SULTAN KUDARAT EDUCATIONAL INSTITUTION

Colleges of Nursing, Education and Midwifery

School of Technical-Vocational Courses
Tacurong City, Sultan Kudarat

“CKD”
(Chronic kidney disease)

Submitted to:
Reynald L. Ecija, RN, RM

Submitted by:
Lee, Chona
Barba, Annika
Barang, Alyssa
Impang, Mark John
Gumboc, Anice Faith
Guiamaludin, Rowaina
Abdulgapor, Haguiar
Jehodo, Feventh Rose
Navarro, Joshua John

December 2018
 TABLE OF CONTENTS

I. Title page

II. Table of contents

III. Acknowledgement

IV. Introduction

V. Objectives

VI. Biographic data

VII. Anatomy/Physiology

VIII. Nursing History

IX. Pathophysiology

X. Patterns of Functioning

XI. Gordon’s patterns of Health care

XII. Physical Assessment

XIII. Diagnostic studies

XIV. Laboratory result

XV. Doctors order

XVI. Med

XVII. NSG. Consideration

XVIII. Bibliography
 ACKNOWLEDGEMENT

Foremost, we would like to express our sincere gratitude to our advisor , Reinald Ecija,

RM, RN for the continuous support of our case research, for his patience, motivation,

enthusiasm, and immense knowledge. His guidance helped us in all the time of

research and writing of this study We could not have imagined having a better mentor

for our study.

Besides our Clinical Instructor, I would like to thank the rest of the case presentation

committee: Princess C. Arandilla RN, RM, Ma. Fe Gadayan RN, MAN and Roy A.

Labanon RN for their encouragement and insightful comments.

Our sincere thanks also goes to Feventh Jehodo, and Mark John Impang , who have

invested their full effort in guiding the team in achieving the goal.

We thank the fellow group mates, Alyssa Barang, Joshua John Navarro, Anice Faith

Gumboc, Haguiar Abdul Gapor, Chona Lee, Rho Guiamaludin and Annika Barba for the

stimulating discussions, for the sleepless nights working their parts before deadlines.

Last but not the least, we would like to thank our families for supporting us spiritually

throughout our life.

 INTRODUCTION

Chronic kidney disease (CKD) is a condition characterized by a gradual loss of

kidney function over time. CKD is also known as chronic renal disease. Chronic kidney

disease, also called chronic kidney failure, describes the gradual loss of kidney function.

Chronic kidney disease includes conditions that damage your kidneys and decrease

their ability to keep you healthy by doing the jobs listed. If kidney disease gets worse,

wastes can build to high levels in your blood and make you feel sick. You may develop

complications like high blood pressure, anemia (low blood count), weak bones, poor

nutritional health and nerve damage. Also, kidney disease increases your risk of having

heart and blood vessel disease. These problems may happen slowly over a long period

of time. Chronic kidney disease may be caused by diabetes, high blood pressure and

other disorders. Early detection and treatment can often keep chronic kidney disease

from getting worse. When kidney disease progresses, it may eventually lead to kidney

failure, which requires dialysis or a kidney transplant to maintain life.

Kidney diseases, especially End Stage Renal Disease (ESRD), are already the 7 th

leading cause of death among the Filipinos. One Filipino develops chronic renal failure

every hour or about 120 Filipinos per million population per year. More than 5,000

Filipino patients are presently undergoing dialysis and approximately 1.1 million people

worldwide are on renal replacement therapy. Reliable estimates reveal that the number

of these patients will double in 2010.

In the past, chronic glomerulonephritis was the most common cause of chronic renal

failure. Today, diabetes mellitus and hypertension have taken center stage in the

causation of ESRD which together account for almost 60% of dialysis patients.

The cost of medical treatment for kidney disease is really exorbitant, beyond the reach

of ordinary patients. Renal transplantation is limited due to the expense and the

shortage of donors. The best that can be done at present is to focus efforts on the

prevention of progression of renal diseases. Strict blood pressure and glycemic control

and adoption of “ healthy lifestyle” play a major role in reducing if not totally controlling

the epidemic of renal failure and this could be achieved through proper education.
 OBJECTIVES

General Objective: 

The purpose of this study is to provide deeper theoretical and practical knowledge and

information about chronic kidney disease.

Specific Objective:

1. To provide information on the related causes of chronic kidney diseases

2. To provide information regarding postpartum care for patients who had the similar

illness of chronic kidney disease

3.To provide a framework of study regarding the subject that can serve as the

foundation of future studies and research

Biographic Data

Name: Patient X

Age: 42 y/o

Sex: Male

Address: Purok Paraiso, Reyes, Banga, South Cotabato

Civil Status: Married

Religion: Roman Catholic

Birth Place: Banga, South Cotabato

Birth Day: November 7, 1976

Admission Data

Date and Time of Admission: November 27, 2018

Attending Physician: Dr. Flohesna

Admission Diagnosis: Chronic Kidney Disease (CKD) secondary to diabetic

nephropathy on top of hypertensive nephropathy

Medical History 2005 – Diabetes Mellitus

 ANATOMY AND PHYSIOLOGY

The kidneys are the primary organs of the urinary system invertebrates. The kidneys

filter the blood, remove the wastes, and excrete the wastes in the urine. About 1,300

milliliters of blood flow through the kidneys each minute (about 400 gallons a day).From

this blood the Malphigian corpuscles (see below) extract about 170 liters of filtrate a

day. As this fluid passes down the uriniferous tubules it is almost all reabsorbed. Only

about 1.5liters are left in the tubules to carry away the waste products. The whole blood

supply passes through the kidneys every 5minutes, ensuring that waste materials don't

build up. The renal artery carries blood to the kidney, while the renal vein carries blood,

now with much lower concentrations of urea and mineral ions, away from the kidney.

