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Pediatrics > Spectrum of renal diseases > Flashcards

Spectrum of renal diseases Flashcards

1
Q

What are the clinical manifestations of nephropathies?

A 
Failure to thrive
abdominal mass
hematuria
asymptomatic proteinuria
hypertension
anemia
polyuria
oligoanura
polydipsia
oedema
acidosis
respiratory distress
enuresis
uti (CAKUT is a risk factor for UTI)
renal osteodystrophy
renal failure
electrolyte abnormalities
Vomiting, Diarrhea
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2
Q

Causes of Glomerulonephritis

A

Causes of idiopathic nephrotic syndrome (MCD, MPGN, MGN, FSGS) and secondary nephrotic syndrome (Hep B, HIV, Hep C, Syphilis, Heavy metals - Gold, Mercury, Obesity)
Congenital (within 3months of life) and Infantile (3m to 1 year) Nephrotic syndrome
Causes of Nephritic syndrome - PIGN, igA nephropathy
Systemic vasculitides with secondary renal involvement - SLE, Henoch Schonlein purpura vasculitis, Anti-neutrophilic cytoplasmic autoantibody vasculitis
Congenital glomerulonephritis - Alport’s

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3
Q

Causes of Cakut

A

Agenesis - Dysplasia - Hypoplasia
Cystic Kidney disease
Obstructive Uropathies - PUJ (commonest), VUJ, PUV
Other causes of non-obstructive urinary tract dilatation - Prune Belly
Reflux nephropathies - VUR, UTI’s
Neurogenic bladder

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4
Q

Where are the kidneys located

A

They are retroperitoneal, between the costovertebral angle.

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5
Q

Describe the functional structure of the kidney

A

Tubules in Interstitium
Glomerulus - Filtration of fluids, solutes and waste

Interstitial cells are mesangial cells - Tissue macrophages in Kidney.

There’s deposit of complement and immunoglobulin in interstitium - stain under immunoflourescence.

Efferent arteriole is narrower than afferent.

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6
Q

Anatomy of the Nephron - Tubules and blood supply

A

Tubules are more susceptible to ischemia and hypoxia, so ATN more common than Cortical necrosis.

Tubules can regenerate.

Peritubular capillaries aid tubules to transform substances and secrete some.

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7
Q

What are the functions of the kidney?

A

*Homepstasis
Water and electrolyte balance
Nitrogenous waste disposal (urea, cr, Uric acid)
Acid base balance

*Hormogenesis
Erythropoietin from the interstitium
Ca2+ & PO42- metabolism via Vit D3 activation (1 hydroxylation - in 1,25 hydroxycholeciferol) - Renal Rickets

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8
Q

What are the consequences of a failed Kidney?

A

Failed homeostatic function
*Accumulation of metabolic waste - raised BUN, SCr: Uraemia (feeling unwell &lack of energy)

  • Failed excretion of daily H+ load - acidosis
  • K+ build up - HyperK+
  • Retention of PO42- & Mg2+ and reciprocal fall of Ca2+ (solubility product - PO4 2.2+ Ca =5)
  • Poor urine output - Fluid retention - Oedema
  • Abnormal urine chemistry (protein and blood) and sediments (sloughed tubular epithelium, RBC cast)
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9
Q

Consequences of a chronically injured Kidney (>3months)

A

Fibrosis - then loss of critical nephron mass - glomerulus and tubules is shed (broad waxy casts - nephron).

Small shrunken kidney.
Impaired synthetic function- decreased erythropoietin production (normochromic anemia)
Decreased production of 1a hydroxyl add - 1,25 vit D3 deficiency - renal osteodystrophy

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10
Q

What are the traditional marker for Kidney Injury

A

Serum Creatinine - endogenous, metabolic product of the muscles, excreted by the Kidney.

Urine output determination
Urine dipstick for proteinuria and blood

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11
Q

What is the issue with SCr as a marker of Kidney injury

A

Creatinine levels rise after ~50% of renal function is lost (time lag before it rises
Levels depends on muscle bulk

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12
Q

What are the newer bio markers for Kidney injury? (Early rise)

A

Neutrophil Gelatinase Associated Lipocalin [Blood and Urine]
AKIM -1 (urine)
Cystatin C (blood)
IL-18

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13
Q

Who is at risk of acute Kidney Injury?

