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PROTEINURIA/NEPHROTIC SYNDROME LEARNING OBJECTIVES: ∙Define proteinuria . ∙Classify proteinuria . ∙Define nephrotic syndrome. PowerPoint PPT Presentation


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PROTEINURIA / NEPHROTIC SYNDROME. Prof. Jameela Kari Dr. Khald Khorshied . PROTEINURIA/NEPHROTIC SYNDROME LEARNING OBJECTIVES: ∙Define proteinuria . ∙Classify proteinuria . ∙Define nephrotic syndrome. ∙Recognize the clinical presentation. ∙Discuss the Causes.

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PROTEINURIA/NEPHROTIC SYNDROME LEARNING OBJECTIVES: ∙Define proteinuria . ∙Classify proteinuria . ∙Define nephrotic syndrome.

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PROTEINURIA / NEPHROTIC SYNDROME

Prof. Jameela Kari

Dr. Khald Khorshied .

PROTEINURIA/NEPHROTIC SYNDROME

LEARNING OBJECTIVES:

∙Define proteinuria.

∙Classify proteinuria.

∙Define nephrotic syndrome.

∙Recognize the clinical presentation.

∙Discuss the Causes.

∙Discuss the investigation.

∙ List the complications.

PROTEINURIA /NEPHROTIC SYNDROME

CONTENTS :

Definition of proteinuria.

Methods of urine collection of urine analysis, 24 hours collection of urine and urine albumin/creatinine ratio.

Steroid Sensitive Nephrotic Syndrome (SSNS) {Investigation, treatment and complications}.

Proteinuria

*Normal range  100mg/m2/day (150mg/day), <4 mg/ m2/hour

*Proteinuria = >4mg/m2/hour

*Nephrotic range  > 1 gm/ m2/day

>40mg / m2/hour

Spot urine for albumin/creatinine ratio (mg:mg)

Normal = <0.2 (0.5 if <2yr) g/g

Nephrotic => 2 g/g

Dipstick test:

negative, trace

1+ (closest to 30 mg/dL)

2+ (closest to 100 mg/dL)

3+ (closest to 300 mg/dL)

4+ (greater than 2,000 mg/dL)

Conditions Particularly Associated with Proteinuria

NON-PATHOLOGIC PROTEINURIA

PATHOLOGIC PROTEINURIA

NON-PATHOLOGIC PROTEINURIA

Excessive protein excretion, not as result of a disease state

Generally less than 1,000 mg/24 hr (1.00 g/24 hr) and is never associated with edema.

Postural (Orthostatic)Proteinuria: Children with this disorder excrete normal or slightly increased amounts of protein in the supine position. In the upright position, the amount of protein in the urine may increase 10-fold or more

Febrile Proteinuria: does not exceed +2 on the dipstick

Exercise Proteinuria: does not exceed +2 on the dipstick


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PATHOLOGIC PROTEINURIA

  • Tubular Proteinuria:

    • Injury to the proximal tubules results in diminished re-absorptive capacity and the loss of these low molecular weight proteins in the urine; rarely exceeds 1 g/24 hr; not associated with edema.

    • May be associated with other defects of proximal tubular function, such as glucosuria, phosphaturia, bicarbonate wasting, and aminoaciduria (FANCONI)

      Glomerular Proteinuria

  • Increased permeability of the glomerular capillary wall

  • Selective (loss of plasma proteins of low molecular weight protein including albumin), primarily in minimal-change nephrosis, or nonselective (loss of albumin and of larger molecular weight proteins such as IgG)

  • Nephrotic range (40mg/m2/hour), non-nephrotic range (4mg/kg/hour)

    PERSISTENT ASYMPTOMATIC PROTEINURIA

  • Persists for 3 mo

  • The amount less than 2 g/24 hr; it is never associated with edema.

  • Causes: postural proteinuria, membranous and membrano-proliferative glomerulonephritis, pyelonephritis, hereditary nephritis, developmental anomalies, and "benign" proteinuria.

  • Investigation: urine culture; measurement of creatinine clearance, 24-hr protein excretion, serum albumin, C3 complement levels, and renal ultrasound

    Indications for Renal Biopsy

    Persistent asymptomatic proteinuria in excess of 1,000 mg/24 hr (1 g/24 hr) or the development of hematuria, hypertension, or diminished renal function.

