Chronic kidney disease diagnosis etiology and management

2. Chronic Kidney Disease
DEFINIATIONS
PATHOGENESIS
CAUSES
CLINICAL FEAURES
DIAGNOSIS
COMPLICATIONS
TREATMENT

3. Definitations
 CKD is defined by the presence of kidney
damage or decreased kidney function for three
or more months, irrespective of the cause
 persistence of the damage or decreased function
for at least three months is necessary to
distinguish CKD from acute kidney disease.

4.  Kidney damage refers to pathologic
abnormalities, whether established via kidney
biopsy or imaging studies, or inferred from
markers such as urinary sediment
abnormalities or increased rates of urinary
albumin excretion.
 Decreased kidney function refers to a
decreased glomerular filtration rate (GFR),
which is usually estimated (eGFR) using
serum creatinine and one of several available
equations

5.  end-stage renal disease or stage 5 CKD
represents a stage of CKD where the
accumulation of toxins, fluid, and
electrolytes normally excreted by the
kidneys leads to death unless the
toxins are removed by renal
replacement therapy, using dialysis or
kidney transplantation

6. Pathogenesis
 two broad sets of mechanisms of damage:
1. Initiating mechanisms specific to the underlying
etiology (e.g., abnormalities in kidney development
or integrity, immune complex deposition and
inflammation in certain types of glomerulonephritis,
or toxin exposure in certain diseases of the renal
tubules and interstitium)
2. Hyperfiltration and hypertrophy of the remaining
viable nephrons, that are a common consequence
following long-term reduction of renal mass,
irrespective of underlying etiology and lead to further
decline in kidney function

8. CKD Risk Factors
 small for gestation
birth weight
 Childhood obesity
 Hypertension
 Diabetes mellitus
 autoimmune disease
 advanced age
 African ancestry
 a family history of
kidney disease
 a previous episode of
acute kidney injury
 presence of
proteinuria
 abnormal urinary
sediment
 Structural
abnormalities of the
urinary tract

9.  Malignancy
 Family History
 Infections like Hep C and HIV
 Nephrotoxics like NSAID
 Metabolic Syndromes
 Cardiovascular disease
 Autosomal Dominant Polycytsic Kideny
disease

10. CKD Risk Factors*
Modifiable
 Diabetes
 Hypertension
 History of AKI
 Frequent NSAID
use
Non-Modifiable
• Family history of kidney
disease, diabetes, or
hypertension
• Age 60 or older (GFR
declines normally with
age)
• Race/U.S. ethnic
minority status
*Partial list
AKI, acute kidney injury

11. ESRD, end stage renal disease
USRDS ADR, 2007
Diabetes and hypertension are
leading causes of kidney failure
Incident ESRD rates, by primary diagnosis, adjusted for age, gender, & race.

12. CKD as a Public Health Issue
 26 million American affected
 Prevalence is 11-13% of adult population in the US
 28% of Medicare budget in 2013, up from 6.9% in 1993
 $42 billion in 2013
 Increases risk for all-cause mortality, CV mortality, kidney
failure (ESRD), and other adverse outcomes.
 6 fold increase in mortality rate with DM + CKD
 Disproportionately affects African Americans and Hispanics
1. NKF Fact Sheets.
http://www.kidney.org/news/newsroom/factsheets/FastFa
cts. Accessed Nov 5, 2014.
2. USRDS. www.usrds.org. Accessed Nov 5, 2014.
3. Coresh et al. JAMA. 2007. 298:2038-2047.
ESRD, end stage renal disease

13. Leading Causes of CKD

14. Causes of CKD

16. Criteria for CKD
 Abnormalities of kidney structure or function,
present for >3 months, with implications for
health
 Either of the following must be present for >3
months:
 ACR >30 mg/g
 Markers of kidney damage (one or more*)
 GFR <60 mL/min/1.73 m2
*Markers of kidney damage can include nephrotic syndrome, nephritic syndrome, tubular
syndromes, urinary tract symptoms, asymptomatic urinalysis abnormalities, asymptomatic
radiologic abnormalities, hypertension due to kidney disease.m²

