Chronic renal failure (CRF) or end stage renal disease (ESRD) is an irreversible deterioration of renal function that results in uremia or azotemia. It is caused by a progressive reduction in kidney function such that the kidneys can no longer maintain homeostasis. This leads to decreased glomerular filtration rate, hypertrophy of remaining nephrons, inability to concentrate urine, further nephron loss, and loss of excretory and non-excretory renal functions. Management of CRF focuses on preserving renal function, alleviating extra-renal manifestations through medications and dialysis, and improving body chemistry through diet and medication.

1. PRESENTED BY
MR.ROMAN BAJRANG
RELIANCE INSTITUTE OF NURSING

2. Edited by :-MR . ROMAN BAJRANG

3. DEFINITION
1.CRF OR ESRD IS A PROGRESSIVE, IRREVERSIBLE
DETERIORATION IN RENAL FUNCTION IN WHICH THE
BODY’S ABILITY TO MAINTAIN METABOLIC AND FLUID
AND ELECTROLYTE BALANCE FAILS RESULTING IN
UREMIA OR AZOTEMIA.
2.CHRONIC OR IRREVERSIBLE RENAL FAILURE IS A
PROGRESSIVE REDUCTION OF FUNCTIONING OF RENAL
TISSUE SUCH THAT THE REMAINING KIDNEY MASS CAN
NO LONGER MAINTAIN THE BODY’S INTERNAL
ENVIRONMENT.

4.  DECREASED RENAL BLOOD FLOW
 SYSTEMIC DISEASES
-DIABETES MELLITUS
-HYPERTENSION
-SLE
-POLYARTERITIS
-SICKLE CELL DISEASE
-AMYLOIDOSIS
-CC GIOMERULONEPHRITIS
-PYELONEPHRITIS
-ARF

5.  OBSTRUCTION OF THE URINARY TRACT
 HEREDITARY LESIONS
-POLYCYSTIC KIDNEY DISEASE
 INFECTIONS
 VASCULAR DISEASES
 MEDICATION OR TOXIC AGENTS
 ENVIRONMENTAL OR OCCUPATIONAL AGENTS
-LEAD
-CADMIUM
-MERCURY
-CHROMIUM

6. PATHPHYSIOLOGY
DUE TO ETIOLOGICAL FACTORS
DECREASED GFR
HYPERTROPHY OF REMAINING NEPHRONS
INABILITY TO CONCENTRATE URINE
FURTHER LOSS OF NEPHRON FUNCTION
LOSS OF NON-EXCRETORY AND EXCRETORY
FUNCTION

7. PATHOPHYSIOLOGY
Decreased renal
blood flow, primary
kidney disease,
damage from other
disease, urine outflow
obstruction
Decreased glomerular
filteration rate
Hypertrophy of
remaining nephrons
Inability to
concentrate urine
Further loss of
nephron function
Loss of excretory
renal function and
non excretoryrenal
function

8. PATHOPHYSIOLOGY OF CHRONIC RENAL FAILURE

9. STAGES OF CHRONIC KIDNEY DISEASE
STAGES 1 WITH NORMAL
OR HIGH GFR
>90 ml/min.
STAGE 2 MILD CKD 60-90 ml/min.
STAGE 3A
STAGE 3 B
MODERATE
CKD
45-59ml/min.
30-44ml/min.
STAGE 4 SEVERE CKD 15-29ml/min.
STAGE 5 END STAGE
CKD
<15ml/min.

10. STAGES OF CRF
1) Reduced Renal reserve
- BUN is high or normal
- Client has no C/M
- 40 to 75 % loss of nephron function
2) Renal Insufficiency
- 75 to 90 % loss of nephron function
- Impaired urine concentration
-Nocturia, mild anemia, increased
creatinine and
BUN
Edited by :-MR . ROMAN BAJRANG

11. 3) Renal failure
- Severe azotemia
- Impaired urine dilution
- Severe anemia
-Electrolyte Imbalances
Hypernatremia
Hyperkalemia
Hyperphosphatemia
4) End Stage Renal Disease
-10 percentage nephrons functioning
-Multisystem dysfunction

12. • DECREASED LIBIDO
• INFERTILITY
• DELAYED HEALING
• INFECTION
• ANEMIA, PALLOR
DISTURBANCES IN
REPRODUCTION
IMMUNE DISTURBANCES
INCREASED PRODUCTION OF
LIPIDS
IMPAIRED INSULINACTION
FAILURE TO PRODUCE
ERYTHROPOIETIN
FAILURE TO CONVERT
INACTIVE FORMS OF
CALCIUM
• ADVANCEDATHEROSCLEROSIS
• ERRATIC BLOOD GLUCOSE LEVEL
• DECREASED CALCIUM ABSORPTION:-
OSTEODYSTROPHYANDHYPOCALCEMIA
LOSS OF EXCRETORY RENAL FUNCTIONS

