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Paediatrics STG > Paediatric Renal Disease > Flashcards

Paediatric Renal Disease Flashcards

1
Q

How are structural abnormalities of KUB detect?

A

Many structural abnormalities of the KUB identified on Antenatal US screening; UTI, VUR, Obstruction have potential to damage the growing kidney
o Chronic disorders may affect growth and development

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2
Q

What is GFR like in infants?

A

GFR is low in newborn infants, especially premature (GFR of 28wks gestation is only 10% term); GFR rises rapidly from 1yrs to 2yrs, when adult rate is achieved

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3
Q

Term Infant Corrected GFR

A

Term infant corrected GFR is about 15-20

o eGFR = k × height (cm) ÷ Creatinine (umol/L); where k is 31 if measured enzymatically, or 40 if using older method

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4
Q

Plasma Urea in Infants

A

Increased in renal failure, often before rise in Creatinine; Also increased in High
Protein diets, Catabolic states, or GI bleeding (=Protein meal)

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5
Q

Radiological Investigations of the Urinary Tract: US KUB

A

Anatomical but not functional information; Useful for visualising dilatation, stones, nephrocalcinosis; Static scan

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6
Q

Radiological Investigations of the Urinary Tract: DMSA

A

(99m-Tc based) – Identify functional defects, such as scars, areas of non-functioning tissues; Sensitive so wait 2/12 after UTI to avoid diagnosis false scars

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7
Q

Radiological Investigations of the Urinary Tract: MCUG

A

Micturating Cystourethrogram (MCUG) – Contrast introduced into bladder by urethral catheter; Visualises anatomy, identify VUR and obstructions

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8
Q

Radiological Investigations of Urinary Tract: MAG3

A

(99m-Tc based) – Dynamic scan measuring drainage to identify obstruction; Furosemide often given; For older children, used to identify VUR

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9
Q

Antenatally detect renal anomalies: Renal Agenesis

A

Oligohydramnios leading to Potter syndrome; Not compatible with life

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10
Q

Antenatally detect renal anomalies: Multicystic Dysplastic Kidney

A

Failure of Ureteric Bud (forms Ureter, Pelvis, Calyces and Collecting Ducts) union with Nephrogenic Mesenchyme; Non-functional, cystic structure with no renal tissue, unconnected with Bladder
o Involution by 2yrs of age; Nephrectomy if remains very large or HTN
o Potter syndrome if bilateral (Due to Oligohydramnios)

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11
Q

Antenatally detect renal anomalies: AR PCKD and AD PCKD

A

AR Polycystic Kidney (Diffuse, bilateral enlargement), AD Polycystic Kidney (Varying cysts)
o Main symptoms are HTN in childhood, Renal Failure in adulthood; Other cystic lesions in Liver, Kidney; Cerebral Aneurysms, Mitral Valve Prolapse

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12
Q

Antenatally detect renal anomalies

A

Other abnormalities include Horseshoe Kidney, Duplex Kidney

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13
Q

Urinary Tract Obstruction

A

Obstruction leads to proximal dilatation – Thickening, Bladder Diverticula etc

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14
Q

Urinary Tract Obstruction : Causes of Unilateral Hydronephrosis

A

PUJ, VUJ obstruction

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15
Q

Urinary Tract Obstruction : Causes of Bilateral Hydronephrosis

A

Bladder neck obstruction, Posterior Urethral valves (boys)

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16
Q

UTI in children: Stats

A

3-7% of girls, 1-2% of boys at least one symptomatic UTI before 6yrs age; 12-30% recurrent

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17
Q

UTI Symptoms

A

Fever and systemic involvement if Pyelonephritis; Cystitis typically non-febrile
• Up to half of patients with UTI have structural abnormalities; Pyelonephritis can damage the growing kidney for scar formation, predisposing to HTN, and progressive CKD if bilateral

