CHRONIC KIDNEY DISEASE

JI SHRESTHA RUJEN
General data
• Name: GH
• Date of admission: JUNE 11 2019
• Age: 20 years
• Sex: Female
• Status: Single
• Date of birth: 8/10/1998
• Occupation: Canteen Helper
• Data source: Patient
Chief complaint:

• Bipedal edema
History of Present illness:

• Patient was apparently well until 2 weeks prior to admission when

she had bipedal edema. No consult done, no medications taken.
• 1 week prior to admission, there was increase in the bipedal edema.
Sought consult at a local clinic, given ciprofloxacin.
• Few hours prior to admission, increase in the edema, sought consult,
admitted
Past medical history
• Medical:
• No Hypertension
• No asthma
• No DM
• No Pulmonary tuberculosis
• Surgical:
• No previous surgeries
• Ob/ gyne: had menarche at age of 14
Family history:

• Paternal: No known medical condition

• Maternal: Hypertension
Personal and social history:

• High school graduate

• Working as a canteen helper
• Non-smoker
• Non-alcoholic
Review of system:

• General: no recent weight change, clothing that fits normal, (+) fatigue
• Skin: (-) cyanosis, (-) pallor, (-) jaundice, (-)itchiness, (-)excessive
sweating
• Head: (-) dizziness, (-) headache, (-) vertigo, (-) seizures (+)facial
edema
• Eyes: (-) bilateral periorbital edema(exophthalmos), (-) abnormal
lacrimation, (-) blurring, (-) visual loss, (-) glaucoma
• Ears: (-) deafness, (-) tinnitus, (-) vertigo, (-) discharge
• Nose and: (-) sinusitis, (-) discharges, (-) epistaxis,
sinuses
• Mouth and Throat: (-)toothache, (-)gum bleeding, (-)sore throat
• Neck: (-)supple, (-)Mass, (-)neck vein distention
 Review of system
• Respiratory: (-) dyspnea, (-) cough, (-)hemoptysis, (-)sputum
• Cardiovascular: (+) easy fatigability, (-)palpitation, (-) syncope, (-) substernal pain
• Gastrointestinal: Appetite good; (-)nausea, (-) vomiting, (-) indigestion. Bowel
movement about once daily,
• Genitourinary: (-)dysuria, (-)urinary frequency, (-)urgency, (-)hematuria, (-)incomplete
bladder emptying, (-)incontinence (+)nocturnal polyuria, (+) foamy urine
• Musculoskeletal: (+) generalized body malaise, (-)edema, (-)swelling of joints, (-)
limitation of movement, (-)low back pain, (-)numbness
• CNS : (-)Headache, (-)vertigo, (-)numbness, (-)loss of memory
• Endocrine: (-)Heat intolerance, (-)cold intolerance, (-)notcuria
• Hematologic : (+)Pallor, (-)Bleeding tendency
PHYSCIAL EXAMINATION

• Vital signs:
• Temp: 37.3 c
• BP: 110/70mmhg
• RR: 22 breath/min
• HR: 66 pulse/min
PHYSICAL EXAMINATION
• General survey: Awake, conscious, coherent
• Skin: skin is pale color, moist, no skin rashes, warm to touch, has a good skin
turgor and elasticity capillary refill <2 seconds.
• HEENT: Edematoscephalic, Anicteric Sclera, Pale palpebral conjunctiva, no
tonsilloparyngeal congestion, no cervical lymphadenopathy,
• Chest and Lungs: symmetrical chest expansion, no retractions, clear breath
sounds
• Heart: Adynamic precordium, Normal Rate, Regular rhythm, no murmur
• Abdomen: Flabby, normoactive bowel sounds, soft, non-tender, hepatomegaly,
no splenomegaly
• Extremities: grossly normal extremities, no cyanosis, no pallor, bipedal edema
grade II, full equal pulses
Pertinent positives
Pertinent positives Pertinent negatives
Bipedal Edema No fever
Facial edema No palpitation
Easy fatigability No dyspnea
Nocturnal polyuria No tachycardia
Foamy urine No headache
Generalized body malaise Anictric sclera
Pallor No vertigo
Fatigue No sensorium loss
No cough
No vomiting
No jaundice
No angina
No murmur
Differential Diagnosis
Infectious
Liver
cirrhosis

