DUMAG, ARIANNE CAMILLE T.

SEC B - GROUP 8
PM WARD (DR. LU)

Date of Interview: April 1, 2023 (3rd hospital day)

Informant: Patient, daughter, and son

I. GENERAL DATA
RO, 69 years old, male, married, unemployed, Filipino, Roman Catholic, born on March
25, 1964 at Ligao, Albay, now currently residing at Pasay City, admitted for the 2nd time last
March 29, 2023 in Pasay City General Hospital.

II. CHIEF COMPLAINT

fever

III. HISTORY OF PRESENT ILLNESS

2 weeks PTA, patient experienced on and off fever with recorded highest temperature
of 39C and lowest of 37C, associated with chills and weakness. No other associated symptoms
such as headache, vomiting, and nausea. He self medicated with Paracetamol that afforded
temporary relief. No consultation done.
1 week PTA, patient sought consultation after his dialysis at Livewell Manila DIalysis,
he was diagnosed with UTI. Patient was prescribed antibiotics, name and dosage not recalled.
Patient was compliant with medication but no relief of symptoms. He self medicated with
Paracetamol, fever was alleviated.
Few hours PTA, still with fever, he went to PCGH, lab done that showed low platelet
count and was subsequently admitted.

IV. PAST MEDICAL HISTORY

Patient claims to have complete childhood vaccination such as BCG, Polio, Tetanus,
Pertussis, and MMR. Adult vaccination includes COVID-19. Patient had chicken pox. mumps,
and measles as a child.
He is a known diabetic and hypertensive for 30 yrs now, maintenance medications
include Metformin and Losartan 100mg. Patient started dialysis last year.
History cataract surgery 5 years ago at Boro hospital, Pasay City. Previous
hospitalization last August 2022 due to fatigue and loss of appetite.
No food or medication allergies. No major accidents and trauma. No history of stroke
and TB.

V. FAMILY HISTORY
Patient’s father died due to hypertension. Patient’s mother died at 50 y/o, due to a
stroke. He is the 3rd among 8 siblings, 4 of them are dead due to unrecalled conditions.
Patient has 6 children all are apparently healthy. Family history of hypertension, DM, and
Arthritis. No other known heredofamilial diseases such as gout, psychiatric problem, seizures
disorder and pulmonary tuberculosis.

VI. PERSONAL & SOCIAL HISTORY

Patient is married for 30 years, he is a college graduate. Previously worked as a brgy
captain. He currently lives in a 4 bedroom condo that is well ventilated with his wife, child and
 apo. Source of drinking water is from a refilling station.Garbage collected weekly. They have a
pet.
He is an ex-smoker for 13 years, and drinks alcohol about 1 bottle of gin per day; eats
3x a day plus merienda, he prefers to eat vegetables. Drinks coffee once every morning, he
used to drink soda but stopped last year. He sleeps around 7-8 hours before but now sleeps
less than 8 hours due to “pangangalay and sumasakit katawan”. He exercises every week,
hobbies include playing basketball. Source of stress is due to occasional family problems.

VII. REVIEW OF SYSTEMS

Constitutional: (+) Fatigue, (+) Chills, (+) Fever, (-) Weight Loss, (-) Weight Gain

Integumentary: (-) Dryness, (-) Rashes, (-) Itchiness, (-) Lumps, (-) Changes In Color

Hair: (-) Increase Hair Fall, (-) Baldness, (-) Excess Hair

Head: (-) Headache, (-) Dizziness, (-) Tenderness, (-) Trauma

Eyes: (-) Blurred Vision, (+) Use Of Glasses/Lenses, (-) Eye Pain, (-) Redness, (-) Double
Vision, (-) Photalgia, (-) Lacrimation

Ears: (-) Hearing Problem, (-) Ear Pain, (-) Itching, (-) Discharge

Mouth And Throat: (-) Dysphagia, (-) Hoarseness, (-) Sore Throat, (-) Odynophagia,
(+) Use Of Dentures, (-) Bleeding Gums, (-) Toothache, (-) Mouth Sores

Neck: (-) Pain, (-) Lump, (-) Stiffness

Breast: (-) Pain, (-) Lump, (-) Discharge

Respiratory: (-) Cough, (-) Sputum, (-) Hemoptysis, (-) Dyspnea, (-) Wheezing, (-) Rales

