Summary of complication of ESRD

1. Complicationof
End StageRenalDisease
Huriah M. Putra, MD

2. THE CASE

3. General Data
• T.A.
• 24 years old
• Female
• Single
• Catholic
• Filipino

4. Chief Complaints
DIFFICULTY OF BREATHING

5. 2 weeks PTC
• Complained of cough, whitish phlegm
• Associated with runny nose
• No fever
• No difficulty of breathing
• No chest pain
• No consult was done

6. 1 week PTC
• Persistence of symptoms
• Sought consult to local clinic
• Sent home without any meds

7. 5 days PTC
• Still with cough, whitish phlegm
• Already associated with orthopnea
(sitting position)
• Sought consult to clinic
• Given mucolytic and sent home

8. Day of admission
• Persistent of symptoms, patient sought
consult to local clinic
• Chest Xray was done
• Transferred to our institution

9. Physical Examination
• Awake, dyspnea
• BP unappreciated; HR 112; RR 42; T
36.8
• Neck vein engorgement (+)
• Crackles all over
• Abdomen soft, nontender
• No edema

10. In the ER
• Norepinephrine 0.1 mcg/kg/min
• Ipratropium bromide + Salbutamol
nebulization 2 doses
• 12 lead ECG ▶ sinus tachycardia
• ABG ▶ FiO2 60%
Ph 7.19
PaCO2 20
PaO2 81
HCO3 7
O2 94%

11. • NaHCO3 50 meq SIVP
• Intubated
• NaHCO3 150 meq in 250 cc D5W x 24o
• Piperacillin-Tazobactam 4.5 gr IV
loading then 2.25 gr IV q8
• BP 150/80
– Furosemide 80 mg IV
FiO2 100%
Ph 7.09
PaCO2 44
PaO2 50
HCO3 13
O2 71%

12. Leukocytes 16.27x 109/L 5.0-10.0
Erythrocytes 2.87x 1012/L 4.2-5.4
Hemoglobin 8.7 g/dL 11.0-15.0
Hematocrit 24.4 % 37.0-47.0
Thrombocytes 559 x 109/L 150-450
Neutrophil 94.2 % 50-70
Lymphocyte 4.3 % 20-40
Monocyte 0.8 % 0-7.0
Eosinophil 0.5 % 0-5.0
Basophil 0.2 % 0-1.0

13. BUN 113 7-18
Creatinine 22.14 0.7-1.3
Sodium 135 136-145
Potassium 5.9 3.5-5.1
Blood Uric Acid 13.4 2.6-6.2
Calcium 6.4 8.5-10.10
Phosphorus 15.4 2.48-4.95
Magnesium 2.19 1.8-2.4
Albumin 2.6 3.4-5.0

14. Impression
• CKD sec to CGN in uremia
• CAP-HR

15. • Patient was scheduled for STAT HD
– Duration 2 hours
– UF 2L + flushing + BT
– BFR 180
– DFR 300
– Loph 18
– Flushing 50 cc Q15

16. CHRONIC KIDNEY DISEASE

17. Chronic Kidney Disease
• Kidney damage or eGFR below 60
ml/min/1.73 m2 persisting for 3 months
• Abnormalities of kidney structure
• Irrespective of the cause

20. Mechanism
• Chronic and sustained insults to the
kidney evolve to progressive kidney
fibrosis with destruction of the normal
microarchitecture of the kidney ▶
replaced by fibrous tissue made of
collagenous extracellular matrix ▶ loss
of function

21. SODIUM ANDWATER HOMEOSTASIS

22. • In normal renal function, tubular
reabsorption of filtered sodium and
water is adjusted; urinary excretion =
intake
• In kidney disease, dietary intake of
sodium > urinary excretion ▶ sodium
retention and ↗ extracellular fluid
volume

23. Sodium
retention
Expansion of
ECFV
Hypertension
Accelerate
nephron injury

24. Na+

26. Expansion of ECFV
• Presents as peripheral edema or
unresponsive hypertension
• Salt restriction
• Combination of diuretics and metolazone
can promote salt excretion
• Diuretic resistance with intractable
edema and hypertension: indication to
initiate dialysis

