Case Report: Chronic Kidney Failure

CASE REPORT
CHRONIC KIDNEY FAILURE
Preceptor :
dr. Hj. Ihsanil Husna, Sp.PD
By :
Bhismo Prasetyo (2012730119)
MEDICAL PROFESSION PROGRAMME DEPT. OF INTERNAL MEDICINE

JAKARTA ISLAMIC HOSPITAL CEMPAKA PUTIH
FACULTY OF MEDICINE AND HEALTH
UNIVERSITY OF MUHAMMADIYAH JAKARTA
2019
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PREFACE
Assalammu’alaikum wr wb,
Alhamdulillah, all praise to Allah SWT The Almighty and The Most Merciful.
Shalawat and salaam to Rasulullah Muhammad Peace Be Upon Him which bring us from
the darkest of time into the lights.
The writer also wish to express his deep and sincere gratitude for those who have
helped in completing this case report with the title “Chronic kidney Disease” to fulfill the
criteria for completing Medical Profession Programme in Internal Medicine Department
of Jakarta Islamic Hospital Cempaka Putih, Faculty of Medicine University of
Muhammadiyah Jakarta.
The writer wish this paper to be useful and add another dimension of knowledge
for the writer himself, medical profession student, and anyone else who never stop in
learning.
The writer acknowledge in the process of making this paper, there are a lot of
mistake and far from perfect, cause perfection are only belong to Allah SWT. All the
critics and advice are needed for the writer for the better of ourselves in this journey to be
the long life learner.
Wassalammu’alaikum wr wb.
Jakarta, August 2019
Writer
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BAB I
MEDICAL STATUS
A. PATIENT’S IDENTITY
Name : Mr. An
Age : 65th years old
Adress : Jl.Cempaka Indah RT10/7, Kemayoran
Marital Status : Married
Religion : Moslem
Date of Admission : July, 5th 2019
Room Number : 7 of Mawar room
MR Number : 00.73.61.XX
B. ANAMNESIS
I did autoanamnesis and alloanamnesis to the his wife in the room on July, 5th
2019.
Chief Complaint
Weakness 2 Weeks Before Entering The Hospital.
Another Complaint
Nausea, vomiting, Epigastric pain, lose of appetite and dry cough.
History of Present Illness
The Patient complaining about the weakness 2 weeks before came to the
Jakarta Hospital Cempaka Putih. The weakness are felt with vomiting ± 500 ml
containing leftover food the frequency 2x, blood(-). Also complaints about the
heartburn, lose of appetite ± 2 days and dry cough 1 week, blood (-) before entering the
hospital. Febris (-).
Patients routinely do hemodialysis at the Jakarta Islamic Hospital Cempaka Putih
with a schedule of Tuesday and Thursday, hemodialysis treatment has been carried out
± 3 years and routinely 2x a week.
Urinary and defecation remains normal. The patient already control to doctor when
doing Hemodialysis, and suggested him to be treated at the hospital.
0
History of Past Ilness
History of the same problem : (+)
History of hypertension : (+)
History of Diabetes Mellitus : (-)
History of Asthma : (-)
History of surgery : (-)
History in The Family

None of his family has same problem.
History of Allergy
Patient has no allergy to food, drugs, and weather.
History of Treatment and Medication

The patient has not take medicine for this complaint.
History of Habits
The patient lives with 4 other people in one house. The patient's home
environment is not dense. The patient have smoking since ± 20 years until now for 1
pack a day. History of drinking alcohol is denied. His wife claimed that patients always
eat regularly and like to eat spicy and fatty until now. Eat vegetables and fruit
sometimes if 1x a week.
C. PHYSICAL EXAMINATION
Generalized State
Patients appear to be moderately ill
Consiciusness
Compos Mentis
Anthropometric Status
Body weight : 49 kg
Body high : 160 cm
1
BMI : IMT 19,14 (Normoweight)
Vital Sign
Blood Pressure : 120/90 mmHg
Heart Rate : 71x/menit
Respiratory Rate : 18x/menit
Temperature : 36.6° C
General Physical Examination

Head : Normocephal, Deformity (-)
Eyes : Anemic Conjungtiva (+/+), Icteric Sclera (-/-)
Nose : Epistaksis (-/-), Secret (-/-), Deviated Septum (-/-),
Mouth : Dry lip mucosa, Cyanosis (-), coated tongue (-)
Neck : Palpable Mass (-), Lymphadenopathy (-)
Thorax
Lungs
Inspection : The movement of the chest symmetrical
Palpation : Same vocal fremitus in dextra et sinistra
Percussion : Sonor
Auscultacion : Vesicular breath sounds + / +, Ronkhi -/-, Wheezing - / -
Heart
Inspection : Ictus cordis not seen in ICS V LMCS
Palpation : Ictus cordis palpable ICS V LMCS
Percussion : Right heart margin: Sternalis line sinistra ICS-V
Left heart margin: Midclavicula line sinistra ICS-V.
Auscultation : Regular 1st & 2nd heart sounds, Murmur (-), Gallop (-)
2
Abdomen
Inspection : Abdominal surface appears convex, distention (+), scar tissue

(-),Spyder Navy (-), Caput Medusa (-).
Auscultation : Bowel sounds are normal
Palpation : Epigastric Pain (+), not palpable enlargement of

the liver and spleen.
Percussion : Tympanic in all abdominal fields, Shifting dullness (-).
Superior Extremity
Acral : warm (+/+)
Edema : (-/-)
Cyanosis : (-/-)
CRT : < 2 second/ < 2 second
Inferior Extremity
Akral : warm (+/+)
Edema : (+/+) minimal
Cyanosis : (-/-)
CRT : < 2 second/ < 2 second
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D.LABORATORY FINDINGS
August 24th 2017 - 00.08
EXAMINATION VALUE UNITS NORMAL
Hemoglobin 8.6 ↓ g/dL 13,2 – 17,3
Hematocrit 26 ↓ % 40 – 52
Leukocyte 6.90 103/uL 3.8 – 10,6
Trombosit 164 103/µl 150 - 440
Eritrosit 2.67 ↓ 106/µl 4,4 – 5,9
MCV 97 Fl 80-100
MCH 32 pg 26-34
MCHC 33 g/dl 32-36
August 24th 2017 - 00.08
Ureum 79 mg/dL 10 – 50
Creatinin 11.8 mg/dL <1.4
Natrium 139 mEq/L 135 – 147
Kalium 3.9 mEq/L 3.5 – 5.0
Clorida 97 mEq/L 94 – 111
Glucose 103 Mg/dL 70-200
1
July, 05th 2019 - 10.17
Hemoglobin 5.3 ↓ g/dL 13,2 – 17,3
E.PROBLEM LIST
 Chronic Kidney Disease
 Anemia et causa Chronic Kidney Disease dd/ Iron deficiency anemia
 Hipertension
F. RESUME
Mr. An, 65 years old came came to the Jakarta Hospital Cempaka Putih
with complaints of weakness for 2 weeks before being hospitalized. The weakness
are felt with vomiting ± 500 ml containing leftover food the frequency 2x,
heartburn (+), lose of appetite ± 2 days and dry cough 1 week before entering the
hospital.
Patients routinely do hemodialysis at the Jakarta Islamic Hospital

Cempaka Putih with a schedule of Tuesday and Thursday, hemodialysis treatment
has been carried out ± 3 years and routinely 2x a week. Urinary and defecation
remains normal. The patient already control to doctor when doing Hemodialysis,
and suggested him to be treated at the hospital.
On Physical Examination:
Awareness : compos mentis
Blood Pressure : 120/90 mmHg
Pulse : 71x / minute
Respiratory Rate : 18x / minute
Temperature : 36.6 ° C
Conjungtiva anemis (+/+)
Dry lip mucosa
2
Epigastric pain (+)
Inferior extremitas edem (+/+) minimal
Laboratory Findings :
August 24th 2017 - 00.08

Hemoglobin 8.6 g/dL (decreased), Hematocrit 26 %(decreased), Eritrosit 2.67
106/µl (decreased) , Ureum 79 mg/dL (increased), creatinine 11.8 mg/dL
(increased )
July 05th 2019 – 10.17

Hemoglobin 5.3 mg/dL (decreased)
D. ASSESMENT
1. Chronic Kidney Disease
S : Nausea and vomiting , anorexia, 2 weeks before hospitalized and

complined about edema in the legs.
O : Vital Sign: BP: 120/90mmHg, HR:71x/minute, RR:18x/minute,

Temperature: 36,6 ° C.
Physical Examination : Dry lip mukosa (+), Epigastric pain (+),

Edem extremitas inferior (+/+) minimal
Laboratory findings :
Ureum 79 mg/dL (increased), Creatinin 11,8 mg/dL (increased)
A : Chronic Kidney Disease
3
P : Planning Diagnostic
- Routine Hematology
- Electrolyt examinations
- Urinalisis
- Renal USG
- Renal biopsy
Planning Non-Therapeutics
- Bed rest
- Monitoring vital signs
- Keep drinking intake
Planning Therapeutics
- IVFD NaCl 0,9% 7 tpm

- Inj deksametason premed
- Inj Rantin 2x1 amp
- Inj Ondancentron 2x1 amp
- CaCO3 tab 3x1
- Folic Acid tab 1x3
- Vit. B.12 tab 3x1
4
2. Anemia et causa Chronic Kidney Disease dd/ Iron deficiency anemia
S : Complained of weakness 4 days before hospitalized.
O :
Vital Sign: BP: 120/90mmHg, HR:71x/minute, RR:18x/minute, Temperature:

