Chronic kidney disease (CKD) is defined as gradual loss of kidney function over months to years. Key risk factors include diabetes, hypertension, family history, and smoking. CKD is usually asymptomatic in early stages. Treatment focuses on controlling blood pressure and blood glucose, limiting proteinuria, treating anemia and bone disease, and slowing progression. The goals are to delay complications by optimizing blood pressure control with ACE inhibitors, ARBs, and other agents and managing associated conditions like anemia, dyslipidemia, mineral bone disorders.

1. CKD/CRF
Dhaval Joshi

2. Definition
• Chronic kidney disease, also called chronic
renal insufficiency or progressive kidney
disease by some
• Defined as a progressive loss of function
occurring over several months to years, and is
characterized by the gradual replacement of
normal kidney architecture with interstitial
fibrosis

4. RF
Susceptibility factors:
• Advanced age
• Reduced kidney mass and low birth weight
• Family history
• Systemic inflammation
• Dyslipidemia

5. RF
Initiation factors:
• DM
• Hypertension
• Glomerulonephritis
Progression factors:
• hyperglycemia
• HTN
• Proteinuria
• Smoking
• Obesity

6. Pathophysiology
• DM
• HTN
• GN

7. CP
• CKD is often asymptomatic, and should be
suspected in individuals with conditions such
as diabetes, hypertension, genitourinary
abnormalities, and autoimmune diseases

8. Symptoms
• Symptoms are generally absent in CKD stages
1 and 2, and may be minimal during stages 3
and 4
• General symptoms associated with stages 1 to
4 include edema, cold intolerance, shortness
of breath, palpitations, cramping and muscle
pain, depression, anxiety, fatigue, and sexual
dysfunction

9. Signs
• Cardiovascular–pulmonary: Edema and
worsening hypertension electrocardiographic
evidence of left ventricular hypertrophy,
arrhythmias, hyperhomocysteinemia, and
dyslipidemia
• Gastrointestinal: Gastroesophageal reflux
disease, weight loss

10. Signs
• Endocrine: Secondary hyperparathyroidism,
decreased vitamin D activation and gout
• Hematologic: Anemia of CKD, iron deficiency,
and bleeding
• Fluid/electrolytes: Hyponatremia,
hyperkalemia, and metabolic acidosis

11. History and Physical Examination
• Careful drug history should be elicited
• Uremic syndrome
• Fundoscopy

12. Laboratory Investigation
• Serum creatinine
• Proteinuria

13. Formula for eGFR

15. Laboratory Investigation
• Serum and urine protein electrophoresis
• Serum concentrations of calcium, phosphorus,
and PTH should be measured to evaluate
metabolic bone disease
• Hemoglobin concentration, iron, B12, and folate
should also be evaluated

16. Imaging Studies
• The most useful imaging study is a renal
ultrasound
• The diagnosis of renovascular disease can be
undertaken with different techniques,
including Doppler sonography or CT or MRI
studies
• Renal biopsy

17. Management

18. GOAL OF THERAPY
• The goal of therapy is to delay the progression of
CKD, thereby minimizing the development or
severity of associated complications including
cardiovascular disease
• Patients generally require a multimodality
treatment approach irrespective of the cause of
their kidney disease
• Therapy with ACEIs and/or ARBs is a key
therapeutic component for almost all patients.

19. Control BP
• Target BP as per JNC-7: <130/80 mmHg
• Results from the MDRD study showed that
further lowering of BP to <125/75 mmHg (or a
mean arterial pressure <92 mmHg) was more
beneficial than usual BP control in patients
with higher rates of urinary protein excretion
(>1 g proteinuria/day)

20. Control BP
• Benefits of ACE inhibitors have been
demonstrated in patients with diabetes who had
some degree of proteinuria, suggesting that use
of ACE inhibitors be considered in this population
regardless of BP
• In patients without diabetes, ACE inhibitors have
been shown to reduce BP, decrease proteinuria,
and slow the progression of kidney disease when
compared with other agents

21. Limitations of ACE inhibitors
• An initial and mild decrease in eGFR is
expected with ACE inhibitor therapy;
therefore, an increase in SrCr of approximately
30% within the first 2 months of therapy is
acceptable
• Hypotension, acute kidney failure, and severe
hyperkalemia are reasons to consider
discontinuing therapy

