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Compiled PPS board reviewer > Renal > Flashcards

Renal Flashcards

1
Q

significant hematuria

A

> 50 rbc per microliter of urine

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2
Q

When does the GFR of a child approach adult values?

A

at 3 yrs old

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3
Q

Between GFR and BUN, which value is affected by state of hydration and nitrogen balance? Which value is primarily influenced by the level of glomerular function?

A

GFR: affected by glomerular function
BUN: hydration and nitrogen balance

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4
Q

The most common cause of gross hematuria

A

bacterial urinary tract infection

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5
Q

Presentation with gross hematuria is usually within 1-2 days after the onset of an apparent viral upper respiratory tract infection and typically resolves within 5 days

A

immunoglobulin A (IgA) nephropathy

  • contrasts to a latency period of 7-21 days occurring between the onset of a streptococcal pharyngitis or impetiginous skin infection and the development of poststreptococcal acute glomerulonephritis
  • the most common chronic glomerular disease
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6
Q

Chronic infection that is the most common cause of membranous nephropathy worldwide

A

MALARIA

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7
Q

Nephropathy presenting in the 2nd decade of life, commonly as nephrotic syndrome. Microscopic hematuria present, some have hypertension, sometimes associated with renal vein thrombosis. Normal C3.

A

Membranous nephropathy

  • dx by renal bx
  • common indications for bx: nephrotic syndrome in a child >10yr or unexplained persistent hematuria with significant proteinuria
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8
Q

Most common etiology of secondary membranous nephropathy

A

SLE or chronic infections (chronic hepB, congenital syphilis, malaria)

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9
Q

PSGN and MPGN both have similar clinical presentations. MPGN can present as acute nephritic syndrome (hematuria, hypertension, renal insufficiency) or nephrotic syndrome. C3 is low in both diseases. How can the two be differentiated?

A

PSGN usually +ASO, with hx of strep infection, C3 level low but resolves in 6-8 wks

MPGN C3 persists beyond 2 mos. In this case, renal bx is warranted for a histopathologic diagnosis

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10
Q

the most common small vessel vasculitis in childhood. It is characterized by a purpuric rash and commonly accompanied by arthritis and abdominal pain

A

Henoch-Schonlein purpura (HSP)

  • 50% of patients with HSP develop renal manifestations, which vary from asymptomatic microscopic hematuria to severe, progressive glomerulonephritis
  • nephritis usually follows onset of the rash, often weeks or even months after the initial presentation of the disease
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11
Q

What is the histopathologic hallmark of crescentic GN?

A

crescents in glomeruli

  • CGN presents as acute nephritis (hematuria, some degree of renal insufficiency, and hypertension) and usually have concomitant proteinuria, often with nephrotic syndrome.
  • If the patient has no extrarenal manifestations and a negative serologic evaluation, and if the biopsy has no immune or EM deposits, the diagnosis is idiopathic, rapidly progressive CGN.
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12
Q

Characterized by pulmonary hemorrhage and glomerulonephritis

usually presents as hemoptysis and acute nephritic syndrome with hematuria, proteinuria, and hypertension

A

Goodpasture disease

  • crescentic GN on biopsy
  • rare in children
  • rapidly progressive course
  • Other diseases that can cause a pulmonary-renal syndrome: SLE, HSP, Wegener granulomatosis, microscopic polyangiitis
  • Goodpasture has serum antibodies directed against GBM (anti–type IV collagen in GBM), and characteristic renal biopsy findings
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13
Q

One of the most common causes of community-acquired acute kidney failure in young children, characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency, usually occuring after an acute gastrointestinal illness (~3wks after onset of GI illness; acute or bloody diarrhea)

A

Hemolytic-Uremic syndrome

  • thrombotic thrombocytopenic purpura (TTP) is also characterized by microangiopathic hemolytic anemia, renal injury and low platelet, but TTP usually has CNS involvement, fever and a more gradual onset
  • diagnosis is mainly clinical
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14
Q

What is the most common form of HUS?