The urine formed passes down the ureter to the bladder. The work of the kidneys is

much more than just the removal of waste, however. Other functions of the kidneys

include:

 Helping control the amount of water lost to the outside world– most important in

land animals.

 Helping regulate the pH (i.e., level of acidity or alkalinity) of the blood and the

general balance of ions in the blood, and hence in the body fluid as a whole.

 Conserving essential substances such as glucose and amino acids.

Parts and Function:

Renal Vein
 This has a large diameter and a thin wall. It carries blood away from the kidney and

back to the right hand side of the heart. Blood in the kidney has had all its urea

removed. Urea is produced by your liver to get rid of excess amino-acids. Blood in the

renal vein also has exactly the right amount of water and salts. This is because the

kidney gets rid of excess water and salts. The kidney is controlled by the brain.

Ahormone in our blood called Anti-Diuretic Hormone (ADH for short)is used to control

exactly how much water is excreted.

Renal Artery

 This blood vessel supplies blood to the kidney from the left hand side of the heart. This

blood must contain glucose and oxygen because the kidney has to work hard producing

urine. Blood in the renal artery must have sufficient pressure or the kidney will not be

able to filter the blood. Blood supplied to the kidney contains a toxic product called urea

which must be removed from the blood. It may have too much salt and too much water.

The kidney removes these excess materials; that is its function.

Pelvis

 This is the region of the kidney where urine collects.

Ureter

the ureter carries the urine down to the bladder.

Medulla
 The medulla is the inside part of the kidney. This is where the amount of salt and water

in your urine is controlled. It consists of billions of loops of Henlé. These work very hard

pumping sodium ions. ADH makes the loops work harder to pump more sodium ions.

The result of this is that very concentrated urine is produced.

Cortex

 The cortex is the outer part of the kidney. This is where blood is filtered. We call this

process "ultra-filtration" or" high pressure filtration" because it only works if the blood

entering the kidney in the renal artery is at high pressure. Billions of glomeruli are found

in the cortex. Aglomerulus is a tiny ball of capillaries. Each glomerulus is surrounded by

a "Bowman's Capsule". Glomeruli leak. Things like red blood cells, white blood cells,

platelets and fibrinogen stay in the blood vessels. Most of the plasma leaks out into the

Bowman's capsules. This is about 160 liters of liquid every 24hours.Most of this liquid,

which we call "ultra-filtrate" is re-absorbed in the medulla and put back into the blood.

Glomerulus and Bowman's Capsule 

 This is where ultra-filtration takes place. Blood from the renal artery is forced into the

glomerulus under high pressure. Most of the liquid is forced out of the glomerulus into

the Bowman's capsule which surrounds it. This does not work properly in people who

have very low blood pressure.

Proximal Convoluted Tubules 

Don't worry about remembering the name for your GCSE biology. Jolly good

though if you can. Proximal means "near to" and convoluted means "coiled up" so this is

the coiled up tube near to the Bowman's capsule. This is the place where all that useful
glucose is re-absorbed from the ultra-filtrate and put back into the blood. If the glucose

was not absorbed it would end up in your urine. This happens in people who are

suffering from diabetes.

Loop of Henlé 

 This part of the nephron is where water is reabsorbed. Kidney cells in this region spend

all their time pumping sodium ions. This makes the medulla very salty; you could say

that this is a region of very low water concentration. If you remember the definition of

osmosis, you will realize that water will pass from a region of high water concentration

(the ultra-filtrate and urine) into a region of low water concentration(the medulla) through

cell membranes which are semi-permeable.

Distal Convoluted Tubules

Distal means "distant" so it is at the other end of the nephron from the Bowman's

capsule. This is where most of the salts in the ultra-filtrate are re-absorbed.

Collecting Duct

Collecting ducts run through the medulla and are surrounded by loops of Henlé. The

liquid in the collecting ducts (ultra-filtrate) is turned into urine as water and salts are

removed from it. Although our kidneys make about 160 liters of urine every 24 hours,
we only produce about ½ litre of urine. It is called a collecting duct because it collects

the liquid produced by lots of nephrons.

