Renal Problems in children Dr. Rim El-Rifai Consultant Paediatrician QMHC October 2005.
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Transcript of Renal Problems in children Dr. Rim El-Rifai Consultant Paediatrician QMHC October 2005.
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Renal Problems in children
Dr. Rim El-Rifai
Consultant Paediatrician
QMHC
October 2005
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Outline
Renal malformations and Common Urological problems
Common Renal Problems Summary
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Introduction
• Developmental disorders account for a wide spectrum of kidney diseases that cause considerable morbidity and mortality in the first years of life
• Childhood kidney disorders can predispose to adult morbidity and mortality
• Chronic renal diseases can affect growth
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Renal Malformations and Common Urological Problems
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Renal malformations
The major causes of end-stage renal failure in children
Can be diagnosed Antenatally Can be part of a syndrome Some have a genetic basis
– Vesico-ureteric reflux
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Types of abnormalities detected antenatally
Abnormalities in the size of the kidneys
Abnormalities in the texture of the renal parenchyma
Visible cysts Hydronephrosis
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Abnormal renal size Large:
– Polycystic kidney disease– Multicysticdysplastic– Cystic dysplasia– Congenital nephrotic syndrome– Renal tumour– Compensatory hypertrophy
Small:– Renal dysplasia/hypoplasia– Damage from obstructive uropathy
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Abnormal Parenchyma
Echobright:– Polycystic disease– Cystic dysplasia– Damage from obstructive uropathy– Glomerulo-cystic disease– Congenital Nephrotic syndrome
Macrocysts:– AD PCKD– TS– Multicystic dysplastic– Cystic dysplasia
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Hydronephrosis
• Obstruction: • PUJO• VUJO/ Megaureter• PUV• Ureterocele
• Non-obstruction: • VUR, • prune-belly s.
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Other renal problems detected antenatally
Duplication of the upper tract Renal agenesis Renal fusion and ectopia
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Diagnosis And Management of Antenatal Hydronephrosis
Diagnosis:– Antenatal screening– Postnatal KUB Ultrasound – MCUG– MAG3 renogram/ DMSA
Management:– Prophylactic antibiotics – Early treatment of UTI and complications– surgery
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Urinary Tract Infections
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Urinary tract infections
One of the most common bacterial infections in childhood (7% of girls- 2% of boys)
Most present to the primary care physician Complications can result in end-stage renal
disease and hypertension Can be as a result of underlying anatomical
abnormalities E-Coli cause 80-90% of first time UTI
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Risk Factors associated with permanent renal damage
Obstruction Vesico-ureteric reflux with dilatation Younger age (< 4 years) Delay of treatment Number of pyelonephritis attacks Uncommon bacteria
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Long-term consequences of reflux nephropathy
Chronic renal failure– Reflux nephrophathy in 13% of patients 5-44 years of
age with ESRF (Australia and New Zealand)– 30% of CRF in children (Wales)– 39% of renal transplants (Ireland)
Hypertension– Need for annual BP monitoring for life
Complications of pregnancy– UTI during pregnancy– Pregnancy induced hypertension– Complicated pregnancies, and worse fetal outcome
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Diagnosis and management of childhood UTI
MSU Early antibiotic therapy Prophylactic antibiotics Imaging: USS, MCUG, DMSA, other Surgery Monitoring of BP annually
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Voiding Dysfunction and The Wet Child
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Normal Sequence of Developing Bladder and Bowel Control
Nocturnal bowel control
Daytime bowel control
Daytime bladder control
Nocturnal bladder control
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Classification: Primary vs secondary
Primary mono-symptomatic nocturnal enuresis Primary Diurnal enuresis
– structural urological abnormalities.– Neuropathic Bladder
Secondary Diurnal enuresis– UTI– Dysfunctional voiding– Concentration abnormalities: IDDM, Diabetes
insipidus– Neuropathic bladder
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Characterization of Voiding Dysfunction
Storage Problem: Failure to Store normal volumes of urine at low pressure & without leakage– Non compliant bladder– overactive bladder– Inadequate sphincter tone during filling
Emptying Problem: Failure to empty completely, on command, efficiently at low pressures– Failure of neurological control of bladder– Bladder muscle failure– Failure of sphincter relaxation during voiding
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Evaluation of Dysfunctional Voiding
History Physical Exam Laboratory Tests Imaging and Urodynamics
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Management of the wet child Treatment of underlying causes:
– UTI– anatomical abnormalities
Bladder training (and bowel) Drugs:
– Anticholinergics – Desmopressin
Other:– Alarms, star charts, – surgery
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Common Renal Problems
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Features of Renal problems Clinical:
– Oedema– Polyuria and polydypsia– Failure to thrive/ short stature– Hypertension
Abnormal investigations– Blood:
» U&E, Albumin, Bone
– Urinalysis» Proteinuria» Haematuria
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Haematuria
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Detection of Haematuria
Visual examination Dipsticks Microscopy
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Causes of gross Haematuria in 150 children: Pediatrics 1977
UTI– Proven 39– Suspected 35
Perineal irritation 16 Trauma 10 Acute nephritis 6 Coagulopathy 5 Stones 3 Tumour 1 Other 35
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IgA Nephropathy
Male predominance More common in 2nd- 3rd decades 2-10% of glomerulonephritides in
UK
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IgA Nephropathy Diagnosis:
– macroscopic haematuria, – asymptomatic microscopic haematuria and
proteinuria, – acute nephritis, – nephrotic syndrome, – mixed nephritic-nephrotic synd.