36,6 ° C.
Physical Examination :
Anemic conjungtiva (+/+)
Laboratory findings : 05/04/2019 (10.17)
Hemoglobin : 5,3 g/dL (decreased)
A : Anemia et causa Chronic Kidney Disease dd/ Iron deficiency anemia
P :
Planning Diagnostic:
HB post ( not checked yet)
Planning Non Therapeutics
Bed Rest
IVFD NaCl 0,9% 7 tpm
Transfusion 600 ml PRC
5
3. Hypertension
S : Headche
O :
Vital Sign:
BP: 130/90mmHg,
HR:71x/minute,
RR:18x/minute,
Temperature: 36,6 ° C.
A : Hypertension
P : Amlodipine 1x10 mg
4. FOLLOW UP
06/07/2019
S Nausea and vomiting , anorexia, 2 weeks before hospitalized and complined

about edema in the legs.
O Vital Signs :
BP : 130/90mmHg,
RR:20x/m,
HR:86x/m,
T:36,6° C
Dry lip mukosa (+), Epigastric pain (+), Edem extremitas inferior (+/+) minimal
Laboratory findings :
6
Ureum 79 mg/dL (increased), Creatinin 11,8 mg/dL (increased)
A Chronic Kidney Disease
P Planning Diagnostic:
- Routine Hematology
- Electrolyt examinations
- Urinalisis
- Renal USG
- Renal biopsy
- Bed Rest
- Monitoring vital signs

- Inj deksametason premed
- CaCO3 tab 3x1
- Vit. B.12 tab 3x1
7
06/07/2019
S Complained of weakness 4 days before hospitalized.
O Vital Signs :
BP : 130/90mmHg,
RR:20x/m,
HR:86x/m,
T:36,6° C
Conjungtiva anemis (+/+)
Laboratory Findings
05/04/2019
Hemoglobin : 5,3 g/dL
A Anemia et causa Chronic Kidney Disease On HD dd/ Anemia et causa Iron
deficiency
- HB post ( not checked yet)
- Bed Rest

- Transfusion 600 ml PRC
8
06/07/2019
S Headache
O Vital Sign:
BP: 130/90mmHg,
HR:71x/minute,
RR:18x/minute,
Temperature: 36,6 ° C
A Hypertension
P Planning Therapeutic
- Amlodipine 1x10 mg
08/07/2019
S Nausea (+), Vomiting(-), weakness (-)
Defecate and urinalysis normal
O Vital Signs:
BP : 120/90,
RR:18x/m,
HR:90x/m,
T:37.0° C
Physical Examination: Dry lip mukosa (+), Epigastric pain (+), Edem
extremitas inferior (+/+) minimal
Laboratory Findings
Hemoglobin : (Not checked yet)
A Chronic Kidney Disease
9
- Hemoglobine examination
- (-)

- CaCO3 tab 3x1
- Vit. B.12 tab 3x1
07/07/2019
S Weakness (+)
O Vital Signs:
BP : 120/90,
RR:18x/m,
HR:90x/m,
T:37.0° C
Conjungtiva anemis (-/-)
Laboratory Findings
Hemoglobin examination : not checked yet

deficiency
10
- (-)

- Vit. B.12 tab 3x1
07/07/2019
S Headache (+)
O Vital Sign:
BP: 120/90mmHg,
HR:71x/minute,
RR:18x/minute,
Temperature: 36,6 ° C
Conjungtiva anemis (-/-)
Laboratory Findings
Hemoglobin examination : not checked yet

deficiency
- (-)
11

- Vit. B.12 tab 3x1
CHAPTER II
LITERATURE REVIEW
2.1. Definition
Chronic kidney disease (CKD) encompasses a spectrum of pathophysiologic
processes associated with abnormal kidney function and a progressive decline in
glomerular filtration rate (GFR). The risk of CKD progression is closely linked to both
the GFR and the amount of albuminuria.1,2,3
2.2. Pathophysiology
The pathophysiology of CKD involves 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) and (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. The
responses to reduction in nephron number are mediated by vasoactive hormones,
cytokines, and growth factors. Eventually, these short-term adaptations of hyperfiltration
and hypertrophy to maintain GFR become maladaptive as the increased pressure and flow
within the nephron predisposes to distortion of glomerular architecture, abnormal
podocyte function, and disruption of the filtration barrier leading to sclerosis and dropout
of the remaining nephrons (Figure 1). Increased intrarenal activity of the renin-
angiotensin system (RAS) appears to contribute both to the initial compensatory
hyperfiltration and to the subsequent maladaptive hypertrophy and sclerosis. This process
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explains why a reduction in renal mass from an isolated insult may lead to a progressive
decline in renal function over many years (Fig. 305-3).1
Figure 1. Left: Schema of the normal glomerular architecture. Right: Secondary glomerular
changes associated with a reduction in nephron number, including enlargement of capillary
lumens and focal adhesions, which are thought to occur consequent to compensatory
hyperfiltration and hypertrophy in the remaining nephrons.
Figure 2. Left: Low-power photomicrograph of a normal kidney showing nomal glomeruli and
healthy tubulointerstitium without fibrosis. Right: Low-power photomicrograph of chronic
kidney disease with sclerosis of many glomeruli and severe tubulointerstisial fibrosis.
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2.3. Risk Factors
Even in individuals with normal GFR. Risk factors include 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, and the presence of proteinuria, abnormal urinary sediment, or
structural abnormalities of the urinary tract. It has been increasingly recognized that one
or more episodes of acute kidney injury are associated with an increased risk of
developing CKD.1
2.4. Staging
Figure 3 provides a staging of CKD stratified by the estimates of both of these
parameters. The dispiriting term end-stage renal disease 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.1,2
Figure 3. Kidney Disease Improving Global Outcome (KDIGO) classification of chronic

kidney disease (CKD)
To stage CKD, it is necessary to estimate the GFR rather than relying on serum
creatinine concentration (Table 1). Many laboratories now report an estimated GFR, or
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eGFR, using one of these equations. These equations are valid only if the patient is in
steady state, that is, the serum creatinine is neither rising nor falling over days.1
Table 1. Recommended Equations for Estimation of Glomerular Filtration Rate (GFR)

Using Serum Creatinine Concentration (SCR), Age, Sex, Race, and Body Weight
The normal annual mean decline in GFR with age from the peak GFR (~120
mL/min per 1.73 m2) attained during the third decade of life is ~1 mL/min per year per
1.73 m2, reaching a mean value of 70 mL/min per 1.73 m2 at age 70, with considerable
inter-individual variability. Although reduced GFR is expected with aging, the lower GFR
signifies a true loss of kidney function with attendant consequences in terms of risk of
CKD complications, and requirement for dose adjustment of medications. The mean GFR
is lower in women than in men. For example, a woman in her eighties with a laboratory
report of serum creatinine in the normal range may have a GFR of <50 mL/min per 1.73
m2. Relatedly, even a mild elevation in serum creatinine concentration often signifies a
substantial reduction in GFR in older individuals.1
Measurement of albuminuria is also helpful for monitoring nephron injury and the
response to therapy in many forms of CKD, especially chronic glomerular diseases. The
cumbersome 24-h urine collection has been replaced by measurement of urinary albumin
to creatinine ratio (UACR) in one and preferably several spot first-morning urine samples
as a measure pointing to glomerular injury. Even in patients with negative conventional
dipstick tests for elevated total protein excretion, UACR above 17 mg albumin/g
creatinine in men and 25 mg albumin/g creatinine in men serves as a marker not only for
early detection of primary kidney disease, but for systemic microvas-cular disease as well.
The presence of albuminuria in general serves as a well-studied screening marker for the
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presence of systemic microvas-cular disease and endothelial dysfunction. A Kidney
Failure Risk (KFR) equation has been devised to predict the risk of progression to stage
5 dialysis-dependent kidney disease. The equation is available on many sites online (for
example, www.kidneyfailurerisk.com) and uses age, sex, region (North American or non-
North American), GFR and the urine albumin/creatinine. It has been validated in several
cohorts around the world, although the risk for progression appears to be greater in North
America, accounting for the regional adjustment in the equation.1
Stages 1 and 2 CKD are usually asymptomatic, such that the recognition of CKD
occurs more often as a result of laboratory testing in clinical settings other than suspicion
of kidney disease. Moreover, in the absence of the risk factors noted above, population-
wide screening is not recommended. With progression to CKD stages 3 and 4, clinical
and laboratory complications become more prominent. Virtually all organ systems are
affected, but the most evident complications include anemia and associated easy
fatigability; decreased appetite with progressive malnutrition; abnormalities in calcium,
phosphorus, and mineral-regulating hormones, such as 1,25(OH)2D3 (calcitriol),
parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23); and abnormalities
in sodium, potassium, water, and acidbase homeostasis. Many patients, especially the
elderly, will have eGFR values compatible with stage 2 or 3 CKD. However, the majority
of these patients will show no further deterioration of renal function. The primary care
physician is advised to recheck kidney function, and if it is stable and not associated with
proteinuria, the patient can usually be followed with interval repeat testing without
referral to nephrologist. However, caution should be exercised in terms of potential
exposure to nephrotoxins or interventions that risk acute kidney injury (AKI) and also
with respect to medication dose adjustment. If repeat testing shows declining GFR,
albuminuria, or uncontrolled hypertension, referral to a nephrologist is appropriate. If the
patient progresses to stage 5 CKD, toxins accumulate such that patients usually
experience a marked disturbance in their activities of daily living, well-being, nutritional
status, and water and electrolyte homeostasis, eventuating in the uremic syndrome.1
2.5. Etiology and Epidemiology

