This document provides information on acute renal injury and chronic kidney disease. It begins with an overview of kidney anatomy and physiology. It then discusses renal failure, defining acute kidney injury and its causes, clinical manifestations, diagnosis, and management. Management involves fluid and electrolyte balance, pharmacological interventions, infection prevention, monitoring, nutrition, and nursing care focused on maintaining homeostasis. The document emphasizes prevention and treatment of complications through diligent monitoring and care.

1. Acute Renal Injury
Chronic Kidney Disease
Presented By:
Monika
M.Sc Nursing 2nd Year
NINE, PGIMER Chandigarh
1

2. Anatomy and physiology of kidney
The urinary system is the main excretory system and consists of following
structures:
• Two kidneys, which secrete urine.
• Two ureters, which conveys the urine from kidney to the urinary bladder.
• The urinary bladder where urine collects and is temporarily stored.
• The urethra through which the urine passes from the urinary bladder to the
exterior.
• The urinary system plays a vital part in maintaining homeostasis of water and
electrolyte concentrations within the body.
• The kidney produce urine that contains metabolic waste products, including
nitrogenous compounds urea and uric acid, excess ions, and some drugs
• Urine is stored in the bladder and excreted by the process of micturition.
2

3. CONT…
• The kidneys lie on the posterior abdominal wall, one on each side of the
vertebral column. Behind the peritoneum and below the diaphragm.
• The right kidney is usually slightly lower than the left, probably, because of
the considerable space occupied by the liver.
• Kidneys are bean shaped organs, about 11 cm long, 6 cm wide, 3 cm thick
and 150 gm weight.
• A sheath of fibrous connective also known as renal fascia encloses the
kidney and the renal fat.
3

4. 4

5. • Organs associated with the kidneys: As the kidneys lie on either side of the
vertebral column, each is associated with a different group of structures.
• RIGHT KIDNEY
• Superiorly: The right adrenal gland.
• Anteriorly: The right lobe of the liver, the duodenum, and the hepatic flexure of the
colon.
• Posteriorly: The diaphragm and the muscles of the posterior abdominal wall.
LEFT KIDNEY
• Superiorly: The left adrenal gland.
• Anteriorly: The spleen, stomach, pancreas, jejunum, and splenic, flexure of the
colon.
• Posteriorly: The diaphragm and muscle of the posterior abdominal wall.
5

6. • Gross structure of the kidney: There are three areas of tissue that can be
distinguished when a longitudinal section of kidney is viewed with the naked
eye.
• An outer fibrous capsule, surrounding the kidney.
• The cortex, a reddish brown layer of tissue immediately below the capsule
and outside the pyramids.
• The medulla, the inner most layer, consisting of pale conical shaped
striations, the renal pyramids.
• The hilum is the concave medial border of the kidney where the renal blood
and lymph vessels, the ureter and nerves enter.
• The renal pelvis is the funnel structure that collects urine formed by the
kidney.
6

7. RENAL FAILURE
• Renal failure is severe impairment or total lack of kidney function, in which
there is an inability to excrete metabolic waste products and water, as well
as functional disturbance of all body systems.
• Renal failure may be acute in onset (developing in hours to days) or chronic
(developing slowly and progressively over a course of several years).
• Renal failure refers to a significant loss of renal function, when only 10
percent of renal function remains, the person is considered to have end-
stage renal disease.
7

8. ACUTE KIDNEY INJURY
(AKI)
8

9. INTRODUCTION
• The term Acute Kidney Injury (AKI) was used for the first time by William
MacNider in 1918 in a situation of acute mercury poisoning, but became the
preferred term in 2004 when ARF was redefined with the now widely
accepted consensus criteria known as RIFLE (an acronym of the Risk-
Injury-Failure-Loss-End stage kidney disease).
• The 2012 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical
Practice Guideline for Acute Kidney Injury (AKI) aims to assist practitioners
caring for adults and children at risk for or with AKI, including contrast-
induced acute kidney injury (CI-AKI). Guideline development followed an
explicit process of evidence review and appraisal.
9

10. DEFINITION
10

11. 11

12. 12

13. ETIOLOGY
13

14. 14

15. 15

16. PHASES OF AKI
16

17. CLINICAL MANIFESTATIONS
- Clinically AKI may progress through phases of onset oliguria, diuresis and recovery.
- In some situations, the patient does not recover from AKI, and chronic kidney disease
results.
• The onset is the initial phase of injury to the kidney. Symptoms which are last for hours to
days.
• Oliguria, when urine output is less than 400 ml/24 hours
• Inability to regulate electrolytes (hyperkalemia, hyponatremia, acidosis, hypocalcemia,
hyperphosphatemia)
• inability to excrete fluid (fluid overload, hypervolemia)
• hematological dysfunction (anemia, platelet dysfunction, leukopenia) cases may require
dialysis.
• The symptoms are nausea, vomiting, cardiac dysrhythmias, ECG changes, Kussmaul's
breathing (rapid, deep respirations) drowsiness, confusion, coma, edema, CCF
pulmonary edema, neck vein distention, hypertension, fatigue, bleeding, infection.
17