Renal biopsy: deposits of IgA (plasma IgA raised in 20%)
Prognosis: – clinical course variable, – 50% recurrence in transplanted kidney
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Alport Syndrome
1. Inherited nephritis, 2. Sensori-neural deafness, 3. Occular defects, 4. less commonly large Platelets.
80-90% X-linked dominant, 10-20% AR
Diagnosis: renal biopsy.
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Alport Syndrome
Treatment: – ACE inhib. or Angiotensin recept. Blockers, – blood pressure control, – Renal transplantation
Prognosis Poor in boys: – proteinuria, hypertension and renal
impairment in late teens. – Hearing loss in adolescent years
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Thin Basement membrane nephropathy
Haematuria Variable clinical course Biopsy DD:
–Alports S.
–benign familial haematuria
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Benign familial haematuria
Microscopic haematuria AD inheritance Normal biopsy Good prognosis
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Proteinuria
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Proteinuria in Renal disease
Dipsticks: correlate better with level of albuminuria
24 hour urinary protein >60mg/m2/day Early morning Urine Protein/creatinine
ratio > 10 –25 mg/mmol Exercise and age related in normal
children
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Causes of proteinuria on dipstick
Artefect: alk. Urine, contamination by vag. Secretions
Benign: – Functional: exercise, cold, fever, congestive heart
failure– Idiopathic: incidental finding: Transient- Intermittent– Orthostatic: transient- fixed (<2 g/24 hr)
Persistent/ non-benign:– Persistent isolated– Disease related
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Disease related Proteinuria
Glomerular mechanisms: increased protein filtration – Damage to basement membrane– Loss of glomerular anion– Increased glomerular permeability
Tubular causes: decreased protein reabsorption
other
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Proteinuria evaluation Exclude non-renal causes History, examination, urinalysis Documentation of proteinuria:
– Dipstick diary: BD for 1/52– 24 hr urine collection– Random Pr:Cr ratio
MSU GFR measurement: est. GFR (Schwartz formula) Immunology/serology: C3-C4, ASOT, anti-hyaloronidase,
ANA, anti-DNA. Blood chemistry: prot, alb, cholest.
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Disease related proteinuria
Renal disease:– Glomerular causes– Tubular causes: hereditary, ATN, heavy metal
poisoning– Secretory proteinuria: neonates, lower urinary tract
Other diseases– Overflow proteinuria– Histuria– other
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Nephrotic Syndrome
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Idiopathic Nephrotic syndrome
More common in boys More common in Arabs and people
from Indian subcontinent Peak incidence 2-5 years Minimal change disease the most
common Genetic component
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Clinical features
Oedema: – gravity related, effusions
BP: – usually normal or low, – paradoxically elevated in 20%
abdominal pain: – hypovolaemia, peritonitis
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Lab. findings
Urine: – large amounts of albumin (>50 mg/kg/day)– microscopic haematuria (23%),
Blood: – Hypoalbuminaemia (<25 g/l), – low IgG, – increased cholesterol, – usually normal U & E, – reduced total calcium, – raised or decreased Hb and Hct
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Investigations of Nephrotic Syndrome
Urine:– Urinalysis and MC&S– Quantification of proteinuria: Early morning Pr:Cr ratio, 24 hr
collection– U- Na if hypovolaemia suspected
Plasma:– U, Cr & E– Albumin, T. Prot., Ca, Phos.– C3, C4, ASOT, ANA– Hep B serology– Varicella IgG status
FBC
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Treatment of SSNS
Admit to hospital Treat associated infection: Penicillin Steroids:
– evidence that longer initial course ( 6-7 mo vs 2-3 mo) protects from frequent relapses
Supporting treatments: diuretics Diet:
– no-added salt, healthy eating, fluid restriction
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Complications of SSNS Infection:
– Low IgG and serum factor B (C3 proactivator), impaired opsonisation and lymphocyte transformation, immunosupression
Thrombosis: – Thrombocytosis, increased clotting factors
(V, VII, VIII, X, Fibrinogen), reduced Antothrombin III, hypovolaemia, steroids
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Complications of SSNS
Acute renal failure: – pre-renal commonly, less common ATN
Hyperlipidaemia: – mechanism poorly understood
Malnutrition Side effects of treatment:
– steroids, alkylating agents, Cyclosporin A, Levamisole
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Indications for renal biopsy in NS
Age < 12 months (continuous or congenital/ infantile NS)
Age > 16 years Persistent hypertension macroscopic haematuria Impaired renal function unresponsive to
correction of hypovolaemia Low C3, C4 Failure to respond to initial course of steroids
