Mksap 16 Q&a Nephro

Front 1

when is coronary artery calcium score indicated?

Back 1

asymptomatic patients with intermediate risk of CAD (10%-20% 10-year risk) --> high score (>400) is an indication for more intensive preventive treatment

Front 2

what is Fanconi syndrome?

Back 2

disease of proximal renal tubules; where BAGUP (bicarbonate, amino acids, glucose, uric acid, phosphate) are passed into the urine, instead of being reabsorbed

Front 3

findings in minimal change disease

Back 3

normal light and immunofluorescence microscopies; effacement of podocyte foot processes on electron microscopy.

Front 4

biopsy findings in primary membranous glomerulopathy

Back 4

diffuse glomerular membrane thickening without cellular infiltration, and coarsely granular deposits of IgG and C3 along the capillary loops by immunofluorescence microscopy. Electron microscopy shows moderate podocyte foot process effacement

Front 5

clinical clue to diagnosis of multiple myeloma

Back 5

elevated total urine protein, (quantifies both albumin and non-albumin protein (paraprotein)) with small amounts of protein on urine dipstick (measures only albumin)

Front 6

when to change HCTZ to furosemide

Back 6

GFR <30, HCTZ becomes ineffective as a diuretic

Front 7

kidney biopsy, what is an acceptable BP?

Back 7

<160/95

Front 8

contraindications to kidney biopsy (7)

Back 8

uncontrolled HTN, coagulopathy, thrombocytopenia, hydronephrosis, atrophic kidney, numerous kidney cysts, and acute pyelonephritis

Front 9

describe FENA in urinary obstruction

Back 9

in early obstruction, urine sodium and FENa may be low; in late obstruction, urine sodium and FENa may be high (tubular damage)

Front 10

lab findings in gentamicin toxicity

Back 10

hypokalemic metabolic alkalosis

Front 11

describe pathophysiology of gentamicin nephrotoxicity

Back 11

Aminoglycosides are divalent cations that activate calcium-sensing receptor in TALOH; this inhibits Na-K-Cl cotransporter, mimicking effect of loop diuretics and leading to hypokalemic metabolic alkalosis

Front 12

fibrosing skin disease caused by an inflammatory reaction to gadolinium that accumulates in the body due to kidney failure

Back 12

nephrogenic systemic fibrosis

Front 13

in DM, when to test for microalbuminuria?

Back 13

annual testing to assess urine albumin excretion in patients with type 1 diabetes of 5 years' duration and in all patients with type 2 diabetes starting at the time of diagnosis by measuring the albumin–creatinine ratio

Front 14

how is microalbuminuria diagnosed?

Back 14

albumin–creatinine ratio of 30 to 300 mg/g; diagnosis requires an elevated albumin–creatinine ratio on two of three random samples obtained over 6 months

Front 15

how do NSAIDs cause hyperkalemia?

Back 15

inhibit renin synthesis, resulting in hyporeninemic hypoaldosteronism, decreased potassium excretion, and hyperkalemia

Front 16

formula for TTKG

Back 16

TTKG = [Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium OR Uffine K / serum K all div by Uosm/Posm

Front 17

how to interpret TTKG?

Back 17

TTKG in patient on normal diet is 8 to 9; >10 in hyperkalemic states, reflecting excretion of excess potassium; if not then prob hypoaldosterone state

Front 18

fevers and leukopenia post kidney transplant

Back 18

CMV infection

Front 19

mechanism of kidney injury due to tenofovir (Viread)

Back 19

drug-related damage to mitochondrial DNA (most significantly in renal tubules causing tubular dysfunction)

Front 20

mechanism of kidney injury due to Bactrim?

