Nephrology Flashcards

1
Q

What is Acute Kidney Injury (AKI)?

A

Inability to clear waste products, leading to a buildup of ‘uremic’ toxins. Inability to maintain electrolyte & acid-base homeostasis. Inability to maintain water homeostasis.

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2
Q

What are the main causes of AKI?

A

Pre-renal, Renal, and Post-renal causes.

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3
Q

Give examples of pre-renal AKI causes.

A

Volume depletion, decreased cardiac output, decreased vascular resistance (sepsis), nephrotic syndrome, liver failure, impaired renal autoregulation.

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4
Q

Give examples of renal AKI causes.

A

Tubules/Interstitium (ischemic tubular injury, nephrotoxic AKI, acute interstitial nephritis), Glomerulus (post-infectious glomerulonephritis), Blood Vessels (Hemolytic Uremic Syndrome, Renal Vein Thrombosis).

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5
Q

Give examples of post-renal AKI causes.

A

UPJ obstruction, ureteric obstruction, intraluminal obstruction, bladder obstruction, cancer.

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6
Q

What is the most common cause of childhood Chronic Kidney Disease (CKD)?

A

Renal dysplasia.

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7
Q

How to manage acute severe hyperkalemia (K+ > 6.5 mmol/L)?

A

Remove K+ intake, cardiac membrane stabilization (Calcium Gluconate or Calcium Chloride), redistribution strategies (Salbutamol, Glucose & Insulin, Sodium Bicarbonate), Removal of K+ via CVVH or HD.

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8
Q

What ECG features are associated with hyperkalemia?

A

Tall peaked T waves, flattened/absent P waves, sine wave, prolonged PR interval, widened QRS complex, bradycardia/VTach/VFib.

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9
Q

What medications should be avoided in hyperkalemia?

A

K+ supplements, K+ sparing diuretics, ACE inhibitors, NSAIDs, Succinylcholine.

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10
Q

What are the indications for dialysis?

A

A: Acidosis, E: Electrolyte abnormalities (hyperkalemia, hyponatremia, hyperphosphatemia), I: Ingestions, O: Fluid overload, U: Uremia.

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11
Q

What is Multicystic Dysplastic Kidney (MCDK)?

A

Failure of union of ureteric bud with renal mesenchyme, resulting in a non-functioning kidney replaced by non-communicating cysts. Often involutes by age 5.

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12
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD) genetics and when does ESRD occur?

A

PKD1 (75-85% of cases) leads to ESRD in 50s, PKD2 leads to ESRD in 70s.

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13
Q

What are key features of Autosomal Recessive Polycystic Kidney Disease (ARPKD)?

A

Presents as neonates or infants, high neonatal mortality, oligohydramnios, large echogenic kidneys. All patients have associated hepatic involvement.

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14
Q

How is hematuria defined?

A

> 5 RBCs per high-power field (HPF) on urinalysis.

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15
Q

What are the signs of Glomerular Hematuria?

A

Brown or ‘tea-colored’ urine, RBC casts, cellular casts, tubular cells, proteinuria ≥ 2+ on dipstick.

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16
Q

What are the signs of Non-Glomerular Hematuria?

A

Red-pink urine, blood clots, no proteinuria or ≤ 2+ on dipstick, normal erythrocytes.

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17
Q

How might Glomerulonephritis present?

A

Asymptomatic microscopic hematuria, asymptomatic microscopic hematuria with proteinuria, acute nephritic syndrome (gross hematuria, AKI, hypertension, edema).

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18
Q

What is Post-streptococcal glomerulonephritis (PSGN)?

A

Most common pediatric GN worldwide, typically affects children 4-12 years old, related to strep-pharyngitis or pyoderma. Presents with acute nephritic syndrome. Diagnosis supported by low C3.

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19
Q

What is Shiga toxin (+) HUS?

A

Primarily affects children <5 years of age. Most often caused by Shiga toxin-producing E.coli 0157:H7 (STEC). Bloody diarrhea is the most common presentation.

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20
Q

What are key features of Pneumococcal HUS?

A

Following invasive S. pneumoniae infection. Presents with severe pneumonia/empyema. Affects infants and young children mostly. High mortality and dialysis rates.

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21
Q

What are key features of Atypical HUS (aHUS)?

A

Mostly complement mediated from genetic mutations. Often triggered by infections. Recurrent in nature with higher risk of CKD/ESRD.

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22
Q

What are key features of IgA Nephropathy?

A

‘Syn-pharyngitic’ GN, gross hematuria around time of URTI, often microscopic hematuria between illnesses. Confirmation with renal biopsy.