13. LOSS OF NON-EXCRETORY RENAL FUNCTIONS
• METABOLICACIDOSIS
DECREASED HYDROGEN
SECRETION ANDDECREASED
BICARBONATE
REABSORPTION
• HYPERPHOSPHATEMIA→DECREASED CALCIUM ABSORPTION→
HYPOCALCEMIA→ HYPER-PARATHYROIDISM→ DECREASEDPOTASSIUM
EXCRETION→ HYPERLKALEMIA
DECREASED PHOSPHATE
EXCRETION
• HYPERKALEMIA
DECREASED POTASSIUM
EXCRETION
• WATER RETENTION CAUSING
• HYPERTENSION, HEART FAILURE, EDEMA
DECREASED SODIUM
REABSORPTION INTUBULE
• UREMIACAUSING
• INCREASED BUN, CREATININE, URIC ACID, PROTEINURA, PERIPHERAL
NERVE CHANGES, PERICARDITIS, PRURITIS, CNS CHANGES,BLEEDING
TENDENCIES
DECREASED EXCRETION OF
NITROGENOUS WASTE

14. CLINICAL MANIFESTATION OF
CHRONIC RENAL FAILURE
 INTEGUMENTORY CHANGES:-
SKIN-VERY DRY BECAUSE OF ATROPHY OF SWEATGLAND.
PRURITIS-EXCORIATED SKIN.
SKIN COLOR-UROCHROMS PIGMENTS.
MUEHRCKE’S LINE
UREMIC FROST

16. MUSCULOSKELETAL
CHANGES
• RENAL OSTEODYSTROPHY
OSTEOPOROSIS
OSTEOSCLEROSIS
OSTEOMALACIA
OSTEITIS FIBROSA

17.  HEMATOLOGIC CHANGES
ANEMIA, FATIGUE,
WEAKNESS, COLD
 HEMATOLOGIC CHANGES
ANEMIA, FATIGUE,
WEAKNESS, COLD
INTOLERANCE ASKIDNEYS
ARE TO PRODUCE
ERYTHROPOIETIN.
HEMOLYSIS, CLOTTING
ABNORMALITIES.
BLEEDING TENDENCIESAS
ACCUMULATION OF
UREMIC INTERFERE WITH
PLATLETADHESIVENESS.

18.  IMMUNOLOGIC CHANGES
MORE
SUSCEPTIBLE TO
INFECTION.
SUPRESSION OF
DELAYED
HYPERSENSITIVITY.

19.  METABOLIC CHANGES
NORMAL RATIO OF BUN TO CREATININE IS 10:1
HYPOPROTEINURIA
INCREASED SERUM URIC ACID
CARBOHYDRATE INTOLERANCE
METABOLIC ACIDOSIS AS KIDNEYS FAIL TOEXCRETE
HYDROGEN IONS.

20.  CHANGES IN MEDICATION
TOXICITY
• MEDICATION TOXICITY
Edited by :-MR . ROMAN BAJRANG

21.  CARDIO-VASCULAR CHANGES
HYPERTENSION
ATHEROSCLEROSIS
LEFT VENTRICULAR DYSTROPHY ANDHEART
FAILURE DUE TO VOLUME OVERLOAD.
ACCELERATED DUE TO ABNORMALLIPID
METABOLISM, ARTERIALCALCIFICATION.

23.  RESPIRATORY CHANGES
PULMONARY EDEMA.
UREMIC LUNG
METABOLIC ACIDOSIS AS A RESULT OF
RESPIRATORY CHANGES TO HYDROGEN IONS.

24.  GASTROINTESTINAL CHANGES
ANOREXIA, NAUSEA, VOMITING
CONSTANT BITTER, METALLIC OR SALTY TASTE
EXPERIENCED.
BREATH- UREMIC FETOR, AMMONIA, FISHY LIKE SMELL.
CONSTIPATION, ULCER.