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18
Q

UTI Causes

A

Typically, bowel flora (e.g. E coli, Klebsiella, Proteus, Pseudomonas, S faecalis) but can also be haematogenous spread, especially in Newborns
o Proteus more common in boys than girls – Predisposes to Phosphate stones due to Urea-splitting to Ammonia, alkalinising the urine
o Pseudomonas indicates present of structural abnormality affecting drainage; Most common in catheterised patients

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19
Q

UTI Presentation in Infants

A

Nonspecific; Fever usually but not always present; Sepsis can set rapidly
o Fever, Vomiting, Lethargy, Irritability, Poor feeding/Faltering growth, Jaundice, Offensive Urine, Febrile Seizure if <6/12

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20
Q

UTI Presentation in Children

A

Dysuria, Frequency and Loin Pain triad more common
o Also, other LUTS (Urgency etc), Fevers, Rigors, Lethargy, Anorexia, Vomiting, Diarrhoea, Haematuria, Offensive/Cloudy urine, Enuresis/Incontinence
o Dysuria alone usually due to Cystitis; Vulvitis in girls, Balanitis in uncircumcised boys
o Symptoms suggestive of UTI can also occur following sexual abuse

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21
Q

UTI Investigations: Urine Dip

A

Urine tested for all infants with unexplained fever >38deg
• Dipstix – Nitrate (Positive result very likely to indicate true UTI, but not all UTI nitrate positive); Leucocyte Esterase (May be negative in UTI, falsely positive if febrile illness; Positive in Balanitis and Vulvo-vaginitis)
• Blood, protein and glucose on Dipstix can identify other diseases e.g. Nephritis, DM

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22
Q

UTI Investigations: Clean Catch

A

Clean-catch into waiting clean pot when nappy removed (recommended); Adhesive plastic bag after careful washing, Catheter if urgent and no urine passed, Suprapubic if severely ill
o In older children – Careful cleaning, collection of midstream urine

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23
Q

UTI Investigation: MC+S

A

MC+S immediately where possible – All children <3yrs with suspected UTI; Otherwise refrigerate to prevent overgrowth
o Culture performed unless both Leucocyte Esterase and Nitrate negative
o >105 CFU bacterial culture of single organism per ml – 90% probability of infection
o Mixed growth – Represents contamination; if doubt, resend sample
o Any growth in catheter or suprapubic specimen is diagnostic of infection

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24
Q

Vesico-Ureteric Reflux

A

Developmental abnormality of VUJ; Lateral displacement of Ureters, enter the bladder directly rather than angle, with shortened or absent Intramural course
o Severe cases may be associated with Renal Dysplasia
• May also occur with Bladder pathology – E.g. Obstruction, or temporarily following UTI
• Mild reflux unlikely to be significant, which might resolve with age; Severe reflux associated with Intrarenal reflux; Scarring if UTI occurs (Reflux Nephropathy)
o Risk of HTN in childhood and early adult life up to 10%

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25
Q

UTI Management

A

Move to only investigate Atypical UTI – Seriously ill, poor urine flow, abdominal/bladder mass, raised Creatinine, Failure to respond to suitable Abx, or atypical organism growth

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26
Q

UTI Management: Initial US KUB

A

Identify serious structural abnormalities and obstruction; Renal defects (non-gold standard for renal scars)

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27
Q

UTI Management: If urethral obstruction suspected

A

If Urethral obstruction suspected (Abnormal bladder in boy) – MCUG promptly
• Functional scanning 3/12 after UTI

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28
Q

UTI Management: Antibiotics

A
  • Infants <3/12 – IV Abx 5-7 days
  • > 3/12, with suspected Pyelonephritis – Oral Abx or IV Abx followed by oral switch
  • Cystitis or Lower UTI – Oral Abx for 3/7
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29
Q

Prevention of UTI: Lifestyle

A
  • High fluid intake, Regular voiding, Double voiding to ensure complete emptying, Treating constipation, Good perineal hygiene
  • Probiotics – Lactobacillus acidophilus reduces pathogenic organisms that can cause invasive disease in the GI tract
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30
Q

