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Management of ckd

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MANAGEMENT OF Pt. WITH CHRONIC KIDNEY DISEASE-CKD PRESENTED BY: INUSAH ADAMS TERNOPIL STATE MEDICAL UNI. UKRAINE. March,2015
Transcript
Page 1: Management of ckd

MANAGEMENT OF Pt. WITH

CHRONIC KIDNEY DISEASE-CKD

PRESENTED BY:

INUSAH ADAMS

TERNOPIL STATE MEDICAL UNI.

UKRAINE. March,2015

Page 2: Management of ckd

PLAN OF PRESENTATION

DEFINITION

ETIOLOGY

PATHOPHYSIOLOGY

CLINICAL PRESENTATION

DIAGNOSIS

TREATMENT

COMPLICATIONS

INDICATIONS FOR DIALYSIS

Page 3: Management of ckd

WHAT IS CHRONIC KIDNEY DISEASE?

It is kidney damage (structurally or functionally) for ≥ 3 months with or without decrease glomerular filtration rate (GFR)

OR

GFR < 60ml/min for ≥ 3 months with or without kidney damage

OR

Persistent microalbuminuria/Persistent proteinuria/Persistent hematuria

OR

Structural abnormalities of the kidneys (polycystic kidney disease, reflux nephropathy) proven by ultrasound

Page 4: Management of ckd

ETIOLOGY OF CHRONIC KIDNEY DISEASE?

Diabetes mellitus

Hypertension

Glomerulonephritis

Pyelonephritis

Renal artery stenosis

Renal calculi

Polycystic kidney disease

Congenital defects of the kidney or bladder

Secondary causes (SLE, rheumatoid arthritis, HIV, drugs-

gold, heroin use etc.)

Drugs (NSAIDS, Aminoglycoside etc.)

Page 5: Management of ckd
Page 6: Management of ckd

PATHOPHYSIOLOGY OF CKD?

Page 7: Management of ckd

PATHOPHYSIOLOGY OF CKD? Regardless of the primary cause of nephron loss, some usually survive

or are less severely damaged

These nephrons then adapt and enlarge, and clearance per nephron

markedly increases.

The RAAS is activated causing renal hypertension

If the initiating process progress, renal failure may ensue with the

rapid development of ESRD.

Focal glomerulosclerosis develops in the glomeruli, and they

eventually become non-functional.

proteinuria markedly increases and systemic hypertension worsens.

Adapted nephrons enhance the ability of the kidney to postpone

uremia, but ultimately the adaptation process leads to the demise of

these nephrons.

Adapted nephrons have not only an enhanced GFR but also enhanced

tubular functions in terms of, for example, potassium and proton

secretion.

Page 8: Management of ckd

Classification of kidney injury RIFLE and the

network criteria

Page 9: Management of ckd

CLINICAL PRESENTATION OF CKD? Asymptomatic in stage 1-3 with GFR > 30ml/min

Symptomatic in stage 4-5 with GFR < 30ml/min

1. Early signs :Polyuria/oliguria, Hematuria, Edema

2. Late signs

a. hypertension

b. Signs of anemia (pallor)

c. Signs of hyperurecemia:

i. Brain ( uremic encephalopathy): low concentration, confusion, lethargy,

asterixis, coma,

ii. Heart: pericarditis

iii. GIT: nausea & vomiting, anorexia, diarrhea

iv. Reproductive system: erectile dysfunction, decreased libido, amenorrhea

v. Blood system: platelet dysfunction with tendency to bleed, infections due to

WBCs dysfunction

vi. peripheral neuropathy: numbness, paraesthesia, restless leg syndrome

vii. Skin: dry skin, pruritus, ecchymosis

viii. Others: fatigue, hiccups, muscle cramps,

Page 10: Management of ckd

DIAGNOSIS OF CKD? Kidney injury with or without decrease GFR for ≥ 3 months

FBC: Anemia (normochromic, normocytic), leukopenia,

thrombocytopenia

Urinalysis:

i. Dipstick proteinuria, if positive, do daily or 24hrs proteinuria test

a. If proteinuria is ≤1g/24hrs, then consider urinary syndrome

b. If proteinuria is 1 to 3g/24hrs, nephritic syndrome/ tubulointerstitial

c. If proteinuria is ≥3.5g/24hrs, consider nephrotic syndrome

i. RBCs, RBC casts, suggests glomerulonephritis

ii. Pyuria or/and WBC casts are suggestive of interstitial

nephritis/pyelonephritis

GFR evaluation; usually decreased

Page 11: Management of ckd

Diagnosis con’t

Biochemical blood test:

i. High creatinine, high BUN

ii. Electrolytes: Hyperkalemia, hyperphosphatemia, hypermagnesemia,

hypocalcemia, low bicarbonate

iii. pH of blood: acidosis (metabolic)

iv. Hypoalbuminemia/hypoproteinemia

Plain abdominal x-ray (useful to look for radio-opaque stones or

nephrocalcinosis)

Renal biopsy (reveals underlying primary cause but may be nonspecific)

Ultrasound findings: small echogenic kidneys in ESRD, hydronephrosis,

polycystic kidneys

Page 12: Management of ckd

Ultrasound findings: small echogenic

kidneys in ESRD

Page 13: Management of ckd

TREATMENT OF CKD?