18. Cont…
The clinical manifestations of acute renal
failure according to body system are:
Urinary
• Decreased urinary output
• Proteinuria
• Casts
• Decreased specific gravity
• Decreased osmolality
• Increased urinary sodium.
Cardiovascular
• Volume overload
• Congestive heart failure
• Hypotension (early)
• Hypertension (after development of fluid
overload)
• Pericarditis
• Pericardial effusion
• Arrhythmias.
Respiratory
• Pulmonary edema
• Kussmaul's respiration
• Pleural effusion.
18

19. Cont….
Gastrointestinal
• nausea and vomiting
• Anorexia
• Stomatitis
• Bleeding
• Diarrhea
• Constipation.
Hematologic anemia (development
within 48 hours)
• Leukocytosis
• Defect in platelet functioning.
Neurologic
• Lethargy
• Convulsions
• Memory impairment.
Others
• Increased susceptibility to infection
• Increased BUN
• Increased creatinine
• Increased potassium
• Decreased pH
• Decreased bicarbonate
• Decreased calcium
• Increased phosphate 19

20. DIAGNOSIS
The most important tool for distinguishing prerenal, intrarenal and postrenal
causes the history, including a thorough review of recent clinical events and
drug therapy.
LABORATICAL TESTS
• Urinalysis is an important diagnostic test.
• Urine sediment containing abundant cells, casts or protein suggests
intrarenal ATN is associated with abundant urinary casts.
• Normal urine sediment is possible in both prerenal and postrenal causes.
Hematuria, Pyuria and crystals may be associated with postrenal causes.
• Urine culture
20

21. Diagnosis Cont….
SEROLOGIC TESTS
• Renal function test
• Serum electrolyte
• Complement ASA testing
• Complete blood count
HISTOPATHIC INVESTIGATIONS
• Renal biopsy
21

22. Cont…
IMAGING INVESTIGATIONS
• CT
• MRI
• Renal ultrasound
• Retrograde pyelogram
• Renal scan
• Renal angiography
22

23. 23

24. Diagnosis andTreatment of
AKI
24

25. MANAGEMENT
25

26. Prevention
• As with any disease process, prevention is the primary intervention.
• Attaining and maintaining adequate hydration and diuresis in high risk
client is crucial, as is the prevention of contributing factors.
• The key elements in preventing AKI occurring are avoidance of
hypovolemia, nephrotoxic drugs and contrast media.
• Correction of the underlying condition, such as hydration for a client
with hypovolemic shock, may be all that is necessary in AKI caused
by prerenal disorders.
26

27. Cont….
• All nephrotoxic drug should be avoided. Such as NSAIDs, antibiotics
(aminoglycosides, vancomycin), amphotericin B, ACE inhibitors, cocaine,
chemotherapeutic agent, acyclovir etc.
• Nephrotoxic drug these accumulate in the renal cortex and can become
highly concentrated, resulting in vasoconstriction, which can lead to acute
tubular necrosis.
• Older patients in the community with identified risk factors are closely
monitored for changes in urine output, or a deterioration in health status
(for example, developing diarrhoea and vomiting or feeling generally unwell
or confused).
• Closely monitor renal function in people with acute illness, especially if
there is less urine output, vomiting and/or diarrhea, or signs.
27

28. Fluid and electrolytes
• In AKI, maintenance of fluid and electrolyte balance is key survival.
• Fluid replacement volume are usually calculated by urine out previous day and
sensible and insensible output also added in daily allotment.
• Diuretics therapy may be used cautiously. Furosemide and mannitol are the drugs
used most often, but furosemide can be nephrotoxic, increasing risk for further
damage.
• Electrolyte replacement is based primarily on urine and serum electrolyte
concentration.
• Hyperkalemia is probably the most dangerous imbalance.
• ECG monitoring are used to check for effects of hyperkalemia or hyperkalemia.
• In most patients with AKI, the priority is to treat hypovolemia and correct electrolyte
imbalances
28

29. Cont..
• If hypovolemia is due to blood or plasma loss, packed red blood cells and
isotonic saline are administered.
• Volume replacement's rates must match volume losses on a 1:1 basis.
• Metabolic acidosis usually results from the accumulation of acid waste
products. Sodium bicarbonate, sodium lactate, or sodium acetate may be
used in the short term to correct this condition. Dialysis is usually used for
severe acidosis.
• Keep accurate records of intake and output.
• Weigh patient daily.
• Administer phosphate binding medications as prescribed. During diuretic
phase.
29

30. Pharmacological
• The use of medications in the treatment of ARF is determined by the underlying cause
and the presenting symptoms.
• Metabolic acidosis is common and is typically treated with sodium bicarbonate.
• Loop diuretics are used to manage potassium levels. Doses of up to 320 mg/day of
furosemide may be required to produce adequate diuretics.
• Renal failure from nephrotoxic or ischemia is treated with agents that increase renal
blood flow. These include renal-dose dopamine, mannitol and loop diuretics.
• Inflammatory states as in acute glomerulonephritis are treated with
glucocorticosteroids.
• NSAIDs and ACE inhibitors are contraindicated in patients with acute renal failure.
• “renal-dose”dopamine(0.5 to 3 ug/kg/min, given as a specific vasodilator to increase
renal blood flow and prevent AKI, does increase urine output but does not affect AKI
outcome or mortality
30