23
Q

What are key features of Thin Basement Membrane Disease?

A

Common cause of persistent or intermittent microscopic hematuria. Kidney Biopsy shows thin glomerular basement membrane.

24
Q

What are key features of Alport Syndrome?

A

Hereditary nephritis, often X-linked. Progressive disorder that often leads to kidney failure. Bilateral sensorineural hearing loss, ocular manifestations.

25
Q

What is considered normal urinary protein excretion?

A

<100 mg/m2/day or <4 mg/m2/hr.

26
Q

What is Glomerular Proteinuria?

A

↑ albumin due to pathological causes (e.g., nephrotic syndrome) or non-pathological/transient causes (e.g., fever, heavy exercise).

27
Q

What is Tubular Proteinuria?

A

Low molecular weight (LMW) proteins.

28
Q

What are the key features of Nephrotic Syndrome?

A

Proteinuria, Edema, Hypoalbuminemia (<25 g/L).

29
Q

What is the initial treatment for Nephrotic Syndrome?

A

Daily prednisone for six weeks followed by alternate day prednisone for an additional six weeks.

30
Q

List some steroid sparing agents and their side effects.

A

Cyclophosphamide (oral) - Leukopenia, hemorrhagic cystitis, gonadal toxicity. Mycophenolate Mofetil (MMF) - GI complaints. Tacrolimus or Cyclosporine - Tremor, hyperK, hypoMg, metabolic acidosis, hypertension, AKI.

31
Q

What is the most important test to determine the etiology of hyponatremia?

A

Urine osmolality.

32
Q

How do you manage SIADH?

A

Identify reversible cause, rule out thyroid & adrenal cause, fluid restriction.

33
Q

How do you treat Symptomatic Hyponatremia?

34
Q

What are the causes of hypernatremia?

A

Water loss (Diabetes insipidus, diarrhea), inability to drink/access water.

35
Q

What should you consider if hypernatremia is present with urine osmolality <600?

A

Central or nephrogenic diabetes insipidus (DI).

36
Q

How do you calculate the Anion Gap?

A

[Na+] – ([HCO3 -] + [Cl-]). Normal AG is 12 +/- 3.

37
Q

What are the main causes of Non Anion Gap Metabolic Acidosis?

A

Diarrhea, Renal tubular acidosis (RTA).

38
Q

What are the key features of Distal RTA (Type 1)?

A

Defective H+ secretion, associated with hypokalemia, hypercalciuria, nephrocalcinosis & hypocitraturia.

39
Q

What are the key features of Proximal RTA (Type 2)?

A

↓ ability to reclaim HCO3, often part of Fanconi syndrome.

40
Q

What is Fanconi Syndrome?

A

Loss of bicarbonate, phosphate, glucose, amino acids, sodium, potassium.

41
Q

What is Cystinosis?

A

AR lysosomal storage disease with accumulation of cystine dimers in lysosomes.

42
Q

What are key features of Bartter Syndrome?

A

Hypokalemia, metabolic alkalosis, hyperaldosteronism, polyuria, hypercalciuria & salt wasting.

43
Q

What are key features of Gitelman Syndrome?

A

Hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, & polyuria. Milder salt wasting compared to Bartter syndrome.

44
Q

How is hypertension identified?

A

BP over 134/90 averaged over 3 readings during office visit. Selection of correct-sized cuff is important.

45
Q

What is White Coat Hypertension?

A

BP ≥ 95th%ile in the clinic but < 95th%ile by 24-hour ABPM.

46
Q

What are the most common causes of secondary hypertension in children?

A

Renal or renovascular causes.

47
Q

What investigations should be conducted for hypertension?

A

Blood chemistry, urinalysis, renal ultrasound, fasting blood glucose, lipid profile, echocardiogram, retinal check.

48
Q

What are the blood pressure goals of hypertension therapy?

A

Children: < 90th percentile for age, gender, height. Adolescents: < 130/80 mmHg.

49
Q

What are the first line medications for hypertension with Chronic Kidney Disease?

A

ACE inhibitor or ARB.

50
Q

How do you treat Hypertensive Urgency?

A

Treat with oral (nifedipine) or IV agents (labetolol, nicardipine, esmolol).

51
Q

What are the first line medications for hypertension with Chronic Kidney Disease?

A

ACE inhibitor or ARB.

52
Q

How do you treat Hypertensive Urgency?

A

Treat with oral (nifedipine) or IV agents (labetolol, nicardipine, esmolol).

53
Q

How do you treat Hypertensive Emergency?

A

Reduce MAP by 25% within minutes to 1-2 hrs. Gradual reduction towards normal in 24-48 hrs.