Prevention of UTI: Antibiotic Prophylaxis

A

Controversial; for <2-3yrs age with congenital abnormalities

o Typically, Trimethoprim, Nitrofurantoin or Cephalexin

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31
Q

Prevention of UTI: Surgery

A
  • Circumcision can be considered in boys – Reduced incidence of UTI
  • Anti-VUR surgery if progression of scarring with UTI
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32
Q

UTI Follow Up

A

BP checked annually if defects present; Urinalysis to check for CKD
• Regular assessment of Renal Growth and Function if bilateral defects

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33
Q

Transient Proteinuria

A

Transient proteinuria may occur during febrile illness or after exercise

34
Q

Persistent Proteinuria

A

Persistent proteinuria is significant – Quantify by measuring Urine Protein-to-Creatinine Ratio, in an early morning sample (Normal PCR<20mg/mmol)
o Common cause of Orthostatic Proteinuria – Proteinuria only when child is upright during the day; Prognosis excellent, no investigation necessary

35
Q

Nephrotic Syndrome

A

• Heavy proteinuria leads to Low Plasma Albumin and Oedema; Unknown cause; Few cases due to systemic diseases (E.g. Henoch-Schönlein, SLE, Malaria) or allergens (e.g. Bee stings)
• Presents as Periorbital Oedema (particularly on waking; Early sign), Scrotal, Vulval, Ankle Oedema, Ascites, Pleural Effusion (leading to SOB)
o Infections, such as Peritonitis, Septic Arthritis or Sepsis due to loss of Ig in urine

36
Q

Minimal Change Disease

A

Called Minimal Change as only minor abnormal Podocyte Fusion seen
More common in Asians, associated with Atopy; Often with respiratory infections

37
Q

Minimal Change Disease: Steroids

A 
Steroid-sensitive Nephrotic syndrome: 85-90% respond to corticosteroid therapy and do not progress to CKD;
Oral steroids (60mg/m2 prednisolone) unless atypical features; Dose tapered over weeks; If no response after 4-6 weeks, or atypical features, Renal biopsy required
38
Q

Minimal Change Disease: Atypical Features

A

Atypical features include Macroscopic Haematuria, Hypertension, Deranged Complement or Renal Function

39
Q

Minimal Change Disease: Complications

A

Hypovolaemia (volume depletion due to Oedema), which leads to risk of Thrombosis and Shock
Thrombosis occurs due to urinary losses of Antithrombotic factors, as well as Thrombocytosis due to Steroids and increased Haematocrit
o Higher risk of infections with capsulated bacteria, especially Pneumococcus; could lead to Spontaneous Bacterial Peritonitis
o Hypercholesterolaemia – Inversely correlated with Serum Albumin

40
Q

Minimal Change Disease: Management of Hypovolemia

A

Can be managed by IV fluid resus; if severe, IV 20% Albumin and Furosemide might improve symptoms, also Albumin SE: Oedema, Hypertension

41
Q

Minimal Change Disease: Rule of Thirds

A

1/3 of patients with MCD resolve directly; 1/3 Infrequently relapse, and 1/3 frequently relapse, becoming steroid-dependent
o Steroid sparing agents include Levamisole, Cyclophosphamide, Tacrolimus, Ciclosporin and Rituximab

42
Q

Steroid Resistant Nephrotic Syndrome

A

Requires specialist Nephrology; Diuretics, Salt restriction, ACE Inhibitors and sometimes NSAIDs improve proteinuria
o Genetic testing available; Can identify specific issues e.g. CoQ10 pathway defect
o Causes include FSGS, MPGN, and Membraneous Nephropathy

43
Q

Congenital Nephrotic Syndrome

A

Presents first three months of life; Most commonly AR, more common in consanguineous; High mortality, usually due to Hypoalbuminaemia

44
Q

Haematuria

A

Microscopy to confirm haematuria; (>10 RBC per hpf); UTI most common cause

45
Q

Glomerular Haematuria

A

Glomerular Haematuria is suggested by brown urine, Deformed RBCs and Casts, and often accompanied by Proteinuria