17. Old Classification of CKD as Defined by Kidney Disease Outcomes
Quality Initiative (KDOQI) Modified and Endorsed by KDIGO
Note: GFR is given in mL/min/1.732 m²
National Kidney Foundation. KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification, and Stratification. Am J Kidney Dis 2002;39(suppl 1):S1-S266
Stage Description Classification
by Severity
Classification
by Treatment
1 Kidney damage with
normal or increased GFR
GFR ≥ 90
2 Kidney damage with
mild decrease in GFR
GFR of 60-89 T if kidney
transplant
3 Moderate decrease in GFR GFR of 30-59 recipient
4 Severe decrease in GFR GFR of 15-29 D if dialysis
5 Kidney failure GFR < 15 D if dialysis
KDIGO, Kidney
Disease: Increasing
Global Outcomes

19. Classification of CKD Based on GFR and
Albuminuria Categories: “Heat Map”

20. Calculations
 Cockcroft-Gault
 Men:CrCl (mL/min) = (140 - age) x wt (kg)
 SCr x 0.81
 Women: multiply by 0.85
 MDRD
 GFR (mL/min per 1.73 m2) = 186 x (SCr x
0.0113)-1.154 x (age)-0.203 x (0.742 if female) x
(1.12 if African-American)

21. Signs & Symptoms
 General
 Fatigue & malaise
 Edema
 Ophthalmologic
 AV nicking
 Cardiac
 HTN
 Heart failure
 Pericarditis
 CAD
 GI
 Anorexia
 Nausea/vomiting
 Dysgeusia
 Skin
 Pruritis
 Pallor
 Neurological
 MS changes
 Seizures

24. Clinical Manifestations
 Stages 1–4 CKD are asymptomatic.
 Symptoms develop slowly with the
progressive decline in GFR, are nonspecific,
and do not manifest until kidney disease is
far advanced (GFR less than 5–10
mL/min/1.73 m2).
 Uremic syndrome.
 Fatigue
 anorexia, nausea
 a metallic taste in the mouth.

25.  Neurologic symptoms such as irritability,
memory impairment, insomnia, restless legs,
paresthesias, and twitching may be due to
uremia.
 Generalized pruritus (without rash)
 decreased libido and menstrual irregularities
 Pericarditis
 Pleuritic chest pain

26. Common physical findings
 Hypertension
 volume overload.
 Uremic signs:
 seen with a profound decrease in GFR (less
than 5–10 mL/min/1.73 m2)
 generally sallow and ill appearance
 halitosis (uremic fetor)
 the uremic encepholopathic signs of
decreased mental status, asterixis,
myoclonus, and possibly seizures

27. Asterixis, Flapping Tremor

29. Lab Findings
 abnormal GFR persisting for at least 3
months.
 Persistent proteinuria or abnormalities
 renal imaging (eg, polycystic kidneys or a
single kidney) are also diagnostic of CKD,
even when eGFR is normal
 Anemia, hyperphosphatemia, hypocalcemia,
 hyperkalemia, and metabolic acidosis

30.  urinary sediment: show broad waxy casts
 dilated,hypertrophic nephrons.
 Proteinuria may be present.
 Quantification of urinary protein is important for
several reasons.
 First, it helps narrow the differential diagnosis of
the etiology of the CKD
 Second, the presence of proteinuria is associated
with more rapid progression of CKD and with
increased risk of cardiovascular mortality

31. Imaging
 small, echogenic kidneys bilaterally (less than
9–10 cm) by ultrasonography
 suggests the chronic scarring of advanced CKD.

32.  Large kidneys:
 adult polycystic kidney disease,
 diabetic nephropathy
 HIV associated
 nephropathy
 plasma cell myeloma
 amyloidosis
 Obstructive uropathy

33. Complications
• CARDIAC
• BONE AND MINERALS
• HEMATOLOGIC
• HYPERKALEMIA
• ACID-BASE DISORDERS
• NEUROLOGIC
• ENDOCRINE

34. Cardiac Complications
 HTN
 CAD
 HF
 Afib
 Pericarditis

35. HTN in CKD
 most common complication of CKD;
 progressive and salt-sensitive
 control of hypertension should focus on both
pharmacologic and nonpharmacologic
therapy (eg, diet, exercise, weight loss,
treatment of obstructive sleep apnea)
 low salt diet (2 g/day)
 Diuretics needed to control HTN
 Initial drug therapy for proteinuric patients
should include ACE inhibitors or ARBs