NURSING HISTORY

PRESENT HEALTH HISTORY

PAST HEALTH HISTORY

Patient X didn’t experience any severe illness when he was a kid. He got all vaccination

that he needs when he was a kid (Diphtheria-Pertussis-Tetanus Vaccine, Oral Polio

Vaccine, Hepatitis B Vaccine, Measles Vaccine). According to him, he had only, minor

cold, cough and fever, which his parents only took him to a faith healer. He remembered

that he got admitted once in a decade due to his rowdy behavior. But one thing that

made him admired by people during his high school days is that he is healthy and has

an appealing body type. Patient G used to be a basketball player which is one of the

factors why he is healthy during his prime years. Until such time that he achieved his

dreams of becoming a sea farer and traveled other parts of the world, where he started

abusing his body. Every night on the ship, he and his co-seafarer’s always had a

drinking session of hard alcoholic drinks. It was his guilty pleasure to fight the loneliness

on board. He even bought boxes of chocolates and soda’s for him to consume daily

every after meal. He couldn’t quit his vices until in the year 2005 he experienced some

symptoms, where he gets dizzy and experiencing polyuria which made him took

himself to a Doctor. He was diagnosed of Diabetes Mellitus Type 2. He was devastated

by it and it drawn him more to his vices. He was given some medication but he only took

it whenever he feels like dying. Due to his recklessness, his situation got even worse.

Instead of having only one disease, it got more complications and it led to CKD, which is

Chronic Kidney Disease. His family got stressed due to the news. During the first year

of having CKD, he decided to make a change in his lifestyle. He started a low sugar and

salt diet. He even followed the Doctor’s orders for him to prolong his life. But it didn’t

take a while when he get back to his previous lifestyle. He started drinking soft drinks

and alcohol again. He was advised to undergo dialysis and it was so bad that he was

ordered to have it three times a week. His wife told him to take the situation seriously
and change his lifestyle for good. However, his wife can’t stop him and he can’t commit

to a healthier pasture.

PATHOPHYSIOLOGY

When discussing the pathophysiology of CKD, renal structural and physiological

characteristics, as well as the principles of renal tissue injury and repair should be taken

into consideration.

Firstly, the rate of renal blood flow of approximately 400 ml/100g of tissue per minute is

much greater than that observed in other well perfused vascular beds such as heart,

liver and brain. As a consequence, renal tissue might be exposed to a significant

quantity of any potentially harmful circulating agents or substances. Secondly,

glomerular filtration is dependent on rather high intra- and transglomerular pressure

(even under physiologic conditions), rendering the glomerular capillaries vulnerable to

hemodynamic injury, in contrast to other capillary beds. In line with this, Brenner and

coworkers identified glomerular hypertension and hyperfiltration as major contributors to

the progression of chronic renal disease. Thirdly, glomerular filtration membrane has

negatively charged molecules which serve as a barrier retarding anionic

macromolecules. With disruption in this electrostatic barrier, as is the case in many

forms of glomerular injury, plasma protein gains access to the glomerular filtrate.

Fourthly, the sequential organization of nephron’s microvasculature (glomerular

convolute and the peritubular capillary network) and the downstream position of the
tubuli with respect to glomeruli, not only maintains the glomerulo-tubular balance but

also facilitates the spreading of glomerular injury to tubulointerstitial compartment in

disease, exposing tubular epithelial cells to abnormal ultrafiltrate. As peritubular

vasculature underlies glomerular circulation, some mediators of glomerular

inflammatory reaction may overflow into the peritubular circulation contributing to the

interstitial inflammatory reaction frequently recorded in glomerular disease. Moreover,

any decrease in preglomerular or glomerular perfusion leads to decrease in peritubular

blood flow, which, depending on the degree of hypoxia, entails tubulointerstitial injury

and tissue remodeling. Thus, the concept of the nephron as a functional unit applies not

only to renal physiology, but also to the pathophysiology of renal diseases. In the fifth

place, the glomerulus itself should also be regarded as a functional unit with each of its

individual constituents, i.e. endothothelial, mesangial, visceral and parietal epithelial

cells - podocytes, and their extracellular matrix representing an integral part of the

normal function. Damage to one will in part affect the other through different

mechanisms, direct cell-cell connections (e.g., gap junctions), soluble mediators such

as chemokines, cytokines, growth factors, and changes in matrix and basement

membrane composition.

The main causes of renal injury are based on immunologic reactions (initiated by

immune complexes or immune cells), tissue hypoxia and ischaemia, exogenic agents

like drugs, endogenous substances like glucose or paraproteins and others, and genetic

defects. Irrespective of the underlying cause glomerulosclerosis and tubulointerstitial

fibrosis are common to CKD.

An overview of the pathophysiology of CKD should give special consideration to

mechanisms of glomerular, tubular and vascular injury.

1.2.1 Mechanism of glomerular impairment

Hereditary defects account for a minority of glomerular disease. A prototype of an

inherited glomerular disease is the Alport’s syndrome or hereditary nephritis, usually

transmitted as an X-linked dominant trait although autosomal dominant and recessive

forms have been reported as well. In its classical X-linked form there is a mutation in the

COL4A5 gene that encodes the α5 chain of type IV collagen located on the X

chromosome. As a consequence, GBM is irregular with longitudinal layering, splitting or

thickening, and the patient develops progressive glomerulosclerosis and renal failure.

Other types of inherited glomerular disease are thin membrane syndrome, nail-patella

syndrome, partial lipodystrophy, and familial lecithin-cholesterol acyltranferase

deficiency.