31. Replace renal function
• When kidney function is severely impaired, dialysis may become necessary
to replace it and maintain health.
• Indications for dialysis include the following:
• Significant volume overload
• Uncontrolled hyperkalemia or acidosis
• Progressive uremia, as evidenced by rising BUN and creatinine concentrations
• Altered central nervous system function
• Pericarditis
• RRT is recommended treatment
31

32. Renal replacement criteria
• Presence of uremic syndrome i.e
• Hyperkalemia (unresponsive to conventional therapy)
• Extraa cellular volume expansion
• Acidosis refractory to medical therapy
• Bleeding diathesis
• Creatinine clearance 10ml/min/1.73m sq
32

33. Infection prevention
• Patient should be monitored carefully for infectious processes, should be
treated.
• Indwelling urethral catheters are usually avoided because of their great
potential for introducing infection.
• If catheter is placed, meticulous catheter care is essential.
• Maintain asepsis for indwelling lines or catheters.
• Maintain proper personal hygiene
33

34. Monitoring
• The care consist of physiological monitoring and assessment.
• To monitoring of progression of manifestations associated with renal failure.
• Assessment finding include pleuritic pain, pericardial friction rub,
tachycardia, and fever.
• To monitor vital sign of patient
• To monitor blood pressure regularly
• To monitor strict intake output chart
• To monitor daily weight
• To monitor fluid electrolyte intake
34

35. Nutrition
• Nutritional support should be directed to ensure adequate nutrition, promote wound healing,
tissue repair, support immune system function and accelerate recovery.
• Provide fluid in small amounts during oliguric phase; gingerable and other effective -scent
soft drinks may be tolerated better than other fluids.
• Provide diet restricted in protein as prescribed.
• The protein biologic value containing the essential amino acids to reduce nitrogenous waste
product.
• A high- calorie diet is usually prescribed.
• High in carbohydrates and fat during protein restrictions.
• Diet may also be low in sodium, magnesium, phosphate and potassium.
• Low in potassium during hyperkalemia, high in potassium during hypokalemia.
• Take measures to relieve nausea (antiemetic and comfort measure).
• If oral intake is not sufficient to meet requirements, tube feeding or TPN, including lipids,
may be instituted. 35

36. PATIENT EDUCATION
In addition, patient and family education to be given to take care of the person with acute renal
failure as follows:
• Causes of renal failure and problems with recurrent failures.
• Identification of preventable environmental or health factors contributing to the illness such as
hypertension and nephrotoxic drugs.
• Prescribed medication regimen, including name of medication, dosage, reason for taking,
desired and adverse effects.
• Prescribed dietary regimen.
• Explanation of risk of hypokalemia, and reportable symptoms (muscle weakness, anorexia,
nausea, vomiting and lethargy).
• Signs and symptoms of returning renal failure (decreased urine output, without decreased
fluid intake, signs of fluid retention and increased weight).
• Signs and symptoms of infection, methods to avoid infection.
• Need for ongoing follow-up care.
• Option for the future, explanation of transplantation and dialysis there is a possibility.
36

37. NURSING MANAGEMENT
• It is important to monitor the vital signs and fluid intake and output. The urine should be
examined for blood, protein, color.
• Assess the general appearance of patient including skin color, edema.
• If patient is receiving dialysis observe or access the site for signs of inflammation.
• Assess the mucous membrane for dryness and inflammation.
• Nurse should monitor client for any complications, fluid and electrolyte imbalance, assess
progress and response to treatment.
• Provide psychological and emotional support to patient and family members.
• It is a duty of nurse to keep informed family members about the patient condition and helps
them to understand the treatment.
• It is a duty of a nurse to maintain fluid and electrolyte balance, monitor fluid intake (IV
medications should be administered), urine output, edema.
• Provide skin care because the skin maybe dry and susceptible to breakdown as a result of
edema.
• Massaging the bony prominences, changing positions frequently.
37

38. NURSING DIAGNOSIS
• Excess fluid volume related to renal failure and fluid retention.
• Risk for infection related to altered immune responses secondary to kidney
failure.
• Imbalanced nutrition pattern less than body requirement related to dietary
restrictions.
• Impaired skin integrity related to edema.
• Anxiety related to disease process and uncertainty of prognosis.
• Deficient knowledge regarding disease condition and treatment.
• Activity intolerance related to fatigue, retention of waste products.
38

39. NURSING INTERVENTIONS
1. Maintaining fluid and electrolytic balance
• Maintain fluid restrictions.
• Monitor intravenous fluid carefully.
• Keep accurate records of intake and output.
• Weigh patient daily.
• Monitor vital signs frequently, including postural signs.
• Assess fluid status of patient frequently.
• Administer phosphate binding medications as prescribed. During diuretic phase.
• Assess for changes in mental status indicative of low serum levels.
• Assess for presence of irregular apical pulses indicative of hypokalemia.
39

