A brief overview of CKD
CKD is defined by kidney damage or eGFR < 60 ml/min/1.73m2 persisting for 3 months. It is classified by KDOQI and KDIGO guidelines, with stages and categories indicating severity. Calculating eGFR involves MDRD and CKD-EPI formulas, but these may have limitations in accurately reflecting true GFR. The progression of CKD is determined by sustained eGFR decline, and the epidemiology reveals a prevalence of 10%-14% with various causes including hereditary and acquired nephropathies.
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A brief overview of CKD Harshani D. Perera Senior Registrar Nephrology SJGH 09.01.2018
CKD definition O Kidney damage or eGFR < 60 ml/min/1.73m2 persisting for 3 months despite the cause O several classifications O KDOQI by National Kidney Foundation O KDIGO by International Society of Nephrology
Classification - CKD O KDOQI (Kidney Disease Outcome Quality Initiative ) guidelines , by NFK O 5 stages of CKD O suffix T for patients with allografts O suffix D for patients on dialysis O 2012 KDIGO guidelines by ISN O 6 categories O G1 to G5 O G3 split in to 3a, 3b O A1, A2, A3 3 levels of albuminuria
Calculating eGFR O MDRD (modification of diet in renal disease formula) : overall MDRD more accurate O CKD-EPI Chronic kidney disease Epidemiology Collaboration) O gender, race, age, Cr : are parameters need in both MDRD , CKD- EPI O Creatinine clearence : by Cockcrofr-Gault Equation : sex, age, weight, Cr, height (remains gold standard after 40 years) less accurate than MDRD in obese and elderly
Limitations classification CKD O Current CKD classification based on eGFR O MDRD , CKD-EPI both are relatively inaccurate in reflecting measured GRF above 60 ml/min O underestimate true GFR , thus over diagnose a large number of people having CKD stage 3 b O Physiological age related decline in kidney function in elderly in absence of associated micro albuminuria seldom progress to ESRF
Progression of CKD O Current classification not determined on progression of CKD O KDIGO suggest , to define Progressive CKD sustained decline in eGFR by 5ml/min per year Or declining eGFR category accompanied by 25% of drop in baseline eGFR
Epidemiology - CKD O Prevalence 10% - 14% among general population O CAUSES : O Hereditary APCKD O Acquired nephropathy : DM , HT, Glomerularnephritis, obstructive nephropathies
Rate of progression vary ! O According to underlying etiology . O Historically DM-nephropathy is the fastest , average decline around 10ml/min per year. O In non diabetic CKD , chronic proteinuria GN having faster progression than low proteinuric CTIN-CKD. O In APCKD, beyond stage 3b , more faster course. O Majority reach from stage 3b to 5 progress to ESRF. O Some patients in CKD-5 remain stable for number of years.
Risk factors - CKD O Modifiable 1. Birth weight 2. Systemic HT 3. Diabetes 4. CVD 5. Albuminuria 6. Obesity / metabolic Xn 7. Dyslipidemia/smoking 8. Hyperuricaemia 9. Nephrotoxins NSAID,herbal, Heavy metal O Non- modifiable Age (older) Race (Non-caucasian) Genetics 1. 2. 3.
Retarding progression of kidney disease ? O Typically natural progression does not proceed until nephron loss exceeds 50%. O Normal solitary kidney is vulnerable to natural progression if condition is congenital or acquired in early life. O LBW esp males progress to ESRF due to defective nephron development.
Proteinuria magnitude and risk of CKD progression Magnitude of proteinuria is the strongest risk factor of CKD progression . O O When it exceeds 500mg/dl it co relate the threshold of natural CKD progression. O Exception is highly selective albuminuria which can persists in nephrotic range even 10 years with out causing structural renal damage.
Non proteinuric CKD O CAUSES O Early phase of diabetic CKD O HT- GS O ADPCK O Chronic NSAIDs O Obstructive uropathy O Nephropathy of aging
Level 1 kidney protective measures Control blood pressure ACEI or ARBS avoid dihydropyridine unless needed for BP control O Control protein intake O O O
Level 2 - recommendations O Restrict NaCl intake and diuretic therapy O NDHP CCB O control each component of metabolic syndrome O Aldosterone antagonists O Allopurinol therapy O control serum PO4 O alkali therapy O Bata blockers O Avoid over anti-coagulation with warfarin
Functions of kidney O Fluid balance O Regulate electrolytes O Blood pressure regulation : RAAS O Ca / P04 regulation- bone metabolism O Acid base balance O Endocrine function erythropoietin / 1 OH CCF / Renin
Management of CKD O Early referral to nephrologist O Aim to slow down the progression : O Management of complications related to CKD O RRT counseling when CKD advances O when eGFR 20 ml/min O Refer to vascular surgeon for access creation if dialysis is decided. O Preserve non-dominant upperlimb for future AVF O Hepatitis B vaccination - dual doses 0,1,6 months
Preventing CKD progression O Most effective intervention is control of blood pressure : O HT is very common among in patients with CKD O Anti HT therapy O Life style modifications : O reduction of salt and alcohol O maintenance of healthy weight O regular exercise
Anti hypertensive therapy O Fluid driven blood pressure (water and Na retention ) rise in advances CKD O Activated RAAS O usually multi drug regimens required. O ACEI and ARBS are first line in proteinuric CKD O risk of hyperkalemia especially during intercurrent illnesses O Choice of drugs depends on co-existing CVD, co- mobidities O Target : 130/80
Dietary advice O Obesity causes rapid progression of CKD, thus need weight loss. O Malnutrition common in CKD , it is multifactorial. O anorexia, acidosis, insulin resistance , inflammation , oxidative stress, urinary protein loss O low serum Albumin, Cholesterol, transferrin are markers O Creatinine may stop rising due to reduction in muscle mass.