A

Critically ill patient requiring ICU care
Hypovolemic patient - Diarrhoea and Vomiting +/- dehydration, Shock, Burns, Septicemia, Nephrotic Syndrome.
Glomerulonephritis
Severe sepsis/Severe malaria
Receiving nephrotoxics including radiographic contrast
Hypoxia - Asphyxia, Pneumonia, Cyanosed, Severe asthma, Status epilepticus/prolonged convulsion

Hemoglobinuria/Myoglobinuria (crushed injury)
Abnormal urinalysis - proteinuria/hematuria, WBC’s/nitrite

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14
Q

Other causes of Kidney injury in Children

A

Chronic malformation of the kidney structure/adjoining urinary tract - CAKUT

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15
Q

Spectrum of Kidney Diseases (1)

A

Inflammatory conditions of the Kidney (Nephritis)

Glomerulo-Nephritis- Nephrotic or nephrotic
Tubulointerstitial Nephritis including pyelonephritis
CAKUT including cystic kidney diseases
Other hereditary nephropathies - cong nephrotic, cong nephritis (Alport), cong TIN (nephronophthisis)

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16
Q

Spectrum of Kidney Diseases - may lead to failure

A

Tubulopathies (eg. cystinosis- Fanconi syndrome, Barters
Metabolic (eg. oxalosis)
Ischemic or toxic injury
Malignancies ( Wilma tumor, leukemia, leukemia

17
Q

Causes of TIN

A

Drug-induced - antibiotics, analgesics, anti-oxide drugs
Hereditary TIN - nephronophthisis

Diagnosis is made when eosinophils infiltrating the kidney, peripheral eosinophilia(red staining white cells) on biopsy.

Eosinophils in urine.

18
Q

The three classical features of Prune Belly Syndrome

A

Wrinkled abdomen (absent abdominal wall)
Cryptorchidism
Hydroureters (with or without Hydronephrosis)

19
Q

What are the Pre-renal causes of AKI

A

Volume loss - Real (loss through vomiting, diarrhea, hemorrhage )or apparent ( septicemia - blood vessels dilate)

20
Q

What are the intrinsic and post renal causes of AKI?

A 
Unresolved pre-renal ARF - uncorrected diarrhea, shock (acute tubular necrosis)
Hypoxia conditions 
Toxins and poisons
Drugs
Glomerulonephritis
Tubulointerstitial nephritis

Post-renal events - any cause of obstructive uropathy

21
Q

What are the causes of Chronic Kidney Disease / End Stage Renal Failure?

A

Unresolved AKI (For 3 months - RF to ESRF)
CAKUT
Progressive renal insult from persistent proteinuria (induced fibrosis in Kidney), nephrotoxic drug use (NSAIDs) infections (HIV), tubular disorders etc.

22
Q

What are the three systems for classifying AKI?

A

RIFLE, AKIN, KDIGO
All are based on changes in SCr from baseline (as proxy for GFR) or urine output

Rationale: To allow for standardized definition and comparison of results.

Also identify the patient who is at risk of kidney injury to allow for more stringent monitoring.

23
Q

What are the general differences between the three classification systems?

A

RIFLE classifies AKI into 5 stages
AKIN and KDIGO classify AKI into 3 stages.
Additional 2 for RIFLE are just outcome measures.

Third criteria for KDIGO combines both RIFLE and AKIN

24
Q

What does RIFLE define AKI (stage 1- Risk of Kidney dysfunction)as?

A

Increase in SCr of 1.5x (not 2)baseline (150% rise) or GFR decreases by 25% within 7 days
Or
Decrease in urine output of <0.5ml/kg/hr over >6 hrs (8hrs for children) -

Measure ace at least 2 times.

25
Q

How many stages does RIFLE classify AKI into?

A 
R- Risk of Kidney dysfunction 
I- injury to the Kidney
F- Failure of Kidney function 
L- Loss of kidney function
E- End stage renal failure
(5 stages)
26
Q

Stage 2 RIFLE classification for AKI (Kidney Injury)

A

SCr has risen by 2%, but not up to 3% (200% rise) or GFR decreases by 50% Or
Urine Output <0.5ml/kg/hr over >12 hrs

27
Q

Stage F, L, ERIFLE definition of AKI

A

Scr has risen >/= 3x baseline (300% rise) OR GFR decreases by 75% OR Scr level > 350úmol/l or acute rise >44úmol/l

Or

Urine output of <0.3ml/kg/hr for 24 hours OR anuria for 12 hours

If it persists for 1 month, you’ve lost function (L) - need for RRT
If it persists for 3 months, you’ve gotten to ESRF (E) - need for RRT

28
Q

How does AKIN define AKI?