40. 2. Maintaining nutrition
• Provide fluid in small amounts during oliguric phase; gingerable and other effective -scent
soft drinks may be tolerated better than other fluids.
• Provide diet. Restricted in protein as prescribed.
• High in carbohydrates and fat during protein restrictions.
• Low in potassium during hyperkalemia, high in potassium during hypokalemia.
• Take measures to relieve nausea (antiemetic and comfort measure).
3. Maintaining rest/activity balance
• Maintain bedrest in the acute phase.
• Assist patient with activities of daily living to conserve energy.
• Promote early ambulation when renal status permits.
• Provide for planned rest periods.
40

41. 4. Prevent injury
• Assess orientation, reorient confused patient.
• During bedrest, keep side rails raised and use padded rails as necessary.
• When patient is ambulatory, assess motor skills and monitor ambulation and
assist patient as necessary.
• Assess patient for signs of bleeding.
• Protect patient from bleeding: instruct patient to use soft tooth brush,
perform guaiac test on stool, emesis and nasogastric returns.
5. Preventing infection
• Avoid source of infection: limit visitors to well adults.
• Assess for signs and symptoms of infection.
• Maintain asepsis for indwelling lines or catheters.
• Perform pulmonary hygiene.
• Turn weak or immobile patients every 2 hours and as needed.
• Provide meticulous skin care.
• Administer prescribed antipruritic agents.
41

42. 6. Facilitate coping
• Encourage development of nurse-patient relationship to assist patient to
express feelings as desired.
• Promote patient independence (autonomy).
• Assist patient to explore alternative way of coping.
42

43. CHRONIC KIDNEY DISEASE
(CKD)
43

44. Definition
According to KDOQI criteria
1. Kidney damage for >3 months, as defined by structural or functional
abnormalities of the kidney, with or without decreased GRF, manifest by either:
-pathological abnormalities; or markers of kidney damage, including
abnormalities in the blood or urine, or abnormalities in imaging tests
2. GFR <60ml/min/1.73m2 for >3 months, with or without kidney damage
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.
44

45. ETIOLOGY
The end result is a systemic disease involving every body organ. The causes of
chronic renal failure include the following:
• Diabetic kidney disease
• Hypertension
• Vascular disease
• Glomerular disease (primary or secondary)
• Cystic kidney diseases
• Urinary tract obstruction or dysfunction
• Recurrent kidney stone disease
• Congenital (birth) defects of the kidney or bladder
• Unrecovered acute kidney injury
45

46. CONT…
Vascular diseases that can cause CKD include the following:
• Renal artery stenosis
• Cytoplasmic pattern antineutrophil cytoplasmic antibody (C-ANCA)–positive
and perinuclear pattern antineutrophil cytoplasmic antibody (P-ANCA)–
positive vasculitides
• ANCA-negative vasculitides
• Atheroemboli
• Hypertensive nephrosclerosis
• Renal vein thrombosis
46

47. CONT…
Primary glomerular diseases include the following:
• Membranous nephropathy
• Alport syndrome
• Immunoglobulin A (IgA) nephropathy
• Focal and segmental glomerulosclerosis (FSGS)
• Minimal change disease
• Membranoproliferative glomerulonephritis (MPGN)
• Complement-related diseases (eg, atypical hemolytic-uremic syndrome
[HUS], dense deposit disease)
• Rapidly progressive (crescentic) glomerulonephritis
47

48. Secondary causes of glomerular disease
include the following:
• Diabetes mellitus
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Mixed connective tissue disease
• Scleroderma
• Granulomatosis with polyangiitis (formerly
known as Wegener granulomatosis)
• Mixed cryoglobulinemia
• Endocarditis
• Hepatitis B and C
• Syphilis
• Human immunodeficiency virus (HIV) infection
• Parasitic infection
• Heroin use
• Gold
• Penicillamine
• Amyloidosis
• Light-chain deposition disease
• Neoplasia
• Thrombotic thrombocytopenic purpura (TTP)
• Shiga-toxin or Streptococcus pneumoniae –
related HUS
• Henoch-Schönlein purpura
• Reflux nephropathy
48

49. Causes of tubulointerstitial disease include the following:
• Drugs (eg, sulfonamides, allopurinol)
• Infection (viral, bacterial, parasitic)
• Tubulointerstitial nephritis and uveitis (TINU) syndrome
• Chronic hypokalemia
• Chronic hypercalcemia
• Sarcoidosis
• Multiple myeloma cast nephropathy
• Heavy metals
• Radiation nephritis
• Polycystic kidneys
• Cystinosis and other inherited diseases
49

50. CONT…
Urinary tract obstruction may result from any of the following:
• Benign prostatic hypertrophy
• Urolithiasis (kidney stones
• Urethral stricture
• Tumors
• Neurogenic bladder
• Congenital (birth) defects of the kidney or bladder
• Retroperitoneal fibrosis
50

51. RISK FACTOR
Non-modifiable
• Age
• Gender
• Race
• Diabetes
• Genetic
Modifiable
• Elevated blood pressure
• Diabetes
• Obesity
• Smoking
• Proteinuria
• Metabolic disturbances
• Dyslipidemia
51