It has been estimated from population data that at least 6% of the adult population
in the United States has CKD at stages 1 and 2. An additional 4.5% of the U.S. population
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is estimated to have stages 3 and 4 CKD. Table 2 lists the five most frequent categories
of causes of CKD, cumulatively accounting for >90% of the CKD disease burden
worldwide. The relative contribution of each category varies among different geographic
regions. The most frequent cause of CKD in North America and Europe is diabetic
nephropathy, most often secondary to type 2 diabetes mellitus. Patients with newly
diagnosed CKD often have hypertension.1,2
Table 2. Leading Categories of Etiologies of CKDa
In Indonesia, prevalence (permil) of CKD based on diagnosis made by doctor as

stated in Riskesdas 2018 showing the prevalence increase as the age and woman has
higher rate than male patient (Figure 4).
Figure 4. Prevalence (permil) of CKD based on diagnosis made by doctor.
2.6. Pathophysiology and Biochemistry of Uremia

Although serum urea and creatinine concentrations are used to measure the
excretory capacity of the kidneys, accumulation of these two molecules themselves does
not account for the many symptoms and signs that characterize the uremic syndrome in
advanced renal failure. Large numbers of toxins that accumulate when GFR declines have
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been implicated in the uremic syndrome. These include watersoluble, hydrophobic,
protein-bound, charged, and uncharged nitrogencontaining non-volatile products of
metabolism. It is thus evident that the serum concentrations of urea and creatinine should
be viewed as being readily measured, but very incomplete surrogate markers for retained
toxins, and monitoring the levels of urea and creatinine in the patient with impaired
kidney function represents a vast oversimplification of the uremic state.1
The uremic syndrome involves more than renal excretory failure. A host of
metabolic and endocrine functions normally performed by the kidneys is also impaired,
and this results in anemia, malnutrition, and abnormal metabolism of carbohydrates, fats,
and proteins. Furthermore, plasma levels of many hormones, including PTH, FGF-23,
insulin, glucagon, steroid hormones including vitamin D and sex hormones, and prolactin
change with CKD as a result of reduced excretion, decreased degradation, or abnormal
regulation. Finally, CKD is associated with increased systemic inflammation. Elevated
levels of C-reactive protein are detected along with other acute-phase reactants, whereas
levels of so-called negative acute-phase reactants, such as albumin and fetuin, decline.
Thus, the inflammation associated with CKD is important in the malnutrition-
inflammation-atherosclerosis/calcification syndrome, which contributes in turn to the
acceleration of vascular disease and comorbidity associated with advanced kidney
disease.1
In summary, the pathophysiology of the uremic syndrome can be divided into
manifestations in three spheres of dysfunction: (1) those consequent to the accumulation
of toxins that normally undergo renal excretion; (2) those consequent to the loss of other
kidney functions, such as fluid and electrolyte homeostasis and hormone regulation; and
(3) progressive systemic inflammation and its vascular and nutritional consequences.1
2.7. Clinical Manifestation

Uremia leads to disturbances in the function of virtually every organ system.
Chronic dialysis can reduce the incidence and severity of many of these disturbances, so
that the florid manifestations of uremia have largely disappeared in the modern health
setting. However, even optimal dialysis therapy is not completely effective as renal
replacement therapy, because some disturbances resulting from impaired kidney function
fail to respond to dialysis.1,2
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2.7.1. Fluid, Electrolyte, and Acid-Base Disorders
Sodium and Water Homeostasis
With normal renal function, tubular excretion of filtered sodium and water
matches intake. Many forms of kidney disease (e.g., glomerulonephritis) disrupt this
balance such that dietary intake of sodium exceeds its urinary excretion, leading to
sodium retention and attendant extracellular fluid volume (ECFV) expansion. This
expansion may contribute to hypertension, which itself can accelerate nephron injury. As
long as water intake does not exceed the capacity for renal water clearance, the ECFV
expansion will be isotonic and the patient will have a normal plasma sodium
concentration. Hyponatremia is not commonly seen in CKD patients but, when present,
often responds to water restriction. The patient with ECFV expansion (peripheral edema,
sometimes hypertension poorly responsive to therapy) should be counseled regarding salt
restriction. Thiazide diuretics have limited utility in stages 3–5 CKD, such that
administration of loop diuretics, including furosemide, bumetanide, or torsemide, may
also be needed. Resistance to loop diuretics in CKD often mandates use of higher doses
than those used in patients with higher GFR. The combination of loop diuretics with
metolazone may be helpful. Diuretic resistance with intractable edema and hypertension
in advanced CKD may serve as an indication to initiate dialysis.1
In addition to problems with salt and water excretion, some patients with CKD
may instead have impaired renal conservation of sodium and water. When an extrarenal
cause for fluid loss, such as gastrointestinal (GI) loss, is present, these patients may be
prone to ECFV depletion because of the inability of the failing kidney to reclaim filtered
sodium adequately. Furthermore, depletion of ECFV, whether due to GI losses or
overzealous diuretic therapy, can further compromise kidney function through
underperfusion, or a “prerenal” state, leading to acute-on-chronic kidney failure. In this
setting, holding or adjusting the diuretic dose or even cautious volume repletion with
normal saline may return the ECFV to normal and restore renal function to baseline.1
Potassium Homeostasis
In CKD, the decline in GFR is not necessarily accompanied by a parallel decline
in urinary potassium excretion, which is predominantly mediated by aldosterone-
dependent secretion in the distal nephron. Another defense against potassium retention in
these patients is augmented potassium excretion in the GI tract. Not with standing these
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two homeostatic responses, hyperkalemia may be precipitated in certain settings. These
include increased dietary potassium intake, hemolysis, hemorrhage, transfusion of stored
red blood cells, and metabolic acidosis. Importantly, a host of medications can inhibit
renal potassium excretion and lead to hyperkalemia. The most important medications in
this respect include the RAS inhibitors and spironolactone and other potassium-sparing
diuretics such as amiloride, eplerenone, and triamterene. The benefits of the RAS
inhibitors in ameliorating the progression of CKD and its complications often favor their
cautious and judicious use with very close monitoring of plasma potassium
concentration.1
Certain causes of CKD can be associated with earlier and more severe disruption
of potassium-secretory mechanisms in the distal nephron, out of proportion to the decline
in GFR. These include conditions associated with hyporeninemic hypoaldosteronism,
such as diabetes, and renal diseases that preferentially affect the distal nephron, such as
obstructive uropathy and sickle cell nephropathy.1
Hypokalemia is not common in CKD and usually reflects markedly reduced
dietary potassium intake, especially in association with excessive diuretic therapy or
concurrent GI losses. The use of potassium supplements and potassium-sparing diuretics
may be risky in patients with impaired renal function, and needs to be monitored closely.1
Metabolic Acidosis
Metabolic acidosis is a common disturbance in advanced CKD. The majority of
patients can still acidify the urine, but they produce less ammonia and, therefore cannot
excrete the normal quantity of protons. Hyperkalemia, if present, further depresses
ammonia production. The combination of hyperkalemia and hyperchloremic metabolic
acidosis is often present, even at earlier stages of CKD (stages 1–3), in patients with
diabetic nephropathy or in those with predominant tubulointerstitial disease or obstructive
uropathy.1
With worsening renal function, the total urinary net daily acid excretion is usually
limited to 30–40 mmol, and the anions of retained organic acids can then lead to an anion-
gap metabolic acidosis. Thus, the non-anion-gap metabolic acidosis seen in earlier stages
of CKD may be complicated by the addition of an anion-gap metabolic acidosis as CKD
progresses. In most patients, the metabolic acidosis is mild; the pH is rarely <7.32 and
can usually be corrected with oral sodium bicarbonate supplementation. Animal and
20
human studies have suggested that even modest degrees of metabolic acidosis may be
associated with the development of protein catabolism. Alkali supplementation may, in
addition, attenuate the catabolic state and possibly slow CKD progression and is
recommended when the serum bicarbonate concentration falls below 20–23 mmol/L. The
concomitant sodium load mandates careful attention to volume status and the need for
diuretic agents.1
2.7.2. Disorders of Calcium and Phosphate Metabolism
The principal complications of abnormalities of calcium and phosphate
metabolism in CKD occur in the skeleton and the vascular bed, with occasional severe
involvement of soft tissues. It is likely that disorders of bone turnover and disorders of
vascular and soft tissue calcification are related to each other (Fig. 305-3).1
Bone Manifestations of CKD
The major disorders of bone disease can be classified into those associated with
high bone turnover with increased PTH levels (including osteitis fibrosa cystica, the
classic lesion of secondary hyperparathyroidism), osteomalacia due to reduced action of
the active forms of vitamin D, and low bone turnover with low or normal PTH levels
(adynamic bone disease) or most often combinations of the foregoing.1
The pathophysiology of secondary hyperparathyroidism and the consequent high-
turnover bone disease is related to abnormal mineral metabolism through the following
events: (1) declining GFR leads to 2115 reduced excretion of phosphate and, thus,
phosphate retention; (2) the retained phosphate stimulates increased synthesis of both
FGF-23 by osteocytes and PTH and stimulates growth of parathyroid gland mass; and (3)
decreased levels of ionized calcium, resulting from suppression of calcitriol production
by FGF-23 and by the failing kidney, as well as phosphate retention, also stimulate PTH
production. Low calcitriol levels contribute to hyperparathyroidism, both by leading to
hypocalcemia and also by a direct effect on PTH gene transcription. These changes start
to occur when the GFR falls below 60 mL/min.1
FGF-23 is part of a family of phosphatonins that promotes renal phosphate
excretion. Recent studies have shown that levels of this hormone, secreted by osteocytes,
increase early in the course of CKD, even before phosphate retention and
hyperphosphatemia. FGF-23 may defend normal serum phosphorus in at least three ways:
(1) increased renal phosphate excretion; (2) stimulation of PTH, which also increases
21
renal phosphate excretion; and (3) suppression of the formation of 1,25(OH)2D3, leading
to diminished phosphorus absorption from the GI tract. Interestingly, high levels of FGF-
23 are also an independent risk factor for left ventricular hypertrophy and mortality in
CKD, dialysis, and kidney transplant patients. Moreover, elevated levels of FGF-23 may
indicate the need for therapeutic intervention (e.g., phosphate restriction), even when
serum phosphate levels are within the normal range.1
Hyperparathyroidism stimulates bone turnover and leads to osteitis fibrosa
cystica. Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and in
advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so
that they appear brown in color, hence the term brown tumor. Clinical manifestations of
severe hyperparathyroidism include bone pain and fragility, brown tumors, compression
syndromes, and erythropoietin (EPO) resistance in part related to the bone marrow
fibrosis. Furthermore, PTH itself is considered a uremic toxin, and high levels are
associated with muscle weakness, fibrosis of cardiac muscle, and nonspecific
constitutional symptoms.1
Adynamic bone disease is increasing in prevalence, especially among diabetics
and the elderly. It is characterized by reduced bone volume and mineralization and may
result from excessive suppression of PTH production, chronic inflammation, or both.
Suppression of PTH can result from the use of vitamin D preparations or from excessive
calcium exposure in the form of calcium-containing phosphate binders or highcalcium
dialysis solutions. Complications of adynamic bone disease include an increased
incidence of fracture and bone pain and an association with increased vascular and cardiac
calcification. Occasionally the calcium will precipitate in the soft tissues into large
concretions termed “tumoral calcinosis” (Fig. 305-4). Patients with adynamic bone
disease often experience the most severe symptoms of musculoskeletal pain, owing to the
inability to repair the microfractures that occur properly as a part of healthy skeletal
homeostasis with regular physical activity. Osteomalacia is a distinct process, consequent
to reduced production and action of 1,25(OH)2D3, leading to non-mineralized osteoid.1
22
Figure 5. Tumoral calcinosThis patient was on hemodialysis for many years and was
nonadherent to dietary phosphorus restriction or the use of phosphate binders. He was
chronically severely hyperphosphatemic. He developed an enlarging painful mass on his arm
that was extensively calcified.
Calcium, Phosphorus, and the Cardiovascular System

