The Case

1
Chronic Renal Failure
Budoor Al Shehhi Aisha Al Shamsi Raya Al
Mazrouei Amna Bedwawi Manal Al Mazrouei
2
Plan..

• Case presentation
• Pathophysiology of Chronic Renal Failure
• Treatment of Chronic Renal Failure

3
Past medical History

• Incidental Proteinuria

• Completely asymptomatic

• 120/ 80

• BP of 156 / 98 mmHg

• The physical examination is otherwise normal

4
Laboratory results
Urinalysis

• Clear amber

• Specific gravity 1.020

• 1.025 1.030

• 2 proteinuria

• Trace blood

• WBC 2-4 per HPF

• 0 4 per HPF

• RBC 4-6 per HPF

• 0 3 per HPF

• No casts

5
Blood tests

• Hgb. 12.0 gm

• 13.5-17.5 gm

• BUN 26mg

• 8-25 mg

• Creatinine 1.5mg

• 0.6-1.5 mg

Normal electrolytes

• 8.5-10.5 mg/dl

• Calcium 9.2 mg

• 3.6-5.3gm/dl

• Albumin 3.9 mg

24 hour urine collection

• 3.1 gm protein

• 90-140mls/min

• Creatinin clearance 60 mls/min

6
Imaging studies

• Chest X-ray

• Normal Ultrasound of the kidneys (Right 11.9 cm,
  Left 12.4 cm)

• No hydronephrosis

7
Present Medical History

• Patient history

• Easy fatiguability
• Anorexia
• Mild pruritis
• Shortness of breath on moderate exertion

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Present Medical History

• Physical examination

• Pallor
• Diffuse scratch marks over his arms, trunk and
  back
• BP 186/108 mmHg
• Elevated JVP
• GII/VI systolic murmur along the left sternal
  border, bilateral basal rales on auscultation of
  the chest, normal abdominal exam and 1 ankle
  edema..

9
Investigations obtained at this present visit
Urinalysis

• clear amber

• 1.025-1.030

• specific gravity 1.017

• 1 proteinuria

• Trace blood

• 0-4/HPF

• WBC 2-4/ HPF

• 0-3/HPF

• RBC 4-6/ HPF

• granular casts 2-4 / HPF

• 0-2/LPF

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Blood tests

• 13.5-17.5 gm/dl

• Hgb. 9.1 gm

• BUN 96mg

• 8-25 mg/dl

• 0.6-1.5 mg/dl

• Creatinine 7.2 mg

• 135-146

• Na 136

• 3.5-5mmol/L

• K 4.8

• 95- 106mmol/ L

• Cl- 107

• 22-30mmol/L

• HCO3- 16.4

• 8.5-10.5 mg/dl

• Calcium 7.1 mg

• 2.5-11.5 U/ml

• Alk P 310 U/ ml

• 3.6-5.3g/dl

• Albumin 3.4 mg

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24 hour urine collection

• 2.1 gm protein

• 82-140ml/min

• Creatinine Clearance 19 ml/min

CXR

• Cardiomegaly

• Mild pulmonary congestion

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• Aetiology of chronic kidney failure
• 1- Congenital inherited diseases
• Polycystic kidney disease
• Alports syndrome
• Congenital hyopplasia
• 2- Glomerular diseases
• Primary Glomerulonephritides including focal
  glomerulosclerosis
• Secondary SLE, Vasculitis, amyloidosis
• 3- Vascular disease
• Arteriosclerosis
• Systemic sclerosis with renal involvement
• Microscopic polyarteritis
• Main and medium- sized vessel vasculitis

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• 4- Tubulointerstitial disease
• Tubulointerstitial nephritis (idiopathic, drugs,
  immune mediated).
• Reflux nephropathy
• TB
• Schistosomiasis
• 5- Urinary Tract Obstruction
• Calculous disease
• Prostatic disease
• Pelvic tumors
• 6- Diabetes mellitus
• 7- Hypertension

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Pathogenesis Clinical manifestations Due to
impaired functions of the kidney
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- breathlessness- fatigue- generalized
swelling- metallic taste- vomiting nausea -
weight loss
In general Chronic renal failure symptoms
includes
- seizures- mental slowness and - confusion-
leg cramps- itching- pale skin color- poor
appetite
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Metabolic changes -Hyperkalemia. -Metabolic
acidosis. -Na water retention. -Haematological
changes(normochromic normocytic anaemia -Mineral
bone changes.
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Hyperkalemia
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• Hyperkalemia
• -manifested when GFR
• -due to decreased renal ability of K excretion.
• -Observed with sudden loads of K from endo. Or
  exo. sources
• k diet
• Drugs (ACI, NSAIDS, K sparing diuretics.
• Type IV RTA.
• Haemolysis, infection truma.
• acidemia lack of insulin.