Back 20

Trimethoprim, particularly in acid urine, blocks the epithelial sodium channel in the cortical collecting duct, leading to increased lumen positive potential, impaired potassium and proton secretion, hyperkalemia, and metabolic acidosis

Front 21

X-linked disease affecting basement membranes due to a collagen protein synthesis defect. Clinical disease is characterized by sensorineural hearing loss, ocular abnormalities, and a family history of kidney disease and deafness

Back 21

Alport syndrome

Front 22

differential diagnosis of combined increased anion gap metabolic acidosis and respiratory alkalosis

Back 22

salicylate toxicity, liver disease, and sepsis

Front 23

ferritin levels that exclude or diagnose iron deficiency

Back 23

>100ng/mL excludes and <15 diagnoses iron def

Front 24

formula for urine potassium–creatinine ratio

Back 24

Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)

Front 25

interpretation of urine K-crea ratio

Back 25

> 20 meq/g c/w kidney potassium wasting, << 15 meq/g suggests extrarenal potassium loss, cellular redistribution, or decreased intake

Front 26

metabolic alkalosis, urine cl levels low, differentials?

Back 26

vomiting or decreased effective arterial blood volume (prior diuretics)

Front 27

metabolic alkalosis, urine Cl levels high, differentials?

Back 27

on diuretics, Bartter or Gitelman syndrome

Front 28

define hypercalciuria

Back 28

urine calcium >300

Front 29

treatment of calcium stones with hypercalciuria

Back 29

thiazide diuretic, promotes distal reabsorption of calcium

Front 30

kidney injury which results when a patient with vascular risk factors and hypertension attains a blood pressure lower than usual measurements

Back 30

normotensive ischemic AKI

Front 31

time frame for AIN to occur

Back 31

1 week after exposure

Front 32

JNC 7 definition of prehypertension

Back 32

average blood pressure reading of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic. Remember goal blood-pressure for people with diabetes regardless of age is a BP less than 130/80.

Front 33

blood pressure that is higher at home than in the office setting

Back 33

Masked hypertension

Front 34

White coat hypertension

Back 34

3 office BP >140/90 mm Hg, 2 home BP <140/90 mm Hg and no target organ damage.

Front 35

Resistant hypertension

Back 35

BP above goal despitee 3 antihypertensives, including 1 diuretic

Front 36

pathophysiology of Gitelman syndrome

Back 36

defect is due to inactivating mutations in the gene for the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule, and the electrolyte profile is analogous to that induced by thiazide diuretics (hypokalemia, hypochloremic metabolic alkalosis)

Front 37

electrolyte and acid base abnormality in diuretic abuse and surreptitious vomiting

Back 37

hypokalemic metabolic alkalosis

Front 38

define gestational hypertension

Back 38

refers to hypertension that develops after 20 weeks' gestation in the absence of proteinuria or other maternal end-organ damage

Front 39

what is preeclampsia?

Back 39

new-onset hypertension accompanied by the development of proteinuria, develops any time after 20 weeks of pregnancy but usually occurs close to term.

Front 40

classic presentation of AIN

Back 40

fever, rash, and eosinophilia with elevated crea (only in 10%)

Front 41

how to interpret fractional excretion of urea

Back 41

<35% prerenal (less influenced by diuretics)

Front 42

propofol-related infusion syndrome is characterized by

Back 42

type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, and J-point elevation or a Brugada-like pattern on EKG

Front 43

treatment of primary membranous glomerulopathy

Back 43

control risk factors - ACEi for HTN and statin if HL

Front 44

differentiate type A and type B lactic acidosis

Back 44

Type A due to tissue hypoperfusion / hypoxia. Type B due to medication / toxin; or in advanced malignancy, liver disease, or G6PD def

Front 45

drugs that cause type B lactic acidosis

Back 45

linezolid, acetaminophen overdose, metformin, the NRTis stavudine and didanosine, propofol, and salicylates

Front 46

kidney stones that will pass and will not pass?

Back 46

5mm or less will pass, 10mm or more will not

Front 47

at what levels of creatine kinase should one suspect rhabdo?

