Nephrology

Question 1

Acid urine pH

Answer 1

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

Question 2

High urine PH

Answer 2

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

Question 3

Primary protein checked by dipstick

Answer 3

Albumin

Question 4

Positive ketones on dipstick

Answer 4

DKA, starvation ketoacidosis, vomiting, pregnancy

Question 5

Glucosuria in the absence of serum hyperglycemia

Answer 5

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

Question 6

Reasons for negative urine nitrite in UTI

Answer 6

Nonconverting organisms like (Enterococcus, Staphylococcus, Streptococcus, Haemophilus_

Question 7

Conditions that cause calcium phosphate crystals

Answer 7

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

Question 8

Evaluation of hematuria in patient older than 35

Answer 8

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

Question 9

Best test for renal artery stenosis other than doppler

Answer 9

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

Question 10

Test for urinary potassium losses

Answer 10

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)

Question 11

Causes of hypophopshatemia

Answer 11

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

Question 12

Newly identified cause of hypomagnesemia

Answer 12

Prolonged use of PPIs

Question 13

Causes of hypomagnesemia

Answer 13

Diuretics 
Cisplatin, calcineurin inhibitors 
VEGF inhibitors 
Alcoholism 
Volume expansion 
DKA

Question 14

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

Answer 14

Metabolic acidosis

1.5(HCO3) + 8 +/-2

Gives you the expected pCO2

Question 15

Treatment of alcoholic ketoacidosis

Answer 15

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

Make sure to give thiamine prior to starting

Question 16

Treatment goal for salicylate toxicity

Answer 16

NaHCO3 w/ goal urine pH 7.5

Question 17

Urine anion gap uses and components

Answer 17

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

Positive = RTA
Negative = Diarrhea

Question 18

Type II RTA

Answer 18

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

Question 19

Fanconi Syndrome

Answer 19

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

Usually associated w/ Type II RTA

Question 20

Type I RTA

Answer 20

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

Question 21

Type IV RTA

Answer 21

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

Question 22

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

Answer 22

Consider Bartter and Gitelman syndromes

Question 23

Timing of rise in creatinine with aminoglycosides

Answer 23

5-7 days after initiation

Can also see loss of pretty much all electrolytes

Question 24

Cisplatin induced AKI

Answer 24

Directly nephrotoxic and also causes renal vasoconstriction

Hypomagnesemia w/ urinary wasting of magnesium is common

Question 25

Goals for treatment in pigment related AKI

Answer 25

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

Question 26

Acute interstitial nephritis w/ NSAIDs or PPI

Answer 26

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

Question 27

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

Answer 27

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

Question 28

Complication with peritoneal dialysis

Answer 28

Peritonitis; will lead to fibrosis and make PD ineffective

Question 29

Med classes renal transplant patients need to be one

Answer 29

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

Question 30

Most common intrinsic renal kidney disease to occur post transplant

Answer 30

FSGS

Question 31

Cancers most common in renal transplant patients

Answer 31

Non melanoma skin cancer Kaposi sarcoma Lymphoproliferative cancers

Question 32

FSGS pathologic mechanism

Answer 32

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

Question 33

Leading cause of nephropathy in white people

Answer 33

Membranous nephropathy

Question 34

Clinical presentation of membranous nephropathy

Answer 34

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

Question 35

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

Answer 35

Possibility of cancer; malignancy detected in 25% of patients within 1 year of diagnosis Perform age appropriate screening

Question 36

Most common glomerular disease worldwide

Answer 36

IgA nephropathy

Question 37

IgA nephropathy pathology

Answer 37

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

Question 38

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

Answer 38

"interferon footprints" *pathognomic for lupus nephritis

Question 39

Membranoproliferative glomerulonephritis classic association?

Answer 39

Hepatitis C