MEDICINE: Chronic Kidney Disease and Dialysis

Dr. Eslaban 03/30/22 1:30-3:30PM

BLOCK
Group 3: Agsaluna, Fuego, Gavan, Jardeleza, Luis

7.5 Assessor: Gavan

OUTLINE
I. Chronic Kidney Disease
 We must also take note about Cockcroft and
A. Stages of CKD Gault formula because the is the one of the
B. Leading Categories common formula that we use in computing the
C. Risk Factors EGFR or serum creatinine clearance.
D. Pathophysiology
E. Clinical Manifestations
F. Diagnosis
G. Treatment
II. Dialysis
H. Hemodialysis
I. Peritoneal Dialysis
I. CHRONIC KIDNEY DISEASE
CHRONIC KIDNEY DISEASE
 Chronic kidney disease (CKD) encompasses a  The one that we usually use is and is more
spectrum of pathophysiologic processes accurate in estimating the GFR of the patient is
associated with abnormal kidney function and a CKD-EPI.
progressive decline in glomerular filtration rate
(GFR). KDIGO CLASSIFICATION
 The difference between AKI and CKD is the time
of onset. For the AKI it should be acute in onset
just within few hours or days or weeks. if we are
talking about CKD. What is the magic number? It
should be more than 3 months.
 The risk of CKD progression is closely linked to
both the GFR and the amount of albuminuria.
 Progressive long-term reduction of nephron
number and function (> 3 months)  decrease
in GFR
 Irreversible while AKI is reversible kidney
function
 Chronic Renal Failure  process of continuing
irreversible reduction in nephron number
→ Typically corresponds to stages 3-5  The parameters used is GFR and Albumin.
 End stage renal disease  Stage 5 Usually, we don’t have the urine albumin results
 If the patient is already in stage 5, the patient is that is why we use the GFR
already a candidate for maintenance renal
replacement therapy by either dialysis or STAGES OF CKD
transplantation  Stages 1 and 2  asymptomatic
RECOMMENDED EQUATIONS FOR ESTIMATION  Stages 3 and 4  clinical and laboratory
OF GLOMERULAR FILTRATION RATE (GFR) complication appear
USING SERUM CREATININE CONCENTRATION → Patients will start to develop manifestations of
(SCR), AGE, SEX, RACE AND BODY WEIGHT uremia
 Normal annual decline in GFR starting age 20-
30 years of 1 ml/min/1.73m2
 Albuminuria
→ Important tool to monitor nephron injury or the
kidney function of the patient
 GFR depending on the age of the patient you
have to calculate/compute for a decreasing GFR
as the patient ages. The normal annual decline
of GFR starts from 20-30 years old. The normal
GFR below 30 years old 120-125 ml/min/1.73m2

1/8
IDCM-MSM-2023
Notes:
 But if you reach 30 years old, you have to expect
that there is a decline in the GFR of 1
ml/min/1.73m2 per year.
 Base line is 120 and if you are 40 years old,
minus 10 to the baseline, expected GFR of a 40-
year-old person is 110. At 70 years old,
expected GFR is 80 ml/min/1.73m2
FIVE LEADING CATEGORIES OF CKD
 Diabetic Nephropathy
→ Now called ‘Diabetic Kidney Disease’
→ Diabetes is the most common cause of CKD
worldwide
 Glomerulonephritis
 Hypertension-associated CKD (includes vascular
& ischemic disease & primary glomerular
disease with associated
→ Hypertensive nephrosclerosis
→ Hypertension - 2nd most common
 Autosomal dominant polycystic kidney disease
 Other cystic & tubulointerstitial nephropathy
→ Chronic pyelonephritis
→ Stones
→ Chronic obstruction of kidney
 Right now
→ Diabetes and Hypertension - the leading
cause of both CKD and ESRD
 In elderly, hypertension is more common due to
Chronic Renal
→ Ischemia (Renovascular Disease)
→ Vascular system of an elderly patient is not
that good, there is already sclerosis due to
atherosclerosis. This patient will develop
chronic renal hypoperfusion, because of
atherosclerosis of BV, most of the time not
only found in kidney but also other parts of the
body
 Genetics (ADPKD, diabetes, FSGS, essential
HPN, medullary cystic disease)
RISK FACTORS
 Hypertension
 Diabetes Mellitus
 Autoimmune Disease
→ SLE - most common
 Old Age
 African Ancestry
 Family History of Renal Disease
 Previous episode of ARF
 Presence of proteinuria, abnormal urinary
sediment, or structural abnormality of urinary
tract
IDCM-MSM-2023
→ Horseshoe kidney
→ Solitary kidneys
→ Double pelvis
 Small for gestation birth weight and childhood
obesity
PATHOPHYSIOLOGY
 2 Mechanisms involved in the pathophysiology
of CKD:
→ Initiating mechanisms specific to the
underlying etiology (immune complex
deposition and inflammation in certain types of
glomerulonephritis, or toxin exposure.)