A

HUS caused by toxin-producing Escherichia coli (shiga toxin of Shigella or verotoxin of E. coli ) that cause prodromal acute enteritis

  • Disease is usually transmitted by undercooked meat or unpasteurized milk or apple cider
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15
Q

Bilateral flank mass in a patient with oligohydramnios, pulmonary hypoplasia, and hypertension and absence of renal cysts by sonography of parents

A

Autosomal recessive polycystic kidney disease

  • this is different from autosomal dominant polycystic kidney disease, which is the most common hereditary human kidney disease
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16
Q

What is the most common cause of persistent proteinuria in school-aged children and adolescents?

A

orthostatic proteinuria

  • asymptomatic
  • dx: collection of first morning urine for 3 consecutive days, do complete urinalysis and spot UPr:UCr; absence of proteinuria confirms diagnosis
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17
Q

Triad of clinical findings characteristic of nephrotic syndrome

A 
hypoalbuminemia
edema
hyperlipidemia
- nephrotic range proteinuria: >2-3 UPr:UCr
- protein excretion of >40 mg/m2/24hr
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18
Q

What is the hallmark of idiopathic nephrotic syndrome?

A

Extensive effacement of podocyte foot processes

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19
Q

Among the idiopathic nephrotic syndromes which one usually does not present with hypertension and gross hematuria

A

Minimal change nephrotic syndrome

  • common in 2-6 yo
  • urinalysis: 3+ to 4+ protein
  • microscopic hematuria in 20%
  • spot UPr:UCr >2
  • serum crea normal
  • serum albumin <2.5 g/dL
  • serum TG and TC elevated
  • C3 normal
  • renal bx not routinely performed
  • 95% steroid responsive (4-6 wks)
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20
Q

Subset of patients that relapse while on alternate day steroid therapy or within 28 days of completing a successful course of prednisone therapy

A

steroid dependent

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21
Q

Patients who respond well to steroid therapy but relapse >=4 times in 12 mos

A

frequent relapsed

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22
Q

Patients who fail to respond to steroid therapy within 8 wks of therapy

A

steroid resistant

  • steroid-resistant nephrotic syndrome are usually caused by FSGS (80%), MCNS or MPGN
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23
Q

What are the most common organisms causing spontaneous bacterial peritonitis in children with nephrotic syndrome?

A

S. pneumoniae and E. coli

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24
Q

What particula vaccines should children with nephrotic syndrome receive?

A

PCV and PPV

  • usually when child is on remission and off prednisone therapy
  • for children on steroids, since they are immunocompromised, avoid giving live vaccines (MMRV, OPV, RV) - may be given one month after discontinuation of prednisone
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25
Q

low molecular weight proteinuria, glycosuria, phosphaturia, aminoaciduria, and proximal RTA

A

Fanconi Syndrome

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26
Q

Rare X-linked disorder characterized by congenital cataracts, mental retardation, and Fanconi syndrome

A

Oculocerebrorenal syndrome of Lowe

  • present in infancy with cataracts, progressive growth failure, hypotonia, and Fanconi syndrome
  • Significant proteinuria is common.
  • Blindness and renal insufficiency often develop
  • Characteristic behavioral abnormalities are also seen, including tantrums, stubbornness, stereotypy (repetitive behaviors), and obsessions.
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27
Q

characterized by a normal anion gap (hyperchloremic) metabolic acidosis in the setting of normal or near-normal glomerular filtration rate

A

Renal Tubular Acidosis

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28
Q

Pathophysiology of RTAI and RTAII

A

Proximal RTA (RTA II) results from impaired bicarbonate reabsorption and distal RTA (RTA I) from failure to secrete acid.

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29
Q

global proximal tubular dysfunction characterized by low molecular weight proteinuria, glycosuria, phosphaturia, aminoaciduria, and proximal RTA

A

Fanconi syndrome

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30
Q

A non–anion gap metabolic acidosis, unremarkabl UA, urine pH is acidic (

A

Proximal type II RTA

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31
Q

damaged or impaired functioning of one or more transporters or proteins involved in the acidification process, including the H+/ATPase, the HCO3−/Cl− anion exchangers, or the components of the aldosterone pathway

A

Distal RTA I

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32
Q

Non-anion gap metabolic acidosis, Urine pH >5.5, hyperchloremia, hypokalemia, hypercalciuria, nephrocalcinosis or nephrolithiasis, Hypocitraturia, Bone disease