Most acquired glomerular disease is triggered by immune mediated injury, metabolic

and mechanical stress. From a pathological and pathogenetic point of view glomerular

diseases can broadly be divided into three groups:

 nonproliferative (without cell proliferation) glomerular diseases without glomerular

inflammation and without deposition of immunoglobulins (minimal change

disease, idiopathic focal, and segmental glomerulosclerosis [FSGS]) or with

deposition of immunoglobulins, but without glomerular inflammation, most likely

because of subepithelial localization of immunoglobulins (e.g., membranous

nephropathy)
  proliferative glomerular diseases with deposition of immunoglobulins leading to

increased cellularity (proliferative glomerulonephrites, e.g., lupus nephritis, IgA

nephropathy, anti-GBM, postinfectious GN), or with severe glomerular injury and

inflammation, but without deposition of immunoglobulins (e.g., pauci-immune

glomerulonephritis).

 heterogenous group of glomerular diseases in systemic diseases like glomerular

disease in diabetes, amyloidosis and paraproteinemia.

The podocyte seems to occupy the central role in the pathogenesis of the first group of

glomerular diseases as well as in diabetic nephropathy. This topic will be elaborated

separately.

In the second group of glomerular diseases with cell proliferation, either deposition of

immune complexes from the circulation or formed in situ lead to activation of intrinsic

renal cells (via Fc receptors and complement cascade activation), resulting in

inflammatory cell recruitment. Futhermore, severe glomerular injury and inflammation

can occur without discernible immune complexes in the glomeruli, as in ANCA

(antineutrophil cytoplasmic antibodies) positive glomerulonephritis. The offending

etiologic agents are mainly unknown, with the rare exception of ß hemolytic streptococci

in poststreptococcal glomerulonephritis, and hepatitis C virus in type 1 cryoglobulinemic

membranoproliferative glomerulonephritis. Most antibody-mediated glomerulonephrites

are initiated by the reactivity of circulatory antibodies and glomerular antigens, whereby

antigens might be the components of normal glomerular parenchyma as in anti-GBM

antibody disease (Goodpasture’ syndrome), or the antigens are planted from the

circulation within the glomeruli as in poststreptococcal glomerulonephritis (the in situ

formation of immune complexes). The immune complexes formed in systemic

circulation can be deposited and trapped in glomeruli (in cryoglobulinemic

glomerulonephritis). Additional mechanism of antibody-mediated glomerular injury, but

without immune complexes in the glomeruli, is represented by circulating autoantibody

against neutrophil cytoplasmatic antigens (ANCA). Reactive oxygen species, protease,

cytokines, chemokines and other inflammatory mediators originating from recruited and

resident inflammatory cells play the key pathogenic roles.

Immune complexes can be deposited in the mesangium (as in IgA nephropathy,

Henoch Schonlein purpura, lupus nephritis class II, postinfectious GN), in

subendothelial (lupus nephritis class III, membranoproliferative GN), or subepithelial

area (idiopatic membranous nephropathy or class V lupus nephritis, postinfectious GN),

or along GBM (as in anti-GBM disease). The site of antibody deposition defines the

response to injury and clinicopathological presentation. A strong inflammatory reaction

occurs only when circulating inflammatory cells can be activated by contact with

immunoglobulins or soluble products released by intrinsic renal cells. Thereby, the

deposition of antibodies in the subendothelial area, mesangium or membrane elicits a

nephritic response, as the position of immune complexes enables activation of

endothelial or mesangial cells which release soluble products and rapidly recruit

leukocytes and platelets from the blood. Leukocyte-derived products, such as cytokines,

lysosomal enzymes, reactive oxygen species, complement components and other,

damage the vascular wall and filtration barrier and attract more leukocytes from the

circulation. The subepithelial position of immune complexes (as in membranous

nephropathy) leads to nephrotic response, as GBM precludes the contact between

immune complexes and inflammatory cells from the circulation. Another reason for this

kind of response is that large fluid flow from vascular lumen to Bowman’s space does

not permit inflammatory mediators formed in the subepithelium to diffuse retrogradely

from epithelial to the endothelial layer and vascular lumen.

Tissue injury after IC deposition is mediated through complement activation resulting in

the formation of C5-9 membrane attack complex which appears to be the major effector

of glomerular injury through release of chemotactic C5a and C3a. C5-9-activated cells

release chemokines and oxidant proteases, and upregulate adhesion molecules.

T-cells also act as mediators of glomerular injury and as modulators of the production of

nephrite/ogenic antibodies, especially in pauci-immune GN. They interact through their

surface receptor/CD3 complex with antigens presented in the clefts of MHC molecules

of endothelial, mesangial and epithelial glomerular cells. This process is facilitated by

the cell-cell adhesion and costimulatory molecules. Once activated, T-cells release

cytokines and other mediators of inflammatory reaction, cytotoxicity and fibrogenesis.

Soluble factors from T cells have been implicated in the pathogenesis of minimal

change disease and focal and segmental glomerulosclerosis, but their identity has yet to

be determined.

TGF-ß and connective tissue growth factor (CTGF) are important in glomerular

fibrogenesis, as they stimulate glomerular cells to produce extracellular matrix (ECM), a

key event in the progression of kidney disease, inhibiting the synthesis of tissue

protease, mostly matrix metalloproteinase, which otherwise degradates matrix proteins.

