Management of chronic kidney disease

1. MANAGEMENT OF CHRONIC
KIDNEY DISEASE
GUIDE: DR Y. JAMRA
CANDIDATE: DR NARESH PATEL

2. Definition:
• CKD is defined as abnormalities of kidney structure or function,
present for >3 months
Criteria for CKD (either of the following present for >3 months)
Markers of kidney damage (one or more) Albuminuria (AER >30 mg/24 hours; ACR >30 mg/g
[>3 mg/mmol])
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular
disorders
Abnormalities detected by histology
Structural abnormalities detected by imaging
History of kidney transplantation
Decreased GFR GFR <60 ml/min/1.73 m2 (GFR categories G3a–G5)

3. CKD is classified based on cause, GFR category, and albuminuria
category (CGA).

4. Screening Tools: eGFR
• Considered the best overall index of kidney function.
• Normal GFR varies according to age, sex, and body size, and declines
with age.
• The NKF(National kidney foundation) recommends using the CKD-
EPI Creatinine Equation (2009) to estimate GFR. Other useful
calculators related to kidney disease include MDRD and Cockroft
Gault.

5. •
.

6. Cockcroft-Gault Formula :
• Creatinine clearance =
[{(140-age)* weight}/ (72*serum creatinine)] *0.85 (if female)
• GFR calculators are available online at www.kidney.org/GFR

7. Small changes make a big difference
Lee A Hebert et al. Kidney International (2001) 59, 1211–1226
•A GFR loss of
> 1 mL/min/year
beginning at age
25 can result in
end-stage renal
disease within a
normal lifespan.

8. Screening Tools: ACR
• Urinary albumin-to-creatinine ratio (ACR) is calculated by dividing
albumin concentration in milligrams by creatinine concentration in
grams.
• Spot urine albumin-to-creatinine ratio for quantification of
proteinuria
• First morning void preferable
• 24hr urine test rarely necessary

9. Etiology of Chronic Kidney Disease

10. CKD -Clinical Manifestations
• Abnormal Sodium-Water metabolism
• Edema, Hypertension
• Abnormal Acid-base abnormalities
• Metabolic Acidosis
• Abnormal hematopoiesis
• Anemia of CKD
• Cardiovascular Abnormalities
• LVH, CAD
• Abnormal Calcium-Phosphorus metabolism
• Hyperphosphatemia, hypocalcemia
• Hyperparathyroidism

11. Fluid and Electrolyte disorder
• Patients with CKD, the tubular reabsorption of filtered sodium and
water is adjusted ,so that urinary excretion matches intake.
• Many form of kidney disease disrupt this balance leading to sodium
retention and extracellular fluid volume(ECFV)
• Dietary salt restriction and use of loop diuretics, occasionally in
combination with metalozone maintain euvolemia
• In contrast overzealous salt restriction or diuretic use can lead to
ECFV depletion and precipitate further decline in GFR.

12. Hyperkalemia
• Decline in GFR doesn’t necessarily parallel decline in urinary potassium
excretion
• Hyperkalemia may precipitate due to increased dietary potassium intake,
protein catabolism, hemolysis, blood transfusion and metabolic acidosis
• RAS inhibitor and potassium sparing diuretics also cause hyperkalemia.
• In diabetic nephropathy and renal disease involving distal nephron such as
obstructive uropathy and sickle cell nephropathy are associated with
earlier and more severe disruption of potassium secreting mechanism in
distal nephron out of proportion to decline in GFR.

13. Hyperkalemia Treatment:
• Respond to reduce dietary potassium
• Stop potassium sparing diuretics (spironolactone)
• Stop or reduce beta blockers, ACE inhibitor/ARBs
• Hypokalemia is not common in CKD.