Edema

Cardiac Renal
(CHD) (CKD)
 Differential diagnoses:
Diagnosis Rule in Rule out
AKI 1. Fatigue 1. Did Not Occur
2. Pitting edema Within Days
2. No Decrease In
Urine Volume
CKD 1. Pallor
2. Pitting Edema
3. Foamy urine
CHD 1. Easy fatigability 1. No palpitation
2. Generalized body 2. No angina
malaise 3. No tachycardia

Liver Cirrhosis 1. Edema 1. No jaundice

2. Lethrgic 2. Anictric sclera
3. Puffy face
 LABORATORY TESTS
BLOOD CHEMISTRY

PARAMETER NORMAL VALUES RESULT

RBS/HGT 2.5-7.2mmol/ L

BUN 2.9-8.2mmol/ L

Creatinine 53.0-106.0 umol/L 1986.79

Na+ 135 – 148 131.9

K+ 3.50 – 5.30 mmol/L 4.36

 HEMATOLOGY
PARAMETERS NORMAL VALUES RESULT

Hemoglobin 135 – 170 g/L 32

Hematocrit 0.390 – 0.500 0.105
WBC Count 4.5-10.5 x 109/ L 5.3
MCV 80-96 86.1
MCHC 334-355 335
MCH 27.5-32.2 26.2
MXD

Poly s 0.55-0.63 0.611

Lymphocytes 0.23 – 0.35
23-35%
0.389
Platelet Count 150,000 – 450,000 138000
Red Blood Cells F: 3.9 – 5.7 x 1012/L 1.22
 CHEMICAL PHYSICAL MICROSCOPIC

Blood: NEGATIVE Color: light yellow Pus cells: 1-4 /HPF

Bilirubin: NEGATIVE Transparency: HAZY Red cells: 1-3 /HPF
Urobilinogen: NEGATIVE Epithelial cells: FEW
Ketone: NEGATIVE A.Urates/Phosphates: FEW
Protein: ++ Mucus Threads:
Nitrite: NEGATIVE Bacteria: FEW
Glucose: TRACE Crystals:
pH: 6.5 Casts:
Specific Gravity: 1.1015
Leukocytes: NEGATIVE
Ascorbic acid:
 HEPATITIS B NON REACTIVE
SURFACE ANTIGEN
(HBsAg)
CXR-AP
Initial impression:

• CKD SECONDARY TO CHRONIC GLOMERULONEPHRITIS , ANEMIA

SECONDARY
CONTENTS
• Brief intro on AKI
• INTRO CKD
• PATHOPHYSIOLOGY OF CKD
• IDENTIFICATION OF RISK FACTOR
• STAGING OF CKD
• CLINICAL AND LABORATORY MANIFESTATION OF CKD
ACUTE KIDNEY INJURY
• Impairment of kidney filtration and excretory function over days to
weeks, resulting in the retention of nitrogenous and other waste
products normally cleared by the kidneys

• Not a single disease, rather, heterogeneous group of conditions that

share common diagnostic features: like increase in serum creatinine
(SCr) concentration associated with a reduction in urine volume
 ETIOLOGY AND PATHOPHYSIOLOGY
• Traditionally been divided into three broad categories: prerenal
azotemia, intrinsic renal parenchymal disease, and postrenal
obstruction
 CHRONIC KIDNEY DISEASE
• Associated with abnormal kidney function and a progressive decline in
glomerular filtration rate (GFR).
• progression is closely linked to both the GFR and the amount of
albuminuria.
 PATHOPHYSIOLOGY OF CKD

• Pathophysiology of CKD involves two broad sets of

mechanisms of damage
• 1. Initiating mechanisms specific to the underlying
etiology
• 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.
• 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.
• process explains why a reduction in renal mass from an isolated insult
may lead to a progressive decline in renal function over many years .
Left: Low-power photomicrograph of a
normal kidney showing normal
glomeruli and healthy
tubulointerstitium without fibrosis.
Right: Low-power photomicrograph of
chronic kidney disease with sclerosis of
many glomeruli and severe
tubulointerstitial fibrosis
(Masson trichrome, 40× magnification).
(Slides courtesy of the late Dr. Andrew
Herzenberg.)
 RISK FACTORS
• Small for gestation birth weight
• childhood obesity
• Hypertension
• diabetes mellitus
• autoimmune disease
• advanced age
• African ancestry
• a family history of kidney disease
• a previous episode of acute kidney injury
• presence of proteinuria
• abnormal urinary sediment
• structural abnormalities of the urinary tract
 STAGING OF CKD
• To stage CKD, it is necessary to estimate the GFR rather than relying on
serum creatinine concentration
WE USED CKD-EPI EQUATION
For our patient
• Equations are valid only if the patient is in steady state
• lower GFR signifies a true loss of kidney function with attendant
consequences in terms of risk of CKD complications
• Mean GFR is lower in women than in men
• Measurement of albuminuria is also helpful for monitoring nephron
injury and the response to therapy in many forms of CKD, especially
chronic glomerular diseases
 CHEMICAL PHYSICAL MICROSCOPIC