27. In face of extrarenal fluid loss..
• Prone to ECFV depletion because
inability to reclaim filtered sodium
• Compromise kidney function through
underperfusion ▶ acute-on-chronic
kidney failure

28. POTASSIUM HOMEOSTASIS

29. • Defense for decline in urinary potassium
excretion:
– Aldosterone-dependent secretion in the
distal nephron
– Augmented potassium excretion in the GI
tract

30. • Hyperkalemia may be precipitated:
– Increased dietary potassium intake
– Protein catabolism
– Hemolysis
– Hemorrhage
– Blood transfusion
– Metabolic acidosis
– RAS inhibitors and potassium sparing
diuretics

31. Hypokalemia
• Not common in CKD
• Reflects markedly reduced dietary
potassium intake, excessive diuretic,
concurrent GI losses

32. METABOLIC ACIDOSIS

33. Metabolic Acidosis in Advanced
CKD
• Caused by failure of the tubular
acidification to excrete normal daily acid
load
• As functional renal mass is reduced;
increase in adaptive ammonia
production and H+ secretion
• Overall production may be decreased
secondary to the decrease in total renal
mass

34. • Majority of patients can still acidify the
urine
• Less ammonia = less proton excretion
• Hyperkalemia will further depresses
ammonia production

35. • eGFR < 30 ml/min, patient may develop
hyperchloremic normal anion gap
metabolic acidosis associated with
normo- or mild hyperkalemia
• eGFR < 15 ml/min, acidosis change to
anion gap metabolic acidosis; inability to
excrete phosphate, sulfate

36. Si & Sy
• Dyspnea as a result of respiratory
compensation
• Aggravates hyperkalemia
• Inhibits protein anabolism
• Accelerates calcium loss from bone (for
buffer of hydrogen ions)

37. Treatment
• NaHCO3 0.5 to 1.5 mmol/kg/day
• Beginning when HCO3
- level is < 22
mmol/L
• If acidosis is refractory to medical
therapy, dialysis needs to be initiated

38. BONEMANIFESTATIONS

39. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)

40. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)

41. Calcium Metabolism
• Calcium metabolism depends on close
interaction of PTH and vitamin D
• Total serum Ca++ tends to decrease as
result of phosphate retention and
decreased production of calcitriol,
intestinal calcium absorption, and
skeletal resistance to PTH
Levels of free calcium within
normal range
Compensatory
hyperparathyroidism

42. Phosphate Metabolism
• Hyperphosphatemia does not evident
before CKD stage 4
• Compensatory hyperparathyroidism and
increases in FGF-23 result in increased
phosphaturia

46. Clinical Manifestations
• Aches and pains, nonspecific; lower
back, hips, legs; aggravated by weight
bearing
• May be confused with gout or
pseudogout and often respond to
NSAIDs

47. • Bone deformities as a consequences of
fractures; sometimes induced by brown
tumors

48. Treatment
• Prevention of hypocalcemia
– Calcium supplements (CaCO3) with
vitamin D
• Control of Phosphate
– Dietary phosphate restriction (0.8 g/kg/day)
– Phosphate binders (calcium-containing
antacids, magnesium salts, aluminium
hydroxide, etc.)

50. Classification
• High bone turnover with increased PTH
levels (osteitis fibrosa)
• Low bone turnover with low or normal
PTH levels (adynamic bone disease and
osteomalacia)

51. • Consequences of inadequately low PTH
levels
• Iatrogenic oversuppression of PTH
results from high dose active vitamin D,
calcium loading, or after
parathyroidectomy

54. Treatment
• Avoid PTH overexpression and restore
adequate PTH levels without
development of secondary
hyperparathyroidism
– Reduction or withdrawal of active
vitamin D
– Reduction of dialysate calcium
concentration

55. ANEMIA

56. • Isolated normochromic, normocytic
anemia
• Observed as early as stage 3 CKD and is
almost universal by stage 4
• Primary cause: insufficient production of
erythropoietin

57. Treatment
• Erythropoietic-stimulating agents
• Adequate bone marrow iron stores
• Adequate supply of other major
substrates and cofactors (e.g., vitamin
B12 and folate)
• Target hemoglobin: 100-115 g/L