Glomerular inflammation can either completely recover or resolve with a variable degree

of fibrosis. The resolution process requires cessation of further antibodies production

and immune complex formation, degradation and removal of deposited and circulating

immune complexes, cessation of recruitment and clearing of inflammatory cells,

dispersing of inflammatory mediators, normalization of endothelial adhesiveness,

permeability and vascular tone, and clearance of proliferating resident glomerular cells.

Nonimmunologic glomerular injury. Hemodynamic, metabolic and toxic injuries can

induce glomerular impairment alone or in conjunction with immunological processes.

Systemic hypertension translated to glomeruli and glomerular hypertension resulting

from local changes in glomerular hemodynamics may cause glomerular injury. The

kidney is normally protected from systemic hypertension by autoregulation which can be

overwhelmed by high blood pressure, meaning that systemic hypertension is translated

directly to glomerular filtration barrier causing glomerular injury. Chronic hypertension

leads to arteriolar vasoconstriction and sclerosis with consequent secondary sclerosis

and glomerular and tubulointerstitial atrophy. Different growth factors like angiotensin II,

EGF, PDGF, and CSGF, TGF-ß cytokine, activation of stretch-activated ion channels

and early response gene are involved in coupling high blood pressure to myointimal

proliferation and vessel wall sclerosis.

Glomerular hypertension is normally an adaptive mechanism in remaining nephrons

to increased workload resulting from nephron loss, whatever the cause. This sustained

intraglomerular hypertension increases mesangial matrix production and leads to

glomerulosclerosis by ECM accumulation. The process is mediated by TGF-ß in the first

place, with a contribution of angiotensin II, PDGF, CSGF and endothelins.

Systemic and glomerular hypertension are not necessarily associated, as glomerular

hypertension may precede systemic hypertension in glomerular disease.

Metabolic injury as that occurring in diabetes is discussed separately.

1.2.2 Mechanism of tubulointerstitial impairment

Regardless of the etiology, chronic kidney disease is characterized by renal fibrosis -

glomerulosclerosis and tubulointerstitial fibrosis. The impairment of the

tubulointerstitium (tubulointerstitial fibrosis and tubular atrophy) is at least as important

as that of the glomeruli (glomerulosclerosis). There is a common consensus that the

severity of tubulointerstitial injury correlates closely (and better than glomerular injury)

with long-term impairment of renal function. This is not surprising, considering that

tubules and interstitium occupy more than 90% of the kidney volume. As very recently

summarized by Fine and Norman, tubulointerstitial fibrosis encompasses a number of

characteristic features including an inflammatory cell infiltrate which results from both

activation of resident inflammatory cells and recruitment of circulating inflammatory

cells; an increase in interstitial fibroblasts due to increased proliferation and decreased

apoptosis of resident interstitial cells, as well as recruitment of cells to the

tubulointerstitium; the appearance of myofibroblasts expressing the cytoskeletal protein

α-smooth muscle actin, which arise by differentiation of resident interstitial fibroblasts

and infiltrating cells and via transdifferentiation; accumulation of extracellular matrix

(ECM) as the net result of increased synthesis of ECM components and decreased

ECM degradation, mostly by specific metalloproteinases that are under the control of

specific inhibitors; tubular atrophy as a consequence of apoptosis and epithelial–

mesenchymal transdifferentiation (EMT); and rarefaction of peritubular capillaries. The

development of fibrosis is associated with an increase in the expression of

proinflammatory, vasoconstrictive and profibrotic factors.

Renal fibrogenesis. The initial insult leads to inflammatory response with the

generation and local release of soluble mediators, an increase in local vascular

permeability, activation of endothelial cells, extravasation of leukocytes along the

endothelium, subsequent secretion of various mediators by infiltrating leukocytes and

tubulointerstitial cells, and activation of profibrotic cells. As a consequence a vicious

cycle of cell stress is initiated generating profibrotic and proinflammatory mediators,

leukocyte infiltration and fibrosis.

Induction and development of the inflammatory response. Leukocytes migrate from

the circulation through postcapillary venules and peritubular capillaries into the

interstitium following gradients of chemoattractants and chemokines. All tubular cells

can generate soluble mediators when stimulated by hypoxia, ischaemia, infectious

agents, drugs, and endogenous toxins like lipids, high glucose, paraproteins or genetic

factors as in cystic renal diseases. Glomerular disease is usually associated with a

variable degree of tubulointerstitial injury and inflammation because tubular cells are

exposed to proteins which are normally not filtered. The factors involved in the formation

of tubulointerstitial inflammatory infiltrates are: proteinuria, immune deposits,

chemokines, cytokines, calcium phosphate, metabolic acidosis, uric acid, lipids, hypoxia

and reactive oxygen species.

The inflammatory infiltrate. Infiltrating inflammatory mononuclear cells are composed

of monocytes/macrophages and lymphocytes, particularly T lymphocytes. CD4-positive

T cells and CD3 T cells carrying chemokine receptors CCR5 and CxCR3 are closely

associated with renal function. This inflammatory cells secrete profibrotic cytokines.

Profibrotic cytokines. Infiltrating inflammatory cells and resident interstitial

macrophages release cytokines which stimulate fibroblasts to become myofibroblasts.