46
Q

Glomerular Haematuria: Causes

A

Acute Glomerulonephritis, Chronic Glomerulonephritis, IgA Nephropathy, Familial Syndromes (e.g. Alport)

47
Q

Lower Urinary Tract Haematuria

A

usually red, Beginning or End of stream, not accompanied by Proteinuria, and unusual in children

48
Q

Lower Urinary Tract Haematuria: Causes

A

Infection, Trauma, Stones, Tumours, Sickle Cell Disease, Renal Vein Thrombosis, Hypercalciuria

49
Q

Haematuria: When to do a renal biopsy

A

Renal Biopsy may be required if significant, persistent Proteinuria, Recurrent Macroscopic Haematuria, Abnormal Renal Function or Abnormal Complement

50
Q

Acute Nephritis: Signs

A

Increased Glomerular Cellularity restricts blood flow, leading to reduced GFR
• Reduced Urine Output, Volume Overload, HTN, Oedema, Nephritic Syndrome

51
Q

Acute Nephritis: Management

A

Managements includes Water and Electrolyte Balance, Use of Diuretics
o Can rapidly progress (Rapidly Progressive GN); If untreated, leads to irreversible CKD; Requires Biopsy and Treatment (e.g. Immunosuppression, Plasma Exchange)

52
Q

Post Streptococcal Nephritis

A

Diagnosed by evidence of recent Streptococcal infection (Raised ASO/Anti-DNAse B), low complement (C3); Long term prognosis is good

53
Q

Henoch Schonlein Purpura

A

Characteristic Skin Rash on Extensor surfaces, Arthralgia, Periarticular Oedema, Abdominal Pain, Glomerulonephritis
3-10yrs; Peaks during Winter, often preceded by URTI; Unknown cause
• Often have fever; Rash symmetrically distributed over Buttocks, Extensor surfaces of Arms, Legs and Ankles; Urticarial rash, rapidly becoming Maculopapular and Purpuric
• Renal Involvement is common, but rarely the first symptom
• Requires long-term follow up to monitor HTN, progressive CKD after interval

54
Q

IgA Nephropathy

A
  • Macroscopic Haematuria often with URTI symptoms
  • Histological findings and URTI like HSP; Might be variant of same pathological progress
  • Better prognosis in children
55
Q

Alport Syndrome

A

X-linked Recessive Disorder – Progresses to End-stage CKD by Early adulthood in Males; Associated with SNHL and Ocular defects

56
Q

AKI

A

Sudden, potentially reversible reduction in Renal Function; Oliguria is usually present

57
Q

Prerenal AKI

A

Caused by circulatory failure or hypovolemia: sepsis, burns, haemorrhage, nephrotic syndrome, gastroenteritis

58
Q

Renal AKI

A

salt and water retention; Blood, proteins and casts are often present in urine
Vascular Causes: HUS, vasculitis, embolus, renal vein thrombosis
Tubular causes: ATN, ischaemia, toxic, obstructive
Glomerular causes: Glomerulonephritis
Interstitial: Interstitial nephritis, pyelonephritis

59
Q

Post renal AKI

A

Due to urinary obstruction
Congenital: Posterior urethral valves
Acquired: Blocked urinary catheter

60
Q

Acute on Chronic RF

A

suggested by Growth Failure, Anaemia, Renal Osteodystrophy (Disordered Mineralisation)

61
Q

Renal Failure Management: Circulation and Fluid Balance

A

Circulation and Fluid Balance meticulously monitored; Investigation by US KUB to identify obstruction, small kidneys in chronic disease, or large, bright kidneys with loss of Cortico-medullary Differentiation in acute processes

62
Q

Prerenal failure Management

A

Hypovolaemia; Urgent correction with Fluid Replacement and Circulatory Support to prevent Acute Tubular Injury and Necrosis

63
Q

Renal Failure Management

A

Restriction of fluid intake, Diuretic challenge if Circulatory Overload
o High calorie, normal protein diet to decrease Catabolism, Uraemia and Hyperkalaemia; Manage metabolic derangements
o If cause not obvious, Renal Biopsy to rule out Rapidly Progressive GN
o Two most common in UK – Haemolytic Uraemic Syndrome, or Acute Tubular Necrosis (typically in setting of Multisystem Failure)

64
Q

Postrenal failure management

A

Assess site of obstruction; Relief by Nephrostomy or Catheterisation; Surgery when fluid volume and electrolytes corrected

65
Q

When is dialysis indicated?