36. HTN in CKD
 ACEi and ARB
 patients must have serum creatinine and potassium
checked within 7–14 days.
 A rise in serum creatinine greater than 30% from baseline
mandates reduction or cessation of the drug
 should not be used in combination
 BP Goal 130/80

37. CAD
 higher risk for death from CVD than the
general population.
 Traditional modifiable risk factors for CVD,
such as hypertension, tobacco use, and
hyperlipidemia, should be aggressively
treated in patients with CKD.
 Uremic vascular calcification involving
disordered phosphorus homeostasis and
other mediators may also be a cardiovascular
risk factor in these patients

38. Atrial Fibrillation
 20% prevalence in patients receiving
dialysis.
 Rate and rhythm management should
be addressed.

39. Heart Failure
 due to hypertension, volume overload, and
anemia
 accelerated rates of atherosclerosis and
vascular calcification resulting in vessel
stiffness
 LVH and HFpEF
 Diuretics and Salt Restriction
 ACE inhibitors and ARBs can be used for
patients with advanced CKD with close
monitoring of blood pressure as well as for
hyperkalemia and worsening kidney function

40. Pericarditis
 uremic patients;
 typical Findings :pleuritic chest pain and a friction
rub.
 significant pericardial effusion may result in
pulsus paradoxus, an enlarged cardiac silhouette
on chest radiograph, and low QRS voltage and
electrical alternans on ECG.
 The effusion is generally hemorrhagic, and
anticoagulants should be avoided if this diagnosis
is suspected.
 Cardiac tamponade can occur; therefore, uremic
pericarditis is a mandatory indication for
hospitalization and initiation of hemodialysis

41. Disorders of Mineral
Metabolism
 metabolic bone disease of CKD refers
to the complex disturbances of calcium
and phosphorus metabolism,
parathyroid hormone (PTH), active
vitamin D, and fibroblast growth factor-
23 (FGF-23) homeostasis

42.  typical pattern seen as early as
CKD stage 3 is
hyperphosphatemia,
hypocalcemia, and
hypovitaminosis D, resulting in
secondary hyperparathyroidism

44.  Bone disease, or renal osteodystrophy, in
advanced CKD is common and there are
several types of lesions. Renal osteodystrophy
can be diagnosed only by bone biopsy, which
is rarely done. The most common bone
disease, osteitis fibrosa cystica, is a result of
secondary hyperparathyroidism and th
osteoclast stimulating effects of PTH
 high-turnover disease with bone resorption and
subperiosteal lesions; it can result in bone pain and
proximal muscle weakness

45.  Adynamic bone disease, or low-bone
turnover, is becoming more common; it may
result iatrogenically from suppression of PTH
or via spontaneously low PTH production
 Osteomalacia is characterized by lack of bone
mineralization
 treatment may involve correction of calcium,
phosphorus, and 25-OH vitamin D levels
toward normal values, and mitigation of
hyperparathyroidism

46.  Declining GFR leads to phosphorus retention.
This results in hypocalcemia as phosphorus
complexes with calcium, deposits in soft
tissues, and stimulates PTH. Loss of renal
mass and low 25-OH vitamin D levels often
seen in CKD patients result in low 1,25(OH)
vitamin D production by the kidney. Because
1,25(OH) vitamin D is a suppressor of PTH
production, hypovitaminosis D also leads to
secondary hyperparathyroidism

47.  first step in treatment of metabolic bone
disease is control of hyperphosphatemia
 dietary phosphorus restriction initially (see
section on dietary management
 oral phosphorus binders if targets are not
achieved
 Oral phosphorus binders block absorption of
dietary phosphorus in the gut and are given
thrice daily with meals

48.  Calciumcontaining binders (calcium
carbonate, 650 mg/tablet, or calcium acetate,
667 mg/capsule, used at doses of one to
three pills per meal) are relatively inexpensive
but may contribute to positive calcium
balance and vascular calcification; overt
hypercalcemia may also occur
 current guidelines suggest limiting their use
in favor of the non-calcium–containing
binders sevelamer carbonate (800–3200
mg/meal) and lanthanum carbonate (500–
1000 mg/meal)