A

An abrupt (within 48hours) absolute increase in Scr of >/= 26.4ûmol/l (0.3mg/dL) OR
%age increase in Scr of >/= 50% (I.e. baseline x1.5) OR
Oliguria of <0.5ml/kg/hr for >6hrs

AKI should only be diagnosed after achieving adequate hydration and after excluding any urinary tract obstruction.

29
Q

Staging of AKI by AKIN Criteria

A

Stage 1
1.5 - 2 fold rise in Scr from baseline (150-200% increase) OR
Any absolute rise of >/= 26.4 ümol/l in 48 hours

Stage 2
>2-3 fold increase in SCr from baseline (200-300% increase)

Stage 3
>3 fold increase in SCr from baseline (>300% rise) OR
Any SCr >/= 354ümol/l with acute rise of at lease 44ümol/l

(Urine output criteria same as RIFLE)

30
Q

How does the KDIGO criteria define AKI?

A
  • Absolute rise in SCr of >/= 26.4 ûmol/l (0.3mg/dL) within 48 hours OR
  • Increase in SCr of 1.5x baseline (%age rise in SCr of >/= 50%) within 7 days OR
  • Oliguria of <0.5ml/kg/hr for > 24hours
31
Q

KDIGO staging of AKI

A

Stage I: 1.5 to <2 fold increase in SCr from baseline

Stage II: >/=2 to <3 fold increase in SCr from baseline

Stage III: >/= 3 fold increase in SCr from baseline

32
Q

Complications of AKI in Failure (RIFLE-F, AKIN III, KDIGO III)

A 
Pulmonary edema (water imbalance)
CCF
Hypertension 
Hyperkalemia
Acidosis
Hyper PO42- & hypoCa2+ - convulsion 
Uraemia if azotemia is severe or prolonged 
Can lead to death
33
Q

Treatment of AKI

A

Consider if the injury is pre-renal, intrinsic or post-renal

Pre-renal - There’s hypovolemia
*Fluid resuscitation (20ml/kg of NS). Repeat hourly if necessary for 1-2 doses

Intrinsic AKI (from tubular necrosis)
Fluid restriction (if Oliguria). Insensible loss [400ml/m2/day] + previous day’s output. If markedly hypervolemjc and anuric, total fluid restriction + diuretic challenge.
Urethral catheterization (low obstruction at urethra)/other urinary diversion procedures for post-renal AKI.
For high obstruction- nephrostomy for massive hydronephrosis
Lower obstruction (PUV) - Vesicostomy

(Also direct treatment at primary cause)

34
Q

How is Hyperkalemia from AKI treated?

A

*Myocardial stabilization (prevent cardiac arrest)
Ca gluconate 10% (0.5ml/kg IV over 5- 10 min). Protects heart from effect of K

*Intracellular K shift
B2 agonist e.g. Salbutamol (nebulize), epinephrine
NaHCO3
Insulin with Dextrose

*K elimination from the body
Kayaxelate (sodium polystyrene - switches Sodium for K)
Dialysis

*Supporting measures
Avoid K-rich diet (banana, coconut, tomato)
Avoid drugs (amoxiclav, AceI) that cause hyperK
35
Q

Indication for Dialysis in AKI in Failure -1

A

*Failure of conservative mgt
Pulmonary edema unresponsive to diuretics
Hyperkalemia not controlled by conservative treatment
Severe metabolic acidosis (can cause heart to stop beating)
* Increase of >20% of initial body weight
* Prolonged Oliguria-Anuria (2-3days)
* Uraemic pericarditis

36
Q

Indications for Dialysis - AKI in Failure 2

A
  • Multisystem failure (liver, brain, kidney, septicemia)
  • Uraemic encephalopathy
  • Severe hyponatremia (<110mmol/l) or hypernatremia (>140mmol/l)
  • Severe uraemia >30mmol/l of blood urea
  • To make room for volume therapy (eg. Transfusion, TPN) in the oligo-anuric patient

Pediatrics (12 decks)

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