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• Hyperkalaemia
• -Normal range of K (3.7-5.2 mmole/L).
• -Normally asymptomatic.
• - In severe cases 7mmol/L.
• tingling around tips fingers.
• loss of tendon jerk.
• abdominal distention.
• arrythmia
• ECG changes

- Tall T-wave, PR interval QRS complexes are
lengthened.
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Metabolic Acidosis
Causes -Inability to produce enough NH3 in
prox.tubules. -In advanced cases, accumulation of
PO4,SO4 other organic anions cause the small
anion gap.
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• Clinical Features
• Hyperventilation.
• Respiratory distress.
• Fatigue.
• Reduced cardiac output.
• Confusion drowsy.

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Increase in ECV -When GFR to excrete Na water. -At higher GFR, may be
due to increase ingestion of Na water. Leads
to -Hypertention. -Oedema.
-Ascites. -CV pulmonary oedema.
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Cont.,

• Hematologic abnormalities
• RBC count
• WBC function
• Clotting and bleeding

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• RBC count
• Normochromic, normocytic anemia ---mainly due to
  low production of erythropoietin low
  erythropoiesis.
• Additional causes

• Toxic uremic effect on bone marrow
• Bone marrow fibrosis due to increased PTH
• Reduced RBC survival hemolysis
• Blood loss due to capillary fragility and poor
  platelet function
• Increased GI blood loss due to dialysis and use
  of heparin
• Decreased dietary intake and absorption of iron

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WBC funtion

• Suppression of leukocytes increased
  susceptibility to infection.

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Clotting Bleeding

• Platelet aggregation, platelet factor III
  prothrombin prolonged bleeding time
  increased tendency of bleeding.

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Secondary hyperparathyroidism

• Causes

• Hyperphosphatemia
• Suppresses hydroxylation of 25-OH vit.D to 1,25
  diOH vit.D

• Hypocalcemia develops because of
• Decreased intestinal calcium absorption
• Calcium binding to high plasma levels of
  phosphate

• Decreased renal production of 1,25 diOH vit.D

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Effects on Bone Renal Osteodystrophy

• High-bone turnover Osteitis fibrosa
• - Due to hyperparathyroidism
• Osteomalacia
• Due to aluminium deposition
• Defective mineralization due to decreased active
  vitamin D
• Adynamic bone disease
• -Predominant bone lesion in chronic peritoneal
  dialysis
• Cysts at the ends of long bones
• -Due to dialysis related amyloidosis from
  beta2-microglubulin accumulation in chronic
  dialysis (8-10 yrs)

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Other manifestations of uremia in ESRD

• Pericarditis cardiac temponade
• Encephalopathy coma death
• Peripheral Neuropathy
• GI symptoms anorexia, nausea, vomiting, diarrhea
• Skin manifestations Pallor, Dryness, Pruritus,
  Ecchymosis
• Easy fatiguability, failure to thrive
• Malnutrition
• Erectile dysfunction, decreased libido,
  amenorrhea.

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Management

• Chronic kidney failure can not be cured but there
  are four goals of therapy
• Slow the progression of disease.
• Treat underlying causes and contributing factors.
• Treat complications of disease.
• Replace lost kidney functions.

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• The previous goals can be achieved by the
  following
• - Blood glucose and blood pressure control
  (ACEI)
• - Diet low protein diet (controversial)
• - Treatment of hyperlipidemia.
• - Avoidance of nephrotoxins such as
• - IV radiocontrast.
• - NSAIDs
• - Aminoglycosides.

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• - Treating the complications
• Fluid retention by diuretics
• Anemia by injections of a recombinant human
  hormone, erythropoietin
• Low calcium by calcium supplements
• Hyperphosphatemia with dietary phosphate binders
  and dietary phosphate restriction.
• Hyperpathayroidism with calcitriol or vitamin D
  analoges.
• Metabolic acidosis with oral alkali supplements.
• - Treating the uremic manifestations by the
  following
• 1- Hemodialysis takes 3-4 hours and usually
  performed about 3 times a week.

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2- Peritoneal dialysis - It is done by putting
2 Liters of dialysis fluid into the abdominal
cavity through a catheter. - The fluid will
balance out electrolytes and toxic waste products
and it needs to be exchanged 4 times a day.

3- Kidney transplant can be from living related
donors,
living unrelated donors or cadavers.
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• Complications of Haemodialysis
• 1- Vascular problems ( CHF)
• 2- Metabolic complications (Hyperparathyroidism)
• 3- Neuromuscular (neuropathy)
• 4- Hematologic (Anemia)
• 5- GI (bleeding)
• 6- Genitourinary ( Sexual dysfunction)
• Complications of peritoneal dialysis
• 1- Infections (Peritonitis)
• 2- New onset diabetes (Hyperglycemia)
• 3- Hypervolemia (Hypertension, pulmonary edema)
• 4- Obesity
• 5- Hypokalemia
• Complications of renal transplantation
• 1- Infections
• 2- Malignancies
• 3- Cardiovascular diseases

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Thank You