25.  REPRODUCTIVE CHANGES
• MENSTURAL IRREGULARITY
• AMENORRORHEA, IMPOTENCE.
ENDOCRINE CHANGES
• HYPOTHYROIDISM

26.  NEUROLOGIC CHANGES
• PERIPHERAL NEUROPATHY- BURNING FAT,GAIT CHANGES, PARAPLEGIA.
• IMPAIRED COGNITIVE FUNCTION.
 PSYCHOLOGICAL CHANGES
• FINANCIAL STRESS
• LIFE-STYLE CHANGES

27. Clinical Manifestations of CRF
 Electrolyte and acid-base balance
 Hematologic System
-Anemia
-Bleeding Tendencies
-Infection
 Metabolic changes
-Waste products accumulation
-Altered CHO metabolism
-Elevated triglycerides

28.  Gastrointestinal changes
-Mucosal Ulcerations
-Stomatitis
-Parotitis
-Gingivitis
-Oesophagitis
-Gastritis
-Colitis
-GI Bleeding
-Diarrhoea
-Constipation
CONTD………

29. CONTD………
-Metallic Taste in mouth
-Anorexia
-Nausea
-vomiting
 Respiratory Changes
-Kussmaul Respiration
-Dyspnea
-Pulmonary oedema
-Uremic Pleuritis

30. -Pleural Effusion
-Uremic Lung
-Cough Reflex is depressed
 Cardio Vascular Changes
-HTN- Leads to
-CHF
-Retinopathy
-Encephalopathy
-Nephropathy
CONTD………

31. -Dysrhythmia
-Peripheral Oedema
-Uremic Pericarditis
 Neurologic Changes
 Manifestations of peripheral
neuropathy
-Burning feet
-Gait changes
-Foot drop
-Paraplegia

32.  Features of CNS involvement
-Forgetfulness
-Inability to concentrate
-Short attention span
-Impaired reasoning
• Musculoskeletal changes
-Osteomalacia
-Osteitis fibrosa
-Osteoporosis
-Oateosclerosis

33.  Integumentary Changes
-Yellow grey discoloration of skin
-Pale
-Dry and scaly
-Pruritis
-Bruising ,Petechial and Purpura
-Hair is brittle
-Nails are thin and brittle

34.  Reproductive Changes
 Women
-Menstrual irregularities
-Infertility
-Decreased libido
 Men
-Impotence
-Testicular atrophy
-Oligospermia
-Decreased libido
-Decreased sperm motility

35.  Endocrine Changes
-Hypothyroidism
-Increased GH and prolactin
 Immunologic changes
-Depression of human antibody
formation
-Decreased function of leukocytes
- Depression of delayed
hypersensitivity

36. DIAGNOSTIC TEST
FOR
CHRONIC RENAL FAILURE
Edited by :-MR . ROMAN BAJRANG

37. DIAGNOSTIC STUDIES
 History and physical examination
 Routine lab measurements
- BUN
- Serum Creatinine
- Serum Electrolytes
- Hematocrit and Hb levels
- Urine Analysis
- Urine Culture

38.  Identification of Reversible Renal Disease
- Renal Ultrasound
- Renal Scan
- C T Scan
- Renal Biopsy

39. MANAGEMENT
1) Preserve the renal function and dialysis
- Controlling the disease process.
- Controlling BP by diet control,
weight control and medication.
- Reducing dietary protein intake.
2) Alleviate extra renal manifestations.
a) Pruritis
- Topical emollient and lotion.
- Antihistamine.
- IV Lidocaine

40. b) Neurological manifestations.
- Safety measures to protect From injury.
- Anticonvulsants.
- Sedatives
c) Hematologic changes:-
Therapy with epoetin alfaThree times a week
and
- supplemental iron, vitamin B12
folic acid.

41. 3) Improve body chemistry.
a) Dialysis
b) Medications
c) Diet

42. a) Dialysis
- Peritoneal dialysis
- Hemodialysis
b) Medications
* Hyperkalemia
- Insulin administration – I/V
- Sodium bicarbonate
- Calcium Gluconate – I/V
- Sodium polystrene
sulfonate(Kayexalate)

43. * Hypertension
- Sodium and fluid restriction
- Anti hypertensive
drugs Diuretics
Beta adrenergic blockers
Ca channel blockers
ACE inhibitors

44. Renal osteodystrophy
- Regulation of calcium,
 Phosphorus and acidosis
1.Treatment of hyperparathyroidism
2. Calciferol
- Paricalcitol (Vitamin D analog)
- Calcium based phosphate binders
Calcium acetate Calcium
carbonate

45. * Anaemia
- Erythropoietin – I/V
subcutaneously
- Epogen ( Epoetin alfa)
- Parental iron
- Folic Acid 1 mg daily
* Diuretics
Given early to stimulate excretion of
water

46. * Vitamins
- Supplemental water soluble
vitamins
c) Diet
* Protein restriction
- 0.6 to 0.75 gm/kg of ideal body
weight/day
- 1.2 to 1.3 gm/kg of ideal body
weight/day once the patient
starts dialysis .