Recent epidemiologic evidence has shown a strong association between
hyperphosphatemia and increased cardiovascular mortality in patients with stage 5 and
earlier stages of CKD. Hyperphosphatemia and hypercalcemia are associated with
increased vascular calcification, but it is unclear whether the excessive mortality is
mediated by this mechanism. Studies using computed tomography (CT) and electron-
beam CT scanning show that CKD patients have calcification of the media in coronary
arteries and even heart valves that appear to be orders of magnitude greater than that in
patients without renal disease. The magnitude of the calcification is proportional to age
and hyperphosphatemia and is also associated with low PTH levels and low bone
turnover. It is possible that in CKD patients ingested calcium cannot be incorporated into
bones with low turnover and, therefore, is deposited at extraosseous sites, such as the
vascular bed and soft tissues. It is interesting in this regard that there is also an association
between osteoporosis and vascular calcification in the general population. Finally,
hyperphosphatemia can induce a change in gene expression in vascular cells to an
osteoblast-like profile, leading to vascular calcification and even ossification.1
Other Complications of Abnormal Mineral Metabolism
Calciphylaxis is a devastating condition seen almost excslusively in patients with
advanced CKD. It is heralded by livedo reticularis and advances to patches of ischemic
necrosis, especially on the legs, thighs, abdomen, and breasts (Fig. 305-5). Pathologically,
23
there is evidence of vascular occlusion in association with extensive vascular and soft
tissue calcification. It appears that this condition is increasing in incidence. Originally it
was ascribed to severe abnormalities in calcium and phosphorus control in dialysis
patients, usually associated with advanced hyperparathyroidism. However, more recently,
calciphylaxis has been seen with increasing frequency in the absence of severe
hyperparathyroidism. Other etiologies have been suggested, including the increased use
of oral calcium as a phosphate binder. Warfarin is commonly used in hemodialysis
patients in whom most direct oral anticoagulants (DOACs) are contraindicated, and one
of the effects of warfarin therapy is to decrease the vitamin K–dependent regeneration of
matrix GLA protein. This latter protein is important in preventing vascular calcification.
Thus, warfarin treatment is considered a risk factor for calciphylaxis, and if a patient
develops this syndrome, this medication should be discontinued and replaced with
another anticoagulant.1
Figure 6. Calciphylaxis. This peritoneal dialysis patient was on chronic warfarin therapy for
atrial fibrilation. She noticed a small painful nodule on the abdomen that was followed by
progressive skin necrosis and ulceration of the anterior abdominal wall. She was treated with
hyperbaric oxygen, intravenous thiosulfate, and discontinuation of warfarin, with slow
resolution of the ulceration.
2.7.3. Cardiovascular Abnormalities

Cardiovascular disease is the leading cause of morbidity and mortality in patients
at every stage of CKD. The incremental risk of cardiovascular disease in those with CKD
compared to the age- and sex-matched general population ranges from 10- to 200-fold,
depending on the stage of CKD. As a result, most patients with CKD succumb to
24
cardiovascular disease (Fig. 305-6) before ever reaching stage 5 CKD. Between 30 and
45% of those patients who do reach stage 5 CKD have advanced cardiovascular
complications. Thus, the focus of patient care in earlier CKD stages should be directed to
prevention of cardiovascular complications.1
Figure 7. U.S. Renal Data System showing increased likelihood of dying rather than starting
dialysis of reaching stage 5 chronic kidney disease (CKD). 1, Detah; 2, ESRD; 3, event-free,
DM; diabetes mellitus.
Ischemic Vascular Disease
The increased prevalence of vascular disease in CKD patients derives from both
traditional (“classic”) and nontraditional (CKD-related) risk factors. Traditional risk
factors include hypertension, hypervolemia, dyslipidemia, sympathetic overactivity, and
hyperhomocysteinemia. The CKD-related risk factors comprise anemia,
hyperphosphatemia, hyperparathyroidism, increased FGF-23, sleep apnea, and
generalized inflammation. The inflammatory state appears to accelerate vascular
occlusive disease, and low levels of fetuin may permit more rapid vascular calcification,
especially in the face of hyperphosphatemia. Other abnormalities seen in CKD may
augment myocardial ischemia, including left ventricular hypertrophy and microvascular
disease. In addition, hemodialysis, with its attendant episodes of hypotension and
hypovolemia, may further aggravate coronary ischemia and repeatedly stun the
myocardium. Interestingly, however, the largest increment in cardiovascular mortality
rate in dialysis patients is not necessarily directly associated with documented acute
25
myocardial infarction but, instead, is the result of congestive heart failure and sudden
death.1
Cardiac troponin levels are frequently elevated in CKD without evidence of acute
ischemia. The elevation complicates the diagnosis of acute myocardial infarction in this
population. Serial measurements may be needed. Therefore, the trend in levels over the
hours after presentation may be more informative than a single, elevated level.
Interestingly, consistently elevated levels are an independent prognostic factor for adverse
cardiovascular events in this population.1
Heart Failure
Abnormal cardiac function secondary to myocardial ischemia, left ventricular
hypertrophy, diastolic dysfunction, and frank cardiomyopathy, in combination with the
salt and water retention often results in heart failure or even pulmonary edema. Heart
failure can be a consequence of diastolic or systolic dysfunction, or both. A form of “low-
pressure” pulmonary edema can also occur in advanced CKD, manifesting as shortness
of breath and a “bat wing” distribution of alveolar edema fluid on the chest x-ray. This
finding can occur even in the absence of ECFV overload and is associated with normal
or mildly elevated pulmonary capillary wedge pressure. This process has been ascribed
to increased permeability of alveolar capillary membranes as a manifestation of the
uremic state, and it responds to dialysis. Other CKD-related risk factors, including anemia
and sleep apnea, may contribute to the risk of heart failure.1
Hypertension and Left Ventricular Hypertrophy
Hypertension is one of the most common complications of CKD. It usually
develops early during the course of CKD and is associated with adverse outcomes,
including the development of ventricular hypertrophy and a more rapid loss of renal
function. Left ventricular hypertrophy and dilated cardiomyopathy are among the
strongest risk factors for cardiovascular morbidity and mortality in patients with CKD
and are thought to be related primarily, but not exclusively, to prolonged hypertension
and ECFV overload. In addition, anemia and the placement of an arteriovenous fistula for
hemodialysis can generate a high cardiac output state and consequent heart failure.1
The absence of hypertension may signify poor left ventricular function. Indeed, in
epidemiologic studies of dialysis patients, low blood pressure actually carries a worse
prognosis than does high blood pressure. This mechanism, in part, accounts for the
26
“reverse causation” seen in dialysis patients, wherein the presence of traditional risk
factors, such as hypertension, hyperlipidemia, and obesity, appear to portend a better
prognosis. Importantly, these observations derive from cross-sectional studies of late-
stage CKD patients and should not be interpreted to discourage appropriate management
of these risk factors in CKD patients, especially at early stages. In contrast to the general
population, it is possible that in late-stage CKD, low blood pressure, reduced body mass
index, and hypolipidemia indicate the presence of an advanced malnutrition-
inflammation state, with poor prognosis.1
The use of exogenous erythropoiesis-stimulating agents can increase 2117 blood
pressure and the requirement for antihypertensive drugs. Chronic ECFV overload is also
a contributor to hypertension, and improvement in blood pressure can often be seen with
the use of dietary sodium restriction, diuretics, and fluid removal with dialysis.
Nevertheless, because of activation of the RAS and other disturbances in the balance of
vasoconstrictors and vasodilators, some patients remain hypertensive despite careful
attention to ECFV status.1
Pericardial Disease
Chest pain with respiratory accentuation, accompanied by a friction rub, is
diagnostic of pericarditis. Classic electrocardiographic abnormalities include PR-interval
depression and diffuse ST-segment elevation. Pericarditis can be accompanied by
pericardial effusion that is seen on echocardiography and can rarely lead to tamponade.
However, the pericardial effusion can be asymptomatic, and pericarditis can be seen
without significant effusion.1
Pericarditis is observed in advanced uremia, and with the advent of timely
initiation of dialysis, is not as common as it once was. It is now more often observed in
underdialyzed, non-adherent patients than in those starting dialysis.1
2.7.4. Hematologic Abnormalities
Anemia
A normocytic, normochromic anemia is observed as early as stage 3 CKD and is
almost universal by stage 4. The primary cause is insufficient production of EPO by the
diseased kidneys. Additional factors are reviewed in Table 3.1
27
Table 3. Causes of Anemia in CKD
The anemia of CKD is associated with a number of adverse pathophysiologic