    Approach to proteinuria

  • History and examination

  • Confirm persistent proteinuria

  • 24 hours for protein

  • Fractional urine collection (orthostatic test)

  • U/Es, creatinine clearance (GFR),serum protein and albumin

  • Strept. Serology, C3, ANA

  • US and further imaging

  • ? Renal biopsy

    Nephrotic syndrome

  • Definition

  • Types:

    • Idiopathic 90%

      • Minimal change (85%)

      • Mesangial proliferation (5%) and membraneous nephropathy.

      • Focal segmental glumerulosclerosis (10%)

    • Secondary 10%

Minimal Change NS

  • More common in boys

  • 2-10years old

  • 2-3/100,000 (UK)

  • oedema "pitting"

  • Weight gain, ascites and/or pleural effusions

  • Declining urine output

Pathophysiology

 glomerular permeability to protein

Edema

 lipids


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Diagnosis

Urine analysis….protein > 2+

24 hours protein excretion

Urine albumin/creatinine (>2 g/g)

Serum Albumin < 25 gm/dl

Increased cholesterol and triglycerides

Other investigations: complements (C3 &C4), U&E, lipids, HepBSAg, ANA & ASO titer.

Nephritis

  • Frank haematuria

  • Hypertension

  • Low complement

  • Non-nephrotic range proteinuria

Nephrotic

  • None or microscopic haematuria (20%)

  • Normal BP

  • Normal complement

  • Nephrotic range proteinuria

  • Complications

  • Hypovalaemia

  • Infection: peritonitis (pneumococci)

  • Thrombosis

  • Management

  • Edema no added salt diet, IV albumin and diuretics if severe (physical discomfort)

  • Hypovolaemia IV albumin

  • STEROID: Prednisolone 60mg/m2/day (Max. 60 mg) or 2mg/kg/day(divided doses) for 6 weeks followed by 40mg/m2 (max. 40 mg)on alternate days for 6weeks. Then taper the dose by 10 mg/m2 on alternate days every 8 days.

  • Excellent prognosis  90% response to steroid

  • If no response after 4 weeks  biopsy

  • If frequent relapsers (2 or more in 6 months) or steroid dependent…consider:

    • Levamisole

    • Cyclophosphamide

    • Cyclosporin /Tacrolimus

  • If steroid resistant  biopsy and referral to pediatric nephrology


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    URINARY TRACT INFECTIONS (UTI).

    LEARNING OBJECTIVES:

    • Define UTI.

    • List the risk factors.

    • List the clinical presentation

    • Recognize how to investigate radiologically.

    • Outline the radiological investigations required.

    • Discuss the management.

      CONTENTS:

    • UTI (Presentation at different ages, investigation and treatment).

    • Congenital renal tract abnormalities (V-U-Reflux).

      …………………………………………………………….

    • Incidence: 0.1% of newborn infants

    • Clinical manifestations are vague and nonspecific (failure to thrive, weight loss, poor feeding, jaundice, diarrhea, and fever)

    • 75% are caused by Escherichia coli, but other enterobacteria and gram-positive cocci are not uncommon.

    • Diagnosis is confirmed by a positive bladder urine culture obtained either by suprapubic aspiration, catheterization or clean catch

    • 25-30% associated with V-U reflux

    • US kidneys, DMSA scan, micturating cystogram

    • TREATMENT. Parenteral antibiotics, usually including an aminoglycoside and ampicillin or a cephalosporin

    • Prophylactic antibiotics until V-U reflux is excluded

    • Older children: girls 6-8%, boys 2% circumcised (0.2%)

    • more specific symptoms (dysuria, abdominal pain, haematuria)

    • Diagnosis: urine culture and colony count: midstream (clean-catch), catheterization, or suprapubic puncture

    • Treatment: antibiotics (Trimethoprium), aminoglycoside and ampicillin or a cephalosporin,

    • 25-30% associated with V-U reflux

    • Reflux will be resolved by 5 years of age in most of the children

    • Recurrent infection leads to renal scars which is permanent  reflux nephropathy (hypertension and impaired renal function)

    • Every child with proved UTI (2nd) needs investigations to exclude V-U reflux and scars.

    • If there is V-U reflux.. Prophylaxis is indicated

    • All ages  US kidneys

    • < 1 year  MCUG to exclude reflux

    • < 5 years  DMSA scan to exclude scars


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    Congenital anomalies of renal tract

    PUV

    Renal agenesis (Potter’s sequence)

    Renal dysplasia

    Horseshoe kidny

    PUJ obstruction

    Prune Belly Syndrome

    Polycystic kidneys

    Ureteric duplication


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