A

Distal RTA Type I

urine pH cannot be reduced to <5.5, despite the presence of severe metabolic acidosis. Loss of sodium bicarbonate distally, owing to lack of H+ to bind to in the tubular lumen (see Fig. 523-1), results in increased chloride absorption and hyperchloremia. Inability to secrete H+ is compensated by increased K+ secretion distally, leading to hypokalemia. Hypercalciuria lead to nephrocalcinosis or nephrolithiasis. Chronic metabolic acidosis also impairs urinary citrate excretion. Hypocitraturia further increases the risk of calcium deposition in the tubules. Bone disease is common, resulting from mobilization of organic components from bone to serve as buffers to chronic acidosis.

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33
Q

impaired aldosterone production (hypoaldosteronism) or impaired renal responsiveness to aldosterone (pseudohypoaldosteronism)

A

Hyperkalemic (Type IV) Renal Tubular Acidosis

Acidosis results because aldosterone has a direct effect on the H+/ATPase responsible for hydrogen secretion. In addition, aldosterone is a potent stimulant for potassium secretion in the collecting tubule; consequently, lack of aldosterone results in hyperkalemia. This further affects acid-base status by inhibiting ammoniagenesis and, thus, H+ excretion

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34
Q

hyperkalemic non–anion gap metabolic acidosis. Urine alkaline or acidic. Elevated urinary sodium levels with inappropriately low urinary potassium levels. Polyuria and dehydration (from salt wasting), growth failure

A

Hyperkalemic (Type IV) Renal Tubular Acidosis

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35
Q

How to compute for blood anion gap?

A

using the formula [Na+] − [Cl− + HCO3−]. Values of 20 are highly suggestive of the presence of an anion gap.

36
Q

mainstay of therapy in all forms of RTA

A

Bicarbonate replacement

37
Q

Tubular Transport Abnormalities characterized by hypokalemic metabolic alkalosis with hypercalciuria and salt wasting

A

Bartter syndrome

defect in sodium, chloride, and potassium transport in the ascending loop of Henle. The loss of sodium and chloride, with resultant volume contraction, stimulates the renin-angiotensin II-aldosterone (RAA) axis. Aldosterone promotes sodium uptake and potassium secretion, exacerbating the hypokalemia. It also stimulates hydrogen ion secretion distally, worsening the metabolic alkalosis. Hypokalemia stimulates prostaglandin synthesis, which further activates the RAA axis.

38
Q

Tubular Transport Abnormalities with hypokalemic metabolic alkalosis, with distinct features of hypocalciuria and hypomagnesemia (presenting as muscle cramps and spasms) more often in adolescents or adults.

A

Gitelman Syndrome (Bartter syndrome variant)

39
Q

features of acute nephritic syndrome

A

Tea- or cola-colored urine, facial or body edema, hypertension, and oliguria

40
Q
  • Gross hematuria within 1-2 days of onset of URTI
  • increased IgA immunoglobulin within mesangial glomerular deposits in the absence of systemic disaease
  • renal biopsy: focal and segmental mesangial proliferation and increased mesangial matrix in the glomerulus; may have cresent formation and sclerosis
A

IgA Nephropathy (Berger Disease)

Therapy
o blood pressure control (ACE-I or ARBs)
o fish oil (omega 3) decreases rate of progression in adults

41
Q
  • hereditary nephritis (X-linked); mutation in type IV collagen (basement membrane
  • asymptomatic microscopic hematuria 1-2 days after URTI
  • bilateral sensorineural hearing loss, ocular abnormalities
  • ANTERIOR LENTICONUS
  • FOAM CELLS
A

Alport syndrome

No therapy

42
Q

extrusion of central portion of lens into anterior chamber. pathognomonic of alport syndrome

A

ANTERIOR LENTICONUS

43
Q

Most common nephrotic syndrome

A

idiopathic nephrotic syndrome (minimal change disease)

Effacement of podocyte foot processes > Increased permeability of glomerular capillary wall > massive proteinuria and hypoalbuminemia

44
Q

Define nephrotic syndrome

A

nephrotic range proteinuria and the triad of clinical findings associated with large urinary losses of protein:

  • hypoalbuminemia,
  • edema
  • hyperlipidemia.
45
Q

Nephrotic range proteinuria is defined as

A

protein excretion of > 40mg/m2/hr or a first morning protein : creatinine ratio of >2-3 : 1

46
Q

2 Modes of classification of acute renal failure

A 
o RIFLE (risk, injury, failure, loss, and end-stage renal disease)
- focus on GFR

o Acute Kidney Injury Network (AKIN)
- categorizes severity by rise in serum creatinine

47
Q

Causes of Pre-renal Failure

A 
o Dehydration 
o Hemorrhage 
o Sepsis 
o Hypoalbumemia 
o Cardiac failure
  • Diminished effective circulating arterial volume, inadequate renal perfusion and a decreased GFR
  • no kidney damage
48
Q

Causes of Intrinsic Renal Failure

A 
o Glomerulonephritis 
o HUS 
o Cortical necrosis 
o Renal Vein thrombosis 
o Rhabdomyolysis 
o Acute interstitial nephritis 
o Tumor Infiltration 
o Tumor lysis syndrome
49
Q

Intrnsic renal failure with tubular cell necrosis due to alterations in intrarenal hemodynamics, tubular obstruction, and passive backleak of the glomerular filtrate across injured tubular cells into the peritubular capillaries.

A

Acute tubular necrosis (ATN)

-occurs most often in critically ill infants, exposed to nephrotoxic and/or perfusion insults.

50
Q

Intrinsic renal failure due to spontaneous or chemotherapy-induced cell lysis in patients with lymphoproliferative malignancies
- caused by obstruction of the tubules by uric acid crystals

A

Tumor lysis syndrome

51
Q

Intrinsic renal failure caused by hypersensitivity reaction to a therapeutic agent or various infectious agents

A

Acute interstitial nephritis

52
Q

Causes of Post-renal Failure

  • Caused by obstruction of the urinary tract.
A 
o Posterior urethral valves 
o Ureteropelvic junction obstruction 
o Ureterovesicular junction obstruction 
o Ureterocoele 
o Tumor 
o Urolithiasis 
o Hemorrhagic cystitis 
o Neurogenic bladder
53
Q

Electrolyte derangement in ARF

A

elevated Crea, BUN, Uric Acid, potassium, phosphate (diminished renal function)

hypocalcemia (hyperphosphatemia)

54
Q

Ecg findings for hyperkalemia

A

peaked T waves, widening of the QRS intervals, ST segment depression, ventricular arrhythmias, and cardiac arrest

55
Q

Treatment for hyperkalemia K>6

A
  • Discontinue K containing fluid, food, drugs

- Sodium polystyrene sulfonate resin (Kayexalate), 1 g/kg, should be given orally or by retention enema

56
Q

Treatment for K>7

A

o Calcium gluconate 10% solution, 1.0 mL/kg IV, over 3-5 min
- Calcium gluconate counteracts the potassium-induced increase in myocardial irritability but does not lower the serum potassium level.

o Sodium bicarbonate, 1-2 mEq/kg IV, over 5-10 min

o Regular insulin, 0.1 U/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
- shifting potassium from the extracellular to the intracellular

57
Q

Glomerular disease with a reduced complement level PELICAN:

A 
Post-streptococcal glomerulonephritis 
Endocarditis (sub-acute) 
Lupus erythematosus 
Idiopatic membranoproliferative glomerulonephritis 
Cryoglobulinemia 
Abscess (visceral) 
Nephritis (shunt)
58
Q

Hematuria: differential

HEMATURIA

A

Hereditary (PCK and OWR) / Henoch Schonlein purpura
Embolism (infective endocarditis)
Malignant HTN
Acute and chronic glomerulonephritis / IgA nephropathy
Tumors / Trauma / Toxic drugs
Urolithiasis
Renal papillary necrosis
Infection (pyelonephritis, cystitis, urethritis)
Anti-coagulants

59
Q

indications for dialysis

AEIOU

A 
Acid-base problems (severe acidosis or alkalosis) 
Electrolyte problems (hyperkalemia) 
Intoxications 
Overload, fluid 
Uremic symptoms
60
Q

Indications for dialysis in ARF include the following:

A

o Volume overload with evidence of hypertension and/or pulmonary edema refractory to diuretic therapy
o Persistent hyperkalemia
o Severe metabolic acidosis unresponsive to medical management
o Neurologic symptoms (altered mental status, seizures)
o Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)
o Calcium:phosphorus imbalance, with hypocalcemic tetany
o Inability to provide adequate nutritional intake because of the need for severe fluid restriction.