Cardiovascular: (-) Chest Pain, (-) Edema, (-) Orthopnea, (-) Paroxysmal Nocturnal
Dyspnea, (-) Palpitations, (-) Cyanosis, Easy Fatigability (-)

Gastrointestinal: (-) Nausea, (-) Abdominal Pain, (-) Hematemesis, (-) Hematochezia, (-)
Diarrhea, (-) Constipation, (-) Loss Of Appetite, (-) Change In Character Of Stool, (-) Pain On
Defecation

Renal: (-) Polyuria, (-) Dysuria, (-) Nocturia, (-) Urgency, (-) Gross Hematuria, (+)
Retention, (-) Flank Pain, (-) Reduced Caliber Or Force Of Urinary Stream, (-) Dribbling, (-) Straining,
(-) Hesitancy

Genitalia: (-) Pain, (-) Swelling, (-) Ulcers, (-) Itching, (-) Discharged

Peripheral Vascular: (+) Leg Cramps, (-) Varicose Veins

Musculoskeletal: (-) Back Pain, (-) Muscle Weakness, (-) Muscle Pain, (-) Joint Pain, (-) Joint
Stiffness, (-) Joint Swelling,
 Neurologic: (-) Paralysis, (-) Numbness, (-) Tremors, (-) Memory Loss, (-) Seizures, (-)
Changes In Mood

Hematologic: (-) Pallor, (-) Easy Bruising, (-) Bleeding

Endocrine: (-) Heat/Cold Intolerance, (-) Excessive Sweating, (-) Polydipsia, (-) Polyphagia

Psychiatric: (-) Nervousness, (-) Hallucinations, (-) Depression, (-) Anxiety

VIII. COMPLETE PHYSICAL EXAMINATION

General Survey
Patient is medium built, well nourished, well developed, conscious, coherent,
cooperative, ambulatory, and not in cardiorespiratory distress.

Vital Signs Anthropometrics

BP HR HT 5’
160/100 mmHg 110/min

RR 30/min T 37.6℃ WT 50 kgs

Integument
The skin is brown in color, warm, dry to touch, has good skin turgor, no superficial
blood vessels, with some hyperpigmentation. Hair is thin, soft, and sparse. CRT is less than 2
seconds.

HEENT

Cranium The head is midline in position with no abnormal head

movement. The skull is normocephalic, oval in shape and
symmetrical. There are no visible lesions, scales, and
deformities.The hair is slightly gray in color. The cranium is
normocephalic and symmetrical. There is no tenderness,
swelling, abnormal prominence, and depression. The hair is
smooth and dry.

Face The face is symmetrical, skin is brown in color, soft and smooth
with no lesions, and with some hyperpigmentation.

Eyes Eyebrows and eyelashes are black in color. Eyelashes are short
and present in both upper and lower eyelids. Conjunctiva is
pink in color. Sclera is anicteric. Iris is round and brown in color.
Pupils are round and symmetrical, can
accommodate, reactive to both direct and indirect light reflex.
 Ears No lesions, nodules, and deformities. Symmetrical, auricle
normal size, patent ear canal. Intact tympanic membrane.
AC>BC

Nose Nose is symmetrical and pointed. No alar flaring. Turbinates are

pinkish, no edema, no swelling, and no secretions.

Mouth Lips are pale and dry in texture. No lesions. Buccal mucosa and
gums are pinkish, moist, with no lesions. Teeth are yellowish
with an incomplete set of teeth. Tongue is whitish in color, in
midline position upon protrusion and retraction, and can move
without difficulty. No tremors, no coating, no lesions noted. The
hard and soft palate is pinkish, no masses, lesions and bony
protuberance.

Neck Skin is fair in color. Normal in size, symmetrical with full range
of motion . Trachea is in the midline. Thyroid is not visible but
palpable with no tenderness, moves with deglutition.

Chest & Lungs

​Skin is fair, no subcutaneous blood vessels seen, no lesions, slightly depressed. No
narrowing or widening of intercostal spaces Equal chest expansion. No tenderness, no masses,
no crepitations. No wheezes, crackles, and rhonchi. On percussion, it is dull all over. Normal
breath sounds.