14. Hyperkalemia Treatment continue…
Large amounts of potassium are found in:
•certain fruits and vegetables (like bananas, melons, oranges, potatoes,
tomatoes, dried fruits, nuts, deep-colored and leafy green vegetables,
and some juices)
•milk and yogurt
•dried beans and peas
•most salt substitutes
•protein-rich foods, such as meat, poultry, pork, and fish

15. Metabolic acidosis
• Mild degree of non-anion gap metabolic acidosis (PH < 7.35)often
present in CKD stage 1-3
• With the worsening renal function non-anion gap metabolic
acidosis complicated by anion gap metabolic acidosis
• Respond to alkali supplementation, typically with sodium
bicarbonate if serum bicarbonate concentration falls below 20-23
mmol/L
• Correction of metabolic acidosis may slow CKD progression and
improve patients functional status by attenuating catabolic state.

16. Hypertension
• Effective reduction in BP with antihypertensive medication can decrease the
urinary excretion of albumin and slow the rate of progression of CKD
• Dual blockade of the renin-angiotensin system with an ACE inhibitor and
angiotensin receptor blocker has been shown to have an additive effect in
reducing albumin excretion.
• Avoid ACE inhibitor and ARB in combination because Risk of impaired kidney
function and hyperkalemia

17. Blood pressure control
• Single most important measure to slow the progress of CKD
• Individualize targets and agents according to age, coexistent CVD, and other
comorbidities
• ACE or ARB
• Diuretics enhance the antihypertensive and antiproteinuric effects of other
agents.

18. ACEi and ARB: Slowing CKD Progression
• ACE inhibitor and ARBs appear to slow the decline of renal function in
a manner beyond reduction in systemic blood pressure
• Check labs after initiation
• If less than 25% SCr increase, continue and monitor
• If more than 25% SCr increase, stop ACEi
• Better proteinuria suppression with low Na diet and diuretics

19. Clinical Practice Guidelines for Management of Hypertension in
CKD
Type of Kidney Disease Blood Pressure
Target
(mm Hg)
Preferred Agents for
CKD, with or without
Hypertension
Other Agents
to Reduce CVD Risk and
Reach Blood Pressure
Target
Diabetic Kidney Disease
<140/90
ACE inhibitor
or ARB
Diuretic preferred, then BB
or CCB
Nondiabetic Kidney
Disease with Urinary
albumin-to-creatinine ratio
(ACR) 30 mg/g
<130/80
Nondiabetic Kidney
Disease with Urinary
albumin-to-creatinine ratio
(ACR) <30 mg/g None preferred
Diuretic preferred, then ACE
inhibitor, ARB, BB or CCB
Kidney Disease in Kidney
Transplant Recipient
CCB, diuretic, BB, ACE
inhibitor, ARB

20. Diabetes and Glycemic Control in CKD
• Target HbA1c ~7.0%
• Improved glycemic control reduces the rate at which
microalbuminuria appears and progresses
• Risk of hypoglycemia increases as kidney function becomes
impaired
• Declining kidney function may necessitate changes to
diabetes medications and renally-cleared drugs

22. Modification of Other CVD Risk Factors in CKD
• Smoking cessation
• Alcohol restriction
• For those who drink alcohol, consume </=2 drink/day in men and </= 1 drink
in women
• Exercise
• 30 -60 minutes of moderate intensity dynamic exercise 4-7 days/ week.
• Weight reduction
• target BMI 18.5 – 24.9 kg/m2 and waist circumference in men <102 cm and
female < 88 cm.

23. Modification of Other CVD Risk Factors in CKD
• Lipid lowering therapy
• In adults >50 yrs : statin when eGFR ≥ 60 ml/min/1.73m2;
:statin or statin/ezetimibe combination when eGFR < 60
ml/min/1.73m2
• In adults < 50 yrs, statin if history of known CAD, MI, DM, stroke
• Aspirin is indicated for secondary but not primary prevention
• Dietary salt restriction less than 5-6 gm daily

24. Anemia in CKD
• Normocytic normochromic anemia is observed as early as stage 3
CKD and is almost universal by stage 4.
• Diagnose anemia in adults and children >15 years with CKD when the
Hb concentration is
<13.0 g/l in males and
<12.0 g/dl in females.
• Anaemia in CKD should include assessment of secondary causes
including iron deficiency.