consequences, including decreased tissue oxygen delivery and utilization, increased
cardiac output, ventricular dilation, and ventricular hypertrophy. Clinical manifestations
include fatigue and diminished exercise tolerance, angina, heart failure, decreased
cognition and mental acuity, and impaired host defense against infection. In addition,
anemia may play a role in growth restriction in children with CKD. Although many
studies in CKD patients have found that anemia and resistance to exogenous
erythropoietic-stimulating agents (ESA) are associated with a poor prognosis, the relative
contribution to a poor outcome of the low hematocrit itself, versus inflammation as a
cause of the anemia and ESA resistance, remains unclear.1
Abnormal Hemostasis
Patients with later stages of CKD may have a prolonged bleeding time, decreased
activity of platelet factor III, abnormal platelet aggregation and adhesiveness, and
impaired prothrombin consumption. Clinical manifestations include an increased
tendency to bleeding and bruising, prolonged bleeding from surgical incisions,
menorrhagia, and GI bleeding. Interestingly, CKD patients also have a greater
susceptibility to thromboembolism, especially if they have renal disease that includes
nephrotic-range proteinuria. The latter condition results in hypoalbuminemia and renal
loss of anticoagulant factors, which can lead to a thrombophilic state.1
2.7.5. Neuromuscular Abnormalities
Central nervous system (CNS), peripheral, and autonomic neuropathy as well as
abnormalities in muscle structure and function are all well-recognized complications of
CKD. Subtle clinical manifestations of uremic neuromuscular disease usually become
28
evident at stage 3 CKD. Early manifestations of CNS complications include mild
disturbances in memory and concentration and sleep disturbance. Neuromuscular
irritability, including hiccups, cramps, and twitching, becomes evident at later stages. In
advanced untreated kidney failure, asterixis, myoclonus, seizures, and coma can be seen.1
Peripheral neuropathy usually becomes clinically evident after the patient reaches
stage 4 CKD, although electrophysiologic and histologic evidence occurs earlier.
Initially, sensory nerves are involved more than motor, lower extremities more than
upper, and distal parts of the extremities more than proximal. The “restless leg syndrome”
is characterized by ill-defined sensations of sometimes debilitating discomfort in the legs
and feet relieved by frequent leg movement. Evidence of peripheral neuropathy without
another cause (e.g., diabetes mellitus) is an indication for starting renal replacement
therapy. Many of the complications described above will resolve with dialysis, although
subtle nonspecific abnormalities may persist.1
2.7.6. Gastrointestinal and Nutritional Abnormalities
Uremic fetor, a urine-like odor on the breath, derives from the breakdown of urea
to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia).
Gastritis, peptic disease, and mucosal ulcerations at any level of the GI tract occur in
uremic patients and can lead to abdominal pain, nausea, vomiting, and GI bleeding. These
patients are also prone to constipation, which can be worsened by the administration of
calcium and iron supplements. The retention of uremic toxins also leads to anorexia,
nausea, and vomiting.1
Protein restriction may be useful to decrease nausea and vomiting; however, it
may put the patient at risk for malnutrition and should be carried out, if possible, in
consultation with a registered dietitian specializing in the management of CKD patients.
Weight loss and protein-energy malnutrition, a consequence of low protein and caloric
intake, is common in advanced CKD and is often an indication for initiation of renal
replacement therapy. Metabolic acidosis and the activation of inflammatory cytokines can
promote protein catabolism. A number of indices are useful in nutritional assessment and
include dietary history, including food diary and subjective global assessment; edema-
free body weight; and measurement of urinary protein nitrogen appearance. Dual-energy
x-ray absorptiometry is now widely used to estimate lean body mass versus fluid weight.
Nutritional guidelines for patients with CKD are summarized in the “Treatment” section.1
29
2.7.7. Endocrine-Metabolic Disturbances
Glucose metabolism is impaired in CKD. However, fasting blood glucose is
usually normal or only slightly elevated, and mild glucose intolerance does not require
specific therapy. Because the kidney contributes to insulin removal from the circulation,
plasma levels of insulin are slightly to moderately elevated in most uremic patients, both
in the fasting and postprandial states. Because of this diminished renal degradation of
insulin, patients on insulin therapy may need progressive reduction in dose as their renal
function worsens. Many anti-hyperglycemic agents, including the gliptins, require dose
reduction in renal failure, and some, such as metformin and sulfonylureas are
contraindicated when the GFR is less than half of normal. A recent 2119 exception is the
class of drugs that inhibit sodium-glucose transport in the proximal tubule, resulting in
glucose lowering, accompanied by striking reductions in kidney function decline and in
cardiovascular events. The stabilization of GFR in many patients with this therapeutic
intervention represents a major, important added beneficial effect of these drugs. Their
long-term stabilizing effect on GFR and urine albumin excretion appears to result from
correction of hyperfiltration early in type 2 diabetes mellitus via re-activation of the
tubuloglomerular feedback loop. This represents a fortunate convergence of
pathophysiology of glomerular hyperfiltration in diabetes with drug discovery.1
In women with CKD, estrogen levels are low, and menstrual abnormalities,
infertility, and inability to carry pregnancies to term are common. When the GFR has
declined to ~40 mL/min, pregnancy is associated with a high rate of spontaneous abortion,
with only ~20% of pregnancies leading to live births, and pregnancy may hasten the
progression of the kidney disease itself. Women with CKD who are contemplating
pregnancy should consult first with a nephrologist in conjunction with an obstetrician
specializing in high-risk pregnancy. Men with CKD have reduced plasma testosterone
levels, and sexual dysfunction and oligospermia may supervene. Sexual maturation may
be delayed or impaired in adolescent children with CKD, even among those treated with
dialysis. Many of these abnormalities improve or reverse with intensive dialysis or with
successful renal transplantation.1
2.7.8. Dermatologic Disturbances
Abnormalities of the skin are prevalent in progressive CKD. Pruritus is quite
common and one of the most vexing manifestations of the uremic state. In advanced
30
CKD, even on dialysis, patients may become more pigmented, and this is felt to reflect
the deposition of retained pigmented metabolites, or urochromes. Although many of the
cutaneous abnormalities improve with dialysis, pruritus is often tenacious. The first lines
of management are to rule out unrelated skin disorders, such as scabies, and to treat
hyperphosphatemia, which can cause itch. Local moisturizers, mild topical
glucocorticoids, oral antihistamines, and ultraviolet radiation have been reported to be
helpful.1
A skin condition unique to CKD patients called nephrogenic fibrosing
dermopathy consists of progressive subcutaneous induration, especially on the arms and
legs. The condition is seen very rarely in patients with CKD who have been exposed to
the magnetic resonance contrast agent gadolinium. Current recommendations are that
patients with CKD stage 3 (GFR 30–59 mL/min) should minimize exposure to
gadolinium, and those with CKD stages 4–5 (GFR <30 mL/min) should avoid the use of
gadolinium agents unless it is medically necessary. However, no patient should be denied
an imaging investigation that is critical to management, and under such circumstances,
rapid removal of gadolinium by hemodialysis (even in patient’s not yet receiving renal
replacement therapy) shortly after the procedure may mitigate this sometimes devastating
complication.1
2.8. Evaluation
2.8.1. Initial Approach
History and Physical Examination Symptoms and overt signs of kidney disease
are often subtle or absent until renal failure supervenes. Thus, the diagnosis of kidney
disease often surprises patients and may be a cause of skepticism and denial. Particular
aspects of the history that are germane to renal disease include a history of hypertension
(which can cause CKD or more commonly be a consequence of CKD), diabetes mellitus,
abnormal urinalyses, and problems with pregnancy such as preeclampsia or early
pregnancy loss. A careful drug history should be elicited. Drugs to consider include
nonsteroidal anti-inflammatory agents, cyclooxygenase-2 (COX-2) inhibitors,
antimicrobials, chemotherapeutic agents, antiretroviral agents, proton pump inhibitors,
phosphate-containing bowel cathartics, and lithium. In evaluating the uremic syndrome,
questions about appetite, weight loss, nausea, hiccups, peripheral edema, muscle cramps,
31
pruritus, and restless legs are especially helpful. A family history of kidney disease,
together with assessment of manifestations in other organ systems such as auditory,
visual, and integumentary, may lead to the diagnosis of a heritable form of CKD (e.g.,
Alport or Fabry disease, cystinosis) or shared environmental exposure to nephrotoxic
agents (e.g., heavy metals, aristolochic acid). It should be noted that clustering of CKD,
sometimes of different etiologies, is often observed within families.1
The physical examination should focus on blood pressure and target organ damage
from hypertension. Thus, funduscopy and precordial examination should be carried out.
Funduscopy is important in the diabetic patient, because it may show evidence of diabetic
retinopathy, which is associated with nephropathy. Other physical examination
manifestations of CKD include edema and sensory polyneuropathy. The finding of
asterixis or a pericardial friction rub not attributable to other causes usually signifies the
presence of the uremic syndrome.1,2
2.8.2. Laboratory Investigation
Laboratory studies should focus on a search for clues to an underlying causative
or aggravating disease process and on the degree of renal damage and its consequences.
Serum and urine protein electrophoresis, looking for multiple myeloma, should be
obtained in all patients >35 years with unexplained CKD, especially if there is associated
anemia and elevated, or even inappropriately normal, serum calcium concentration in the
face of renal insufficiency. In the presence of glomerulonephritis, autoimmune diseases
such as lupus and underlying infectious etiologies such as hepatitis B and C and HIV
should be tested. Serial measurements of renal function should be obtained to determine
the pace of renal deterioration and ensure that the disease is truly chronic rather than acute
or subacute and hence potentially reversible. Serum concentrations of calcium,
phosphorus, vitamin D, and PTH should be measured to evaluate metabolic bone disease.
Hemoglobin concentration, iron, vitamin B12, and folate should also be evaluated. A 24-
h urine collection may be helpful, because protein excretion >300 mg may be an
indication for therapy with ACE inhibitors or ARBs.
2.8.3. Imaging Studies
The most useful imaging study is a renal ultrasound, which can verify the presence
of two kidneys, determine if they are symmetric, provide an estimate of kidney size, and
rule out renal masses and evidence of obstruction. Because it takes time for kidneys to
32
shrink as a result of chronic disease, the finding of bilaterally small kidneys supports the
diagnosis of CKD of long-standing duration. If the kidney size is normal, it is possible
that the renal disease is acute or subacute. The exceptions are diabetic nephropathy (where
kidney size is increased at the onset of diabetic nephropathy before CKD supervenes),
amyloidosis, and HIV nephropathy, where kidney size may be normal in the face of CKD.
Polycystic kidney disease that has reached some degree of renal failure will almost always
present with enlarged kidneys with multiple cysts. A discrepancy >1 cm in kidney length
suggests either a unilateral developmental abnormality or disease process or renovascular
disease with arterial insufficiency affecting one kidney more than the other. The diagnosis
of renovascular disease can be undertaken with different techniques, including Doppler
sonography, nuclear medicine studies, or CT or magnetic resonance imaging (MRI)
studies. If there is a suspicion of reflux nephropathy (recurrent childhood urinary tract
infection, asymmetric renal size with scars on the renal poles), a voiding cystogram may
be indicated. However, in most cases, by the time the patient has CKD, the reflux has
resolved, and even if still present, repair does not improve renal function. Radiographic
contrast imaging studies are not particularly helpful in the investigation of CKD.
Intravenous or intraarterial dye should be avoided where possible in the CKD patient,
especially with diabetic nephropathy, because of the risk of radiographic contrast dye–
induced renal failure. When unavoidable, appropriate precautionary measures include
avoidance of hypovolemia at the time of contrast exposure, minimization of the dye load,
and choice of radiographic contrast preparations with the least nephrotoxic potential.
Additional measures thought to attenuate contrast-induced worsening of renal function
include judicious administration of sodium bicarbonate–containing solutions and N
acetylcysteine.1
2.8.4. Kidney Biopsy
In the patient with bilaterally small kidneys, renal biopsy is not advised because
(1) it is technically difficult and has a greater likelihood of causing bleeding and other
adverse consequences, (2) there is usually so much scarring that the underlying disease
may not be apparent, and (3) the window of opportunity to render disease-specific therapy
has passed. Other contraindications to renal biopsy include uncontrolled hypertension,
active urinary tract infection, bleeding diathesis (including ongoing anticoagulation), and
severe obesity. Ultrasound-guided percutaneous biopsy is the favored approach, but a
33
surgical or laparoscopic approach can be considered, especially in the patient with a single
kidney where direct visualization and control of bleeding are crucial. In the CKD patient
in whom a kidney biopsy is indicated (e.g., suspicion of a concomitant or superimposed
active process such as interstitial nephritis or in the face of accelerated loss of GFR), the
bleeding time should be measured, and if increased, desmopressin should be administered
immediately prior to the procedure.1,2
A brief run of hemodialysis (without heparin) may also be considered prior to
renal biopsy to normalize the bleeding time.
2.9. Diagnosis Workup

