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MKSAP > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Acid urine pH

A

High protein diet
Increases risk for uric acid stones
Type IV distal RTA

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2
Q

High urine PH

A

Urease-splitting organisims (proteus), type I and II RTA, increased risk for struvite stones

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3
Q

Primary protein checked by dipstick

A

Albumin

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4
Q

Positive ketones on dipstick

A

DKA, starvation ketoacidosis, vomiting, pregnancy

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5
Q

Glucosuria in the absence of serum hyperglycemia

A

Indicates proximal tubule dysfunction (myeloma, drug exposure, Fanconi syndrome)

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6
Q

Reasons for negative urine nitrite in UTI

A

Nonconverting organisms like (Enterococcus, Staphylococcus, Streptococcus, Haemophilus_

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7
Q

Conditions that cause calcium phosphate crystals

A

Distal RTA, tumor lysis syndrome (also causes uric acid crystals)

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8
Q

Evaluation of hematuria in patient older than 35

A

CT urography or noncontrast, helical CT if stone suspected

Bladder US is reasonable if wanting a cheap and fast screen but gold standard is above

If negative, cystoscopy is needed

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9
Q

Best test for renal artery stenosis other than doppler

A

MR angiography (can even get without contrast if really needed)

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10
Q

Test for urinary potassium losses

A

Spot K+/Cr ratio: <13 indicates hypokalemia due to lack of intake or GI losses

Otherwise, consider other causes like aldosteronism, diuretic use, RTA, Barter/Gitelman (diuretic mimicry)

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11
Q

Causes of hypophopshatemia

A 
Refeeding syndrome 
Insulin treatment
Respiratory alkalosis 
Meds (calcium, antacids) 
Diarrhea/renal wasting (>100mg/24hrs or check FEPo4 with MD calc) 
Hyperparathyroidism
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12
Q

Newly identified cause of hypomagnesemia

A

Prolonged use of PPIs

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13
Q

Causes of hypomagnesemia

A 
Diuretics 
Cisplatin, calcineurin inhibitors 
VEGF inhibitors 
Alcoholism 
Volume expansion 
DKA
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14
Q

For what acid-base disorder is Winter’s Formula used?

A

Metabolic acidosis

1.5(HCO3) + 8 +/-2

Gives you the expected pCO2

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15
Q

Treatment of alcoholic ketoacidosis

A

IV saline AND D5w; need insulin secretion and suppression of glucagon release

Make sure to give thiamine prior to starting

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16
Q

Treatment goal for salicylate toxicity

A

NaHCO3 w/ goal urine pH 7.5

17
Q

Urine anion gap uses and components

A

Used to differentiate normal anion gap acidosis and need a urine Na, K, and Cl

Positive = RTA
Negative = Diarrhea
18
Q

Type II RTA

A

Proximal tubule fails to resorb HCO3 leading to acidosis

Can have acidic urine still since distal nephron is still intact

Tx: Alkalinize the urine; consider thiazides

19
Q

Fanconi Syndrome

A

Glycosuria, phosphaturia, aminioaciduria, hypouricemia all due to failure of the proximal renal tubule

Usually associated w/ Type II RTA

20
Q

Type I RTA

A

Failure of DCT to secrete H+

Known causes include lithium, Wilsons, dysproteinemias

Associated with urinary potassium wasting and hypocitraturia which predisposes to renal calculi

Tx: Potassium citrate

21
Q

Type IV RTA

A

Caused by aldosterone deficiency or resistance seen with diabetic nephropathy (due to hyporeninism), ACEi/ARB, heparin, and COX-2 inhibitors

Tx: Underlying cause; can consider fludrocortisone, thiazides, loop diuretics

22
Q

Patient not on diuretics but has metabolic alkalosis and high urine chloride

A

Consider Bartter and Gitelman syndromes

23
Q

Timing of rise in creatinine with aminoglycosides

A

5-7 days after initiation

Can also see loss of pretty much all electrolytes

24
Q

Cisplatin induced AKI

A

Directly nephrotoxic and also causes renal vasoconstriction

Hypomagnesemia w/ urinary wasting of magnesium is common

25
Q

Goals for treatment in pigment related AKI

A

Fluid resuscitate w/ goal UOP 200-300cc/hr

Additionally, could alkalinize the urine if no improvement to prevent cast formation, however, if patient becomes hypocalcemia or alkalotic, may need to discontinue

26
Q

Acute interstitial nephritis w/ NSAIDs or PPI

A

Classic triad of fever, rash, and eosinophilia is rarely ever present with these two common medications

27
Q

Labs to check w/ AMS and history is suggestive of ingestion

A

HCO3, serum osmols and osmol gap, urine osmol gap, UA for crystals (calicum oxalate w/ polyethylene glycol or excessive orlistat)

28
Q

Complication with peritoneal dialysis

A

Peritonitis; will lead to fibrosis and make PD ineffective

29
Q

Med classes renal transplant patients need to be one

A

Calcineurin inhibitors (tacrolimus, cyclosporine)
Antimetabolites (Mycophenolate or Azathioprine)
Glucocorticoids

30
Q

Most common intrinsic renal kidney disease to occur post transplant

A

FSGS

31
Q

Cancers most common in renal transplant patients

A

Non melanoma skin cancer
Kaposi sarcoma
Lymphoproliferative cancers

32
Q

FSGS pathologic mechanism

A

Immunologic injury from leukocytes producing a factor that directly targets podocytes causing glomerular detachment; associated w/ APOL1 gene in african americans and obese people

33
Q

Leading cause of nephropathy in white people

A

Membranous nephropathy

34
Q

Clinical presentation of membranous nephropathy

A

Slowly progressive edema w/ labs showing nephrotic stuff, however, renal fnxn remains mostly intact (as opposed to FSGS)

Patient’s are also more prone to thrombotic complications, especially when albumin <2.8

35
Q

What should you consider when a patient is diagnosed w/ membranous nephropathy?

A

Possibility of cancer; malignancy detected in 25% of patients within 1 year of diagnosis

Perform age appropriate screening

36
Q

Most common glomerular disease worldwide

A

IgA nephropathy

37
Q

IgA nephropathy pathology

A

Deficient IgA1-producing cells cause galactose deficient IgA to be attack by antibodies and form deposited immune complexes producing microscopic/gross hematuria or can become more aggressive and look like a traditional glomerulonephritis

38
Q

Tubloreticular inclusions in glomerular endothelial cell cytoplasm on EM of kidney biopsy

A

“interferon footprints”

*pathognomic for lupus nephritis

39
Q

Membranoproliferative glomerulonephritis classic association?

A

Hepatitis C

MKSAP (15 decks)

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