Back 47

>5000

Front 48

abnormal ARR

Back 48

>25 considered abnormal

Front 49

when to start bicarbonate therapy in CKD?

Back 49

Stage 4-5 with bicarb 15-20 (delays progression of CKD)

Front 50

treatment of hyperoxaluria

Back 50

calcium carbonate supplements

Front 51

When to consider evaluating for secondary causes of HTN? (6)

Back 51

young age, no family history, no risk factors, rapid onset, abrupt change, endocrine abnormality

Front 52

Indications for rasburicase (being that it is more expensive) (2)

Back 52

high risk for tumor lysis syndrome or very high UA levels in chemo

Front 53

NOTE: Plain AXR has no role in

Back 53

the acute diagnosis of kidney stones.

Front 54

NOTE: There is no role for the routine measurement of

Back 54

EPO in CKD.

Front 55

How does GFR relate to creatinine?

Back 55

inversely proportional; 50% reduction in GFR = doubling of serum crea

Front 56

medications that block tubular secretion of creatinine (resulting in higher crea without change in GFR)

Back 56

TMP, cimetidine

Front 57

alternative marker of GFR that is less influenced by age, gender, muscle mass, and body weight compared with serum creatinine

Back 57

cystatin C

Front 58

high urinalysis pH

Back 58

strict vegetarians, distal RTA (Type 1), urease–splitting organisms (Proteus and Pseudomonas)

Front 59

urine dipstick reads negative or trace for protein but shows increased positivity for protein by the SSA test

Back 59

consider multiple myeloma – presence of urine light chains or Ig not detected by urine dipstick

Front 60

at what serum glucose does glucosuria occur?

Back 60

180–200 mg/dL

Front 61

differential diagnosis for (+) ketones

Back 61

DKA, starvation / alcoholic ketoacidosis; salicylate toxicity, isopropyl alcohol poisoning

Front 62

ketones detected by urinalysis

Back 62

acetoacetate, not B–OH

Front 63

when is nitrites (+)?

Back 63

GN UTI (Kleb, E. coli, Proteus, Pseudomonas)

Front 64

differentials for (+) urobilinogen in urinalysis

Back 64

hemolytic anemia or hepatic necrosis (NOT obstructive causes)

Front 65

differentials for (+) bilirubin in urinalysis

Back 65

severe liver disease or obstructive jaundice

Front 66

sterile pyuria differentials

Back 66

M. tuberculosis, AIN, kidney stones, kidney transplant rejection

Front 67

common causes of AIN

Back 67

antibiotics, NSAIDs, PPI

Front 68

differentials for urine eosinophil (+) in urinalysis

Back 68

allergic reaction, atheroembolic disease, RPGN, small vessel vasculitis, UTI, prostatic disease, parasitic infections

Front 69

blood in urine: isomorphic RBCs

Back 69

tumor, stone or infection. The fact that the RBCs are isometric by definition determines their origins not at the glomeruli level.

Front 70

blood inurine: acanthocytes and RBC casts

Back 70

GN, severe interstitial nephritis, ATN

Front 71

casts in urinalysis

Back 71

hyaline casts – hypovolemia; pigmented granular (muddy brown) casts – tubular injury; RBC casts – GN; WBC casts – tubulointersitial inflammation of kidney, pyelonephritis

Front 72

urine crystal shapes

Back 72

-Calcium oxalate: envelope / dumbell / needle

-Calcium phos: prism, needle, star–like clump

-Uric acid: rhomboid / needle / rosette

-Struvite or Mag ammonium phos: coffin

-Cystine: Hexagonal

Front 73

Nephrotic–range proteinuria

Back 73

protein–creatinine ratio greater than 3.5 mg/mg

Front 74

ADA recommendation: when to check urine albumin–crea ratio in DM?

