1. MANAGEMENT OF Pt. WITH
CHRONIC KIDNEY DISEASE-CKD
PRESENTED BY:
INUSAH ADAMS
TERNOPIL STATE MEDICAL UNI.
UKRAINE. March,2015
2. PLAN OF PRESENTATION
DEFINITION
ETIOLOGY
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
DIAGNOSIS
TREATMENT
COMPLICATIONS
INDICATIONS FOR DIALYSIS
3. 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
7. 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.
9. 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,
10. 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
11. 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
13. 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
14. 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
15. 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%
16. 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
17. 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
21. 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