→ Progressive mechanism involving
hyperfiltration and hypertrophy of remaining
viable nephrons, a common consequence of
long-term reduction of renal mass.
Why is there a hyper filtration and hypertrophy
of viable nephrons? This is to overcompensate.
Because there is already damage of some
nephrons so these remaining viable nephrons
would compensate by hyperfiltration and
would eventually hypertrophies which is
helpful initially, however in the long rung
hyperfiltration and hypertrophy would lead to
nephrosclerosis.
 Underlying cause --- reduction of renal mass---
ESRD
 Azotemia - retention of waste products (BUN
and Creatinine) but without clinical symptoms
this is more of a laboratory diagnosis
 Uremia - Multiorgan system derangement
associated with clinical manifestations this is
already a clinical diagnosis. This has already a
lot of clinical manifestations that would make you
think that this patient has uremia. There is
already a multi-organ problem in cases of uremia.
Uremia may already be seen in Stages 3, more
so in Stage 5.
CLINICAL MANIFESTATIONS
ELECTROLYTE ABNORMALITIES
 Hyperkalemia - most common
→ Cardiac arrythmia for both hyper and
hypokalemia
→ Hypokalemia may also cause paralysis
 Severe hypocalcemia may lead to seizure and
convulsion
 Hypo and hypernatremia
→ Common manifestation is obtundation
→ The patient’s sensorium is decreased and
sometimes endstage would lead to coma
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Notes:
ACID-BASE ABNORMALITIES
 Metabolic acidosis
FLUID OVERLOAD
 Anemic patient
HYPERTENSION
 Most common complication of CKD & ESRD
→ Major cause of uremia is volume overload
→ Goals of Treatment:
o To slow the progression of CKD
o To prevent extra-renal complication of
HPN
CARDIAC ABNORMALITIES
 It is the leading cause of morbidity and mortality.
 Pericarditis, arrhythmia, accelerated
atherosclerosis. CHF and ischemic CVD
 Cardiovascular complications risk 10-200 fold
depending on the stage of CKD, other risk
factors and comorbid conditions
 Pericarditis is due to retained metabolic toxins
(absolute indication of urgent initiation of dialysis
or intensification of dialysis prescription)
 Accelerated atherosclerosis is due to HPN,
hyperlipidemia, glucose intolerance, chronic
increase of Cardiac output, metabolic vascular &
myocardial calcification (Lifetime Statin Therapy)
 Ischemic cardiovascular disease is due to
occlusive coronary heart, cerebrovascular &
peripheral vascular disease
 Actually, all organs of the body are affected by
uremia. Because this nitrogenous waste product
would accumulate in the blood and all organs in
the body.
HEMATOLOGIC ABNORMALITIES
 Anemia - usually normochromic, normocytic.