Cardiovascular
​Upon inspection, there is no bulging nor depression of the pericardium. Carotid artery
pulses are palpable, strong and bounding. Radial artery, pulses palpable, strong and bounding.
Right & Left brachial artery pulse are palpable, strong, and bounding. Femoral artery not
palpated. Adynamic precordium, apex beat at 5th LICS MCL. No heaves, thrills and lifts. Apex
beat is at the 5th intercostal space left midclavicular line. S1 is loudest at the apex and S2 is
loudest at the base. No S3, S4, and extra heart sounds. Pulse rate is 110 bpm, regular
rhythm.

Abdomen
Upon inspection, the abdomen is globular, symmetrical, no skin lesions, no
superficial veins, no scars, no striae, the umbilicus is inverted, and no visible peristalsis.
Abdominal circumference is 89cm at the level of umbilicus. On auscultation, 23 bowel sounds,
no bruits and no friction rub. On light palpation, no tenderness. On deep palpation, no
tenderness . The liver, spleen, and kidneys are not palpable. On percussion, it was tympanitic
for the whole abdomen. Traube’s space is intact, no obliteration, no splenomegaly. Negative
for fluid wave test and shifting dullness.

Extremities
Upper Extremities
Patient’s skin is dry and brown in color, nail beds are pinkish, there is no swelling of
nail folds, no lesions, no edema, no tenderness, and no bone deformities seen. Intact range of
motion. There are no noted lesions on both lateral upper arms, no gross deformities. There is
no pain felt upon palpation on the sternoclavicular joint, acromion, coracoid process, and
greater tuberosity.

Lower Extremities
The skin is dry and brown in color, no gross deformities, lesions, and nodules.
Presence of bipedal pitting edema, grade 3. Posteriorly, cervical spine is concave, no joint
tenderness, no stiffness, no crepitations. There are no noted discoloration of the knee, no
nodules, no tenderness, no crepitations. Flexion and extension of the knee are normal and
without pain.

Neuro Exam

Cerebrum: The patient was conscious, coherent, and cooperative. He was oriented as to
person, time and place. He was able to demonstrate object recall, had no difficulty to follow
simple and complex commands, and able to do calculation, intact immediate, recent and
remote memory.

Cerebellum: Patient was able to execute a finger-nose test.

Cranial Nerves:

CN I Intact

CN II Both pupils are equally reactive to light and accommodation.

CN II / III Pupils are equally round and respond to direct light and
consensual stimuli

CN III / IV / V Patient has full extraocular muscle movements

CN V Able recognize sensations of pain and light touch bilaterally

on the face, able to demonstrate normal and force in the
muscle of mastication

CN VII Able to demonstrate different facial expression

CN VIII Patient was able to repeat words whispered to her and able
to localize the sound.

CN IX / X Uvula is at the midline. Gag reflex was not assessed, Both

sides of the pharyngeal wall are symmetrical, no hoarseness
of voice noted.

CN XI No fasciculation, tremors or atrophy noted. Patient was not

able to shrug her shoulders symmetrically.

CN XII Tongue is at the midline and symmetrical when protruded,

no atrophy nor involuntary movement observed.
 Motor Function: No muscle atrophy/hypertrophy, no fasciculation noted. There is no rigidity
and involuntary muscle movement noted. Patient has good muscle tone.
Reflexes: DTR are normal. Biceps, triceps, knee and ankle are 2+. Patient is negative for
Babinski.
Sensory: Intact sensation for pain, crude touch and position sensation for both upper and
lower extremities.
Meningeal: Brudzinski, Kernig’s sign, and nuchal rigidity are all negative.

IX. PRIMARY DIAGNOSIS & DIFFERENTIAL DIAGNOSIS

PRIMARY IMPRESSION: ESRD SECONDARY TO HYPERTENSION
Basis:
● On dialysis
● infection (immune system compromised)
● High blood pressure
● History of DM and hypertension (uncontrolled)
● Fatigue
● Tachycardia
● Tachypnea

Differential Diagnosis

RULE IN RULE OUT

RPGN (+) fever (-) hematuria

(+) prodromal illness (-) history of pharyngitis or
(+) fatigue tonsilitis
(+) hypertension
(+) tachycardia
(+) tacypnea