52. STAGES OF CHRONIC RENAL FAILURE
• Chronic kidney disease (CKD) means that your kidneys have been
irreversibly damaged and the extent of the damage will only increase over
time. There are five stages of CKD. CKD stage 5 refers to End Stage Renal
Disease (ESRD), also known as kidney failure. Stages of CKD according to
NKF:
52

53. Stages Description GFR (ml/min/1.73 m Action
Stage 1 At increased risk for CKD
Kidney damage with normal or ↑GFR
≥90(with CKD risk factor)
≥90
-Screening CKD risk reduction
Diagnosis and treatment
-Normal kidney function but urinalysis or structural
abnormalities may indicate kidney disease.
Stage 2 Kidney damage with mild ↓GFR 60-89 -Estimation of progression
-Mildly reduced kidney function, and other findings (as for
stage 1) point to kidney disease
Stage 3 Moderate ↓GFR 30-59 -Evaluation and treatment of complications
-Moderately reduced kidney function
Stage 4 Severe ↓GFR 15-29 -Preparation for renal replacement therapy
-Severely reduced kidney function
Stage 5 Kidney failure < 15 (or dialysis) -Renal replacement (if uremia present)
-Very severe or End Stage Renal Disease (ESRD)
* All GFR values are normalized to an average surface area (size) of 1.73 m2
53

54. PATHOPHYSIOLOGY
The pathogenesis of CKD involves
disorientation and destruction of
nephrons with progressive loss of
renal function.
As the total GFR decreases and
clearance is reduced, serum
urea nitrogen and creatinine
levels increase. Remaining
functioning nephrons
hypertrophy as they filter a
larger load of solutes.
A consequence is the
kidneys lose their ability to
concentrate urine
adequate.
To continue excreting the
solutes, a large volume of dilute
urine may be passed, which
make the client susceptible to
fluid depletion.
54

55. The tubules gradually
lose their ability to
reabsorb electrolytes.
occasionally, the result
is salt wasting, in which
urine contains large
amount of sodium,
which lead to more
polyuria.
As renal damage
advances and the number
of functioning nephrons
declines, to total GFR
decreases further. Thus
the body becomes unable
to rid itself to excess
water, salt, and other
waste products through
the kidneys.
When the GFR is less
than 10 to 20ml/min, the
effect of uremic toxins on
the body becomes
evident. If the disease is
not treated by dialysis or
transplantation, the
outcomes of CKD is
uremia and death.
55

56. 56

57. CLINICAL MANIFESTATIONS
• As renal function progressively deteriorates every body system becomes
involved.
• The clinical manifestations are a result of retained resistances, including
urea, creatinine, uremia, is a syndrome that incorporates all the
disturbances seen in the various systems throughout the body in chronic
renal failure.
• The body system manifestation in chronic renal failure causes signs,
symptoms and assessment parameters as followings
57

58. CONT…
Hematopoietic system:
• Affected may be due to decreased
erythroproteins by the kidney
• Decreased survival time of RBCS
• Bleeding
• Blood loss during dialysis
• Mild thrombocytopenia
• Decreased activity of platelets
• Anemia
• Fatigue
• Ecchymosis
• Assessment parameters include
hematocrit, hemoglobin, platelet
count and observing for bruising,
hematemesis or melena.
58

59. CONT…
Cardiovascular system:
• affected may be due to fluid
overload, Renin-angiotensin
mechanism; overload anemia
• chronic hypertension, calcification of
soft tissues, uremic toxins of
pericardial fluid and fibrin formation
on epicardium.
• Hypervolemia
• Hypertension
• Tachycardia
• Dysrhythmias
• CCF
• Pericarditis
• For which monitoring of vital signs,
body weight, ECG, heart sounds,
electrolytes pain is needed.
59

60. CONT…
Respiratory system:
• affected due to compensatory
mechanisms for metabolic acidosis,
uremic toxins, uremic lung and fluid
overload.
• Tachypnea
• Kussmauls respirations
• Tenacious sputum
• Pain with coughing elevated
temperature
• Hilar pneumonitis
• Pleural friction rub
• Pulmonary edema
• For which needs respiratory
assessment, arterial blood gas
results readings, inspection of oral
mucosa, monitoring vital signs and
pulse oximetry.
60

61. CONT…
Gastrointestinal systems:
affected may be due to change in
platelet activity, serum uremic toxins,
electrolyte imbalances and urea
converted to ammonia by saliva.
• Anorexia
• Nausea
• Vomiting
• Gastrointestinal bleeding
• Abdominal distention
• Diarrhea
• Constipation
• Which need monitoring of intake and
output, hematocrit, hemoglobin,
guaic test for all stools, assessment
for quality of stools, assess for
abdominal pain
61

62. CONT…
Neurological system:
affected due to uremic toxins,
electrolyte imbalance, cerebral
swelling, resulting from fluid shifting.
• Lethargy
• Confusion
• Stupor
• Coma
• Sleep disturbances
• Unusual behavior
• Asterixis
• Muscle irritability
• This requires monitoring level of
consciousness, level of orientation,
reflexes, EEG and electrolyte levels.
62