Blood: NEGATIVE Color: light yellow Pus cells: 1-4 /HPF

Bilirubin: NEGATIVE Transparency: HAZY Red cells: 1-3 /HPF
Urobilinogen: NEGATIVE Epithelial cells: FEW
Ketone: NEGATIVE A.Urates/Phosphates: FEW
Protein: ++ Mucus Threads:
Nitrite: NEGATIVE Bacteria: FEW
Glucose: TRACE Crystals:
pH: 6.5 Casts:
Specific Gravity: 1.1015
Leukocytes: NEGATIVE
Ascorbic acid:

• Urinalysis Shows Increase Protein Level Indicating Albuminuria

• Presence of albuminuria in general serves as a well-studied
screening marker for the presence of systemic microvascular
disease and endothelial dysfunction.
Stages
• Stages 1 and 2 CKD - usually asymptomatic, Recognition of CKD
occurs often as a result of laboratory testing in clinical settings other
than suspicion of kidney disease
• 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)
• abnormalities in sodium, potassium, water, and acid- base homeostasis
Stages
• 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.
Etiology
Pathophysiology
• Although serum urea and creatinine concentrations are used to mea-
sure 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.
• 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
• the pathophysiology of the uremic syndrome can be divided into
manifestations in three spheres of dysfunction
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;
• (3) progressive systemic inflammation and its vascular and nutritional
consequences.
 CLINICAL AND LABORATORY MANIFESTATIONS OF
CKD AND UREMIA
• FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
• Sodium and Water Homeostasis
• Many forms of kidney disease (e.g., glomerulonephritis) disrupt this balance
such that dietary intake of sodium exceeds its urinary excretion
• 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.
 BLOOD CHEMISTRY

PARAMETER NORMAL VALUES RESULT

RBS/HGT 2.5-7.2mmol/ L

BUN 2.9-8.2mmol/ L

Creatinine 53.0-106.0 umol/L 1986.79

Na+ 135 – 148 131.9

K+ 3.50 – 5.30 mmol/L 4.36

FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS

• Potassium Homeostasis
• 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.
• Hypokalemia is not common in CKD and usually reflects markedly reduced
dietary potassium intake, especially in association with exces- sive diuretic
therapy or concurrent GI losses.
 BLOOD CHEMISTRY

PARAMETER NORMAL VALUES RESULT

RBS/HGT 2.5-7.2mmol/ L

BUN 2.9-8.2mmol/ L

Creatinine 53.0-106.0 umol/L 1986.79

Na+ 135 – 148 131.9

K+ 3.50 – 5.30 mmol/L 4.36

• Metabolic Acidosis
• Metabolic acidosis is a common disturbance in advanced CKD.
• 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.
• 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.
• most patients, the metabolic acidosis is mild; the pH is rarely <7.32 and can
usually be corrected with oral sodium bicarbonate supplementation
 Bone Manifestations of CKD
• The major disorders of bone disease can be classified into those
associated with high bone turn over 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.
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 cardiovascular disease .
■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.
• anemia may play a role in growth restriction in children with CKD.
 HEMATOLOGY
PARAMETERS NORMAL VALUES RESULT
THE RESULT SHOWS
Hemoglobin 135 – 170 g/L 32
NORMOCYTIC
Hematocrit 0.390 – 0.500 0.105
NORMOCHROMIC
WBC Count 4.5-10.5 x 109/ L 5.3
ANEMIA INDICATING
MCV 80-96 86.1 RENAL DISEASE
MCHC 334-355 335
MCH 27.5-32.2 26.2
MXD

Poly s 0.55-0.63 0.611

Lymphocytes 0.23 – 0.35
23-35%
0.389
Platelet Count 150,000 – 450,000 138000
Red Blood Cells F: 3.9 – 5.7 x 1012/L 1.22
REFERENCES
• 20TH EDITION HARRISON PRINCIPLE OF INTERNAL MEDICINE
• https://www.kidney.org/