49. Phosphate Binders
 Once serum phosphorus levels are controlled,
active vitamin D (1,25[OH] vitamin D, or
calcitriol) or other vitamin D analogs are used
by nephrologists to treat secondary
hyperparathyroidism in advanced CKD and
ESRD.
 Serum 25- OH vitamin D levels should be
measured and brought to normal prior to
considering administration of active vitamin
D

50.  Typical calcitriol dosing is 0.25 or 0.5 mcg
orally daily or every other day. Cinacalcet
targets the calcium-sensing receptors of the
parathyroid gland and suppresses PTH
production.
 Cinacalcet, 30–90 mg orally once a day, can
be used if elevated serum phosphorus or
calcium levels prohibit the use of vitamin D
analogs; cinacalcet can cause serious
hypocalcemia, and patients should be closely
monitored for this complication

51. Hematologic Complications
CKD
ANEMIA
COAGULOPATHY

52. Anemia in CKD
 due to decreased erythropoietin production
 Anemia Of Chronic Disease:
 high levels of hepcidin, which blocks GI iron
absorption and mobilization of iron from body
stores
 thyroid function tests, serum vitamin B12
levels, and iron stores (ferritin and iron
saturation) should be checked
 In CKD, a serum ferritin below 100–200
ng/mL or iron saturation less than 20% is
suggestive of iron deficiency

53.  Iron stores may be repleted with oral or parenteral
iron; iron therapy should probably be withheld if the
serum ferritin is greater than 500–800 ng/mL, even if
the iron saturation is less than 20%.
 Oral therapy with ferrous sulfate, gluconate, or
fumarate, 325 mg once daily, is the initial therapy In
pre-ESRD CKD
 those who do not respond due to poor GI absorption
or lack of tolerance, intravenous iron (eg, iron sucrose
or iron gluconate) may be necessary

54.  Erythropoiesis-stimulating agents (ESAs, eg,
recombinant erythropoietin [epoetin alfa or
beta] and darbepoetin) are used to treat the
anemia of CKD if other treatable causes are
excluded
 starting dose of epoetin alfa is 50 units/kg
(3000–4000 units/dose) once or twice a week,
and darbepoetin is started at 0.45 mcg/kg
and administered every 2–4 weeks; epoetin
beta is given every 2–4 weeks

55. ESAs
 Intravenous
 Subcutaneous darbopoetin
 Hypertension is a common complication of treatment
with ESAs

56. Coagulopathy
 bleeding diathesis that may occur in stage 4–
5 CKD
 is mainly due to platelet dysfunction
 Treatment is required only in patients who are
symptomatic
 Desmopressin (25 mcg intravenously every 8–
12 hours for two doses) is a short-lived but
effective treatment for platelet dysfunction
and it is often used in preparation for surgery
or kidney biopsy
 Dialysis improves the bleeding time

57. Hyperkalemia
 stages 4–5
 Cardiac monitoring is indicated for any ECG
changes seen with hyperkalemia or a serum
potassium level greater than 6.0–6.5 mEq/L or
mmol/L
 Chronic hyperkalemia is best treated with
dietary potassium restriction (2 g/day) and
minimization or elimination of any
medications that may impair renal potassium
excretion
 Diuretics

58. Acid Base Disorders
 Damaged kidneys are unable to excrete the 1
mEq/kg/day of acid generated by metabolism of
dietary animal proteins in the typical Western diet
 Metabolic Acidosis
 Decreased GFR
 proximal or distal tubular defects may contribute
to or worsen the acidosis
 Excess hydrogen ions are buffered by bone; the
consequent leaching of calcium and phosphorus
from the bone contributes to the metabolic bone
disease

59.  Chronic acidosis can also result in muscle
protein catabolism as well as growth
retardation in children with CKD and may
accelerate progression of CKD
 Reduction of dietary animal protein and
increased fruit and vegetable intake, and the
administration of oral sodium bicarbonate (in
doses of 0.5–1.0 mEq/kg/day divided twice
daily and titrated as needed) are strategies to
bring serum bicarbonate levels toward
normal

60. Neurologic Complications
 Uremic encephalopathy does not occur until GFR
falls below 5–10 mL/min/1.73 m2
 Symptoms begin with difficulty in concentrating
and can progress to lethargy, confusion, seizure,
and coma.
 Physical findings may include altered mental
status, weakness, and asterixis. These findings
improve with dialysis
 peripheral neuropathies (stocking-glove or
isolated mononeuropathies), erectile dysfunction,
autonomic dysfunction, and restless leg syndrome
 These may not improve with dialysis therapy