63. CONT…
Skeletal system:
• May be affected due to decreased calcium absorption and decreased phosphate
excretion.
• These give rise to renal osteodystrophy, renal rickets, joint pains, retarded growth.
• It needs assessment of levels of serum phosphorus, serum calcium, and for joint
pain.
Skin:
• May be affected due to anemia, retained pigment, decreased size of sweat glands,
decreased activity of oil glands, dry skin, phosphate deposits and excretion of
metabolic waste products through the skin.
• These give rise to pallor, pigmentation, pruritis, ecchymosis, excoriation and uremic
frost, which needs observation for bruising
• Assessment of color and integrity of skin and observe for scratching.
63

64. CONT…
Genitourinary system:
• affected due to damaged nephron.
• This gives rise to decreased urine output, decreased urine specific gravity, proteinuria,
casts and cells present in the urine, and decreased urine sodium.
• which requires monitoring of intake and output, serum creatinine, BUN, serum
electrolytes, urine-specific gravity and urine electrolytes.
Reproductive system:
• may be affected due to hormonal abnormalities, anemia, hypertension, malnutritions
and medication.
• This leads to infertility, decreased libido, erectile dysfunction, amenorrhea, and
delayed puberty.
• which require monitoring intake and output, vital signs, hematocrit and hemoglobin.64

65. CONT…
Psychological:
• changes including personality and behavioral changes, emotional liability,
withdrawal and depression are commonly observed.
• Fatigue and lethargy contribute to the patient's feeling of sickness.
• The changes and body image caused by edema, integumentory
disturbances, and access devices (fistulas, catheters) lead to further anxiety
and depression.
65

66. DIAGNOSTIC MEASURES
• When a patient is diagnosed as having chronic renal insufficiency,
conservative therapy is attempted before maintenance of dialysis begins.
Because of the multisystem effects, chronic renal failure may have serious
abnormalities in laboratory values and which are characteristics of person
with CKD. Diagnostic measures as I have discussed previously in AKI
diagnostic measures.
66

67. MANAGEMENT
67

68. PREVENTION
Primary prevention
• Measures aim to eliminate or
reduce exposure to factors which
cause ill health or disease.
• For CKD this involves strategies
to reduce the incidence and
prevalence of risk factors such as
diabetes and high blood pressure,
in order to reduce the number of
people at risk of developing CKD.
Secondary prevention
• Measures for early detection of
disease to allow prompt and
effective intervention to prevent
the disease becoming
established.
• Early detection and effective
intervention in the early stages of
kidney damage are essential to
prevent or delay the development
of CKD.
68

69. CONT…
Tertiary prevention
• Strategies are focused on management of established disease to prevent
progression and reduce or delay long-term complications, impairment or
disability.
• Management of CKD aims to prevent or delay further kidney damage and
loss of kidney function, and hence reduce the incidence and prevalence of
ESKD and other complications.
• In those who do develop ESKD, good management during kidney
replacement therapy not only reduces suffering and death, but also
improves quality of life.
69

70. High Risk Factor management
• Among people with diabetes and high blood pressure, blood sugar and blood
pressure control have been shown to lower the risk of developing kidney disease.
• Several studies have shown the possibility for preventing or delaying the start of
diabetic kidney disease by treating patients who have diabetes with blood pressure-
lowering drugs. In addition to lowering blood pressure, these medications reduce
protein in the urine, a risk factor for developing kidney disease.
• Managing blood sugar, blood pressure, and cholesterol levels is very important
because these are all risk factors for heart disease and stroke.
• Because having kidney disease increases the chances of also having heart disease
and stroke, early detection and treatment of kidney disease is important for people
with diabetes to help prevent or delay cardiovascular death and kidney failure.
70

71. Initial management of patient with chronic renal failure is focused
on controlling symptoms, preventing complications and delaying
the progression of renal failure.
The treatment goals for the person whose CRF
are:
• Stabilization of the internal environment as
demonstrated by Mental alertness, attention
span, and appropriate interactions.
• Absence or control of peripheral and
pulmonary edema.
• Control of electrolyte balance within a limits.
• Control of protein catabolism and protein
metabolic wastes as normal parameters.
• Absence of joint inflammation and pain.
• Control of anemia
• Absence of infection.
• Absence of bleeding.
• Blood pressure controlled at
• <140/90 mm Hg sitting and
• < 10 mm Hg postural change in standing.
• Control of coexisting disease including heart
failure, anemia, dehydration.
• Absence of toxicity from inadequately
excreted medications.
• Nutrient intake sufficient to maintain positive
nitrogen balance.
• Anorexia and nausea are controlled.
• Pruritis controlled.
71