22. ARB
• Losartan
• Irbesartan
• Valsartan
• Candesartan

23. Other agent
• Aliskiren is the first available agent in a new
class of antihypertensives that targets the
renin-angiotensin-aldosterone system (RAS)
by inhibiting renin
• Limited clincial trails

24. Control Blood pressure
• Target: 130/80 mmHg
Drug options:
ACE inhibitors
ARBs
CCBs
Diuretics

25. Control Blood pressure
• Use ACEIs or ARBs as tolerated, with close
monitoring for renal deterioration and for
hyperkalemia
• With every dose change, serum creatinine levels
need to be monitored. If serum creatinine levels
increase more than 30% from baseline after
adding RAS blockers, RAS blockers should be
stopped

26. Dosing
• Benazepril 10 mg once daily
• Ramipril 2.5 mg once daily
• Enalapril 20 mg once daily
• Losartan: 50 mg once daily

27. Combinational therapy
• A recent study prospectively evaluated the use of
losartan 100 mg daily alone, trandolapril 3 mg
daily alone, or the combination of the two in 336
patients with nondiabetic kidney diseases
• The primary end point, time to doubling of serum
creatinine or ESRD, was observed in 11% of
combination therapy patients and in 23% of each
of the single-agent treatment groups

28. Referance
165. Nakao N, Yoshimura A, Morita H, Takada M,
Kayano T, Ideura T. Combination treatment of
angiotensin-II receptor blocker and
angiotensin- converting-enzyme inhibitor in
non-diabetic renal disease (COOPERATE): A
randomised controlled trial. Lancet
2003;361:117–124

31. Control Blood pressure
• The ARBs, although evaluated to a lesser
extent than ACEIs, appear to have similar
efficacy in terms of kidney protection in
patients with several forms of
glomerulonephritis
• Proteinuria reduction on the order of 25% to
47% was shown with ARB therapy

32. Control Blood pressure
• The combination use of ARBs with ACEIs has
been proposed and preliminary data suggest
that this approach is safe and results in a
greater decrease in proteinuria than that seen
with either agent alone
• The CCBs are also effective treatments for
hypertension in patients with nondiabetic CKD

33. Control Blood pressure
• If proteinuria is present, the use of ACEIs, ARBs, and
possibly nondihydropyridine CCBs may be superior to
conventional agents in decreasing proteinuria and
glomerular hypertension
• β-Blockers may offer benefits in the treatment of
diabetic nephropathy as demonstrated by the United
Kingdom Prospective Diabetes Study, which showed
similar effects of atenolol and captopril on
decreasing the incidence of albuminuria in patients
with diabetes

34. Treatment of Dyslipidemia
• Hyperlipidemia common in patients with CKD
• Elevated triglyceride, total cholesterol, LDL
cholesterol, and decreased HDL cholesterol levels
are generally observed
• The predominance of triglyceride-rich apo-B
lipoproteins may contribute to the progression of
kidney disease and is also a risk factor for the
development of cardiovascular morbidity and
mortality

35. Tretment options
• Statins: decreased proteinuria and
preservation of eGFR in a small number of
patients with CKD
• Despite uncertainty of therapy to delay
progression, treatment of dyslipidemia should
be considered, because abnormal lipid
metabolism predisposes patients to
cardiovascular disease

36. Suggestions from Guidlines (NKF-
K/DOQI)
• Hydroxymethylglutaryl-coenzyme A (HMG-CoA)
reductase inhibitors, which are necessary to
lower LDL cholesterol, may have added
cardiovascular benefits
• Fibrates should be used cautiously in patients
with CKD, because all agents in this class are
renally metabolized, and all are eliminated
primarily via the renal route leading to a possible
increase risk ofmyositis and increase in SrCr

37. Control of Blood Glucose
• It is recommended that plasma values for
preprandial glucose be kept in the 5.0–7.2
mmol/L (90–130 mg/dL) range and
hemoglobin A1C should be < 7%
• As the GFR decreases with progressive
nephropathy, the use and dose of oral
hypoglycemics needs to be reevaluated

38. Control of Blood Glucose
INTENSIVE INSULIN THERAPY:
• The DCCT was the first study to show the long-
term benefits of intensive insulin therapy (IIT) on
kidney and other diabetes-related outcomes
• IIT was achieved by administration of three or
more times daily insulin injections or by insulin
pump infusion so as to attain preprandial and
postprandial blood glucose levels of 70 to 120
mg/dL and <180 mg/dL, respectively

39. Control of Blood Glucose
INTENSIVE INSULIN THERAPY:
• IIT effectively reduced the incidence of
microalbuminuria as compared to standard
therapy in both the primary prevention and
secondary prevention groups, as described
previously
• However, IIT was associated with at least one
episode of hypoglycemia in 65% of patients as
compared to 35% in the standard treatment
group.

