Chronic kidney disease (CKD) is defined as decreased kidney function over a period of three months or more. It can cause complications such as anemia, metabolic acidosis, hyperkalemia, and cardiovascular disease as kidney function declines. Treatment involves managing the underlying cause, restricting dietary intake of sodium, potassium, and phosphorus, treating complications pharmacologically, and potentially performing long-term dialysis or kidney transplantation for end-stage renal disease. Nursing care focuses on fluid management, dietary modifications, treatment of complications, and health education.

1. CHRONIC KIDNEY DISEASE
AND ITS MANAGEMENT
BY RAJEE RAVINDRAN
PEER GROUP PRESENTATION
ON

2. What is CKD ?
It is a term that encompasses all degrees of decreased renal
function, from damaged–at risk through mild, moderate, and severe
chronic kidney failure.
CRF

3. 8
GLOBAL BURDEN
DISEASE 2015

4. A Global health awareness campaign focusing on the importance of the
kidneys and reducing the frequency and impact of kidney disease and its
associated health problems worldwide.

5. ANATOMY AND
PHYSIOLOGY OF
KIDNEY

6. FUNCTIONS OF KIDNEY

10. DEFINITION
CKD is a condition in which there is either kidney damage or a decreased
glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least 3
months.
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.
The Kidney Disease
Outcomes Quality
Initiative (KDOQI) of
the National Kidney
Foundation (2002)

11. STAGING OF CKD

12. CRITERIA FOR ESTABLISHMENT OF CKD
•Albuminuria (albumin excretion> 30 mg/24hror 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

13. CAUSES

14. PATHOPHYSIOLOGY
TOTAL
GLOMERULAR
FILTRATION
RATE

15. CLINICAL MANIFESTATIONS
• Patients with CKD stages 1-3 are generally asymptomatic
• sodium and water imbalance
 Peripheral edema
 Pulmonary edema
 Hypertension
 Congestive heart failure
• Hyperkalemia due to either extracellular shift of potassium (as in
acidemia) or lack of insulin in DM.
• Metabolic acidosis
Malaise
Potentially fatal cardiac arrhythmias

16. CLINICAL MANIFESTATIONS
• Proteinuria
Protein-energy malnutrition
Loss of lean body mass
Muscle weakness
• Azotemia (nitrogen in blood) and Uremia (urea in blood)
Uremic frost (Due to its high systemic circulation, urea is excreted in eccrine sweat at high
concentrations and crystallizes on skin as the sweat evaporates)
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

17. CLINICAL MANIFESTATIONS
Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea
Skin manifestations: Dry skin, pruritus, ecchymosis
Fatigue, increased somnolence, failure to thrive
Malnutrition
Sexual dysfunction such as Erectile dysfunction, decreased libido, amenorrhea
Coagulopathies (Platelet dysfunction with tendency to bleed)
Hyperphosphatemia

18. CLINICAL MANIFESTATIONS
Hypocalcemia due to 1,25 dihydroxyvitamin D3 deficiency
Secondary hyperparathyroidism
Renal osteodystrophy
Vascular calcification
Left ventricular hypertrophy
Calciphylaxis (calcium accumulates in small blood vessels of the fat and skin
tissues)
Abnormalities in bone turnover, mineralization, volume, linear growth, or strength
Renal osteodystrophy (defective bone development)

19. CLINICAL MANIFESTATIONS
Reduction in erythropoietin
Anemia
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

20. DIAGNOSIS
• History
• Physical examination
• Urine
Volume: Usually less than 400 mL/24 hr (oliguria) or urine is absent (anuria).
Color: Abnormally cloudy urine may be caused by pus, bacteria, fat, colloidal
particles, phosphates, or urates. Dirty, brown sediment indicates presence of
RBCs, hemoglobin, myoglobin, porphyrins.

21. DIAGNOSIS
Specific gravity: Less than 1.015 (fixed at 1.010 reflects severe renal damage).
Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and
urine/serum ratio is often 1:1.
Blood
• BUN/Creatinine: GFR and creatinine clearance decrease while serum creatinine
(more sensitive indicator of renal function) and BUN levels increase. Creatinine
level of 12 mg/dL suggests ESRD. A BUN of >25 mg/dL is indicative of renal
damage.
• CBC: Anemia is present. Hemoglobin usually less than 7–8 g/dL.
• RBCs: Life span of red blood cells decreased because of erythropoietin
deficiency & azotemia.

22. DIAGNOSIS
• Proteins (especially albumin): Decreased serum level may reflect protein loss via
urine, fluid shifts, decreased intake, or decreased synthesis because of lack of
essential amino acids.
• Serum osmolality: Higher than 285 mOsm/kg; often equal to urine.
• sodium: May be low (if kidney “wastes sodium”) or normal (reflecting dilutional
state of hypernatremia).
• Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue
release (RBC hemolysis). In ESRD, ECG changes may not occur until potassium
is 6.5 mEq or higher. Potassium may also be decreased if patient is on
potassium-wasting diuretics or when patient is receiving dialysis treatment.