Causes of Anemia:
→ Decrease EPO production (main reason)
→ Diminished RBC survival - (Normal is 120
days)
→ GI bleed & other bleeding diathesis due to
prolonged BT, decreased PC, abnormal
platelet aggregation & adhesiveness, impaired
prothrombin consumption
→ Iron deficiency - patient have poor appetite
→ Hyperparathyroidism / bone marrow fibrosis
→ Chronic inflammation - (inc CRP)
→ Folate or Vitamin B12 deficiency
→ Hemoglobinopathy
IDCM-MSM-2023
→ Comorbid conditions
 Changes in leukocyte formation & function,
susceptible to infection (due to acidosis,
hyperglycemia, CHON-calorie malnutrition,
serum/tissue hyperosmolarity due to azotemia)
NEUROMUSCULAR ABNORMALITIES
 Peripheral neuropathy – firm indication to initiate
RRT (renal replacement therapy)
→ Once the patients develop peripheral
neuropathy, you really need to convince the
patient to initiate RRT as soon as possible just
like pericarditis. Although peripheral
neuropathy is not as urgent as pericarditis, but
yet it is already a firm indication to start renal
therapy
 Impaired sensorium
→ Sometimes it will start as insomnia
→ Ask the patient how was his/her sleep
→ The first neurologic abnormality is usually
insomnia
→ Later on, as the disease progresses ten the
sensorium impaired, they would become
lethargic until such time that in the terminal
stages will develop into coma
 Coma in terminal stages
Dialysis complications:
 Dialysis dementia
→ This is usually found who is already on chronic
dialysis for a year
→ Chronic dialysis complication
→ Aluminum intoxication – a major contributor
→ Before, some of the phosphate binders that
were used contains aluminum. But now, this is
seldom seen because we are no longer using
this aluminum compound
 Dialysis disequilibrium syndrome
→ Noted on 1st few dialysis
→ Associated with rapid decrease in BUN
→ We usually prescribe dialysis in a gentle way
during the 1st few sessions even the blood flow
rate is low
GASTROINTESTINAL ABNORMALITIES
 Nausea and vomiting, anorexia, hiccups
 Uremic fetor – uriniferous odor of the breath
associated with unpleasant taste (breakdown of
urea in saliva to NH3)
→ Because the patient has already a lot of urea
in the body
3/8
Notes:
→ Remember that urea is nitrogenous waste
products and they are accumulated inside the
body even in saliva
→ The patient will usually complain having a bad
breath even though their oral hygiene is good
→ Bad breath can only be improved by starting
dialysis
 Uremic gastroenteritis (mucosal ulcerations
brought about by waste products)
NUTRITIONAL ABNORMALITIES
 Protein-energy malnutrition is a consequence of
low protein and caloric intake in CKD patients
→ We have to remember that common
manifestation of uremia is anorexia
→ Most of the time they would not eat, because if
they eat, they would have nausea or vomit
 Indication for initiation of RRT
ENDOCRINE
 Secondary to hyperparathyroidism (due to
increased calcium impaired Vit. D3)
 Abnormal glucose intolerance
 Insulin metabolism
 Nutritional abnormality
→ FEMALE: decrease estrogen, amenorrhea,
abortions
→ MALE: impotence, oligospermia, decrease
testosterone
→ ADOLESCNETS: impaired sexual maturation
DERMATOLOGIC ABNORMALITIES
 Uremic frost – fine white powder found on skin
surface (evaporation of urea in sweat)
→ Uremic frost and uremic fetor – you can see
this when the patient is ABOUT to start
dialysis
 Uremic pruritus – give phosphate binders
→ Because of the accumulation of phosphorous
beneath the skin
 Hemochromatosis – slate-gray-bronze
discoloration of skin
→ Very common in those who receive multiple
blood transfusions
IDCM-MSM-2023
 Nephrogenic fibrosing dermopathy –
progressive subcutaneous induration
prominently seen in the arms and legs
→ Gray nodule-like, very common among
patients who are under dialyzed, mga permi
ga absent, those who have financial problem
BONE MANIFESTATIONS
Classified into:
High bone turnover with elevated PTH level
 Osteitis fibrosa cystica – classic lesion of
secondary hyperparathyroidism
Low bone turnover with low or normal PTH levels
 Adynamic bone disease and Osteomalacia
DIAGNOSIS
 History and PE
 Laboratory Tests
→ CBC
→ Serum electrolytes
→ ABG
→ Uric Acid
→ Creatinine
→ BUN
→ Imaging studies (The most useful imaging
study is renal ultrasound)
→ Renal biopsy
o Renal biopsy reserved for patients with
near normal kidney size and possibility of
reversibility is tenable, and clarification of
underlying disease may alter medication
o Not advised in a patient with bilateral small
kidneys because:
o It is technically difficult and has a
greater likelihood of causing bleeding
and other adverse consequences
o There is usually so much scarring that
the underlying disease may not be
apparent
o The window of opportunity to render
disease-specific therapy has passed.