40. Control of Blood Glucose
INTENSIVE INSULIN THERAPY:
• A meta-analysis of 16 clinical studies showed a
benefit in reducing the frequency and severity
of diabetic complications, and delaying the
development and progression of diabetic
nephropathy with intensive blood glucose
control in type 1 diabetes

41. Oral Hypoglycemics
• SU
• Metformin (except in stage 4 and 5)

42. ANEMIA OF CHRONIC KIDNEY
DISEASE
• Caused by a decreased production of EPO
• Type: Normochromic – Normocytic
• Characterized by pallor and fatigue

43. ANEMIA OF CHRONIC KIDNEY
DISEASE
• A direct correlation between eGFR and
hematocrit has been demonstrated with a
3.1% decrease in hematocrit for every 10
mL/minute/1.73m2 decline in eGFR
• A higher prevalence of anemia occurs in the
population with an eGFR <60 mL/minute/1.73
m2

44. ANEMIA OF CHRONIC KIDNEY
DISEASE
• LVH has been observed in approximately 30%
of patients with eGFR 50 to 75
mL/minute/1.73m2 (stages 2 and 3 CKD) and
in up to 74% of patients at the start of dialysis
(stage 5 CKD)

45. ANEMIA OF CHRONIC KIDNEY
DISEASE
• A more complete workup for anemia of CKD is
recommended for patients with an eGFR of
<60 mL/minute/1.73 m2
• This workup includes monitoring of
hemoglobin and hematocrit, assessment of
iron indices with correction if iron deficiency is
present, and evaluation for sources of blood
loss, such as bleeding from the GI tract

46. ANEMIA OF CHRONIC KIDNEY
DISEASE
• Identification and management of iron
deficiency through regular follow-up testing
and iron supplementation is essential for
adequate RBC production

47. Other factors contribute to Anemia
• Shortened RBC life span secondary to uremia
• Blood loss from frequent phlebotomy and HD
• GI bleeding
• Severe hyperparathyroidism
• Protein malnutrition
• Accumulation of aluminum
• Severe infections and
• Inflammatory conditions

48. Goals of Therapy
• NKF-K/DOQI guidelines recommend a target
of ≥11 g/dL for hemoglobin (≥33% for
hematocrit) in patients with CKD receiving ESA
therapy
• Because iron deficiency is the primary cause
of ESAhyporesponsiveness, assessment of iron
status is essential before initiating
erythropoietic therapy

49. Iron status
• The two tests that best evaluate iron status
are the transferrin saturation percent (TSAT), a
measure of iron immediately available for
erythropoiesis, and serum ferritin, a measure
of storage iron

50. TSAT determination

51. Interpretation
• The goal of iron replacement therapy is to maintain the
TSAT >20% and a serum ferritin >100 ng/mL for CKD
stages 2 through 4 and >200 ng/mL for CKD stage 5 to
provide sufficient iron for erythrocyte production
• Values below these targets are indicative of absolute
iron deficiency
• A functional iron deficiency may exist when ferritin is
>500 ng/mL, TSAT is <20%, and anemia persists despite
appropriate ESA therapy. In these cases, iron
supplementation may lead to improved erythropoiesis

52. Iron therapy
• Administration of IV iron requires IV access
and frequent outpatient visits, which are
drawbacks to therapy with IV iron in CKD stage
3 and 4
• A recent trial examined an accelerated dosing
regimen (500 mg given on two consecutive
days) of IV iron sucrose to address these
issues

54. Common infusion-related effects
• Hypotension
• Myalgias
• Arthralgias

55. Potential Drug-drug interactions – oral
iron
• Antacids
• Quinolones

56. IV Iron
• The IV iron preparations currently available are
iron dextran (In- FeD, DexFerrum), sodium ferric
gluconate complex in sucrose (Ferrlecit), and iron
sucrose (Venofer)
• The dextran products have caused anaphylactic
reactions and, as a result, have a FDA mandated
black box warning that requires administration of
a 25 mg test dose followed by a 1-hour
observation period before the total dose of iron is
infused