61. Endocrine Complicaions
 Decreased renal elimination of insulin in advanced
CKD confers risk for hypoglycemia in treated diabetic
patients
 Doses of oral hypoglycemics and insulin may need
reduction. The risk of lactic acidosis with metformin is
due to both dose and eGFR; it should be discontinued
when eGFR is less than 30 mL/min/1.73 m2
 Decreased libido and erectile dysfunction are common

62.  Men have decreased testosterone levels;
women are often anovulatory.
 Women with serum creatinine less than 1.4
mg/dL are not at increased risk for poor
outcomes in pregnancy; however, those with
serum creatinine greater than 1.4 mg/dL may
experience faster progression of CKD with
pregnancy
 pregnancy can occur in this setting; however,
fetal mortality approaches 50%, and babies
who survive are often premature

63. Treatment
SLOWING PROGRESSION
DIETARY MODIFICATION
MEDICAL MANAGEMENT
MANAGEMENT OF ESRD

64. Slowing the Progress
 Treat underlying cause CKD
 Control of diabetes should be aggressive in early CKD
 Blood pressure control is vital to slow progression of
all forms of CKD;
 agents that block the renin-angiotensin-aldosterone
system are particularly important in proteinuric
patients.
 Obese patients :lose weight.
 Risks for AKI should be minimized or avoided.
 treatment of metabolic acidosis and of hyperuricemia

65. Goals of Care in CKD
 Slow decline in kidney function
 Blood pressure control1
 ACR <30 mg/g: ≤140/90 mm Hg
 ACR 30-300 mg/g: ≤130/80 mm Hg*
 ACR >300 mg/g: ≤130/80 mm Hg
 Individualize targets and agents according to age,
coexistent CVD, and other comorbidities
 ACE or ARB
*Reasonable to select a goal of 140/90 mm Hg, especially for moderate albuminuria (ACR 30-300 mg/g.)2
1) Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. Kidney Int Suppl.
(2012);2:341-342.
2) KDOQI Commentary on KDIGO Blood Pressure Guidelines. Am J Kidney Dis. 2013;62:201-213.

66. Slowing CKD Progression: ACEi or
ARB
 Risk/benefit should be carefully assessed in the elderly and
medically fragile
 Check labs after initiation
 If less than 25% SCr increase, continue and monitor
 If more than 25% SCr increase, stop ACEi and evaluate for RAS
 Continue until contraindication arises, no absolute eGFR cutoff
 Better proteinuria suppression with low Na diet and diuretics
 Avoid volume depletion
 Avoid ACEi and ARB in combination1,2
 Risk of adverse events (impaired kidney function, hyperkalemia)
1) Kunz R, et al. Ann Intern Med. 2008;148:30-48.
2) Mann J, et al. ONTARGET study. Lancet. 2008;372:547-553.

67. Goals of Care in CKD: Glucose
Control
 Target HbA1c ~7.0%
 Can be extended above 7.0% with comorbidities or
limited life expectancy, and risk of hypoglycemia
 Risk of hypoglycemia increases as kidney function
becomes impaired
 Declining kidney function may necessitate changes to
diabetes medications and renally-cleared drugs
NKF KDOQI. Diabetes and CKD: 2012 Update.
Am J Kidney Dis. 2012 60:850-856.

68. Modification of Other CVD
Risk Factors in CKD
 Smoking cessation
 Exercise
 Weight reduction to optimal targets
 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
Kidney Disease: Improving Global Outcomes
(KDIGO) CKD Work Group. Kidney Int Suppls.
2013;3:1-150.