Back 74

typ1DM x 5 years; all type 2 DM at time of diagnosis

Front 75

ADA definition of microalbuminuria

Back 75

urine albumin–creatinine ratio of 30 to 300 mg/g; two of three random samples over 6 months

Front 76

transient proteinuria differentials

Back 76

fever, rigorous exercise

Front 77

proteinuria increases during the day and decreases at night when the patient is recumbent

Back 77

orthostatic proteinuria

Front 78

diagnostic test for orthostatic proteinuria

Back 78

split urine collection

Front 79

imaging used in the evaluation of hematuria

Back 79

CT urography, MR urography, US, IVP

Front 80

which urinary tract imaging to choose in hematuria

Back 80

CT uro for high–risk patients with preserved GFR; MR uro when GFR 30–60; US in <40y/o with no RF for urologic malignancy; noncontrast abd CT if stones suspected; IVP no longer recommended

Front 81

hematuria ffd by negative evaluation of upper urinary tract, next step

Back 81

cystoscopy; assess for lower ureteral, bladder or urethral causes

Front 82

gold standard for quantifying the glomerular filtration rate and renal plasma flow

Back 82

radionuclide kidney clearance scanning

Front 83

when to order MRI of kidneys

Back 83

mass lesions and cysts

Front 84

test of choice for the evaluation of urologic bleeding in patients at high risk for bladder cancer with an estimated GFR above 60 mL/min/1.73 m2

Back 84

CT urography

Front 85

can identify non–uric acid–containing kidney stones

Back 85

KUB xray

Front 86

Indications for kidney biopsy

Back 86

suspected glomerular pathology such as glomerulonephritis and the nephrotic syndrome, acute kidney injury of unclear cause, and kidney transplant dysfunction

Front 87

Contraindications to kidney biopsy

Back 87

bleeding diatheses, active infection of the genitourinary system, hydronephrosis, atrophic kidneys, and uncontrolled hypertension; relative C/I: solitary kidney, severe anemia, and chronic anticoagulation

Front 88

abnormal serum osmolal gap

Back 88

>10 mosm/kg H20; reflects the presence of unmeasured solutes

Front 89

Formula: plasma Osmolality (mosm/kg H2O)

Back 89

2 × Sodium (meq/L) + Glucose (mg/dL)/18 + BUN (mg/dL)/2.8

Front 90

normal effective osmolality

Back 90

275–295 mosm/kg H204 to 6 meq/L (4–6 mmol/L) over the first 24 hours is sufficient

Front 91

goal rise in sodium in patients with symptomatic hyponatremia

Back 91

4–6 meq/L over 1st 24 hours

Front 92

conditions causing pseudohyponatremia

Back 92

Hyperglobulinemia or severe hyperlipidemia

Front 93

most common form of hyponatremia

Back 93

hypotonic hyponatrmeia

Front 94

causes of hypertonic hyponatremia

Back 94

marked hyperglycemia or exogenously administered solutes such as mannitol or sucrose

Front 95

first step in the evaluation of hyponatremia

Back 95

check plasma osmolality – normal in pseudohyponatremia (check chol, TG, serum total Pr)

Front 96

how is cause of hypotonic hyponatremia established

Back 96

history, vol status, urine osmolality, urine sodium level

Front 97

Uosm for primary polydipsia and hyponatremia

Back 97

<100

Front 98

mechanism of hyponatremia in beer potomania

Back 98

water excretion is in part solute dependent, chronic ETOH + low solute intake = decrease free water excretion; hyponatremia develops in setting of modest increases in fluid intake

Front 99

when does reset osmostat occur?

Back 99

quadriplegia, TB, advanced age, pregnancy, psych disorders

Front 100

how to distinguish reset osmostat from SIADH

Back 100

document excretion of dilute urine following a water load

Front 101

What is cerebral salt wasting?