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Other Nephrotic Syndromes
Steroid-resistant NS:– Focal segmental glomerulosclerosis and
minimal change disease: rising incident in African-American children
– Membranoproliferative (mesangiocapillary) glomerulonephritis: uncommon
– Membranous nephropathy: very rare Congenital/ Infantile NS
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Acute Nephritis Syndrome
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Acute Nephritis Syndrome
Acute glomerular injury and inflammation with decreased GFR and Na and water retention
Urinalysis: – Haematuria + Albuminuria + red cell casts
Most common cause: – Acute post-streptococcal Glomerulo-
nephritis (APSGN) 80%
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Other causes of acute nephritis
IgA Nephropathy HSP Membranoproliferative Glomerulonephritis Lupus nephritis ANCA-positive vasculitis Chronic infections:
– Shunt nephritis, Infective endocarditis, Hep B, Hep C, HIV nephropathy
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Acute post-Streptococcal Gromelunephritis
(APSGN)
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APSGN
Post throat or skin infection – nephritogenic group A beta-haemolytic
streptococcus Risk of APSGN is 10-15%, (40% within
families)
AB’s do not prevent GN but important to prevent further spread of bacteria
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APSGN
Age: 5-15 years More common in males Antigen-antibody related nephritis Abrupt onset 7-14 days after throat
infection and 3-6 weeks after skin infection
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Renal involvement in APSGN
Mild asymptomatic Haematuria
Acute renal failure with oligo-anuria
(rarely necessitating dialysis)
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Clinical features of APSGN Acute fluid overload
– Peripheral oedema– Pulmonary oedema– Congestive heart failure
Hypertension Haematuria (micro +/- macro) Proteinuria Renal function impairment
– Oliguria– Elevated plasma creatinine
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Investigations
Urinalysis:– M C &S, – early morning Pr: Cr ratio
Bacteriology: – throat swab, – ASOT, – Streptozyme essay ( strptolysin O,
streptokinase, DNAse B, Hyaloronidase, NADase antibodies)
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Investigations
Immunology: – C3 and C4– (ANCA, ANA and double straded DNA Ab, GBM
Ab)
Renal function: – U Cr &E, acid-base, plasma proteins, Ca and
phos.
Haematology: – FBC, blood film
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Management
Eradication of organism Treatment of renal failure: supportive
Indications for in-patient management: Hypertension Oedema Oliguria Elevated plasma creatinine Electrolyte abnormalities
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Clinical course and long term prognosis
Most symptoms subside in 2-3 weeks C3 back to normal in 8-12 weeks Microscopic haematuria +/- low grade
proteinuria can persist for 1-2 years
Excellent prognosis overall in children
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Renal manifestations of Systemic Disorders
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Childhood vasculitis Systemic symptoms: malaise, fever weight
loss– purpuric skin rash– Haematuria and red cell casts– Arthropathy– Serositis– Unexplained cardiac or pulmonary disease
Lab: anaemia, leukocytosis, thrombocytosis, raised ESR or CRP, ANCA +ve
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Henoch-Schönlein Purpura
Multisystem small vessel systemic vascultitis
Prominent cutaneous component
Most common vasculitis in children
14/100 000 of children Most favourable outcome
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HSP nephritis
Incidence varies greatly (20-61%)
Up to 2 months from presentation
Isolated haematuria- acute nephritis picture
Treatment supportive Steroids in severe GI, Immunosuppressant for
severe renal involvement
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Prognosis: HSP nephritis
Risk of chronic renal impairment <2% overall
CRF – up to 10% in patients referred to Nephrologist– Picture of nephritic/nephrotic nature and
crescentic changes on biopsy– Late deterioration in renal function well
recognised: long term FU needed
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Other vasculitis syndromes
SLE Kawasaki disease Takayasu’s arteritis Polyarteritis nodosa Wegenr’s granulomatosis
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Other renal manifestations of systemic diseases
Cystic Fibrosis– Nephrotoxic drugs– Tubulo-interstitial nephritis– IgA Nephropathy
Diabetes Mellitus– microalbuminuria
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Summary
Antenatal screening can detect a significant number of renal and urological abnormalities
Prevention and treatment of reflux nephropathy can prevent ESRD
Nephro-Urological problems in childhood are reasonably common
Spectrum of childhood nephro-urological problems extend through adolescent age necessitating close collaboration with adult nephrologists