8.·       In a 5 years crosssectional study on Heavy smokers(>30pack/year) revealed that Smoking is thefactor for CKD 9·       Smoking increase themortality in dialysis patients although there was not a corresponding increasedrisk of Cardiovascular events 10.ALCOHOL:-Progressof CKD to ESRD is more due to consumption of alcohol 11. Alcohol consumption of more than twoalcoholic drinks per day, on average, was associated with an increased risk ofkidney failure in the general population 12 DiabetesMellitus: -In2000, India (31.

7 million) topped the world with the highest number of peoplewith diabetes mellitus followed by china and US 13. Recent 2015data of WHO India states that about 69.2 million people are living with diabetes(8.

7%) in India 14.Mechanisms that lead to kidney disease in diabetes include hyperfiltration injury, advanced glycosylation end products, and reactive oxygen species15. Pathogenic changes that are associated with diabetic nephropathyare due to hormones such as transforming growth factor-beta and angiotensin II16.

   AGE: – However, relatively little is known about the clinical courseof CKD in older individuals. Renal damage is common in elderly peopleof aged above 6517,18,19. Age is recognised as independent riskfactor for renal disease 20. According to the National Kidney FoundationKidney Disease Outcomes Quality Initiative(k/DOQUI) Guidelines- Elderlypopulation were screened, more than one-half of subjects are and found as CKDstages 3-5(GFR 60ml/min per 1.73m2) 2110 yearsfollow up study revealed that Age group 50above are prone to CKD and Age 60above are at CKD stage-III or ESRD, irrespective of their gender 22 HYPERTENSION:- SALT restriction should be indicated inantihypertensive therapy and diuretic therapy for better outcomes 23Experimentalanimal model shows that hypertension can be lead to kidney damage, which isbecause of decrease ability of kidney to eliminate salt. Experiment was done ondogs that was found that 70% of kidney damage is seen and developinghypertension with in few days.

Due to increase intake of salt may lead toHypertension thus in-turn leads to the progression of CKD disease 24.  In another experimental study, high salt dietis given to the rats which shows high increase in levels of transforming growthfactor beta, polypeptides associated with kidney fibrosis thus leads to kidney damage25. oxidative stress played an important role in the production ofrenal damage 26. TREATMENT:  Treatment ofchronic kidney disease (CKD) can slow itsprogression to end-stage renal disease (ESRD). Angiotensin-converting enzyme(ACE) inhibitors and angiotensin-II receptor blockers are used in order tomaintain blood pressure in CKD27. National kidney foundation was suggesting that combinationtherapy like ARB’s and ACE inhibitors can be used to decline the proteinuria inthe patients who are with renal disease 28. By monitoring thecreatinine levels in early stages if (serum creatinine>1.

4 mg/dl)then we can choose the ACE inhibitors and we can stop the progress of thedisease with mono therapy of ACE inhibitors. Thus we can prevent progression ofdisease 29Combinationtherapy of ACE inhibitors and ARB’s is better option for complete blockade ofRAAS which gives better Reno protection. A study shown that patients with stable hypertension andadvanced CKD, who are receive therapy with angiotensin-converting enzyme (ACE) inhibitorsand angiotensin-II receptor blockers exhibit an association withlow risk of long-term dialysis 30.Pentoxifylline is Reno-protective drug whenit is given in combination with Angiotensin-convertingenzyme (ACE) inhibitors and angiotensin-II receptor blockers, we can decreasethe progress of CKD stages 30.A mono-therapy of short acting Dihydropyridinecalcium channel blockers(CCB`s) worsens proteinuria and accelerate renal damagein both animal models and human with hypertension or diabetes. But when we giveNon-dihydropyridine CCB`s in combination with ACE inhibitors. It acts as Reno-protective31VITAMIN-D SUPPLEMENTATION:Vitamin-D involves numerous regulatory processesin the body 32.

Vitamin-D is observed in the form of calciferol, hydroxylationof calciferol occurs in Liver then it forms into 25-hydroxycalciferaol. This25-hydroxycalciferaol undergoes one more hydroxylation in kidney and develops1,25 dihydroxycalciferol.Vitamin-D is not only restricted to its classicalfunction of maintaining Calcium and phosphatehomeostasis but also Vitamin-D plays crucial role in cell differentiation andanti-proliferative factors with action upon different tissues i.e., includes immunesystem, renal system and cardio vascular system 33-34.

 IRONSUPPLEMENTS:Kidney maintains RBC by erythropoietinproduction, Impaired production of erythropoietin by failing kidneys leads toanaemia condition 35.Ironbased phosphate binders have greater absorption properties, could representnovel approach for correcting anemia and hyperphosphatemia in CKD patients36. CONCLUSION: Involvementof Clinical pharmacist in the therapy, can guide the physician about propercombination of drug therapy in order to stop the progression of CKD and thusdecrease in pill burden may attains medication adherence.