Back 101

syndrome of hypotonic hyponatremia that may complicate subarachnoid hemorrhage or neurosurgery

Front 102

risk factors for acute hyponatremia

Back 102

pos–op hypotonic fluids; use of thiazides, use of ecstacy, overhydration with extreme exercise, primary polydipsia

Front 103

treatment of symptomatic hyponatremia

Back 103

hypertonic saline in symptomatic SIADH; NS for hypovolemic hyponatremia; seizure or coma – 100ml or 2ml/kg bolus infusions of 3% NS, repeated up to 2x as needed

Front 104

maximum rate of correction of hyponatremia

Back 104

not >10 meq/l within 24 hours or 18 within 48 hours

Front 105

clinical features of osmotic demyelination syndrome

Back 105

progressive quadriparesis, speech and swallowing disorders, coma, locked–in syndrome (IRREVERSIBLE)

Front 106

treatment of asymptomatic hyponatremia

Back 106

fluid restriction in SIADH or hypervolemic hyponatremia

Front 107

causes of diabetes insipidus

Back 107

decreased release of ADH (central diabetes insipidus); ADH resistance (nephrogenic diabetes insipidus); and metabolism of ADH by circulating vasopressinase (gestational diabetes insipidus)

Front 108

define polyuria

Back 108

urine volume >3L/24h

Front 109

diff Dx of polyuria

Back 109

DI, primary polydipsia, osmotic diuresis

Front 110

urine osmolality in osmotic diuresis, primary polydipsia and DI

Back 110

>300 in osmotic diuresis; <200 in Di and primary polydipsia

Front 111

effect of water deprivation testing in primary polydipsia and DI

Back 111

increases urine osmolality to ~600mosm/kg H20; <200 in DI

Front 112

effect of desmopressin in central DI / gestational DI / nephrogenic DI

Back 112

rise to 600 mosm/kg H20 except in nephrogenic DI

Front 113

treatment of hypernatremia

Back 113

in shock, NS – avoid boluses; estimate water deficit, D5 water

Front 114

rate of correction of hypernatremia

Back 114

no more than 10 meq/L to avoid cerebral edema

Front 115

estimated water deficit formula

Back 115

Total Body Water [0.6 in Men and 0.5 in Women × Body Weight (kg)] × [(Serum Sodium/140 [or target serum sodium]) – 1]

Front 116

treatment of central and gestational DI

Back 116

intranasal desmopressin

Front 117

treatment of nephrogenic DI

Back 117

thiazide diuretics (increase prox Na and water reabsorption); d/c lithium if possible or add amiloride

Front 118

DDx of hypokalemia

Back 118

cellular redistribution, kidney (diuretics) or GI losses, decreased intake

Front 119

conditions that result in increased intracellular uptake of serum K

Back 119

marked leukocytosis (myeloprolif disorders), B2 agonists, epinephrine, insulin, Vit B12 repletion, systemic alkalosis; toxicity to barium, chloroquine, quetiapine, risperidone

Front 120

rare syndrome that presents with acute episodic muscle weakness, often following a high carbohydrate meal or strenuous exercise

Back 120

hypokalemia periodic paralysis

Front 121

this amount of 24 hour urine K excretion suggests ongoing urinary potassium losses

Back 121

>30meq/L

Front 122

formula for urine potassium–crea ratio

Back 122

(meq/g) = Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)

Front 123

interpretation of urine K–crea ratio

Back 123

>20 in kidney potassium wasting, <15 suggests cellular reditribution, decreased intake or extrarenal K loss

Front 124

used for patients with concomitant metabolic acidosis due to renal tubular acidosis and hypokalemia

Back 124

potassium citrate

Front 125

the most efficient intervention that enhances intracellular potassium uptake

Back 125

IV insulin +/– glucose

Front 126

evolution of EKG changes in hyperkalemia

Back 126

peaked T waves with a shortened QT interval initially, followed by an increased PR interval and QRS duration, decreased P wave amplitude, and eventually a sinoventricular pattern heralding ventricular standstill

Front 127

NOTE: Severe leukocytosis (leukocyte count >120,000/microliters [120 × 109/L]) and thrombocytosis (platelet count >600,000/microliters [600 × 109/L])

Back 127

can result in the release of intracellular potassium in serum specimens.