The most important initial diagnostic step is to distinguish newly diagnosed CKD
from acute or subacute renal failure, because the latter two conditions may respond to
targeted therapy. Previous measurements of serum creatinine concentration are
particularly helpful in this regard. Normal values from recent months or even years
suggest that the current extent of renal dysfunction could be more acute, and hence
reversible, than might otherwise be appreciated. In contrast, elevated serum creatinine
concentration in the past suggests that the renal disease represents a chronic process. Even
if there is evidence of chronicity, there is the possibility of a superimposed acute process
(e.g., ECFV depletion, urinary infection or obstruction, or nephrotoxin exposure)
supervening on the chronic condition. If the history suggests multiple systemic
manifestations of recent onset (e.g., fever, polyarthritis, rash), it should be assumed that
renal insufficiency is part of an acute systemic illness.1
Although kidney biopsy can usually be performed in early CKD (stages 1–3), it
is not always indicated. For example, in a patient with a history of type 1 diabetes mellitus
for 15–20 years with retinopathy, nephrotic-range proteinuria, and absence of hematuria,
the diagnosis of diabetic nephropathy is very likely and biopsy is usually not necessary.
However, if there were some other finding not typical of diabetic nephropathy, such as
hematuria or white blood cell casts, or absence of diabetic retinopathy, some other disease
may be present and a biopsy may be indicated.1
In the absence of a clinical diagnosis, kidney biopsy may be the only recourse to
establish an etiology in early-stage CKD. However, as noted above, once the CKD is
advanced and the kidneys are small and scarred, there is little utility and significant risk
34
in attempting to arrive at a specific diagnosis. Genetic testing is increasingly entering the
repertoire of diagnostic tests, since the patterns of injury and kidney morphologic
abnormalities often reflect overlapping causal mechanisms, whose origins can sometimes
be attributed to a genetic predisposition or cause.1
2.10. Treatment
2.10.1. Chronic Kidney Disease
Slowing The Progression of CKD
There is variation in the rate of decline of GFR among patients with CKD.
However, the following interventions should be considered in an effort to stabilize or
slow the decline of renal function.1
Reducing Intraglomerular Hypertension and Proteinuria
Increased intraglomerular filtration pressures and glomerular hypertrophy
develop as a response to loss of nephron number. This response is maladaptive, as it
promotes the ongoing decline of kidney function even if the inciting process has been
treated or spontaneously resolved. Control of glomerular hypertension is important in
slowing the progression of CKD. Moreover, elevated blood pressure increases proteinuria
by increasing its flux across the glomerular capillaries. Conversely, the renoprotective
effect of antihypertensive medications is gauged through the consequent reduction of
proteinuria. Thus, the more effective a given treatment is in lowering protein excretion,
the greater the subsequent impact on protection from decline in GFR. This observation is
the basis for the treatment guideline establishing 130/80 mmHg as a target blood pressure
in proteinuric CKD patients.1
Several controlled studies have shown that ACE inhibitors and ARBs are effective
in slowing the progression of renal failure in patients with advanced stages of both
diabetic and nondiabetic CKD, in large part through effects on efferent vasodilatation and
the subsequent decline in glomerular hypertension. In the absence of an anti-proteinuric
response with either agent alone, combined treatment with both ACE inhibitors and ARBs
has been considered. The combination is associated with a greater reduction in proteinuria
compared to either agent alone. Insofar as reduction in proteinuria is a surrogate for
improved renal outcome, the combination would appear to be advantageous. However,
there is a greater incidence of acute kidney injury and adverse cardiac events from such
35
combination therapy. On balance, therefore, ACE inhibitor plus ARB therapy should be
avoided. A progressive increase in serum creatinine concentration with these agents may
suggest the presence of renovascular disease within the large or small arteries.
Development of side effects may mandate the use of second-line antihypertensive agents
instead of ACE inhibitors or ARBs. Among the calcium channel blockers, diltiazem and
verapamil may exhibit superior antiproteinuric and renoprotective effects compared to
the dihydropyridines. At least two different categories of response can be considered: one
in which progression is strongly associated with systemic and intraglomerular
hypertension and proteinuria (e.g., diabetic nephropathy, glomerular diseases) and in
which ACE inhibitors and ARBs are likely to be the first choice; and another in which
proteinuria is mild or absent initially (e.g., adult polycystic kidney disease and other
tubulointerstitial diseases), where the contribution of intraglomerular hypertension is less
prominent and other antihypertensive agents can be useful for control of systemic
hypertension.1
MANAGING OTHER COMPLICATIONS OF CKD
Medication Dose Adjustment
Although the loading dose of most drugs is not affected by CKD because renal
elimination is not used in the calculation, the maintenance doses of many drugs will need
to be adjusted. For those agents in which >70% excretion is by a nonrenal route, such as
hepatic elimination, dose adjustment may not be needed. Some drugs that should be
avoided include metformin, meperidine, and oral anti-hyperglycemics that are eliminated
by the kidney. NSAIDs should be avoided because of the risk of further worsening of
kidney function. Many antibiotics, antihypertensives, and antiarrhythmics may require a
reduction in dosage or change in the dose interval. Several online Web-based databases
for dose adjustment of medications according to stage of CKD or estimated GFR are
available (e.g., http://www.globalrph.com/ 2121 index_renal.htm). Nephrotoxic
radiocontrast agents and gadolinium should be avoided or used according to strict
guidelines when medically necessary as discussed above.1
PREPARATION FOR RENAL REPLACEMENT THERAPY
Temporary relief of symptoms and signs of impending uremia, such as anorexia,
nausea, vomiting, lassitude, and pruritus, may sometimes be achieved with dietary protein
36
restriction. However, this carries a risk of malnutrition, and thus plans for more long-term
management should be in place.1
Maintenance dialysis and kidney transplantation have extended the lives of
hundreds of thousands of patients with CKD worldwide. Clear indications for initiation
of renal replacement therapy for patients with CKD include uremic pericarditis,
encephalopathy, intractable muscle cramping, anorexia, and nausea not attributable to
reversible causes such as peptic ulcer disease, evidence of malnutrition, and fluid and
electrolyte abnormalities, principally hyperkalemia or ECFV overload, that are refractory
to other measures.1
Recommendations for the Optimal Time for Initiation of Renal Replacement
Therapy
Because of the individual variability in the severity of uremic symptoms and renal
function, it is ill-advised to assign an arbitrary urea nitrogen or creatinine level to the need
to start dialysis. Moreover, patients may become accustomed to chronic uremia and deny
symptoms, only to find that they feel better with dialysis and realize in retrospect how
poorly they were feeling before its initiation.1
Previous studies suggested that starting dialysis before the onset of severe
symptoms and signs of uremia was associated with prolongation of survival. This led to
the concept of “healthy” start and is congruent with the philosophy that it is better to keep
patients feeling well rather than allowing them to become ill with uremia and then
attempting to return them to better health with dialysis or transplantation. Although recent
studies have not confirmed an association of early-start dialysis with improved patient
survival, there may be merit in this approach for some patients. On a practical level,
advanced preparation may help to avoid problems with the dialysis process itself (e.g., a
poorly functioning fistula for hemodialysis or malfunctioning peritoneal dialysis catheter)
and, thus, preempt the morbidity associated with resorting to the insertion of temporary
hemodialysis access with its attendant risks of sepsis, bleeding, thrombosis, and
association with accelerated mortality.1
Patient Education
Social, psychological, and physical preparation for the transition to renal
replacement therapy and the choice of the optimal initial modality are best accomplished
with a gradual approach involving a multidisciplinary team. Along with conservative
37
measures discussed in the sections above, it is important to prepare patients with an
intensive educational program, explaining the likelihood and timing of initiation of renal
replacement therapy and the various forms of therapy available, and the option of
nondialytic conservative care. The more knowledgeable that patients are about
hemodialysis (both in-center and home-based), peritoneal dialysis, and kidney
transplantation, the easier and more appropriate will be their decisions. Patients who are
provided with education are more likely to choose homebased dialysis therapy. This
approach is of societal benefit because home-based therapy is less expensive and is
associated with improved quality of life. The educational programs should be commenced
no later than stage 4 CKD so that the patient has sufficient time and cognitive function to
learn the important concepts, make informed choices, and implement preparatory
measures for renal replacement therapy.1
Exploration of social support is also important. Early education of family
members for selection and preparation of a home dialysis helper or a biologically or
emotionally related potential living kidney donor should occur long before the onset of
symptomatic renal failure.1
Kidney transplantation offers the best potential for complete rehabilitation,
because dialysis replaces only a small fraction of the kidneys’ filtration function and none
of the other renal functions, including endocrine and anti-inflammatory effects.
Generally, kidney transplantation follows a period of dialysis treatment, although
preemptive kidney transplantation (usually from a living donor) can be carried out if it is
certain that the renal failure is irreversible.1
2.10.2. Fluid, Electrolyte, and Acid-Base Disorders
Dietary salt restriction and the use of loop diuretics, occasionally in combination
with metolazone, may be needed to maintain euvolemia. Water restriction is indicated
only if there is a problem with hyponatremia.1
Hyperkalemia often responds to dietary restriction of potassium, the use of
kaliuretic diuretics, and avoidance of both potassium supplements (including occult
sources, such as dietary salt substitutes) and dose reduction or avoidance of potassium-
retaining medications (especially angiotensin-converting enzyme [ACE] inhibitors or
angiotensin receptor blockers [ARBs]). Kaliuretic diuretics promote urinary potassium
excretion, whereas potassium-binding resins, such as calcium resonium, sodium
38
polystyrene or patiromer can promote potassium loss through the GI tract and may reduce
the incidence of hyperkalemia. Intractable hyperkalemia is an indication (although
uncommon) to consider institution of dialysis in a CKD patient. The renal tubular acidosis
