1. Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function lasting more than 3 months, including decreased glomerular filtration rate (GFR) <60 mL/min/1.73m2 or markers of kidney damage. 2. Dietary management of CKD involves restricting sodium, potassium, phosphorus, and fluid intake depending on the stage of disease. Protein intake is usually moderately restricted. 3. Common complications of CKD include anemia, bone mineral disorders, cardiovascular disease, electrolyte abnormalities, acidosis, and hypertension. Treatment involves controlling risk factors and managing complications through diet, medications, dialysis or transplant.

1. Management of CKD
Dr ARUN

2. Criteria for definition CKD
CKD is defined as abnormalities of kidney structure or function , present for more than 3 months,
with implications for health. These may include the following:
● Markers of kidney damage
Albuminuria (ACR more than equal to 30mg/ 24h).
Urine sediment abnormalities
Electrolyte abnormalities due to tubular disorders
Abnormalities detected through histology
Structural abnormalities detected through imaging
History of kidney transplant
● Decreased GFR < 60ml/min/1.73m2

3. DIET
● Adequate calories , vitamin and iron.
● Low sodium diet - restrictions of sodium intake to less than 2.3g/day.(volume
overload pts and hypertensive pts)
● Low potassium diet - 2 to 3 g/day ( oliguric pts and hyperkalemic pts), avoid coconut
water, banana)
● Low phosphorous diet - avoid dairy products.
● Protein usually moderate - if pts in early ckd not on RRT (0.8-0.9g/kg/day)
If pts with ckd and RRT (1.1-1.3g/kg/day)
● Fluid restriction - early stages not much of restriction
● Late stages mostly in volume overload state, hypervolmeic hyponatremia

4. Diabetes and CKD
● Most common risk of hypoglycemia - mostly insulin and oha’s (sulphonylureas) are
not metobilized , exception glipizide which is renofriendly and do not cause
hypoglycemia.
● We can reduce the dose of insulin and avoid sulphonylureas.
● Metformin : risk of lactic acidosis,acute uremia and contraindicated in pts with gfr
<30ml
● Gliptans are safe , mainly linagliptan( metobolised through liver) and also studies
shows that it will help in decrease in proteinuria.
● SGLT2 inhibitors - gfr upto 60 ml can be given below that less efficacy commonly
used are CANAGLIFOSIN and EMPAGLIFOSIN and also slow down CKD
progression.
● Meglinitides not recommended
● Incretins will cause renal impairment and not used in renal failure.
● Most safest is INSULIN if gfr less than 30ml stop oha and switch to insulin.

7. Cardiovascular manifestation
● Leading cause of mortality in CKD patients
● 50% of ESRD patients die from a cardiac disease
● In younger patients there is 500 fold higher risk in comparison to age
related controls.
● Prevalence of HTN in a CKD Patients is 90%.
● HTN directly correlates with LVH , which in turn directly correlates with
diastolic dysfunction.
● HTN is also a risk factor for CAD

8. Hypertension and ckd
● Low sodium diet
● Anti hypertensive of choice are ACE inhibitors and ARBS
● It will help in reduction of proteinuria and ckd progression.
● Contraindiacation : if potassium > or= 5.5 meq
● Serum creatinine increase by >30 per from the baseline.
● Target blood pressure in CKD is <130/80 mmhg.

9. ● Metabolic acidosis - sodium bicarbonate are used and target should be 22-24
● Increase potassium - low potassium diet and potassium binders are given
mostly we use SPS( sodium polyesterene sulfonate),SPS exchanges sodium
for potassium and binds it in the gut, primarily in the large intestine,
decreasing the total body potassium level by approximately 0.5-1 mEq/L.
● Patiromer recently approved drug by FDA. Powder form 8.4g/16.8/25.2g/
packet.
● Mao: binds and remove potassium from GI tract particularyat colon and also
increases fecal excretion.
● Volume overload : with diuretics (loop diuretics and can increases the dose
accordingly)

10. Anemia and CKD
● Target :10 -11.5 g/dl
● Usually seen in stage 3 to 5 ckd - 57% incidence
● Usually it will contribute to LVH, develops diastolic dysfunction and leads to cardiac
failure .
● Independently influence the rate of fall in GFR.
Why anemia??
● 1) Due to absolute or relative deficiency of EPO
● 2) anemia of chronic disease
● 3) decrease number of RBC ( survival time decreased in ckd)
● 4) iron deficiency anemia
● 5) increased PTH will cause bone marrow fibrosis
● 6) uremic bleeding

12. How to correct anemia??
● 1 step : reticulocyte production index
If it is less than 2 confirms hypoproliferative anemia
● 2nd step : check MCV ( low or normal)
● 3rd step : check serum ferritin and percentage saturation of transferrin.
● If both are low give iron first. Because there is no use of giving EPO if
iron levels are not corrected.
● So iron therapy indicated if serum ferritin less than 200mg/dl and TSAT
<20%
● Iron therapy : iron sucrose, Ferric carboxymaltose(500 mg / 1 gram) and iron
isomaltose.