Recommendation - diet O Reduce protein intake slow the CKD progression evidence based. O Protein energy malnutrition is common. O KDIGO protein 0.8 g/KBW/day when GFR < 30 ml/min O Avoid high protein intake >1.3g/KBW/d in patients at risk of CKD progression. O Salt restriction : < 5g NaCl (90mmol) per day. O In stage 4,5 restrict K ,and PO4 .
Anemia in CKD O Common in stage 3a and above O low Epo levels O reduced availability of iron O chronic inflammation Monitor Hb levels annually till stage 3 a , then 6 monthly in advanced CKD. O
Recommendation - anemia O Rule out other causes of anemia O Fe studies, blood picture, Vit B12, foalte levels, stool occult blood, UGIE / LGIE O IV Iron : when T. Sat < 30 % O Correct deficiencies , if Hb still < 10g/dl, start EAS ( Erythropoetin stimulating agents) If benefits overweigh potential harm increased risk of stroke/thromboembolism, malignancies, hypertension
Benefits of anemia correction O Cardio- vascular benefits : regression of LVH, reduction of myocardial ischemia, reduced HR / CO O Increased quality of life : improved O exercise capacity, sleep patterns, immune functions, cognition, depression O Target Hb < 11.5 g/dl should be maintained. O Hb > 11.5 carry higher risk of cardiovascular events : stroke/ MI
Bone and mineral metabolism O Renal bone disease may already be manifested in CKD stage 3 b, and well established in ESRF. O Even it is well established patient may remain asymptomatic. O Active early management of CKD-BMD will prevent some of cardio-vascular complications.
Recommendations - BMD O check serum ionized Ca, PO4 , intact PTH levels when eGFR < 45 ml/min O optimal PTH target : 3 times upper range O correct hyperphosphatemia, hypocalcemia, and Vit D deficiency O Vit D suppliments / analogue O Phosphate binders O dietary phosphate restriction (dairy products, processed foods )
Complications of BMD O Coronary vessels calcification higher cardio-vascular risk O Heart valve calcification O soft tissue calcifications calciphilaxis : indicating very poor prognosis in CKD. O Renal osteodystrophy
Metabolic acidosis in CKD O Failure of H+ excretion , may be compounded by accumulation of organic acids and bicarbonate loss in interstitial kidney diseases. O clinical manifestations rare till stage 5, dyspnoea occur due to respiratory compensation .
Metabolic acidosis O aggravate hyperkalemia O inhibits protein anabolism O accelerate Ca loss from bone O correction of acidosis also slow the progression of kidney disease O KDIGO - recommends if HCO3 < 22 mmol/L oral bicarbonate supplementations to maintain HCO3 level above 22 .
Cardiovascular risk O high prevalence of CVD among CKD patients. O most likely to die due to CV event than progress to ESRF. O KDIGO recommends :level of coronary care should not be reduced by their CKD state. O Anti platelets in secondary prevention of CVD. O accelerate atherosclerosis : lipid lowering drugs for all above 50 yr, and young CKD patients with additional risk factors for dyslipidemia.
Risk of infection O Infection is second commonest cause of death in ESRF. O state of chronic immunosuppression ,defect in both cellular and humoral immunity. O Annual influenza vaccine when eGFR < 30 O Pneumococal vaccine for those who are high risk O Hepatitis vaccination : early as possible , preferably eGFR > 30
Avoid risks of AKIs among CKD O All patients with CKD are at increased risk of AKI O Avoid nephrotoxins: NSAIDs, aminoglycosides, vancomycin , drugs causing interstitial nephritis O Iodinating contrast for imaging better avoid unless benefits outweigh the risk of contrast AKI. O poor renal perfusion : volume depletion , over diuresis , diarrhoea, vomiting O sepsis O heart failure , MI, tachyarrythmias
Increased bleeding risk O Uremic platelet dysfunction O mild to moderate thrombocytopenia is commonly seen among ESRF O Inadequate dialysis O anemia O Heparin use for dialysis Options :adequate hemodialysis, correction of anemia, platelet transfusion, cryopercipitate, desmopressin nasal spray, tranexamic acid
Timing and initiation of RRT O All patients with eGFR < 20 , or who are likely to progress to ESRF in 12 months should receive education and counseling to aid their decision on best RRT modality. O If HD is preferred AVF referrel O If PD is preferred CAPD catheter insertion 3 weeks prior. O Kidney transplant : Pre-emptive is the best , offer when eGFR <20 , before dialysis. O explore the possibility of live donor if KT opted.
Conservative Management O Potential burden of commencing RRT in terms of O high short term mortality rates O Recurent hospitalizations O Time spent for travelling O Limited improvement of quality of life O Multiple co-morbidities O Advanced malignancy O Offer active medical management and follow up with out starting dialysis. O distressful advanced uremic symptoms need palliative care to facilitate suffering free death.
Conclusion O Rising global trend of CKD during last few decades. O Diagnosis of CKD is challenging and by exclusion of AKI when there is no baseline Cr available. O CKD management guidelines are freely available which is helpful to provide standards of care. O Asses the progression of CKD O Delay the progression of CKD while managing CKD related complication. O Early referral to nephrologist and on time RRT counseling are key in successful management.