and subsequent anion-gap metabolic acidosis in progressive CKD will respond to alkali
supplementation, typically with sodium bicarbonate. Recent studies suggest that this
replacement should be considered when the serum bicarbonate concentration falls below
20–23 mmol/L to avoid the protein catabolic state seen with even mild degrees of
metabolic acidosis and to slow the progression of CKD.1
2.10.3. Disorders of Calcium and Phosphate Metabolism
The optimal management of secondary hyperparathyroidism and osteitis fibrosa
is prevention. Once the parathyroid gland mass is very large, it is difficult to control the
disease. Careful attention should be paid to the plasma phosphate concentration in CKD
patients, who use of phosphate-binding agents. These are agents that are taken with meals
and complex the dietary phosphate to limit its GI absorption. Examples of phosphate
binders are calcium acetate and calcium carbonate. A major side effect of calcium-based
phosphate binders is calcium accumulation and hypercalcemia, especially in patients with
low-turnover bone disease. Sevelamer and lanthanum are non-calcium-containing
polymers that also function as phosphate binders; they do not predispose CKD patients to
hypercalcemia and may attenuate calcium deposition in the vascular bed.1
Calcitriol exerts a direct suppressive effect on PTH secretion and also indirectly
suppresses PTH secretion by raising the concentration of ionized calcium. However,
calcitriol therapy may result in hypercalcemia and/or hyperphosphatemia through
increased GI absorption of these minerals. Certain analogues of calcitriol are available
(e.g., paricalcitol) that suppress PTH secretion with less attendant hypercalcemia.1
Recognition of the role of the extracellular calcium-sensing receptor has led to the
development of calcimimetic agents that enhance the sensitivity of the parathyroid cell to
the suppressive effect of calcium. This class of drug, which includes cinacalcet, produces
a dose-dependent reduction in PTH and plasma calcium concentration in some patients.1
Current National Kidney Foundation Kidney Disease Outcomes Quality Initiative
guidelines recommend a target PTH level between 150 and 300 pg/mL, recognizing that
very low PTH levels are associated with adynamic bone disease and possible
consequences of fracture and ectopic calcification.1
39
2.10.4. Cardiovascular Abnormalities
Management of Hypertension
The overarching goal of hypertension therapy in CKD is to prevent the extrarenal
complications of high blood pressure, such as cardiovascular disease and stroke. Although
a clear-cut generalizable benefit in slowing progression of CKD remains as yet unproven,
the benefit for cardiac and cerebrovascular health is compelling. In all patients with CKD,
blood pressure should be controlled to levels recommended by national guideline panels.
In CKD patients with diabetes or proteinuria >1 g per 24 h, blood pressure should be
reduced to <130/80 mmHg, if achievable without prohibitive adverse effects. Salt
restriction should be the first line of therapy. When volume management alone is not
sufficient, the choice of antihypertensive agent is similar to that in the general population.
ACE inhibitors and ARBs appear to slow the rate of decline of kidney function in a
manner that extends beyond reduction of systemic arterial pressure and that involves
correction of the intraglomerular hyperfiltration and hypertension. Occasionally,
introduction of ACE inhibitors and ARBs can actually precipitate an episode of acute
kidney injury, especially when used in combination in patients with ischemic
renovascular disease. Slight reduction of GFR (<30% of baseline) may signify a salutary
reduction in intra-glomerular hypertension and hyperfiltration, and, if stable over time,
can be tolerated with continued monitoring. Progressive decline in GFR should prompt
discontinuation of these agents. The use of ACE inhibitors and ARBs may also be
complicated by the development of hyperkalemia. Often the concomitant use of a
combination of kaliuretic diuretics (e.g., furosemide with metolazone), or a potassium-
lowering GI tract binder, such as patrimer, can improve potassium excretion in addition
to improving blood pressure control. Potassium-sparing diuretics should be used with
caution or avoided altogether in most patients.1
The recent movement to even lower blood pressure targets in the general
population may not be applicable to patients with CKD, who often lack autoregulation to
maintain GFR in the face of low perfusion pressure. If a patient experiences sudden
decline in kidney function with intensification of antihypertensive therapy, consideration
should be given to reducing therapy.1
Management of Cardiovascular Disease
40
There are many strategies available to treat the traditional and nontraditional risk
factors in CKD patients. Although these have proved effective in the general population,
there is little evidence for their benefit in patients with advanced CKD, especially those
on dialysis. Certainly hypertension, and dyslipidemia promote atherosclerotic disease and
are treatable complications of CKD. Renal disease complicated by nephrotic syndrome is
associated with a very atherogenic lipid profile and hypercoagulability, which increases
the risk of occlusive vascular disease. Because diabetes mellitus and hypertension are the
two most frequent causes of advanced CKD, it is not surprising that cardiovascular
disease is the most frequent cause of death in dialysis patients. The role of “inflammation”
may be quantitatively more important in patients with kidney disease, and the treatment
of more traditional risk factors may result in only modest success. However, modulation
of traditional risk factors may be the only weapon in the therapeutic armamentarium for
these patients until the nature of inflammation in CKD and its treatment are better
understood.1
Pericardial Disease
Uremic pericarditis is an absolute indication for the urgent initiation of dialysis or
for intensification of the dialysis prescription in those already receiving dialysis. Because
of the propensity to hemorrhage in pericardial fluid, hemodialysis should be performed
without heparin. A pericardial drainage procedure should be considered in patients with
recurrent pericardial effusion, especially with echocardiographic signs of impending
tamponade. Non-uremic causes of pericarditis and effusion include viral, malignant,
tuberculous, and autoimmune etiologies. It may also be seen after myocardial infarction
and as a complication of treatment with the antihypertensive drug minoxidil.1
2.10.5. Hematologic Abnormalities
Anemia
The availability of recombinant human ESA has been one of the most significant
advances in the care of renal patients since the introduction of dialysis and renal
transplantation. Its routine use has obviated the need for regular blood transfusions in
severely anemic CKD patients, thus dramatically reducing the incidence of transfusion-
associated infections and iron overload. Frequent blood transfusions in dialysis patients
also lead to the development of alloantibodies that can sensitize the patient to donor
kidney antigens and make renal transplantation more problematic.1
41
Adequate bone marrow iron stores should be available before treatment with ESA
is initiated. Iron supplementation is usually essential to ensure an optimal response to
ESA in patients with CKD because the demand for iron by the marrow frequently exceeds
the amount of iron that is immediately available for erythropoiesis (measured by percent
transferrin saturation), as well as the amount in iron stores (measured by serum ferritin).
For the CKD patient not yet on dialysis or the patient treated with peritoneal dialysis, oral
iron supplementation should be attempted. If there is GI intolerance or poor GI
absorption, the patient may have to undergo IV iron infusion. For patients on
hemodialysis, IV iron can be administered during dialysis, keeping in mind that iron
therapy can increase the susceptibility to bacterial infections, and that the adverse effects
of free serum iron are still under investigation. In addition to iron, an adequate supply of
other major substrates and cofactors for red cell production must be ensured, including
vitamin B12 and folate. Anemia resistant to recommended doses of ESA in the face of
adequate iron stores may be due to some combination of the following: acute or chronic
inflammation, inadequate dialysis, severe hyperparathyroidism, chronic blood loss or
hemolysis, chronic infection, or malignancy.1
Randomized, controlled trials of ESA in CKD have failed to show an
improvement in cardiovascular outcomes with this therapy. Indeed, there has been an
indication that the use of ESA in CKD may be associated with an increased risk of stroke
in those with type 2 diabetes, an increase in thromboembolic events, and perhaps a faster
progression of renal decline. Therefore, any benefit in terms of improvement of anemic
symptoms needs to be balanced against the potential cardiovascular risk. Although further
studies are needed, it is quite clear that complete normalization of the hemoglobin
42
concentration has not been demonstrated to be of incremental benefit to CKD patients.
Current practice is to target a hemoglobin concentration of 100–115 g/L.1
Abnormal Hemostasis
Abnormal bleeding time and coagulopathy in patients with renal failure may be
reversed temporarily with desmopressin (DDAVP), cryoprecipitate, IV conjugated
estrogens, blood transfusions, and ESA therapy. Optimal dialysis will usually correct a
prolonged bleeding time.1
Given the coexistence of bleeding disorders and a propensity to thrombosis that
is unique in the CKD patient, decisions about anticoagulation that have a favorable risk-
benefit profile in the general population may not be applicable to the patient with
advanced CKD. One example is warfarin anticoagulation for atrial fibrillation; the
decision to anticoagulate should be made on an individual basis in the CKD patient
because there appears to be a greater risk of bleeding complications.1
Certain anticoagulants, such as fractionated low-molecularweight heparin, may
need to be avoided or dose-adjusted in these patients, with monitoring of factor Xa
activity where available. It is often more prudent to use conventional unfractionated
heparin, titrated to the measured partial thromboplastin time, in hospitalized patients
requiring an alternative to warfarin anticoagulation. The new classes of oral
anticoagulants are all, in part, renally eliminated and need to be avoided or dose adjusted
in the face of decreased GFR.1
2.11. Prognosis
Patients with chronic kidney disease (CKD) generally experience progressive loss
of kidney function and are at risk for end-stage renal disease (ESRD). The rate of
progression depends on age, the underlying diagnosis, the success of implementation of
secondary preventive measures, and the individual patient. Timely initiation of chronic
renal replacement therapy is imperative to prevent the uremic complications of CKD that
can lead to significant morbidity and death.3
43
REFERENCES
1 Bargman JM, Skorecki KL. Chronic Kidney Disease. In Jameson JL, et al. ed.
Harrison’s Principles of Internal Medicine 20th edition. New York: McGraw-Hill
Medical Publishing Division. 2008: 2111-21.
2 Amend WJ, Vincenti FG. Chronic Renal Failure & Dialysis. In Tanagho E. &
McAninch J.W. ed. Smith’s General Urology 17th edition. New York: McGraw-
Hill Medical Publishing Division. 2018: 536-8.
3 Arora P. Chronic Kidney Disease [cited 2019 6 April]. Available from:
https://emedicine.medscape.com/article/238798-overview.
4 Kemenkes RI. Riskesdas 2018.
44