A

Dialysis indicated where conservative management fails, Hyperkalaemia, Severe Hypo or Hypernatraemia, Pulmonary Oedema or Severe HTN, Severe Metabolic Acidosis or MOF

66
Q

Metabolic Acidosis Treatment

A

Sodium Bicarbonate

67
Q

Hyperphosphatemia

A

Calcium Carbonate

Dietary restriction

68
Q

Hyperkalaemia

A 
Calcium gluconate if EEG changes
Salbutamol
Calcium Exchange resin
Dietary restriction 
Dialysis
69
Q

Haemolytic Uraemia Syndrome

A

Triad of AKI, Microangiopathic Haemolytic Anaemia (MAHA) and Thrombocytopaenia

70
Q

Haemolytic Uraemia Syndrome: Cause

A

Typically, secondary to Verocytotoxin producing E coli O157:H7; Prodrome of bloody diarrhoea; Organisms preferentially damage Renal Endothelial cells
o Platelets consumed in ensuing Intravascular Thrombogenesis; MAHA from RBC circulating into damaged microvasculature; Brain, Pancreas and Heart involvement

71
Q

Haemolytic Uraemia Syndrome: Prognosis and Follow up

A

If supported early, good prognosis; Long term follow-up for Proteinuria, HTN, and CKD

72
Q

Atypical HUS

A

No diarrhoea prodrome, may be familial; Frequently relapses
o High risk of HTN, progressive CKD, Mortality; Eculizimab (Anti-C5 Mab) greatly improves prognosis but expensive; Plasmapheresis alternatively

73
Q

Undescended testes

A

Most become arrested along their normal pathway of descent; 5% of Term infants, more common in Premature; by 3/12, only 1% still undescended
o Small, spontaneous rate of descent = Delayed decision to operate
o Diagnosis made during routine examination of the newborn
o Examination should be made in warm environment, with warm hands; Testis may be delivered by gentle pressure along line of Inguinal Canal

74
Q

Palpable Undescended Testes

A

Usually seen/felt in groin but unable to manipulate to scrotum
o If palpated below External Inguinal ring but outside scrotum – Ectopic Testis

75
Q

Impalpable Undescended Testis

A

May be in Inguinal Canal, Intra-Abdominal, or Absent
o If Bilaterally Impalpable – Establish Karyotype to exclude disorders of sexual development
o 10% of Impalpable Testis regressed and absent; Laparoscopy for diagnosis

76
Q

Retractile Testes

A

Testis may also be retractile – Can be manipulated into testis without tension easily; Action of Cremasteric muscle pulling up the testis
o Follow-up as some require surgery to place
into scrotum

77
Q

Management of Undescended Testes

A

Orchidopexy (Surgical placement of testis into Scrotum) for Cosmetic reasons, reduce risk of Trauma and Torsion, Fertility (Temperature for Spermatogenesis, important if bilateral; Evidence if delaying beyond 2 years adversely affects development) and Malignancy

78
Q

Operating on Undescended Testes: Timing

A

Timing depends on local surgical and anaesthetic facilities; Typically, before or around 1yr age, since beyond then spontaneous descent unlikely
o Adverse effects to Testicular Growth, Hormonal Function and Spermatogenesis if waiting until older

79
Q

Groin Approach to Undescended Testes

A

Opening Inguinal Canal like Herniotomy, Mobilisation of Testis while preserving Ductus Deferens and Vasculature, and Placement into Scrotal Sac

80
Q

How are intraabdominal testis managed?

A

Intra-abdominal Testis managed laparoscopically; might require staged approach

Paediatrics STG (17 decks)

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