14. Nephrology Flashcards
Name: Common Manifestations of Renal Disease in NEONATE (3)
- Flank Mass
- Hematuria
- Anuria/Oliguria
Name: Common Manifestations of Renal Disease in CHILD and ADOLESCENT (8)
- Cola/Red-Coloured Urine
- Gross Hematuria
- Edema
- HTN
- Polyuria
- Proteinuria
- Oliguria
- Urgency
Name common causes in neonates: Flank Mass (3)
- Hydronephrosis
- polycystic disease (autosomal dominant or recessive subtypes)
- tumour
Name common causes in neonates: Hematuria (4)
- Renal vein thrombosis
- Asphyxia
- Malformation
- Trauma
Name common causes in neonates: Anuria/Oliguria (3)
- Bilateral renal agenesis
- obstruction
- asphyxia
Name common causes in child/adolescent: Cola/Red-Coloured Urine (3)
- Acute GN (post-streptococcal, HSP, IgA nephropathy, etc.)
- hemoglobinuria (hemolysis)
- myoglobinuria (rhabdomyolysis)
Name common causes in child/adolescent: Gross Hematuria (3)
- Urologic disease (nephrolithiasis, trauma, etc.)
- UTI
- acute GN
Name common causes in child/adolescent: Edema (5)
- Nephrotic syndrome
- nephritis
- acute/chronic renal failure
- consider cardiac
- liver disease
Name common causes in child/adolescent: HTN (3)
- GN
- renal failure
- dysplasia (consider coarctation, drugs, endocrine causes)
Name common causes in child/adolescent: Polyuria (5)
- DM
- central and nephrogenic DI
- renal Fanconi’s syndrome (genetic/metabolic/acquired causes)
- hypercalcemia
- polyuric renal failure (renal dysplasia)
Name common causes in child/adolescent: Proteinuria (3)
- Orthostatic
- nephrotic syndrome (MCD, etc.)
- GN
Name common causes in child/adolescent: Oliguria (4)
- Dehydration
- ATN
- interstitial nephritis
- acute or chronic kidney disease (i.e. renal failure)
Name common causes in child/adolescent: Urgency (2)
- UTI
- vulvovaginitis
Name triad of: Hemolytic Uremic Syndrome (3)
- non-immune microangiopathic hemolytic anemia
- thrombocytopenia
- acute renal injury
Describe epidemiology: Hemolytic Uremic Syndrome (2)
- annual incidence of 1-2 per 100,000 in Canada
- most common cause of acute renal failure in children
Describe etiology: Hemolytic Uremic Syndrome (2)
- diarrhea positive HUS: 90% of pediatric HUS from E.coli O157:H7, shiga toxin, or verotoxin
- diarrhea negative HUS: other bacteria, viruses, drugs, familial/genetic
Describe pathophysiology: Hemolytic Uremic Syndrome (5)
- toxinbinds, invades, and destroys colonic epithelial cells, causing bloody diarrhea
- toxin enters the systemic circulation, attaches to, and injures endothelial cells (especially in kidney),
- causing a release of endothelial products (e.g. von Willebrand factor, platelet aggregating factor)
- platelet/fibrin thrombi form in multiple organ systems (e.g.kidney,pancreas,brain,etc.) resulting in thrombocytopenia
- RBCs are forced through occluded vessels, resulting in fragmented RBCs (schistocytes) that are removed by the reticuloendothelial system (hemolytic anemia)
Describe clinical features: Hemolytic Uremic Syndrome (7)
- initial presentation of abdominal pain and diarrhea, followed by bloody diarrhea;
- within 5-7d begins to show signs of anemia, thrombocytopenia, and renal insufficiency
- pallor
- jaundice (hemolysis)
- edema
- petechiae
- HTN
Describe investigations: Hemolytic Uremic Syndrome (7)
- CBC (anemia, thrombocytopenia)
- blood smear (schistocytes)
- electrolytes
- renal function
- urinalysis (microscopic hematuria)
- stool cultures
- and verotoxin/shigella toxin assay
Describe management: Hemolytic Uremic Syndrome (4)
- mainly supportive: nutrition, hydration, ventilation (if necessary), blood transfusion for symptomatic anemia
- monitor electrolytes and renal function: dialysis if electrolyte abnormality (hyperkalemia) cannot be corrected, fluid overload, or uremia