23. DIAGNOSIS
• Magnesium, phosphorus: Elevated.
• Calcium/phosphorus: Decreased.
• ABGs: pH decreased. Metabolic acidosis (less than 7.2) occurs because of loss
of renal ability to excretehydrogen and ammonia or end products of protein
catabolism.
• Antinuclear antibodies (ANA) to screen for for systemic lupus erythematosus
• 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); a positive P-ANCA
result is also helpful in the diagnosis of microscopic polyangiitis

24. DIAGNOSIS
• KUB x-rays: Demonstrates size of kidneys/ureters/bladder and presence of obstruction
(stones).
• Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters.
• Renal arteriogram: Assesses renal circulation and identifies extravascularities, masses.
• Voiding cystourethrogram: Shows bladder size, reflux into ureters, retention.
• Renal ultrasound: Determines kidney size and presence of masses, cysts, obstruction in
upper urinary tract.
• Renal biopsy: May be done endoscopically to examine tissue cells for histological
diagnosis.
• Renal endoscopy, nephroscopy: Done to examine renal pelvis; flush out calculi,
hematuria; and remove selected tumors.
• ECG: May be abnormal, reflecting electrolyte and acid-base imbalances.
• X-ray of feet, skull, spinal column, and hands: May reveal demineralization/ calcifications
resulting from electrolyte shifts associated with CRF

25. COMPLICATIONS
• Secondary hyperparathyroidism
• Vascular dysfunction
• Left ventricular hypertrophy

26. NON PHARMACOLOGICAL MANAGEMENT
• oxygen support if required.
• restrict dietary protein to less than 40gm/day. Restrict sodium and
potassium, phosphate intake
• Water and electrolyte balance: Daily fluid intake should be
according to previous urine output+600
• Daily weight monitoring
• General health advice

27. PHARMACOLOGICAL MANAGEMENT
• Treatment of underlying condition (eg: Diabetes mellites,
hypertension, autoimmune diseases etc)
• Treatment of fluid overload: Diuretics (Furosemide oral/IV 40-120mg
daily
• Treatment of hypocalcaemia- calcium citrate 1g/day, Vitamin D
supplement; 2 tablets (800IU) once daily.
• phosphorus binders to treat hyperphosphatemia- Phosphate
binders
• Treatment of hyperkalemia

28. PHARMACOLOGICAL MANAGEMENT
• calcium acetate/ calcium carbonate 2 capsules orally with food.
• Antihypertensive and cardiovascular agents (digoxin and dobutamine) manage
hypertension. They have also been found to reduce the risk of major
cardiovascular events such as myocardial infarction, stroke, heart failure, and
death from cardiovascular disease. The goal of BP< 130/80mmHg. ACE inhibitors
such as lisinopril, oral, 5-40 mg daily or ramipril, oral, 2.5-10mg daily. ARBs such
as losartan, oral, 25-100mg daily or valsartan, oral 80-160mg daily.
• Statins to treat hypercholesterolemia
• Anti-seizure agents (IV diazepam or phenytoin) are used for seizures
• Replacement of Erythropoietin (Epogen) is used to treat anemia associated
ESRD. A target hemoglobin level of 9–12 g/dL is recommended. Inj Erythropoietin
50-100 units IV/SC 3 times weekly. Tab Ferrous sulphate 200mg 3 times daily

29. PHARMACOLOGICAL MANAGEMENT
• Replacement of Calcitriol
• 10% calcium gluconate, IV, 10-20ml over 2-5 minutes.
• Regular insulin, IV, 10 units in 50-100 ml glucose 50%.
• Treatment of pruritis
• Capsaicin cream or cholestyramine
• Treatment of bleeding
• Desmopressin 0.3 mcg/kg IV over 15-30 mins
• Nutritional therapy. Dietary intervention includes careful regulation of protein
intake, fluid intake to balance fluid losses, sodium intake to balance sodium
losses, and some restriction of potassium.
• Dialysis (Haemodialysis or Peritoneal Dialysis)

30. SURGICAL MANAGEMENT
• The renal artery of the new kidney, previously branching from the
abdominal aorta in the donor, is often connected to the external iliac
artery in the recipient.
• The renal vein of the new kidney, previously draining to the inferior
vena cava in the donor, is often connected to the external iliac vein
in the recipient
• The donor ureter is anastomosed with the recipient bladder.

31. NURSING MANAGEMENT

32. SUMMARY

33. CONCLUSION
Chronic kidney disease results in worse all-cause mortality which increases as kidney
function decreases. While renal replacement therapies can maintain people
indefinitely and prolong life, the quality of life is negatively affected. Kidney
transplantation increases the survival of people with stage 5 CKD when compared to
other options; however, it is associated with an increased short-term mortality due to
complications of the surgery.

34. BIBLIOGRAPHY
Brunner and Sudharth’s Text book of Medical Surgical Nursing, Vol I, 11th edition. Lippincott Williams and Wilkins, 2008
Black, M Joyce, Medical Surgical Nursing: Clinical ManageMent of positive outcomes, Vol I, 8th edition, Saunders and
Elsevier publications, 2009
Lewis, Medical Surgical Nursing: Assessment and Management Of Clinical Problems, 6th edition, mosby
publications,2004
https://emedicine.medscape.com/article/318436-overview (Assessed on 09/08/2019)
https://www.hindawi.com/journals/jir/2018/2180373/ abs (Assessed on 11/08/2019)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6315879 (Assessed on 11/08/2019)
https://en.wikipedia.org/wiki/Chronic_kidney_disease (Assessed on 05/08/219)

35. ANY DOUBTS

36. EVALUATION

37. THANK YOU