47. * Water restriction
Patient not receiving dialysis – 600ml +
an amount equal to the previous days
urine out put
Patients on dialysis – fluid intake is
adjusted so that weight gains are not
more than 1 to 3 kg between dialysis

48. * Phosphate restriction
- 1000 mg/day
- Phosphate rich foods are
Diary products (milk, Ice
cream, cheese etc.)
* Potassium restriction
2 to 4 gm/day
(Sources are – orange,bamnana,
beans, legumes melons, tomatoes, etc.)

49. * Sodium restriction
- 2 to 4 gm/day
(Sources are – pickled foods,
soups, soya sauce
canned
etc. )
* Calcium
If serum ca levels are low,
calcium intake isadequate
important.
* Magnesium
Mild Mg restriction may be
imposed

50. MEDICAL MANAGEMENT
OF CHRONIC RENAL
FAILURE
Edited by :-MR . ROMAN BAJRANG

51. MEDICAL MANAGEMENT OF CRF
• HYPERKALEMIA
• PERICARDITIS
• HYPERTENSION
• ANEMIA
PREVENT
COMPLICATIONS-

52. ADMINISTRATION OF:-
ANTI-HYPERTENSIVES
ERYTHROPOIETIN
IRON SUPPLEMENTS
PHOSPHATE BINDINGAGENTS
CALCIUM SUPPLEMENTS
ADEQUATE DIALYSIS

53. • FLUID ALLOWANCE 500-600ml MORE
THAN THE PREVIOUS DAY 24hrs. URINE
OUTPUT.
• CARBOHYDRATE & FAT INTAKE 40-
50kcal/kg/day.
• DIET RESTRICTION PROTEIN 1g/kg/day.
• VITAMIN SUPPLEMENTS.
DIETARY INTERVENTIONS:-

54. • DIALYSIS THERAPY
• POTASSIUM REMOVAL
• POTASSIUM RESTRICTED DIET
HYPERKALEMIA:-
(KAYEXALATE)

55. HYPERPHOSPHATEMIA &
HYPOCALCEMIA PREVENTION &
TREATMENT:-
ALUMINIUM BASED ANTACIDS.
CARBONATE-CARBONATE AND
PHOSPHATE BINDING ANTACIDS.

56. NEUROLOGICAL ABNORMALITIES
• OBSERVE FOR SLIGHT TWITCHING,
HEADACHE, DELIRIUM, SEIZURES.
• IV DIAZEPAM OR PHENYTOIN.
ANEMIA
• EPOGEN (RECOMBINANT HUMAN
ERYTHROPOIETIN)

57. SURGICAL
MANAGEMENT

59. 1. FLUID VOLUME EXCESS
RELATED TO DECREASED URINE
OUTPUT, DIETARY EXCESS &
RETENSION OF SODIUM AND
WATER SECONDARY TO DISEASE
PROCESS.

60. 2. ALTERED NUTRITION LESS
THAN BODY REQUIREMENT
RELATED TO ANOREXIA, NAUSEA,
VOMITING, DIETARY RESTRICTION,
ALTERED ORAL MUCUS
MEMBRANES SECONDARY TO
DISEASE PROCESS.

61. 3. ACTIVITY INTOLERANCE
RELATED TO FATIGUE,
RETENTION OF WASTE
PRODUCT AND DIALYSIS
PROCEDURES SECONDARY
TO CHRONIC RENAL FAILURE.

62. 4. SELF-ESTEEM DISTURBANCE
RELATED TO DEPENDANCY,
ROLE CHANGE, CHANGE IN
BODY IMAGE AND CANGE IN
SEXUAL FUNCTION SECONDARY
TO DISEASE PROCESS.

63. 5. RISK FOR HYPERKALEMIA,
PERICARDITIS, PERICARDIAL
EFFUSION, PERICARDIAL
TEMPONATE, HYPERTENSION,
ANEMIA, BONE DISEASE,
METASTATIC CALCIFICATION
RELATED TO DISEASE PROCESS.

64. 6. KNOWLEDGE DEFICIT
REGARDING CONDTION
AND TREATMENT
MODALITIES RELATED
TO DISEASE PROCESS.

65. 7. RISK FOR
IMPAIRED SKIN
INTEGRITY RELATED
TO EDEMA, DRY SKIN
AND PRURITIS

66. 8. RISK OF INFECTION
RELATED TO INDEWELLING
PERITONEAL CATHETER,
VENI-PUNCTURE
CONNECTION OF TUBING
DURING HEMODIALYSIS.

67. Edited by :-MR . ROMAN BAJRANG