Dengue (+) on & off fever (high (-) rash

grade)
(+) fatigue
(+) tachycardia
(+) tachypnea

X. PATHOPHYSIOLOGY & EPIDEMIOLOGY

PATHOPHYSIOLOGY
● The pathophysiology of CKD involves two broad mechanisms of damage:
○ (1) specific initiating mechanisms particular to the underlying etiology (e.g.,
genetic abnormalities in kidney development, immune complex deposition, and
inflammation in certain types of glomerulonephritis, or toxin exposure in
certain diseases of the renal tubules and interstitium), and
○ (2) nonspecific mechanisms involving hyperfiltration and hypertrophy of the
remaining viable nephrons, which are common consequences of long-term
reduction of renal mass, irrespective of underlying etiology. The responses to
 reduction in nephron number are mediated by vasoactive hormones,
cytokines, and growth factors. Eventually, the 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.
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 explains why
a reduction in renal mass from an isolated insult may lead to a progressive
decline in renal function over many years and the efficacy of pharmacologic
approaches that attenuate this response

EPIDEMIOLOGY
● In 2017, 697.5 million cases of CKD (all stages) were recorded worldwide, for a global
prevalence of 9.1%. From 1990 to 2017, the global all-age prevalence of CKD
increased 29.3%, whereas the age-standardized prevalence remained stable.
● Globally, 1.2 million people died from CKD in 2017. The global all-age mortality rate
from CKD increased 41.5% from 1990 to 2017. Diabetic nephropathy accounted for
almost a third of disability-adjusted life years (DALYs) from CKD. Most of the burden of
CKD was concentrated in the three lowest quintiles of the Socio-demographic index
(SDI)

● The estimated prevalence of CKD stages 3–5 in LMICs in Asia was found it resembles
the global CKD stages 3–5 prevalence of 10.6%, and approximately 1 in every 10
people was affected by CKD (range from 0.7% to 61.4%). The prevalence of CKD
stages 3–5 reported in this study was higher in south Asia (13.5%) and western Asia
(13.1%) than those in south-east Asia (12.0%) and east Asia (8.6%).
● People had an increased risk of CKD stages 3–5 if they were elderly, had less than high
school education, suffered from obesity, hypertension, diabetes, hypertriglyceridemia,
hypercholesterolaemia, low levels of HDLc, hyperuricaemia, anemia, history of CHD,
history of stroke, history of CVD, family history of CKD, and NSAIDs medication use.

XI. DIAGNOSTICS

● 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
■ Should be obtained in all patients >35 years with unexplained CKD,
especially if there is associated anemia and elevated serum calcium
concentration
○ Serum albumin levels
■ Patients may have hypoalbuminemia due to malnutrition, urinary
protein loss, or chronic inflammation
○ Lipid profile
■ Patients with CKD have an increased risk of cardiovascular disease
○ Complete blood count (CBC)
 ○ Serum Creatinine and BUN
■ To check and compute GFR level
○ Urinalysis
■ To check for albumin levels in urine
○ Imaging studies - Renal ultrasonography
■ Should be done to look for hydronephrosis or involvement of the
retroperitoneum with fibrosis, tumor, or diffuse adenopathy
○ Kidney tissue biopsy
■ Indicated when kidney impairment and/or proteinuria approaching the
nephrotic range are present and the diagnosis is unclear after
appropriate workup.

XII. MANAGEMENT

INTERVENTION

INTERVENTION GOALS

● Exercise & lifestyle • Ifobese, aim for 5%weight loss

• Moderate intensity physical activity for at least
150minutes per week, or to a level compatible with their
cardiovascular and physical tolerance
• Complete smoking cessation

● Dietary modification • Salt restriction: <5g/day (equivalent to <2g/day or 90

mEq of Na• per day)
• Energy requirements: 25-35kcal/kg/day in CKD G1-5D&
posttransplantation who are metabolically stable

● Dietary modification • No CKD but at risk (solitary kidney, polycystic kidney,

DM, HPN): moderately low protein diet (0.8-1.0g/kg/day)
• CKD G3-5,metabolically stable, nondiabetic, not on
dialysis:
● Low protein diet (LPD): 0.55-0.60 g/kg/day, OR
● Supplemented very low protein diet (sVLPD):
0.28-0.43 g/kg/day with ketoanalogues of amino
acid (KAA)supplementation
• CKD G3-5,diabetic, not on dialysis: o.6-o.8 g/kg/day
• CKD G5 on maintenance HD/PD, with or without DM:
1-1.2g/kg/day