 Ultrasound-guided percutaneous biopsy
→ Favored approach
 Indications for kidney biopsy
→ Suspicion of concomitant or superimposed
active process such as interstitial nephritis
→ Accelerated loss of GFR
→ Bleeding time should be measured and
desmopressin administered if kidney biopsy is
indicated in a CKD patient
4/8
Notes:
→ Brief run of hemodialysis without heparin may
also be considered prior to renal biopsy to
normalize bleeding time
Contraindications of Kidney Biopsy
 Bilateral small kidneys
 PKD (polycystic kidney disease)
→ induce hemorrhage
 Uncontrolled HPN
 Urinary tract or perinephric infection
 Bleeding diathesis
 Respiratory distress
 Morbid obesity
 Establishing the Diagnosis and Etiology of CKD
→ Most important initial diagnostic step in the
evaluation of a patient presenting with
elevated serum creatinine is to distinguish
newly diagnosed CKD from acute or subacute
renal failure
 Acute
→ If normal values from recent months and even
years
→ If history suggests multiple systemic
manifestations of recent onset (e.g., fever,
polyarthritis, and rash)
 Chronic
→ Elevated serum creatinine concentration in the
past
→ Evidence of metabolic bone disease with
hyperphosphatemia, hypocalcemia, and
elevated PTH
→ Elevated bone alkali phosphatase
→ Normochromic, normocytic anemia
→ Reduced kidney size (<8.5cm)
 Renal biopsy
→ Can be performed in early CKD (Stages 1-3)
 Ischemic Nephropathy
→ Presence of long-standing hypertension
→ Evidence of ischemic disease (cardiac or
peripheral vascular disease)
o Finding of non-nephrotic proteinuria in the
absence of urinary blood or red cell casts
TREATMENT
 Treat the underlying cause
 Diet Modification
→ Protein Restriction ~0.6 g/Kg/day; may retard
progression of renal disease if initiated early
→ Energy Req. is 35 Kcal/Kg/day
→ Low Sodium, Low Purine, Low Potassium (if
hyperkalemic), Low Phosphorus
IDCM-MSM-2023
 Treat anemia – ESA (erythropoietin stimulating
agent)
→ target is hemoglobin of 100-115 g/L
 Hypertension control
 Correction of electrolytes and acid-base
disorders (start sodium bicarbonate when
bicarbonate level falls below 20-23 mmol/L
 Renal Replacement Therapy –
dialysis/transplant
SLOWING THE PROGRESSION OF CKD
 Following interventions should be considered in
an effort to stabilize or slow the decline of renal
function
 Reducing intraglomerular hypertension and
proteinuria
TREATMENT FOR SLOWING THE PROGRESSION
OF CKD
 Antihypertensive therapy
→ 125/75 mmHg target blood pressure in
proteinuric CKD patients
→ ACE inhibitors and ARBs
→ Calcium channel blockers
→ Diltiazem
SLOWING PROGRESSION OF DIABETIC RENAL
DISEASE
 Diabetic nephropathy is now the leading cause
of CKD requiring renal replacement therapy in
many parts of the world.
Control of Blood Glucose
 Target pre-prandial glucose: 5.0—7.2 mmol/L
(90-130 mg/dl)
 Target HbA1c: <7%
Control of Blood Pressure and Proteinuria
 Microalbuminuria precedes the decline in GFR
and heralds renal and cardiovascular
complications
 Testing for microalbumin is recommended in all
diabetic patients
 Antihypertensive agents reduce albuminuria and
diminishes its progression even in normotensive
diabetic patients
Protein Restriction
 Slows the rate of renal decline at earlier stages
of renal disease protein-mediated
hyperfiltration contributes to ongoing decline in
renal function in many different forms of renal
disease
5/8
Notes:
 Daily protein intake of between 0.60 and 0.75
g/kg per ay
 At least 50% of the protein intake be of high
biologic value
 0.9 g/kg per day might be recommended
 Sufficient energy intake to prevent protein-
calorie malnutrition
 35kcal/kg is recommended
CRITERIA FOR INITIATING PATIENTS ON
MAINTENANCE DIALYSIS
 Uremia
 Intractable Hyperkalemia
 Persistent ECF volume expansion despite
diuretic therapy
 Acidosis refractory to medical therapy
 Bleeding Diathesis
 Creatinine Clearance or GFR <10 ml/min/1.72m2
II. DIALYSIS
DIALYSIS
 Indicated for both ARF & CKD
 Hemodialysis / peritoneal dialysis / CRRT / Slow
Low-Efficiency Dialysis
 CRRT & SLED are specific for the management
of AKI
 CRRT is done continuously
 SLED is done for over 6-12 hours
 Hemodialysis is done for 3-4 hours
 Peritoneal dialysis (CAPD or CCPD)
 The decision to initiate dialysis usually depends
on a combination of the PX’s symptoms,
comorbid conditions, and laboratory parameters.