- steroids are not helpful
- antibiotics are contraindicated as death of bacteria leads to increased toxin release and worse clinical course
Describe prognosis: Hemolytic Uremic Syndrome (2)
- death in <5% of cases,
- 5-25% long term renal damage (HTN, proteinuria, decreased renalfunction)
Define: Nephritic Syndrome (3)
- acute or chronic syndrome affecting the kidney, characterized by glomerular injury and inflammation
- defined by hematuria (>5 RBCs per high-powered microscope field), presence of dysmorphic RBCs, and RBC casts on urinalysis
- often accompanied by at least one of proteinuria (<50mg/kg/d), edema, HTN, azotemia, and oliguria
Describe presentation: Nephritic Syndrome (6)
PHAROH
- Proteinuria (<50 mg/kg/d)
- Hematuria
- Azotemia
- RBC casts
- Oliguria
- HTN
Describe epidemiology: Nephritic Syndrome (1)
highest incidence in children aged 5-15 yr old
Describe etiology: Nephritic Syndrome (2)
- humoral immune response to a variety of etiologic agents → immunoglobulin deposition → complement activation, leukocyte recruitment, release of growth factors/cytokines → glomerular inflammation and injury → porous podocytes → hematuria + RBC casts ± proteinuria
- HTN secondary to fluid retention and increased renin secretion by ischemic kidneys
Name: Major Causes of Nephritic Syndrome
Describe clinical features: Nephritic Syndrome (3)
- often asymptomatic; some overlap in clinical findings for nephritic and nephrotic syndrome
- gross hematuria, mild-moderate edema, oliguria, HTN
- signs and symptoms suggestive of underlying systemic causes (e.g.fever,arthralgias,rash,dyspnea, pulmonary hemorrhage)
Describe investigation: Nephritic Syndrome (3)
- urine
- dipstick (hematuria, 0 to 2+ proteinuria) and microscopy (>5 RBCs per high-powered microscope field, acanthocytes, RBC casts)
- first morning urine protein/creatinine ratio (<200 mg/mmol)
- blood word
- CBC, electrolytes, Cr, BUN, albumin
- impaired renal function (⬆️ Cr and BUN) resulting in ⬆️ pH and electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia)
- mild anemia on CBC (secondary to hematuria)
- hypoalbuminemia (secondary to proteinuria)
- appropriate investigations to determine etiology: C3/C4 levels, serologic testing for recent streptococcal infection (ASOT, anti-hyaluronidase, anti-streptokinase, anti-NAD, anti-DNAse B), ANA, anti-DNA antibodies, ANCA, serum IgA levels, anti-GBM antibodies
- renal biopsy should be considered only in the presence of acute renal failure, no evidence of streptococcal infection, normal C3/C4
Describe management: Nephritic Syndrome (3)
- treat underlying cause
- symptomatic
- renal insufficiency: supportive (dialysis if necessary), proper hydration
- HTN: salt and fluid restriction (but not at expense of renal function), ACEI or ARBs for chronic persistent HTN (not acute cases because ACEI or ARBs may decrease GFR further)
- edema: salt and fluid restriction, possibly diuretics (avoid if significant intravascular depletion)
- corticosteroids if indicated: IgA nephropathy, lupus nephritis,etc.
Describe prognosis: Nephritic Syndrome (2)
- dependent on underlying etiology
- complications include HTN, heart failure, pulmonary edema, chronic kidney injury (requiring renal transplant)
Define: Nephrotic Syndrome (4)
clinical syndrome affecting the kidney, characterized by
- significant proteinuria
- peripheral edema
- hypoalbuminemia
- hyperlipidemia
Describe epidemiology: Nephrotic Syndrome (1)
highest incidence in children 2-6 yr old, M>F
Name types of Nephrotic Syndrome (3)
- Primary (idopathic)
- Secondary
- Congenital: congenital nephropathy of the Finnish type, Denys-Drash syndrome,etc.