61
Q

Define Chronic Kidney Disease

A

Renal injury (proteinuria) and/or a glomerular filtration rate <60ml/min/1.7m3 for >3 mo

62
Q

High-turnover bone disease caused by secondary hyperparathyroidism in CKD patients

A

osteitis fibrosa cystica

63
Q

gold standard to determine GFR

A

Inulin clearance

64
Q

antihypertensive drugs of choice in CKD

A

ACE and Angiotensin II receptor blocker

65
Q

Diuretic of choice in CKD

A

Loop diuretics furosemide

66
Q

MOST COMMON serious bacterial infection in infants <24 mo of age who have fever without an obvious focus

A

Clinical pyelonephritis

67
Q

Dysuria, urgency, frequency, suprapubic pain, incontinence, malodorous urine without fever

A

Cystitis

68
Q

Abdominal, back or flank pain; Fever, malaise, nausea, vomiting, occasional diarrhea

Fever may be the ONLY manifestation

A

Clinical pyelonephritis

69
Q

Positive urine culture w/o any manifestation

A

Asymptomatic bacteriuria

70
Q

Diagnosis of UTI based on urinalysis

A

> 100,000 colonies of a single pathogen OR 10,000 colonies and the child is symptomatic, UTI is considered

71
Q

Treatment for Acute cystitis

A

o TMP-SMX (3-5 day course)
- effective against most strains of E.coli
o Nitrofurantoin (5-7mkday in 3-4 divided doses)
- effective against Klebsiella and Enterobacter
o Amoxicillin (50mkday)
- effective but with no clear advantage

72
Q

Treatment for Pyelonephritis

A

10-14 day course of broad spectrum antibiotics

o ceftriaxone 50-75mkday
o cefotaxime 100 mkday
o ampicillin 100 mkday
* with aminoglycoside like gentamicin 3-5mkday
o Cipropfloxacin
- alternative agent for resistant organisms like Pseudomonas in >17 yo

73
Q

Recurrent UTI-prophylaxis against reinfection

A

TMP-SMX, trimethoprim or nitrofurantoin at 30% of the normal therapeutic dose once a day

74
Q

What is the 1999 AAP guidelines on febrile UTI?

A

2mo to 2 yr with a febrile UTI, renal sonogram and VCUG or radionuclide cystogram is recommended

75
Q

Diagnosis of urethritis

A

o Mucoid or purulent urethral discharge
o ≥5 WBC per HPF of urethral secretions
o ≥10 WBC per HPF of first void urine specimen
o Positive FVU leukocyte esterase test
o Gram-negative intracellular diplococci on microscopy

76
Q

Diagnosis for vaginitis

A

o Elevated pH >4.5 is common in Bacterial vaginitis or trichomoniasis
o Motile or dead T vaginalis under the microscope, clue cells for Bacterial vaginitis
o Yeast or pseudohyphae for Candida spp seen in KOH specimens

77
Q

Treatment for chlamydia

A

o Azithromycin

o Doxycycline

78
Q

Treatment for N. gonorrhoeae

A

o Ceftriaxone

o Cefixime

79
Q

Treatment for T. pallidum

A

Benzathine penicillin

80
Q

Treatment for H. ducreyi

A

o Azithromycin
o Ceftriaxone
o Ciprofloxacin
o Erythromycin

81
Q

Treatment for C. trachomatis

A

Doxycycline

82
Q

Treatment for Calymmatobacterium granulomatis (donovanosis or granuloma inguinale)

A

Doxycycline

83
Q

Treatment for Trichomonas vaginalis

A

o Metronidazole

84
Q

Treatment for Phthirus pubis (pubic lice) and Sarcoptes scabiei

A

Permethrin 1%

85
Q

Define hematuria

A

at least 5 rbc per microliter of urine

Compiled PPS board reviewer (60 decks)

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