 Unless a living donor is identified, transplantation
is deferred by necessity, due to the scarcity of
cadaveric donor organs (median waiting time, 3–
6 years at most transplant centers).
 Dialytic options include hemodialysis and
peritoneal dialysis (PD)
HEMODIALYSIS
 Employs a process of diffusion across a
semipermeable membrane to remove unwanted
substances from the blood while adding
desirable components
 (-) hydrostatic pressure on the dialysis side for
fluid removal (ultrafiltration)
 Most patients require 9-12 hours/week
 BFR ranges from 250-500 ml/minute- vol of
heparinized blood filtered in dialyzer per unit
of time.
IDCM-MSM-2023
 Dialysate flows in an opposite counter-current
direction at 500–800 mL/min
 Hemodialysis requires direct access to the
circulation, either via a native arteriovenous
fistula (the preferred method of vascular access),
usually at the wrist (a “Brescia-Cimino” fistula);
an arteriovenous graft, usually made of
polytetrafluoroethylene; a large-bore intravenous
catheter; or a subcutaneous device attached to
intravascular catheters.
• Blood is pumped though hollow fibers of an
artificial kidney (the “dialyzer”) and bathed with a
solution of favorable chemical composition
(isotonic, free of urea and other nitrogenous
compounds, and generally low in potassium).
THREE ESSENTIAL COMPONENTS
TO HEMODIALYSIS
Dialyzer
 Is a plastic chamber with the ability to perfuse
blood and dialysate compartments
simultaneously at very high flow rates
Dialysate
 The potassium concentration of dialysate may
be varied from 0 to 4 mmol/L depending on the
predialysis serum potassium concentration.
 The usual dialysate calcium concentration is
1.25 mmol/L (2.5 mEq/L).
 The usual dialysate sodium concentration is
136–140 mmol/L.
Blood Delivery System
 Composed of the extracorporeal circuit and the
dialysis access.
 Most patients undergo dialysis thrice weekly,
usually for 3–4h.
 The efficiency of dialysis is largely dependent on:
→ Duration of dialysis,
→ Blood flow rate,
→ Dialysate flow rate, and;
→ Surface area of the dialyzer
DIALYSIS ACCESS:
FISTULA, GRAFT, CATHETER
 FISTULAS have the highest long-term patency
rate (Permanent access)
 GRAFTS & CATHETERS are used among
persons with smaller caliber veins
 Urea Clearance Rate ranges from 200-350
ml/minute
 Dose of hemodialysis depends on:
→ Patient size
→ Residual renal function
6/8
Notes:
→ Dietary protein intake
o Inc in CHON intake = Inc. Creatinine
→ Degree of anabolism or catabolism
→ Presence of comorbid conditions
*The dialysis prescription is not uniform for all
patients, so you have to individualize your patients.
 Hemodialysis adequacy is based on decreased
BUN concentration during dialysis treatment
→ Urea Reduction Ratio (URR)
o 1- (post/pre-dialysis plasma urea level ratio)
→ KT/V
o Where:
 K = urea clearance rate
 T = time spent on dialysis
 V = size of urea pool presented by urea
distribution volume which is roughly
equal to total body water
 Minimal standards:
→ URR = 65%
→ KT/V = 1.2
*Most of the time we use KT/V. Before we really
need to compute for KT/V. RIght now, medyo high-
tech na ang mga machines ta right now so they can
already check for the KT/V of the patient. Once the
KT/V is below 1.2 then you have to adjust because
that means that your patient is under-dialysed. The
adequacy of your patient is not that good. So you
have to check and review your dialysis prescription.
 Hemodialysis removes both low and high
molecular weight solutes.
COMPLICATIONS OF HEMODIALYSIS
 Hypotension - most common especially among
diabetic patients
→ Causes:
o Excessive ultrafiltration with inadequate
compensatory vascular filling (most
common)
 If you noticed that your patient
develops every time that they undergo
hemodialysis, try to check the
ultrafiltration prescription that you give
to the patient, then you have to
decrease.
o Impaired vasoactive or autonomic
responses
o Osmolar shifts
 During hemodialysis, urea and other
toxins are also moving which would
cause sudden shift of the fluids
between cells.