Describe etiology: Nephrotic Syndrome PRIMARY (2)
primary (idiopathic): nephrotic syndrome in the absence of systemic disease (most common cause in pediatrics)
- glomerular inflammation ABSENT on renal biopsy: MCD (85%), focal segmental glomerular sclerosis
- glomerular inflammation PRESENT on renal biopsy: membranoproliferative GN, IgA nephropathy
Describe secondary: Nephrotic Syndrome PRIMARY (6)
nephrotic syndrome associated with systemic disease or due to another process causing glomerular injury (<10% in pediatrics)
- autoimmune: SLE, DM, rheumatoid arthritis
- genetic: sickle cell disease, Alport syndrome
- infections: hepatitis B/C, post-streptococcal, infective endocarditis, HUS, HIV
- malignancies: leukemia, lymphoma
- medications: captopril, penicillamine, NSAIDs, antiepileptics
- vasculitides: HSP, granulomatosis with polyangiitis
Describe clinical features: Nephrotic Syndrome (4)
- non-specific symptoms such as irritability, malaise, fatigue, anorexia, or diarrhea
- edema
- often first sign; detectable when fluid retention exceeds 3-5% of body weight
- starts periorbital and often pretibial → edematous areas are white, soft, and pitting
- gravity dependent: periorbital edema ⬇️ and pretibial edema ⬆️ over the day
- anasarca may develop (i.e. marked periorbital and peripheral edema, ascites, pleural effusions, scrotal/labial edema)
- decrease in effective circulating volume (e.g. tachycardia, HTN, oliguria,etc.)
- foamy urine is a possible sign of proteinuria
Describe investigation: Nephrotic Syndrome (3)
- urine
- urine dipstick (3 to 4+ proteinuria, microscopic hematuria) and microscopy (oval fat bodies,hyaline casts)
- first morning urine protein/creatinine ratio (>200 mg/mmol)
- blood work
- diagnostic: hypoalbuminemia (<25 g/L), hyperlipidemia/hypercholesterolemia (total cholesterol >5
mmol/L)
* secondary: electrolytes (hypocalcemia, hyperkalemia, hyponatremia), renal function (⬆️BUN and Cr), coagulation profile (⬇️PTT) * appropriate investigations to rule out secondary causes: CBC, blood smear, C3/C4, ANA, hepatitis B/C titres, ASOT, HIV serology, etc. * consider renal biopsy if: HTN, gross hematuria, ⬇️renal function, low serum C3/C4, no response to steroids after 4 wk of therapy, frequent relapses (\>2 in 6 mo), presentation before first yr of life (high likelihood of congenital nephrotic syndrome), presentation ≥12 yr (rule out more serious renal pathology than MCD)
Describe management: Nephrotic Syndrome (7)
- MCD: oral prednisone 2 mg/kg/d (or equivalent) for up to 12 wk → varicella status should be known before starting
- consider cytotoxic agents, immunomodulators, or high-dose pulse corticosteroid if steroid resistant
- symptomatic
- edema: salt and fluid restriction, possibly diuretic (avoid if significant intravascular depletion); furosemide + albumin for anasarca
- hyperlipidemia: generally resolves with remission; limit dietary fat intake; consider statin therapy if persistently nephrotic
- hypoalbuminemia: IV albumin and furosemide not routinely given; consider if refractory edema
- abnormal BP: control BP; fluid resuscitation if severe intravascular depletion; ACEI or ARBs for persistent HTN
- diet: no added salt; monitor caloric intake and supplement with Ca2+ and Vit D if on corticosteroids
- daily weights and BP to assess therapeutic progress
- secondary infections: treat with appropriate antimicrobials; antibioticprophylaxis not recommended; pneumococcal vaccine at diagnosis and varicella vaccine after remission; varicella Ig + acyclovir if exposed while on corticosteroids
- secondary hypercoagulability: mobilize, avoid hemoconcentration due to hypovolemia, prompt sepsis occur
Name: Side Effects of Long-Term Steroid Use (10)
- Increasedappetite
- Weight gain
- Dorsal hump
- Impaired growth