Treatment objectives

• To detect chronic kidney disease early in susceptible individuals.

• To control hypertension

• To control blood glucose

• To treat other underlying causes

• To prevent complications and further worsening of kidney function

Page 14: Management of ckd

Non-pharmacological treatment

Admit patient especially in stage of exacerbation

Diet: Restrict dietary protein to< 40 g/day, Restrict Na+, K+, PO4-

intake, avoid potassium containing foods e.g. banana

Water and electrolyte balance:

i. Daily fluid intake = previous day’s urine output + 600 ml (for

insensible losses)

ii. Strict fluid input and output chart

Daily weighing

General health advice e.g. smoking cessation

• Avoid nephrotoxins e.g. NSAIDs , Herbal medication

Page 15: Management of ckd

Pharmacological treatment Treatment of underlying condition (diabetes, HPT, autoimmune d’ses etc.)

Treatment of fluid overload

Diuretics: Furosemide, oral /IV, 40-120 mg daily

Treatment of hypertension (goal of BP<130/8OmmHg):

i. ACEIs- Lisinopril, oral, 5-40 mg daily Or Ramipril, oral, 2.5-10 mg daily Or

ii. ARBs- Losartan, oral, 25-100 mg daily or Valsatan, oral, 80-160 mg daily

Treatment of anemia

i. Injection erythropoietin 50-100units IV/SC 3times weekly

Treatment is initiated at Hb <10g/dl

i. Tab. Ferrous sulphate 200mg 3times daily

Treatment of hyperkalaemia/metabolic acidosis

• 10% Calcium gluconate, IV, 10-20 ml over 2-5 minutes Plus

• Sodium Bicarbonate, IV, 8.4% 50mEq, over 5 minutes Plus

• Regular Insulin, IV, 10 units in 50-100 ml Glucose 50%

Page 16: Management of ckd

Pharmacological treatment con’t…

Treatment of hyperphosphatemia:

i. Phosphate binders (calcium acetate/ calcium carbonate 2 capsules (1334mg )

orally with food)

Treatment of hypocalcemia:

i. Calcium citrate 1g/day

ii. Vitamin D supplement; 2 tablets (800 IU) once daily

Treatment of pruritus:

Capsaicin cream or cholestyramine

Treatment of bleeding:

Desmopressin 0.3 mcg/kg IV over 15-30mins

Page 17: Management of ckd

Renal replacement therapy (RRT)

Dialysis (hemodialysis or peritoneal dialysis)

Kidney transplant with immunosuppressant usage

hemodialysis= peritoneal dialysis in terms of efficiency

But hemodialysis is superior to peritoneal dialysis due to the

complication (peritonitis then subsequent septic shock) associated with

peritoneal dialysis

Indications for dialysis are:

1. fluid overload

2. severe acidosis

3. hyperkalemia

4. pericarditis

5. encephalopathy

Page 18: Management of ckd

Hemodialysis: 3-4hrs, 3 times per week

(Monday, Wednesday and Friday)

Page 19: Management of ckd

Peritoneal dialysis

Page 20: Management of ckd

Kidney transplant

plus immunosuppressant therapy

Page 21: Management of ckd

Complications of CKD? Anemia: due to lack of erythropoietin

Metabolic acidosis (severe): due to lack of NH3 production by kidneys which is

involved in acid-base buffer

Hyperkalemia: due to lack of excretion

Pericarditis: due to uremia

Osteodystrophy (osteitis fibrosa cystica): due to lack of 1,25-

dihydroxycholecalciferol and also Secondary hyperparathyroidism

Fluid overload (anasarca): lack of excretion and Na+ retention

Encephalopathy: due to uremia

Hypertension: due to activation of RAAS. HPT is the common cause of death

due to myocardial infarction. Maintain BP <130/80

Infections: uremia prevents degranulation of the neutrophils and so

myeloperoxidase can’t be released to destroy bacteria

Bleeding tendencies: due to platelets dysfunction from effects of uremia

Page 22: Management of ckd

Stay healthy


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