The most important profibrotic factors involved in renal fibrogenesis are angiotensin II,

TGF-ß1, CTGF, PDGF, FGF-2 (fibroblast growth factor -2), EGF, ET-1, tryptase mast

cell. Angiotensin II induces TGF- ß synthesis in tubular epithelial cells and fibroblast. AII

induces hypertrophy in tubular epithelial cells together with connective tissue growth

factor (CTGF), independently of TGF- ß. It is currently assumed that TGF-ß1 is the key

cytokine in renal fibrogenesis.

Fibroblast proliferation and activation. Fibroblasts proliferate and become active

following infiltration of inflammatory cells into the tubulointerstitial space. To express α-

smooth muscle actin, the fibroblasts must be activated by cytokines (mostly derived

from infiltrating macrophages), change their phenotype and transit from fibroblasts to

myofibroblasts. The important mitogens for renal fibroblast are PDGF, bFGF-2 and

others, but no single profibrotic „master cytokine„ has been identified so far.

Epithelial-mesenchymal transition. Phenotypic conversion of epithelial cells into

mesenchymal cells is known as the epithelial-mesenchymal transition. Evidence for

EMT in human disease comes from utilization of mesenchymal marker proteins such as

vimentin or S100A4, the human analogue of fibroblast-specific protein-1. The

expression of these mesenchymal marker proteins in tubular epithelial cells was well

correlated with renal function in IgA nephropathy, lupus nephritis and chronic allograft
failure. TGF-ß1 is thought to be the most potent inducer of EMT, which may be induced

by a variety of factors other than cytokines.

It has been shown lately that hypoxia-inducible factor-1 (HIF-1), considered to be

master regulator of the adaptive response controlling expression of hundreds of genes,

also stimulates EMT, which explains why hypoxia results in fibrosis and progressive

renal failure. Hypoxia as a consequence of peritubular capillaries loss has been

frequently observed in chronic kidney disease. It alters proximal tubular epithelial (PTE)

matrix metabolism, promoting ECM accumulation, with a switch to production of

interstitial collagen and suppression of matrix degradation. Exposure of PTE to hypoxia

induces transition to myofibroblastic phenotype, whereas more prolonged exposure

leads to mitochondrial injury and apoptosis consistent with the loss of tubular cells in

vivo. In PTE, hypoxia also induces expression of fibrogenic factors. Reports from

biopsies carried out in patients with diabetic nephropathy, IgA nephropathy, polycistic

kidney disease, and chronic allograft nephropathy have confirmed increased expression

of HIF, supporting the hypothesis that hypoxia is an important contributory factor in the

pathogenesis of CKD in humans. Furthermore, changes in HIF expression correlate

with the extent of tubulointerstitial injury.

Proteinuria and tubulointerstitial damage. Proteinuria can damage tubulointerstitium

through multiple pathways including direct tubular toxicity, changes in tubular epithelial

metabolism, induced cytokine and chemokine synthesis, and increased expression of

adhesion molecules. (Abbate). Excess protein reabsorption in proximal tubule may

exceed lysosomal processing capacity, lead to lysosomal rupture and result in direct

tubular toxicity. There is a great variability in tubular toxicity induced by proteinuria. For
example, patients with nephrotic range proteinuria exclusively consisting of albuminuria

as in minimal change disease, rarely exhibit tubulointerstitial damage. Different

experimental models have demonstrated generation of chemotactic factor for

macrophages, secretion of chemokines such as monocyte chemoattractant protein-1

and RANTES, and expression of fractalkine (a chemokine promoting mononuclear cell

adhesion). In addition to inducing chemokine secretion proteinuria may induce secretion

of TGF-ß as well as that of adhesion intercellular adhesion molecule-1 and vascular

adhesion molecule-1. In a study reporting on results from 119 renal biopsies the

formation of interstitial infiltrates and the degree of tubulointerstitial fibrosis was

associated with the level of expression of adhesion molecules.

The reversibility of renal fibrosis was demonstrated in different animal studies with

relatively mild degrees of fibrosis. In this context BMP-7, which offers strategy to

prevent the progression of renal disease and possibly even reverse fibrosis, has been

extensively studied. However, only Fioretto has given evidence of reversibility of

tubulointerstitial fibrosis in humans in a small group of patients with type 1 diabetes who

underwent pancreas transplantation.

 PRACTICE ESSENTIALS

Chronic kidney disease (CKD)—or chronic renal failure (CRF), as it was historically

termed—is a term that encompasses all degrees of decreased renal function, from

damaged–at risk through mild, moderate, and severe chronic kidney failure. CKD is a

worldwide public health problem. In the United States, there is a rising incidence and

prevalence of kidney failure, with poor outcomes and high cost

CKD is more prevalent in the elderly population. However, while  younger patients with

CKD typically experience progressive loss of kidney function, 30% of patients over 65

years of age with CKD have stable disease.  

CKD is associated with an increased risk of cardiovascular disease and chronic renal

failure. Kidney disease is the ninth leading cause of death in the United States.

The Kidney Disease Outcomes Quality Initiative (KDOQI) of the National Kidney

Foundation (NKF) established a definition and classification of CKD in 2002.   The

KDOQI and the international guideline group Kidney Disease Improving Global

Outcomes (KDIGO) have subsequently updated these guidelines.  These guidelines

have allowed better communication among physicians and have facilitated intervention

at the different stages of the disease.