72. MEDICAL MANAGEMENT
• are used to control blood pressure, regulate electrolytes and control intravascular fluid
volume accordingly as prescribed.
• Vitamin D: A person with CKD develops a high PTH, activated vitamin D given to suppress
PTH production
• Calcium supplement: hypocalcemia more often observed in stage 5.
• Phosphate binder: Hyperphosphatasemia is an independent predictor of cardiovascular
disease and mortality in patients with advanced chronic kidney disease (stage 4 and 5) and is
due to impaired phosphate excretion by the kidney. 1 - 3 It is typically managed with oral
phosphate binders in conjunction with dietary phosphate restriction.
• Laxatives: Laxative use was independently associated with lower risk of hyperkalemia during
the last 1-year pre-ESKD period, finds a recent study.
• Diuretic: Diuretics are useful in the management of most patients with CKD. They reduce
ECF volume; lower blood pressure; potentiate the effects of ACE inhibitors, Angiotensin II
receptor blockers and other antihypertensive agents; and reduce the risk of CVD in CKD.
Choice of diuretic agents depends on the level of GFR and need for reduction in ECF
volume. 72

73. CONT…
• Antihypertensive: CKD is associated with both stimulation of the RAS and ECF volume
overload. ACE inhibitors and Angiotensin II receptor blockers are generally effective
antihypertensive agents in CKD; as single agents, they lower SBP and DBP by
approximately 10 to 15 mm Hg and 5 to 10 mm Hg, respectively.
• Topical emollients: Uremic pruritus, which is frequently encountered in patients with CKD, is
considered to be an inflammatory systemic disease rather than a local skin disorder.
Treatment options for uremic pruritus include emollients, topical capsaicin cream, ultraviolet
B phototherapy, gabapentin.
• Sedative/ anticonvulsants: Due to complexities of metabolism, protein-binding, renal
elimination, and other pharmacokinetic parameters, the dosing of antiepileptic drugs (AEDs)
in patients with chronic kidney disease (CKD) or end stage renal disease (ESRD) deserves
special attention
• Iron, vitamin: A vitamin and mineral supplement with iron, vitamin B12, and folic acid. To
treat anemia and nutritional deficiency.
• Dialysis: When kidney function is severely impaired, dialysis may become necessary to
replace it and maintain health. In chronic or end stage kidney failure, kidneys do not get
better and will need dialysis for the rest of the life.
73

74. SURGICAL MANAGEMENT
Renal transplant
• The best treatment foe ESRD is renal transplant.
• The transplanted organ can come from either a live donor or deceased donor.
Stem cells in renal modelling
• It is generally accepted that the Reno protective activity of stem cells (both in acute
and chronic renal disease models) is due to stem cell secretion of cytokines and
other molecules that inhibit inflammation and fibrosis and promote endogenous
repair processes including angiogenesis.
• Recently, stem cell-based therapies have been proposed as an alternative approach
to augment and restore renal function. In this study, we used to human-derive
amniotic fluid stem cells (AFSCs) to treat CKD in a rat model and demonstrated that
AFSC treatment facilitated positive effects in terms of improvements
of renal function.
74

75. Patient and family teaching
• Relationship between symptoms and their causes.
• Relationships among diet, fluid restriction, medication and blood
chemistry values.
• Preventive health care measures: oral hygiene, prevention of infection
and avoidance of bleeding.
• Dietary regimen, including fluid restrictions, i.e.
• Prescribed sodium, potassium, phosphorus and protein restrictions.
• Label reading and identifying nutritional content of foods.
• Use of small frequent feedings to maintain nutrient intake when anorexia or
nauseated.
• Fluid prescription and sources of fluid in diet.
• Avoidance of salt substitute containing potassium.
75

76. CONT…
• Monitoring of fluid excess.
• Accurate measurements and recording of intake and outputs.
• Monitoring weight gain and edema.
• Medication
• Action, doses, purpose and side effects of prescribed medications.
• Avoidance of over-the-counter (OTC) drugs, especially aspirin, cold medication
and NSAIDs.
• Planning for gradual increase in physical activity including rest
periods to conserve energy.
• Measures to control pruritis.
• Planning for following health care.
• Symptoms requiring immediate medical attention: changes in urine output,
edema, weight gain, dyspnea, infection, increased symptoms of uremia.
• Need for continual medical follow-up.
76

77. NURSING MANAGEMENT
- Nurse should obtain a complete history of any existing renal disease or
family history of renal disease because some kidney disorders have a
hereditary basis.
- Nursing is directed toward assessing fluid status and identifying potential
sources of imbalance, implementing a dietary program to ensure proper
nutritional intake within the limit of the treatment regimen
- Promoting positive feelings by encouraging increased self-care and greater
independence.
77

78. NURSING DIAGNOSIS
• Excess fluid volume related to decreased urine output, dietary excesses, and
retention of sodium and water.
• Imbalance nutrition less than body requirement related to anorexia, nausea,
vomiting, dietary restrictions, and altered oral membrane.
• Fatigue related to anemia, metabolic state and dietary restriction.
• Activity intolerance related to fatigue, retention of waste products, and dialysis
procedure.
• Grieving related to loss of kidney function as evidenced by expression of feelings
of sadness, anger, inadequacy hopelessness.
• Anxiety related to disease process therapeutic interventions and uncertainty of
prognosis.
• Deficient knowledge regarding condition and treatment.
• Risk of infection related to suppressed immune system, access sites and
malnutrition secondary to dialysis and uremia.
78