Front 128

how to diagnose pseudo–hyperkalemia related to leukocytosis

Back 128

by repeating a serum potassium measurement in a sample carefully transported to the laboratory without agitation immediately following phlebotomy or measurement of whole blood potassium in uncentrifuged specimens using ion–specific electrodes also confirms the diagnosis

Front 129

what does TTKG estimate?

Back 129

the ratio of the potassium level in the CCD to that in the peritubular capillary; capacity of kidney to excrete K in the setting of hyperK

Front 130

formula for TTKG

Back 130

[Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium

Front 131

how to interpret TTKG

Back 131

>10 under normal conditions; < 10 indicates kidney defect in K excretion

Front 132

how is IV calcium given in hyperkalemia?

Back 132

every 5 minutes until ECG changes resolve

Front 133

When is IV calcium contraindicated in hyperkalemia?

Back 133

digoxin toxicity

Front 134

onset and duration of effect of glucose insulin solution in hyperkalemia

Back 134

within 10 minutes and is sustained for 4 to 6 hours

Front 135

Caveat with using sodium polystyrene sulfate in hyperkalemia

Back 135

use sorbitol–free preparation – sorbitol implicated in GI necrosis and bleeding

Front 136

treatment of mild–moderate hyperkalemia

Back 136

dietary potassium restriction to less than 2500 mg/d

Front 137

DDx of hypophosphatemia

Back 137

chronic alcohol use, critical illness, malnutrition

Front 138

presentation of hypophosphatemia

Back 138

<2 symptomatic weakness, <1 resp muscle weakness, hemolysis, rhabdomyolysis

Front 139

when to correct low phos with IV?

Back 139

<1

Front 140

NOTE: When hypophosphatemia is due to increased cellular uptake or extrarenal phosphate loss,

Back 140

the 24–hour urine phosphate excretion is less than 100 mg/dL (32.3 mmol/L) and the fractional excretion of phosphate is less than 5%

Front 141

risks of IV phosphate treatment

Back 141

hypocalcemia and AKI. Because serum phosphate and calcium have an inverse relationship.

Front 142

maximum dose of intravenous phosphate

Back 142

doses of phosphate should be restricted to 80 mmol over 12 hours

Front 143

DDx of hyperphosphatemia

Back 143

advanced CKD, increased cell turnover, cell injury, or exogenous phosphate administration

Front 144

normal reference range for the anion gap

Back 144

8 to 10 meq/L ± 2 meq/L

Front 145

correction of anion gap in hypoalbuminemia

Back 145

For every 1 g/dL (10 g/L) decrease in serum albumin, for example, the expected or “normal” anion gap falls by approximately 2.3 meq/L (2.3 mmol/L).

Front 146

define lactic acidosis

Back 146

serum lactate level greater than 4 mg/dL

Front 147

MOA fomepizole

Back 147

inhibitor of alcohol dehydrogenase that prevents the formation of toxic acid metabolites

Front 148

formula for corrected bicarbonate

Back 148

24– change in AG

Front 149

interpretation of delta delta

Back 149

if measured HCO3 > corrected bicarb – concomitant MAlk in addition to HAGMA; if measured HCO3 < corrected – concomitant NAGMA + HAGMA

Front 150

What is the goal blood pressure for person younger than 80 years?

Back 150

Less than 140/90

Front 151

And what hemoglobin should erythropoietin stimulants be started in CKD?

Back 151

Less than 10. With a target hemoglobin level of 10 to 11.

Front 152

Acetazolamide causes kidney excretion of what:

Back 152

Bicarb and sodium

Front 153

When to start dual antihypertensive therapy?

Back 153

When blood pressure more than 20 points above goal blood pressure based on age.

Front 154

How long to treat UTI and patience with autosomal dominant polycystic kidney disease?