57. Dosing
• The dose of IV iron recommended to correct absolute
iron deficiency is a total dose of 1 g administered in
divided doses or over a prolonged period to minimize
the risk of adverse effects
• For iron dextran, the approved dose is 100 mg
increments, administered over 10 dialysis sessions for
patients on HD to provide a total of 1 g
• Larger doses of 500 mg up to the total 1-g dose have
been safely administered over a longer infusion period
of 4 to 6 hours

58. Iron salts
• Sodium ferric gluconate and iron sucrose are
the most widely used iron products in the CKD
population

59. Newer agent
• Ferumoxytol, a semisynthetic carbohyrdrate-coated, magnetic
iron oxide preparation, is in phase III clinical trials for use in
patients with CKD requiring iron supplementation
• A potential advantage of ferumoxytol is that higher doses can
be safely administered over a shorter period (17 seconds)
• There is also a proposed reduced immunologic sensitivity,
resulting in less risk for anaphylactic type reactions compared
with the other available high molecular weight IV iron
products (e.g., iron dextran)

60. Role of other vitamin
supplemenatation
• Low serum folate concentrations and
macrocytosis, is relatively uncommon in
patients with early kidney disease, but occurs
most often in patients on dialysis, because
folic acid is removed by dialysis
• Therefore, the daily prophylactic
administration of the water-soluble vitamins,
including 1 mg of folic acid, is recommended

61. Role of other vitamin
supplemenatation
• Routine use of the fat-soluble vitamin A is
discouraged, because hypervitaminosis A may
develop, contributing to anemia
• Several multivitamin preparations devoid of
vitamin A (e.g., Nephrocaps) are available for
patients with kidney failure

62. Role of other vitamin
supplemenatation
• Pyridoxine (vitamin B6) deficiency can also occur
in both dialyzed and nondialyzed patients with
CKD. Significant similarities are seen between this
deficiency and the symptoms of uremia, which
include skin hyperpigmentation and peripheral
neuropathy
• Current multivitamin products for patients with
stage 5 CKD contain adequate amounts of
pyridoxine to prevent deficiency

63. ESA Therapy
• Human erythropoietin or epoetin, the
exogenous form of EPO, is produced using
recombinant technology
• Epoetin alfa stimulates the proliferation and
differentiation of erythroid progenitor cells,
increases hemoglobin synthesis, and
accelerates the release of reticulocytes from
the bone marrow

64. ESA Therapy
• According to the NKF-K/DOQI guidelines for
anemia management, SC administration is
preferred because lower doses can be
administered less frequently and cost is lower
than with IV administration

65. ESA Therapy - Dosing
• Starting doses for SC administration are 80 to 120
U/kg/wk (∼6,000 U/wk), whereas IV starting
doses are 120 to 180 U/kg/wk (∼9,000 U/wk)
• Based on the half-life of epoetin alfa (8.5 hours
IV, 24.4 hours SC), the total weekly dose is usually
divided into smaller doses, administered one to
three times per week with SC administration and
three times per week for IV administration in
patients on HD

66. ESA Therapy - Dosing
• For patients being converted from IV to SC
administration whose hemoglobin is within
the target range, the SC dose is usually two-
thirds the IV dose
• For patients not yet at the target hemoglobin,
a SC dose equivalent to the IV dose is
recommended

67. ESA Therapy – Practice points
• Patients receiving epoetin alfa SC should be
instructed on the appropriate administration
technique, which includes rotating the sites
for injection (e.g., upper arm, thigh, abdomen)

68. ESA Therapy – Extended therapy
• Extended dosing intervals for SC
administration of epoetin alfa have been
evaluated in patients with CKD who are not
having dialysis
• Doses of 10,000 U once weekly to 40,000 U
once every 4 weeks have been shown to
maintain target hemoglobin values for those
patients with CKD not on dialysis

69. DARBEPOETIN ALFA
• Darbepoetin alfa’s longer half-life relative to
epoetin alfa offers the potential advantage of
less frequent dosing to maintain target
hemoglobin values