79. NURSING INTERVENTIONS
1. Maintain fluid and electrolyte balance.
• Monitor for fluid and electrolyte excess.
• Assess intake and output every 8 hours.
• Weigh patient every day.
• Assess presence of and extent of edema.
• Auscultate breach sounds.
• Monitor cardiac rhythm and blood pressure every 8 hours.
• Assess level of consciousness with the interval of every 8 hours.
• Encourage patient to remain within prescribed fluid restriction.
• Provide small quantities of fluid spaced over the day to stay within fluid
restrictions.
• Encourage a diet high in carbohydrate and within the prescribed sodium,
potassium, phosphorus and protein limits.
• Administer phosphate-binding agents with meals as prescribed.
79

80. 2. Prevent infection or injury.
• Promote meticulous skin care.
• Encourage activity within prescribed limits but avoid fatigue.
• Protect confused person from injury.
• Protect person from exposure to infectious agents.
• Maintain good medical/surgical asepsis during treatment and procedures.
• Avoid aspirin products.
• Encourage use of soft tooth brush.
80

81. 3. Promote comfort.
• Medicate patient as needed for pain.
• Medicate with prescribed antipruritic use of emollient bath, keep skin moist,
and control environmental temperature to modify pruritis.
• Encourage use of damp cloth to keep lips moist, give good oral hygiene.
• Encourage rest for fatigue, however, encourage self-care as tolerated.
• Provide calm and supportive atmosphere.
4. Assist with coping in lifestyle and self-concept
• Promote hope.
• Provide opportunity for patient to express feelings about self.
• Identify available community resources.
81

82. RESEARCH ARTICLES:
1. Watanabe S. (2017) Low-protein diet for the prevention of renal failure
• This artical said that The prevalence of chronic kidney disease (CKD) is estimated to
be 8–16% worldwide, and it is increasing. CKD is a risk factor for heart attack and
stroke, and it can progress to kidney failure requiring dialysis or transplantation.
Recently, diabetic nephropathy has become the most common cause of CKD. In
Japan, the cumulative probability of requiring hemodialysis by the age 80 years is 1/50
in males and 1/100 in females. The number of patients under hemodialysis in Japan
exceeded 320,000 in 2014, among which 38,000 were newcomers and 27,000 died.
• The annual medical costs of hemodialysis are 1.25 trillion yen in Japan, representing
4% of the total national medical expenditures in 2014. A low-protein diet (less than 0.5
g/kg b.wt.) is a very effective intervention. Low-protein rice (1/10 to 1/25 of the normal
protein contents) is helpful to control the consumption of proteins, decreasing at the
same time the intake of potassium and phosphate.
• Protein restriction is indicated as soon as the eGFR becomes lower than 60
ml/min/1.73 m2 body surface, in order, to slow disease progression. The newly
developed low-protein Indica rice is expected to help many CKD patients in China and
Southeast Asia.
82

83. 2. Karen M Van de Velde-Kossmann (2018) Skin Examination: An Important
Diagnostic Tool in Renal Failure Patients
• This artical said Renal failure is common in the United States with an
estimated prevalence of 660,000 treated end-stage renal disease patients in
2015 [<xref ref-type="bibr" rid="ref1">1</xref>]. Causes of renal failure are
many, and complications from renal failure, underlying disease, and
treatment are not infrequent. Examples of common skin manifestations
include xerosis, pigmentary change, and nail dystrophies. Frequent disease-
specific skin changes may be helpful in the diagnosis of primary disorders
leading to renal disease or severity of disease including bullosis
diabeticorum, sclerodactyly, or leukoctoclastic vasculitis. Some cutaneous
changes, such as the multiple angiokeratomas of Fabry disease or the
plexiform neurofibromas of neurofibromatosis, are pathognomonic of genetic
disorders, which often lead to renal failure. Careful examination of the skin
can provide crucial clues to diagnosis of renal failure causation and aid in
monitoring complications.
83

84. REFERANCES LIST
• Basavanthappa BT. “Medical Surgical Nursing”. 2nd Edition. Jaypee Publisher ,2009. Pp 1041-1055
• Sethi Deepak, Rani Kirti. “Medical Surgical Nursing I & II”. 1st Edition. Jaypee Publisher ,2016. Pp 782-799
• Basavanthappa BT. “Medical Surgical Nursing (2volumes)”. 3st Edition. Jaypee Publisher ,2015. Pp 1128, 1169-
1184
• Black M Joyce et al, “Medical Surgical Nursing”. 7th Edition. Volume I. Elsevier Publisher 2005. Pp 941-968
• https://www.ncbi.nlm.nih.gov.elibpgimer.remotexs.in/pmc/articles/PMC5406621/
• http://pubmed.ncbi.nlm.nih.gov.elibpgimer.remotexs.in/29478059/
• https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf
• https://nkfs.org/kidney-failure/chronic-kidney-disease-ckd/
• https://emedicine.medscape.com/article/238798-overview#a6
• https://www.cdc.gov/kidneydisease/prevention-
risk.html#:~:text=%20Prevention%20%26%20Risk%20Management%20%201%20Get,blood%20pressure...%2
04%20Managing%20CKD.%20%20More%20
• https://liebertpub.com/doi/10.1089/ten.TEA.2018.0371
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