- Behavioural changes
- Risk of infection
- Salt and water retention
- HTN
- Bone demineralization
- Skin striae
Describe prognosis: Nephrotic Syndrome (3)
- generally good: 80% of children responsive to corticosteroids
- up to 2/3 experience relapse, often multiple times; sustained remission with normal kidney function usually by adolescence
- complications: ⬆️ risk of infections (spontaneous peritonitis, cellulitis, sepsis); hypercoagulability due to decreased intravascular volume and antithrombin III depletion (PE, renal vein thrombosis); intravascular volume depletion, leading to hypotension, shock, renal failure; side effects of drugs
Define HTN (1)
sBP and/or dBP ≥95th percentile for sex, age, and height on ≥ 3occasions
Define pre-HTN (2)
- sBP and/or dBP ≥90th percentile but <95th percentile
- or BP≥ 120/80 irrespective of age, gender, and height
Fill table
Describe epidemiology: Hypertension in Childhood (2)
- prevalence: 3-5% for HTN, 7-10% for pre-HTN; M>F
- increasing prevalence of pre-HTN over the last 25 +yr
Describe etiology: Primary HTN (3)
- diagnosis of exclusion
- most common in older children (≥10 yr), especially if positive family history, overweight, and only mild HTN
- responsible for ~90% of cases of HTN in adolescents, rarely in young children
Describe etiology: Secondary HTN (2)
- identifiable cause of HTN (most likely etiology depends on age)
- responsible for majority of childhood HTN
Name: Etiology of Secondary HTN by Age Group
Name risk factors primary HTN (6)
- male gender
- positive family history
- obesity
- obstructive sleep apnea
- African American
- prematurity/LBW
Name risk factors secondary HTN (4)
- history of renal disease
- abdominal trauma
- family history of autoimmune diseases
- umbilical artery catheterization
Name: Signs of Secondary HTN (6)
- Edema (renal parenchymal disease)
- Abdominal or renal bruit (RAS)
- Differential 4 limb BP/diminished femoral pulses (coarctation)
- Abdominal mass (Wilms’, neuro blastoma)
- Goitre/skin changes (hyperthyroidism)
- Ambiguous genitalia (CAH)
Describe clinical features: Hypertension in childhood (3)
often asymptomatic, but can include
- FTT
- fatigue
- epistaxis
Name: symptoms of hypertensive emergency (6)
- neurologic:
- headache
- seizures
- focal complaints
- change in mental status
- visual disturbances
- cardiovascular:
- symptoms of MI or heart failure (chest pain, palpitations, cough, SOB)
Describe physical exam: Hypertension childhood (7)
- measure BP with correct cuff size
- BMI
- full neurologic exam
- ophthalmoscopy,
- precordial exam
- peripheral pulses
- perfusion status
Describe Investigations: Hypertension childhood (6)
- laboratory
- urine dipstick for hematuria and/or proteinuria (renal disease), urine catecholamines (pheochromocytoma, neuroblastoma)
- blood work: renal function tests (electrolytes, Cr, BUN), consider renin and aldosterone levels (RAS, Conn’s syndrome, Wilms’ tumour)
- other specific hormones if indicated on history and physical
- imaging:
- Echo (coarctation, heart function)
- abdomina lU/S (RAS, abdominal mass)
- renal radionucleide imaging (renal scarring)
Describe management: Hypertension childhood (5)
- treat underlying cause
- non-pharmacologic: modify concurrent cardiovascular risk factors (weight reduction,exercise,salt restriction, smoking cessation)
- pharmacologic: gradual lowering of BP using thiazide diuretics; no antihypertensives havebeen formally studied in children; if hypertensive emergencies use hydralazine, labetalol, sodium nitroprusside
- management of end-organ damage (e.g.retinopathy,LVH)
- consider referral to specialist
Describe prognosis: Hypertension childhood (5)
end-organ damage (similar to adults) including
- LVH
- CHF
- cerebrovascular insults
- renal disease
- retinopathy