IDCM-MSM-2023
o Overzealous use of antihypertensive
agents
 Patients undergoing hemodialysis are
advised not to take their
antihypertensive medications BEFORE
undergoing the procedure. We just
advise them to bring their
antihypertensive meds during dialysis
to the dialysis unit so that if incase the
BP would increase, then we can advise
them to take their medicine at that
particular time.
o Reduced cardiac reserve
 Especially in patients that have poor
cardiac function where the ejection
fraction is very low.
 Rapid change in electrolytes leading to
arrhythmia
→ Usually due to hypokalemia during
hemodialysis; really needs to be checked
because it can cause cardiac arrest
 Disequilibrium syndrome
 Dementia
 Use of heparin
→ We use anticoagulants to avoid clotting of
blood during hemodialysis. This use of heparin
may lead to some form of hemorrhage,
especially when your patient would develop a
sudden drop in the hemoglobin. So if the
hemoglobin is stable with those of the
erythropoietin that you are giving to them and
suddenly there is a significant drop in the
hemoglobin, then you have to look for some
form of bleeding anywhere in the body.
→ May lead to subdural hematoma,
retroperitoneal, GI, pericardial & pleural
hemorrhages
 Malnutrition
→ HD may affect and increase catabolism &
allow amino acid loss through the membrane.
ADVANTAGES OF HEMODIALYSIS
 Short treatment time
→ The patient will just sit there for 4 hours, and
after 4 hours, the dialysis is finished. The
patient may go home after that.
 Minimal interruption of lifestyle between
treatment
 Rapid clearance rate
→ For those patients with very severe volume
overload, like patients with pulmonary edema
(they already have difficulty of breathing &
7/8
Notes:

hypoxemia), then you need to do HD because  Catheter-associated nonperitonitis infections

it has a rapid clearance rate of fluid compared
to peritoneal dialysis.
PERITONEAL DIALYSIS
 Infusion of dextrose containing solution (1.5 - 3L)
into the peritoneal cavity and allowed to dwell for
a period of time (2-4 hours)
→ We have the continuous ambulatory peritoneal
dialysis (CAPD), and we do exchanges for
approximately 4-5 times a day, so that’s why
it’s more tiring to do than HD.
 Involves the process of diffusion through a
semipermeable membrane (peritoneum); the
peritoneum is the dialyzer
ADVANTAGES OF PERITONEAL DIALYSIS
 Avoidance of heparinization
→ If the patient has a bleeding problem, then you
can do PD because there is no need for you to
use heparin.
 Avoidance of vascular surgery
 Slower clearance rate
 More amenable to self-treatment
→ More advantageous to those patients who are
living far from a place with a hemodialysis
center.
(Tunnel Infection)
 Weight gain & other metabolic disturbances
→ Fluid that is infused to the patient contains
glucose, so that’s why the patient would gain
weight. If the patient is diabetic, you need to
monitor the sugar frequently.
 Residual Uremia (patients with no residual
kidney function)
→ Clearance is usually very slow. If the patient
develops residual uremia, you need to advise
them to shift to HD.
PROGNOSIS
 5-year survival rate of patients on both kinds of
dialysis (USA) is ~35-40%
 Deaths are due mainly to cardiovascular
diseases (~40%) and infections (~10%)
 Important predictors of death:
→ Older age
→ Male sex
→ Non-black race
→ Diabetes mellitus
→ Malnutrition
→ Underlying heart disease

DISADVANTAGES OF PERITONEAL DIALYSIS

 Longer treatment time
 Should not be used in patients with severe
pulmonary disease
→ Because you are infusing 1.5-3L of fluid into
the peritoneal cavity. This would increase the
intraperitoneal pressure, and would further
increase the pulmonary pressure.
 Should not be used in patients with extensive
abdominal adhesions due to surgery
 Inadequate clearance in patients with
scleroderma, vasculitis,malignant hypertension,
peritoneal fibrosis, or in heavy patients (70 kg) References:
with no residual renal functions
 Doctor’s lecture
COMPLICATIONS OF PERITONEAL DIALYSIS  Hiliusa trans
 Peritonitis
→ Elevated PF leukocyte count = 100/µL (50%
PMN)
→ This particular complication also depends on
the hygiene of the patient.
 The most common culprit organisms in
peritonitis are Gram (+) cocci (Staphylococci)

IDCM-MSM-2023 8/8