The guidelines define CKD as either kidney damage or a decreased glomerular filtration

rate (GFR) of less than 60 mL/

. Whatever the underlying etiology, once the loss of nephrons and reduction of

functional renal mass reaches a certain point, the remaining nephrons begin a process

of irreversible sclerosis that leads to a progressive decline in the GFR.  

Staging

The different stages of CKD form a continuum. The stages of CKD are classified as

follows:

 Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m 2)

 Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m 2)

 Stage 3a: Moderate reduction in GFR (45-59 mL/min/1.73 m 2)

 Stage 3b: Moderate reduction in GFR (30-44 mL/min/1.73 m 2)

 Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m 2)

 Stage 5: Kidney failure (GFR < 15 mL/min/1.73 m 2 or dialysis)

In stage 1 and stage 2 CKD, reduced GFR alone does not clinch the diagnosis,

because the GFR may in fact be normal or borderline normal. In such cases, the

presence of one or more of the following markers of kidney damage can establish the

diagnosis

 Albuminuria (albumin excretion >30 mg/24 hr or albumin:creatinine ratio >30

mg/g [>3 mg/mmol])

 Urine sediment abnormalities

  Electrolyte and other abnormalities due to tubular disorders

 Histologic abnormalities

 Structural abnormalities detected by imaging

 History of kidney transplantation in such cases

Hypertension is a frequent sign of CKD but should not by itself be considered a marker

of it, because elevated blood pressure is also common among people without CKD.

In an update of its CKD classification system, the NKF advised that GFR and

albuminuria levels be used together, rather than separately, to improve prognostic

accuracy in the assessment of CKD. More specifically, the guidelines recommended the

inclusion of estimated GFR and albuminuria levels when evaluating risks for overall

mortality, cardiovascular disease, end-stage kidney failure, acute kidney injury, and the

progression of CKD. Referral to a kidney specialist was recommended for patients with

a very low GFR (< 15 mL/min/1.73 m²) or very high albuminuria (>300 mg/24 h).

Patients with stages 1-3 CKD are frequently asymptomatic. Clinical manifestations

resulting from low kidney function typically appear in stages 4-5.

Signs and symptoms

Patients with CKD stages 1-3 are generally asymptomatic. Typically, it is not until

stages 4-5 (GFR < 30 mL/min/1.73 m²) that endocrine/metabolic derangements or

disturbances in water or electrolyte balance become clinically manifest.

Signs of metabolic acidosis in stage 5 CKD include the following:

 Protein-energy malnutrition

 Loss of lean body mass

 Muscle weakness

Signs of alterations in the way the kidneys are handling salt and water in stage 5 include

the following:

 Peripheral edema

 Pulmonary edema

 Hypertension

Anemia in CKD is associated with the following:

 Fatigue

 Reduced exercise capacity

 Impaired cognitive and immune function

 Reduced quality of life

 Development of cardiovascular disease

 New onset of heart failure or the development of more severe heart failure

 Increased cardiovascular mortality

Other manifestations of uremia in end-stage renal disease (ESRD), many of which are

more likely in patients who are being inadequately dialyzed, include the following:

 Pericarditis: Can be complicated by cardiac tamponade, possibly resulting in

death if unrecognized

 Encephalopathy: Can progress to coma and death

 Peripheral neuropathy, usually asymptomatic

 Restless leg syndrome

 Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea

 Skin manifestations: Dry skin, pruritus, ecchymosis

 Fatigue, increased somnolence, failure to thrive

 Malnutrition

 Erectile dysfunction, decreased libido, amenorrhea

 Platelet dysfunction with tendency to bleed

Screen adult patients with CKD for depressive symptoms; self-report scales at initiation

of dialysis therapy reveal that 45% of these patients have such symptoms, albeit with a

somatic emphasis.

See Clinical Presentation for more detail.

Diagnosis

Screening

American College of Physicians guidelines on screening for CKD include the following

recommendations:
  Do not screen for CKD in asymptomatic adults without risk factors for CKD

(grade: weak recommendation, low-quality evidence).

 Do not test for proteinuria in adults with or without diabetes who are currently

taking an angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin II-

receptor blocker (ARB)(grade: weak recommendation, low-quality evidence).

Laboratory studies

Laboratory studies used in the diagnosis of CKD can include the following:

 Complete blood count (CBC)

 Basic metabolic panel

 Urinalysis

 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

Evidence of renal bone disease can be derived from the following tests:

 Serum calcium and phosphate

 25-hydroxyvitamin D

 Alkaline phosphatase

 Intact parathyroid hormone (PTH) levels

In certain cases, the following tests may also be ordered as part of the evaluation of

patients with CKD:

 Serum and urine protein electrophoresis and free light chains: Screen for a

monoclonal protein possibly representing multiple myeloma

  Antinuclear antibodies (ANA), double-stranded DNA antibody levels: Screen for

systemic lupus erythematosus

 Serum complement levels: Results may be depressed with some

glomerulonephritides

 Cytoplasmic and perinuclear pattern antineutrophil cytoplasmic antibody (C-

ANCA and P-ANCA) levels: Positive findings are helpful in the diagnosis of

granulomatosis with polyangiitis (Wegener granulomatosis); P-ANCA is also

helpful in the diagnosis of microscopic polyangiitis

 Anti–glomerular basement membrane (anti-GBM) antibodies: Presence is highly

suggestive of underlying Goodpasture syndrome

 Hepatitis B and C, human immunodeficiency virus (HIV), Venereal Disease

Research Laboratory (VDRL) serology: Conditions associated with some

glomerulonephritides

Imaging studies

Imaging studies that can be used in the diagnosis of CKD include the following:

 Renal ultrasonography: Useful to screen for hydronephrosis, which may not be

observed in early obstruction or dehydrated patients; or for involvement of the

retroperitoneum with fibrosis, tumor, or diffuse adenopathy; small, echogenic

kidneys are observed in advanced renal failure

 Retrograde pyelography: Useful in cases with high suspicion for obstruction

despite negative renal ultrasonograms, as well as for diagnosing renal stones

  Computed tomography (CT) scanning: Useful to better define renal masses and

cysts usually noted on ultrasonograms; also the most sensitive test for identifying

renal stones

 Magnetic resonance imaging (MRI): Useful in patients who require a CT scan but

who cannot receive intravenous contrast; reliable in the diagnosis of renal vein

thrombosis

 Renal radionuclide scanning: Useful to screen for renal artery stenosis when

performed with captopril administration; also quantitates the renal contribution to

the GFR

Biopsy

Percutaneous renal biopsy is generally indicated when renal impairment and/or

proteinuria approaching the nephrotic range are present and the diagnosis is unclear

after appropriate workup.

Management

Early diagnosis and treatment of the underlying cause and/or institution of secondary

preventive measures is imperative in patients with CKD. These may slow, or possibly

halt, progression of the disease.The medical care of patients with CKD should focus on

the following:

 Delaying or halting the progression of CKD: Treatment of the underlying

condition, if possible, is indicated

 Diagnosing and treating the pathologic manifestations of CKD

 Timely planning for long-term renal replacement therapy

The pathologic manifestations of CKD should be treated as follows:

 Anemia: When the hemoglobin level is below 10 g/dL, treat with erythropoiesis-

stimulating agents (ESAs), which include epoetin alfa and darbepoetin alfa after

iron saturation and ferritin levels are at acceptable levels

 Hyperphosphatemia: Treat with dietary phosphate binders and dietary phosphate

restriction

 Hypocalcemia: Treat with calcium supplements with or without calcitriol

 Hyperparathyroidism: Treat with calcitriol or vitamin D analogues or calcimimetics

 Volume overload: Treat with loop diuretics or ultrafiltration

 Metabolic acidosis: Treat with oral alkali supplementation

 Uremic manifestations: Treat with long-term renal replacement therapy

(hemodialysis, peritoneal dialysis, or renal transplantation)

Indications for renal replacement therapy include the following:

 Severe metabolic acidosis

 Hyperkalemia

 Pericarditis

 Encephalopathy

 Intractable volume overload

 Failure to thrive and malnutrition

 Peripheral neuropathy

 Intractable gastrointestinal symptoms

 In asymptomatic patients, a GFR of 5-9 mL/min/1.73 m²,  [2] irrespective of the

cause of the CKD or the presence or absence of other comorbidities.

 GORDON’S FUNCTIONAL HEALTH PATTERNS

Pattern Before Hospitalization During Analysis and

Hospitalization Interpretation
Self-Perception/ Self Patient felt he is still strong Patient feels a little Normal concern
Concept and okay weak and wants to regarding on his
go back to his daily body strength and
life routine accepted his fate.
Role Relationship Patient primary support are Patient primary Patient is
Pattern his wife, children and his support are his wife dependent on his
whole family only wife

Sexuality and Patient believed his still able Patient has to take Normal reaction on
Reproductive Health to have sexual activities with a break from it and sex and
his wife focus on his health reproductive health
betterment because of his age
(early 40’s)
Cognitive Perceptual There are no problems in There are no Normal cognitive
Pattern hearing but visual acuity, problems in hearing patterns except the
especially on the left eye is but visual acuity, left eye
blurry especially on the
left eye is blurry
Coping Stress Psychosocial: Psychosocial: Patient X display
Perceptual Pattern Ego Integrity Vs. Despair Ego Integrity Vs. normal
Despair psychosocial,
Psychosexual: psychosexual and
Genital Psychosexual: cognitive
Genital development and
Cognitive: has emotional
Formal, he can still stability.
Formal Operation, He talks talk to his wife and
to his family and friends the other patient
Value Belief Pattern He does basketball coaching
and a player as well
Elimination Patient X cannot void
anymore and regularly
defecates at least once a day bathroom to take a
Sleep Rest Pattern Patient X has an average of
8 hours continuous sleep
Safe Environment No Allergies
Nutrition Patient X is able to eat and
finish one full course meal
and able to eat any kinds of
fruits
Patient X is place in Patient has strong
a hospital bed and religious belief and
took some is not afraid to die.
medication while he
waits for his
hemodialysis
Patient X can still Patient X cannot
walk to the void
dump
Patient X has an Patient X can still
average of 8 hours have 8 hours of
continuous sleep sleep since he is in
a private room with
an old patient man
No Allergies Normal
Patient fluid is IV fluids are given
usually controlled for hydration and
since he can’t take diet of the patient
so much liquid due is not so restricted.
to his kidney failure.