● Avoid and prevent AKI ● Manage AKI risk during intercurrent illness or
during procedures that are likely to increase AKI
risk

PHARMACOLOGIC
● BP should be lowered if ≥140/90 mm Hg and treated to a target <130/80 mm Hg
(<140/80 in elderly patients)
● RAS-inhibitors are first-line drugs because they reduce albuminuria in addition to
BP control.
○ ACE-inhibitors and ARBs are first line anti-hypertensive agents.
○ Optimal renoprotective doses:
■ Losartan 100 mg daily
 ■ Candesartan 16 mg daily
■ Irbesartan 900 mg daily
■ Valsartan 320-640 mg daily
■ Lisinopril 40 mg daily

○ Caution: may cause reversible hyperkalemia & AKI especially in advanced CKD &
renovascular hypertension

● CCBs and diuretics (loop-diuretics if eGFR <30 ml/min/1.73m2) can be added.

○ Diuretics
■ Useful in CKD because there is decrease in filtered load of salt & fluid when
there is reduced GFR
■ Loop diuretics: preferred in dissipating edema & in treating HPN, acidosis, &
hyperkalemia
■ Avoid exceeding ceiling doses of loop diuretics to prevent AKI, ototoxicity, &
electrolyte imbalance

GFR Ceiling Dose

FUROSEMIDE BUMETANIDE

GFR 20-50 ml/min ● 80-160 mg IV or 160 mg PO ● 6 mg IV or PO

GFR <20 ml/min ● 200 mg IV or 200 mg PO ● 10 mg IV or PO

● eGFR, microalbuminuria and blood electrolytes should be monitored.

XIII. COMPLICATIONS & PROGNOSIS

COMPLICATIONS

Complications due to ESRD

○ Coronary heart disease- is a significant complication of chronic kidney disease and is

the most common cause of death in this population. Patients on dialysis have a 10 to
30 times higher cardiovascular mortality risk than the general population.
○ Peripheral vascular disease
○ Hypertension
○ Mineral and bone disorders (secondary to hyperparathyroidism, vitamin D deficiency)
○ Hyperuricemia
○ Metabolic acidosis
○ Hyperphosphatemia
○ Hypoalbuminemia
○ Anemia
○ Decreased libido, erectile dysfunction

Complications due to Vascular Access/Dialysis

○ Bleeding
○ Local or disseminated intravascular infection
 ○ Graft occlusion
○ Electrolyte abnormalities after dialysis
○ Dialysis dementia
○ Dialysis disequilibrium syndrome

PROGNOSIS

● End-stage renal disease is a progressive disorder, and timely renal replacement therapy is
necessary to prevent death. The disorder is associated with numerous hospitalizations,
increased healthcare costs, and metabolic changes. The mortality rates for patients with
end-stage renal disease are significantly higher than those without the disease. Even with
timely dialysis, the death rates vary from 20% to 50% over 24 months. The most common
cause of death is hyperkalemia, followed by adverse cardiac events.
● Mortality rates are higher for men than women; similarly, Blacks are more prone to death due
to ESRD than Whites. The highest mortality rate is within the first six months of starting
dialysis. The 5-year survival rate for a patient undergoing long-term dialysis in the United
States is approximately 35% and about 25% in patients with diabetes.
● In children, puberty is delayed in both genders, and low vitamin D levels are common, an
independent risk factor for death.

REFERENCES:

Jameson, J. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., & Loscalzo, J. (2022).
In Harrison's Principles of Internal Medicine (21st ed.,). essay, McGraw-Hill Education.

Pradeep Arora, M. (2023, May 26). Chronic kidney disease (CKD). Practice Essentials,
Pathophysiology, Etiology. https://emedicine.medscape.com/article/238798-overview#a5

Suriyong, P., Ruengorn, C., Shayakul, C., Anantachoti, P., & Kanjanarat, P. (2022, February
25). Prevalence of chronic kidney disease stages 3-5 in low- and middle-income countries in
Asia: A systematic review and meta-analysis. PloS one.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8880400/