26. Anaemia continue….
• Iron replacement is often effective in anaemia of CKD as initial
therapy.
• ESA (erythropoiesis stimulating agents): Start ESA if Hb <10 g/dl, and
maintain Hb <11.5 g/dl. Ensure adequate Fe stores.
• Before initiation of ESA therapy iron saturation should be maintained
at 30 -50 % and serum ferritin at 200-500 ng/ml.
• In addition to iron adeqaute supply of vitamin B12 and folic acid
should be assured.

27. CKD-MBD (Mineral and Bone Disorder)
• Serum calcium , phosphate and PTH should be measured for adults
with stage 4-5 CKD and for with stage 3 CKD with progressive decline
in renal functions.
• Serum phosphate and serum calcium level should be maintained
within the normal range.
• Target PTH levels in CKD is 150-300 pg/ml.

28. Pathophysiology of Secondary Hyperparathyroidism
Decline GFR
Phosphate retention : hyperphosphatemia
Increase PTH
hyperparathyroidism
Increase synthesis of
FGF-23 by osteocytes
Suppression of calcitriol
production by kidney
Decrease level of
ionised Calcium

29. FGF-23 maintain normal serum phosphate level by
• Increase serum phosphate excretion
• Stimulation of PTH , which increase phosphate excretion
• Suppression of calcitriol leading to diminished phosphorus absorption
from GI tract.
FGF-23 is also an independent risk factor for LVH and mortality in CKD,
dialysis and renal transplant patients.

30. Bone Manifestations
• Osteitis fibrosa cystica- due to secondary
hyperparathyroidism
• Adynamic bone disease and osteomalcia-
low or normal PTH
• Occasionally calcium will precipitate
in soft tissue in large concentration
termed “TUMORAL CALCINOSIS”

31. Calciphylaxis
• Calcific uremic arteriolopathy is a
devasting condition seen almost in
patients with advanced CKD and heralded
by livedo reticularis and ischemic necrosis
patches, especially in legs, thigh,
abdomen and breast.
• Pathologically, vascular and extensive soft
tissue calcification.

32. CKD-MBD :Prevention
• Restriction of dietary phosphate:
Large amounts of phosphorus are found in:
•dairy products such as milk, cheese, yogurt, ice cream, and pudding
•nuts and peanut butter
•dried beans and peas, such as kidney beans, split peas, and lentils
•beverages such as cocoa, beer, and dark cola drinks
•bran breads and bran cereals
•processed, convenience, and fast foods, including some meats

33. CKD-MBD : Prevention continue…
• Use of calcium based phosphate binders- calcium carbonate and
calcium acetate and non-calcium based phosphate binders sevalamer
and lanthanum.
• Calcium based phosphate binder have risk of developing
hypercalcemia.
• Prescribe vitamin D analogue if serum level of intact PTH > 53 pg /ml

34. Renal replacement therapy
• Indication:
• Uremic symptoms: anorexia and nausea, impaired nutritional status,
increased sleepiness, and decreased energy level, attentiveness, and
cognitive tasking
• Presence of Hyperkalaemia unresponsive to conservative measure
• Severe metabolic acidosis refractory to medical therapy
• Uremic pericarditis
• Encephalopathy
• Persistent extracellular volume expansion despite of diuretic therapy
• Asymptomatic patients with eGFR 5-9 ml/min/1.73 m2

35. Treatment Options for Renal Replacement
Therapy
There are essentially two options to a patient facing ESRD:
1- Dialysis
2- Transplantation, which has been clearly shown to be the best
treatment option

36. Dialysis Options
• They have to choose between
• hemodialysis and
• peritoneal dialysis
- Hemodialysis can be done at home with a machine that is smaller than
the traditional in-hospital/outpatient clinic machine.
- Peritoneal dialysis can either be done with a cycler or manually

37. Immunizations
CDC recommend following immunization in patients with CKD on
dialysis
• Influenza vaccine annually for all CKD patients
• Pneumococcal vaccine for patients with ESRD
• O, 2 months
• Booster at 5 year
• Hepatitis B vaccine
• O, 1,2, 6 month (2 ml)