69. Detect and Manage CKD
Complications
 Anemia
 Initiate iron therapy if TSAT ≤ 30% and ferritin ≤ 500 ng/mL
(IV iron for dialysis, Oral for non-dialysis CKD)
 Individualize erythropoiesis stimulating agent (ESA) therapy:
Start ESA if Hb <10 g/dl, and maintain Hb <11.5 g/dl. Ensure
adequate Fe stores.
 Appropriate iron supplementation is needed for ESA to be
effective
 CKD-Mineral and Bone Disorder (CKD-MBD)
 Treat with D3 as indicated to achieve normal serum levels
 2000 IU po qd is cheaper and better absorbed than 50,000 IU
monthly dose.
 Limit phosphorus in diet (CKD stage 4/5), with emphasis on
decreasing packaged products - Refer to renal RD
 May need phosphate binders

70. Detect and Manage CKD
Complications
• Metabolic acidosis
o Usually occurs later in CKD
o Serum bicarb >22mEq/L
o Correction of metabolic acidosis may slow CKD progression
and improve patients functional status1,2
• Hyperkalemia
o Reduce dietary potassium
o Stop NSAIDs, COX-2 inhibitors, potassium sparing diuretics
(aldactone)
o Stop or reduce beta blockers, ACEi/ARBs
o Avoid salt substitutes that contain potassium
1) Mahajan, et al. Kidney Int. 2010;78:303-309.
2) de Brito-Ashurst I, et al. J Am Soc Nephrol.
2009;20:2075-2084.

71. Dietary Managment
 Salt and water Restriction
 Intake of greater than 3–4 g/day can lead to
hypertension and hypervolemia, whereas intake of
less than 1 g/day can lead to volume depletion and
hypotension. A goal of 2 g/day of sodium is
reasonable for most patients
 Protein Restriction
 Reduced intake of animal protein to 0.6–0.8
g/kg/day may slow CKD progression and is likely
not harmful in the otherwise well-nourished
patient

72.  Potassium Restriction
 Restriction is needed once the GFR has
fallen below 10–20 mL/min/1.73 m2, or
earlier if the patient is hyperkalemic
 should limit their intake to less than 50–60
mEq/day (2 g/day).
 An aggressive bowel regimen should be
instituted for patients with hyperkalemia
(more than two bowel movements daily),
since a higher percentage of potassium is
excreted through the GI tract as GFR
declines

73.  Phosphorus Restriction
 Guidelines suggest lowering elevated serum phosphorus
levels toward normal in all stages of CKD.
 Dietary phosphate restriction to 800–1000 mg/day is the
first step
 Processed foods and cola beverages are often preserved
with highly bioavailable phosphorus and should be
avoided.
 Foods rich in phosphorus such as eggs, dairy products,
nuts, beans, and meat may also need to be limited,
although care must be taken to avoid protein
malnutrition.
 When GFR is less than 20–30 mL/min/1.73 m2, dietary
restriction is rarely sufficient to reach target levels, and
phosphorus binders are usually required

74. Medical Managment
 Dosages of drugs should be adjusted for GFR.
 Insulin doses may need to be decreased
 Magnesium-containing medications, such as
laxatives or antacids, and phosphorus-containing
medicines (eg, cathartics) should be avoided.
 Active morphine metabolites can accumulate in
advanced CKD; this problem is not encountered
with other opioid agents.
 Drugs with potential nephrotoxicity (NSAIDs,
intravenous contrast, as well as others noted in
the Acute Kidney Injury section) should be
avoided

75. Common Medications Requiring
Dose Reduction in CKD
 Allopurinol
 Gabapentin
 CKD 4- Max dose 300mg qd
 CKD 5- Max dose 300mg qod
 Reglan
 Reduce 50% for eGFR< 40
 Can cause irreversible EPS with chronic use
 Narcotics
 Methadone and fentanyl best for ESRD patients
 Lowest risk of toxic metabolites

76. • Renally cleared beta blockers
o Atenolol, bisoprolol, nadolol
• Digoxin
• Some Statins
o Lovastatin, pravastatin, simvastatin. Fluvastatin,
rosuvastatin
• Antimicrobials
o Antifungals, aminoglycosides, Bactrim, Macrobid
• Enoxaparin
• Methotrexate
• Colchicine

77. Treatment of ESRD
• DIALYSIS
• Hemodialysis
• Peritoneal dialysis
• KIDNEY TRANSPLANT
• MEDICAL MANAGMENT

78. Treatment of ESRD
 GFR declines to 5–10 mL/min/1.73 m2,
renal replacement therapy
(hemodialysis, peritoneal dialysis, or
kidney transplantation) is required to
sustain life
 Referral to a nephrologist should take
place in late stage 3 CKD, or when the
GFR is declining rapidly.