70. Dosing
• Studies in patients with early CKD (stages 3
and 4) determined that starting SC doses of
0.45 mcg/kg administered once per week and
0.75 mcg/kg once every other week were
effective in achieving target hemoglobin and
hematocrit values in patients who had not
previously received erythropoietic therapy

71. Epoietin to Darbepoetin conversion
• In patients on dialysis converted from epoetin
alfa to darbepoetin alfa (IV and SC),
darbepoetin maintained target hemoglobin
values when administered less frequently (i.e.,
one dose every week in patients previously
receiving epoetin alfa three times per week
and one dose every other week in patients
previously receiving epoetin once weekly)

72. Epoietin to Darbepoetin conversion
• The approved starting dose of darbepoetin
alfa in patient who have not previously
received epoetin therapy is 0.45 mcg/kg given
either IV or SC once weekly
• Patients who are already receiving epoetin
therapy may be converted to darbepoetin alfa
based on the current total weekly epoetin
dose

74. Therapy related problems
• Hypertension (most common)
• Failure to elicit a response to erythropoietic
therapy requires evaluation of factors that
cause resistance, such as iron deficiency,
infection, inflammation, chronic blood loss,
aluminum toxicity, malnutrition, and
hyperparathyroidism

75. Therapy related problems
• Resistance to erythropoietic therapy has been
observed in patients receiving ACE inhibitors,
although data are conflicting
• Rare cases of antibody formation to epoetin
therapy have been reported

76. CONTINUOUS ERYTHROPOIETIN
RECEPTOR ACTIVATOR (CERA)
• Continuous erythropoietin receptor activator
(Mircera) has completed phase III of its clinical
development program and has received an
approval letter from the FDAfor use in patients
withCKDwith anemia
• CERA is twice the molecularweight of EPO
because of the addition of a single 30-kd polymer
chain into the erythropoietin molecule resulting
in a considerably longer elimination half-life
compared with EPO (130 hours vs. 4–28 hours).

77. CONTINUOUS ERYTHROPOIETIN
RECEPTOR ACTIVATOR (CERA)
• This allows for extended interval dosing of
biweekly and once monthly
• It has an efficacy and safety profile
comparable to available ESA. The approved
dosing of CERA is pending the release of the
FDA-approved package insert

78. SECONDARY HYPERPARATHYROIDISM AND
RENAL OSTEODYSTROPHY
• Renal osteodystrophy (ROD) is the term used
to describe the skeletal manifestations that
occur as kidney function declines
• Collectively, ROD refers to specific bone
abnormalities that include osteitis fibrosa
(most common pattern), osteomalacia,
osteosclerosis, and osteopenia

79. SECONDARY HYPERPARATHYROIDISM AND
RENAL OSTEODYSTROPHY
• Hyperphosphatemia, hypocalcemia,
hyperparathyroidism, decreased production of
active vitamin D, and resistance to vitamin D
therapy are all frequent problems in CKD that
can lead to the secondary complication of
ROD

80. SECONDARY HYPERPARATHYROIDISM AND
RENAL OSTEODYSTROPHY
• The chronic effects of hyperparathyroidism on
the skeleton lead to bone pain, fractures, and
myopathy
• In children, these effects may be particularly
severe and usually retard growth
• The metabolic acidosis of kidney disease also
contributes to a negative calcium balance in the
bone

81. Dietary Restriction of Phosphorus
• During the early stages of kidney disease (eGFR
<60 mL/minute/1.73 m2), dietary phosphorus
should be reduced to 800 to 1,000 mg/day
(∼60% of normal) through restriction of meat,
milk, legumes, and carbonated beverages to
achieve normal phosphorus concentrations
• Patients requiring dialysis have less dietary
phosphorus restriction with a recommended
phosphorus intake of approximately 800 to 1,200
mg/day

82. Phosphate-Binding Agents
• Phosphate-binding agents limit phosphorus
absorption from the GI tract by binding with the
phosphorus present from dietary sources
• Therefore, these agents must be administered
with meals
• Available binders include products that contain
calcium, lanthanum, aluminum, or magnesium
cations or the polymer-based agent, sevelamer
hydrochloride (Renagel)

83. Calcium containing Agents
• Calcium carbonate and calcium acetate
• Compared with calcium carbonate, calcium
acetate binds about twice the amount of
phosphorus for the same amount of calcium
salts
• Ca. Citrate – Not recommanded in CKD