Case Report: Chronic Kidney Failure

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Case Report: Chronic Kidney Failure

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CASE REPORT

CHRONIC KIDNEY FAILURE

MEDICAL PROFESSION PROGRAMME DEPT. OF INTERNAL MEDICINE

Jakarta, August 2019

History of Present Illness

History in The Family

History of Treatment and Medication

General Physical Examination

Inspection : Ictus cordis not seen in ICS V LMCS

Palpation : Ictus cordis palpable ICS V LMCS

Percussion : Right heart margin: Sternalis line sinistra ICS-V

Left heart margin: Midclavicula line sinistra ICS-V.

Inspection : Abdominal surface appears convex, distention (+), scar tissue

Auscultation : Bowel sounds are normal

Palpation : Epigastric Pain (+), not palpable enlargement of

Percussion : Tympanic in all abdominal fields, Shifting dullness (-).

Acral : warm (+/+)

CRT : < 2 second/ < 2 second

Akral : warm (+/+)

Edema : (+/+) minimal

CRT : < 2 second/ < 2 second

EXAMINATION VALUE UNITS NORMAL

Hemoglobin 8.6 ↓ g/dL 13,2 – 17,3

Leukocyte 6.90 103/uL 3.8 – 10,6

Trombosit 164 103/µl 150 - 440

Eritrosit 2.67 ↓ 106/µl 4,4 – 5,9

MCHC 33 g/dl 32-36

August 24th 2017 - 00.08

EXAMINATION VALUE UNITS NORMAL

Creatinin 11.8 mg/dL <1.4

Natrium 139 mEq/L 135 – 147

Kalium 3.9 mEq/L 3.5 – 5.0

Clorida 97 mEq/L 94 – 111

Glucose 103 Mg/dL 70-200

EXAMINATION VALUE UNITS NORMAL

Hemoglobin 5.3 ↓ g/dL 13,2 – 17,3

 Anemia et causa Chronic Kidney Disease dd/ Iron deficiency anemia

Patients routinely do hemodialysis at the Jakarta Islamic Hospital

August 24th 2017 - 00.08

July 05th 2019 – 10.17

S : Nausea and vomiting , anorexia, 2 weeks before hospitalized and

O : Vital Sign: BP: 120/90mmHg, HR:71x/minute, RR:18x/minute,

Physical Examination : Dry lip mukosa (+), Epigastric pain (+),

Ureum 79 mg/dL (increased), Creatinin 11,8 mg/dL (increased)

A : Chronic Kidney Disease

- IVFD NaCl 0,9% 7 tpm

S : Complained of weakness 4 days before hospitalized.

Vital Sign: BP: 120/90mmHg, HR:71x/minute, RR:18x/minute, Temperature:

Anemic conjungtiva (+/+)

Laboratory findings : 05/04/2019 (10.17)

Hemoglobin : 5,3 g/dL (decreased)

A : Anemia et causa Chronic Kidney Disease dd/ Iron deficiency anemia

HB post ( not checked yet)

Planning Non Therapeutics

IVFD NaCl 0,9% 7 tpm

Transfusion 600 ml PRC

S Nausea and vomiting , anorexia, 2 weeks before hospitalized and complined

A Chronic Kidney Disease