79. Dialysis
 should be considered when GFR is near 10
mL/min/1.73 m2
 uremic symptoms are present
 Fluid overload unresponsive to diuresis
 refractory hyperkalemia
 Acidosis pH< 7.1

80. Hemodialysis
 Vascular access : arteriovenous fistula (the
preferred method) or prosthetic graft
 indwelling catheter
 Infection, thrombosis, and aneurysm
formation are complications seen more often
in grafts than fistulas
 Staph Aureus
 three times a week, 3-5 hour
 Home hemodialysis is often performed more
frequently (3–6 days per week for shorter
sessions) and requires a trained helper

81. Peritoneal Dialysis
 peritoneal membrane is the “dialyzer.”
Dialysate is instilled into the peritoneal cavity
through an indwelling catheter; water and
solutes move across the capillary bed that lies
between the visceral and parietal layers of the
membrane into the dialysate during a “dwell.”
After equilibration, the dialysate is drained,
and fresh dialysate is instilled—this is an
“exchange.

82.  Common Complication: Peritonitis
 nausea and vomiting, abdominal pain, diarrhea or
constipation, and fever
 The normally clear dialysate becomes cloudy; and
a diagnostic peritoneal fluid cell count greater
than 100 white blood cells/mcL with a differential
of greater than 50% polymorphonuclear
neutrophils is present
 Staph Aureus and Streptococci and Gram –
 either vancomycin or a first-generation
cephalosporin (cefazolin) plus a third-generation
cephalosporin (ceftazidime)
 Culture Results

83. Kidney Transplantation
 Many patients with ESRD are otherwise
healthy enough to be suitable for
transplantation

84. Medical Managment
 some patients are not candidates for kidney
transplantation and may not benefit from
dialysis
 patients with ESRD who elect not to undergo
dialysis or who withdraw from dialysis,
progressive uremia with gradual suppression
of sensorium results in a painless death
within days to months

85.  Hyperkalemia may intervene with a
fatal cardiac dysrhythmia.
 Diuretics, volume restriction, and
opioids may help decrease the
symptoms of volume overload.
 Involvement of a palliative care team is
essential

86. Prognosis
 most common cause of death is cardiac
disease (more than 50%)
 Others are infection, cerebrovascular disease,
and malignancy.
 Diabetes, advanced age, a low serum
albumin, lower socioeconomic status, and
inadequate dialysis are all significant
predictors of mortality;
 high FGF-23 levels are a marker for mortality
in ESRD

87. When to Refer
 A patient with stage 3–5 CKD should be
referred to a nephrologist for management in
conjunction with the primary care provider.
 A patient with other forms of CKD such as
those with proteinuria greater than 1 g/day
or polycystic kidney disease should be
referred to a nephrologist at earlier stages

88. *Significant albuminuria is defined as ACR ≥300 mg/g (≥30 mg/mmol) or AER ≥300 mg/24 hours, approximately
equivalent to PCR ≥500 mg/g (≥50 mg/mmol) or PER ≥500 mg/24 hours
**Progression of CKD is defined as one or more of the following: 1) A decline in GFR category accompanied by a 25%
or greater drop in eGFR from baseline; and/or 2) rapid progression of CKD defined as a sustained decline in eGFR of more
than 5ml/min/1.73m2/year. KDOQI US Commentary on the 2012 KDIGO Evaluation and Management of CKD
Indications for Referral to Specialist Kidney Care Services
for People with CKD
• Acute kidney injury or abrupt sustained fall in GFR
• GFR <30 ml/min/1.73m
2
(GFR categories G4-G5)
• Persistent albuminuria (ACR > 300 mg/g)*
• Atypical Progression of CKD
**
• Urinary red cell casts, RBC more than 20 per HPF sustained
and not readily explained
• Hypertension refractory to treatment with 4 or more
antihypertensive agents
• Persistent abnormalities of serum potassium
• Recurrent or extensive nephrolithiasis
• Hereditary kidney disease

89. When to Admit
 Admission should be considered for
decompensation of problems related to CKD,
such as worsening of acid-base status,
electrolyte abnormalities, and volume
overload, that cannot be appropriately
treated in the outpatient setting.
 Admission is appropriate when a patient
needs to start dialysis and is not stable for its
outpatient initiation