13. ESA( erythropoietin stimulating agents)
● Indicated only if S.ferritin more than 500 and TSAT > 25%.
● Hemoglobin less than 10gmdl
● 1st gen : Epoietin alpha given 50-100 units / kg. 3 times per week in
dialysis patients and once weekly in ckd.
● 2 nd gen : Darbopoetin ( 0.45mg/kg/ once a week) iv or sc and dosing
can be extended to every 4th week on reaching the target level of hb.

14. CKD- mineral bone disease
A systemic disorder of mineral and bone metabolism due to CKD ,
manifested by either one or combination of the following
● Abnormalities of calcium, phosphorus,PTH or vitamin D
metabolism
● Abnormalities in bone turnover, mineralization, volume, linear
growth or strength
● Vascular or other soft tissue calcification.

15. CKD and mineral bone disease
3 major disease and major abnormalities
3 major disease
● High bone turnover disease: 90% (osteitis fibrous cystica)
● Low bone turnover disease : 10% (adynamic bone disease)
● Miscellaneous: Osteomalacia and osteoporosis.
3 major abnormalities
● Biochemical abnormalities
● Bone changes
● Calcification

16. High bone turnover disease
● Secondary hyperparathyroidism is the major cause.
● Usually GFR will be less than 50-70 ml/my
● As GFR declines tendency for phosphorus to increase by FGF-23
● Phosphorus can convert normal endothelial cells to osteoblasts.
FGF-23
● Produced by osteocytes, which will inhibit Na/p cotransport at PCT
● It will increases phosphorus excretion
● Receptor for FGF23 is
● But the same time it will inhibit 1alpha hydroxylase enzymes(which helps in converting 25
hydroxylase D3 to 1,25 hydroxylase D3) causing decreased calcium and phosphorus
absorption from GIT.

17. Ckd patients with secondary hyperparathyroidism :
● Decreased serum calcium.
● Decreased calcitriol
● Decreased kotho resistance
Features of high bone turnover disease
● Increased PTH ( normal is 50 - 100pg ) in CKD ( 150 to 300pg/ml)
● Increase phosphorus (>5.5) but target will be less than 5.5 mg/dl
● Decreased adjusted serum calcium (<8.4) target will be 8.4 to 9.5mg/dl
● Decreased calcitriol
● Features: bone pain, fractures, increased bone mass with decreased mineralization.

18. Low bone turnover disease
● Also known as adynamic bone disease
● Seen in 19%of cases
● PTH decreases and bone mass will decrease
● PTH markedly reduced due to increase calcium from exogenous route or high
calcium dialysate.
Features
● Decreased PTH <200pg/ml due to increased calcium exogenous
● Widespread medical calcification
● Death due to coronary calcification
● Decreased bone mass and high secondary mineralization.

19. Management CKD-MBD
Low bone turnover:
● Stop calcium/ vitamin D
● Low calcium or zero calcium dialysate.
● Vitamin k2 analogues.
High bone turnover :
● Most common wil be low serum calcium and high phosphorus combination
● Control by dietary restrictions ( avoid dairy products)
● Phosphate binders

20. Phosphate binders
● Calcium based :calcium
carbonate
300-1200mg/8hourly
orally
● calcium acetate 667 mg
● Non calcium based :
metal based -
LANTHANUM
(500/750/1000mg)
● Non metal based:
SEVALAMER
(400mg/800 mg)

22. Vitamin d supplement
● Active vitamin D- calcitriol 0.25mcg to 1 mcg PO daily.
● 19- nor 1,25dihydroxyvitamin D2 paricalcitol 1-5 mcg PO daily in pre
dialysis patients or 2-10 mcg iv with each dialysis pts.
● It is an synthetic vit D analog with lower incidence of hypercalcemia.
● Doxerxcakciferol 1-5 mcg in pre dialysis pts or 5-20mcg thrice weekly
with dialysis.

23. Cinacalcet
● Increased serum calcium
● Increased serum phosphorus
● Increased PTH (>1000)
● All mainly due to tertiary hyperparathyroidism
● Can be treated with cinacalcet which is calcium receptor agaonist
● Which will down regulate PTH
● dose will be 30mg-120mg PO.

24. Parathyroidectomy
Indication
● Serum PTH >800pg/dl
● Tertiary hyperparathyroidism
● Parathyroid adenoma
● Severe hypercalcemia not controlled with medications
● Severe extra skeletal calcification.

25. Take home (CKD)
● GFR and stages
● Uremic symptoms
● Anemia
● Bone mineral changes
● Blood pressure
● Cardiac
● Diuretics usage
● Electrolytes
THANK YOU