84. Calcium containing Agents – Equations
for dosing adjustmnet

85. Calcium containing Agents – Practice
Points
• Nausea, diarrhea, and constipation – common
SEs
• Intercations with FQs and oral iron
• If the calcium products are being used as
supplementation to treat hypocalcemia or
osteoporosis, they should be taken between
meals to enhance intestinal absorption

86. Non Calcium based phospherus
binders
• Sevelamer
• Lanthanum carbonate
• Aluminum, or magnesium preparations

87. Sevelamer
• Now considered a first-line agent in patients with
stage 5CKD
• Also lowers LDL and total serum cholesterol
• Coadministration of calcium (900 mg/day
elemental calcium) with sevelamer resulted in
greater decreases in both phosphorus and PTH
than either agent alone without significant
increases in serum calcium

88. Sevelamer - Dosing
• Sevelamer is available as a 403 mg capsule
and as 400-mg and 800-mg tablets
• The starting dose is variable and depends on
the baseline serum phosphorus concentration
(800 mg TID with meals if serum phosphorus
is <7.5 mg/dL; 1,600 mg TID with meals if
serum phosphorus is >7.5 mg/dL)

89. Sevelamer - Dosing
• Based on studies showing similar reductions in
serum phosphorus, 800 mg of sevelamer is
considered equivalent to 667 mg of calcium
acetate (169 mg elemental calcium)

90. LANTHANUM CARBONATE
• Lanthanum is supplied as chewable tablets for
oral administration in four strengths: 250, 500,
750, and 1,000 mg
• The recommended initial total daily dose is 750
to 1,500 mg given with meals and dosage
titration up to a maximal dosage of 3,000 mg
daily should be based on serum phosphate levels
• The most frequent adverse events reported in
clinical trials are nausea and vomiting

91. Less common Agents
• Aluminum–phosphate complex
• Magnesium hydroxide
• Magnesium carbonate

93. Vitamin D
• Calcitriol is available as an oral formulation
(Rocaltrol) or IV formulation (Calcijex).
Administration of calcitriol by either the oral
or IV route may be based on conventional
dosing (usually 0.25–0.5 mcg/day) or pulse
dosing (intermittent dosing of 0.5 to 2.0 mcg
two to three times per week)

94. Vitamin D
• Higher doses (e.g., 4 mcg three times per
week) are generally required to reduce PTH
secretion in more severe sHPT (PTH >1,000
pg/mL)

95. VITAMIN D ANALOGS
• Currently approved agents for managing sHPT
in the United States are paricalcitol (Zemplar),
also referred to as 19-nor-1,25-
dihydroxyvitamin D2, and
• Doxercalciferol (Hectorol), or 1-α-
hydroxyvitamin D2. Doxercalciferol requires
conversion to the active form (1-α-,25-
dihydroxyvitamin D2) by the liver

96. Gastrointestinal Complications
• Gastrointestinal abnormalities are extremely
common in patients with CKD and include
anorexia, nausea, vomiting, hiccups,
abdominal pain, GI bleeding, diarrhea, and
constipation
• Metoclopramide (lower dose 5 mg, caution for
extrapyramidal side effects)

97. Gastrointestinal Complications
• Cisapride (Propulsid), a prokinetic agent that has
restricted access, is contraindicated in patients
with kidney disease because its use is associated
with the development of arrhythmias in this
population
• Drug-induced nausea and vomiting always should
be considered, because patients with CKD often
take multiple drugs and are at risk for drug
toxicity because of diminished kidney function
(e.g., digitalis intoxication).

98. Neurologic Complications
• Due to PTH and uremic toxins
• PTH may enhance the entry of calcium into
the brain and peripheral nerves
• Treatment: TCA, Anticonvulsants

99. Dermatologic Complications
• Several dermal abnormalities have been
observed in patients with CKD, including
hyperpigmentation, abnormal perspiration,
skin dryness, and persistent pruritus
• Of these, uremic pruritus can be the most
bothersome for the patient and may lead to
repeated scratching and skin excoriation

100. Dermatologic Complications
• Oral antihistamines (e.g., hydroxyzine)
• 2nd line: Cholestyramine, ultraviolet B (UVB)
phototherapy, and oral administration of
activated charcoal

101. THANK U !!