Back 154

Cipro for 2 to 4 weeks

Front 155

Most important thing to do to prevent tumor lysis syndrome?

Back 155

Intravenous fluids at 250 mL per hour if possible

Front 156

What is the most common primary nephrotic syndrome?

Back 156

Focal segmental glomerulosclerosis. This condition as a predilection for African-Americans. Typically these patients at minimal edema.

Front 157

Type of kidney disease seen with lupus?

Back 157

Proliferative lupus nephritis

Front 158

What is the most common primary nephrotic syndrome?

Back 158

Focal segmental glomerulosclerosis. This condition as a predilection for African-Americans.

Front 159

How soon to follow up on blood pressure in pre-hypertension?

Back 159

Recheck in 1 year

Front 160

What type of alcohol poisoning should Fomepizole be used?

Back 160

Methanol and Ethylene glycol

Front 161

I what pH is sodium HCO3 generally indicated in?

Back 161

Persistent severe acidemia with pH less than 7.15

Front 162

What test is done in the patient's home to confirm resistant hypertension?

Back 162

Ambulatory blood-pressure monitoring

Front 163

Conditions associated with lead toxicity:

Back 163

-CKD
-Hypertension
-Gout

Front 164

Best test for lead toxicity:

Back 164

Chelation mobilization testing

Front 165

NOTE: beta blockers are no longer universally recommended as first-line agents to treat hypertension in the absence of compelling indication such as history of MI or heart failure.

Back 165

X

Front 166

When to add Allopurinol in patients with recurrent uric acid stones?

Back 166

After recurrent stones despite alkalinization (treatment with potassium citrate) of the urine.

Front 167

Type of kidney injury caused by amyloidosis?

Back 167

Nephrotic syndrome. Amyloidosis also affects the heart typically causing a restrictive cardiomyopathy and subsequent heart failure.

Front 168

Describe liddle syndrome:

Back 168

-Early onset hypertension
-Metabolic alkalosis
-Hypokalemia

in this condition renin and aldosterone are suppressed. Treated with amiloride or triamterene.

Front 169

When his GFR calculation using chronic disease epidemiology collaboration equation best?

Back 169

When GFR thought to be greater than 60. Use

Front 170

How does dysmorphic RBCs look in glomerular hematuria:

Back 170

Round in shape but with blebs protruding from their membranes.

Front 171

Urine cast seen in acute interstitial nephritis (AIN)

Back 171

Leukocyte casts

Front 172

You're in cast seen in acute tubular necrosis (ATN)?

Back 172

Muddy brown casts

Front 173

Type of acute kidney injury seen with Intravenous bisphosphonate therapy?

Back 173

Acute tubular necrosis

Front 174

Characteristics of type 1 renal tubular acidosis:

Back 174

-Normal anion gap metabolic acidosis
-hypokalemia
-Alkaline urine pH (>6)
-Nephrocalcinosis
-Urine ammonia less than 30

Front 175

Lab values seen a laxative abuse:

Back 175

-Normal anion gap metabolic acidosis
-Hypokalemia

Front 176

Characteristics of proximal (type 2) renal tubular acidosis:

Back 176

A defect in the regeneration of bicarbonate in the proximal tubule's.

-Normal anion gap metabolic acidosis
-Hypokalemia
-Glucosuria in setting of normal plasma glucose
-Renal phosphate wasting
-Acidic urine pH unlike that scene and type 1 RTA

Front 177

When his GFR calculation using chronic disease epidemiology collaboration equation best?

Back 177

When GFR thought to be greater than 60. Use modification of diet in renal disease study equation at lower GFRs.

Front 178

Target blood pressure for people with diabetes regardless of age:

Back 178

Less than 130/80

Front 179

How does dysmorphic RBCs look in glomerular hematuria:

Back 179

Round in shape but with blebs protruding from their membranes.

Front 180

What is the normal urine albumin to creatinine ratio?

Back 180

Less than 30

Front 181

What is the normal urine protein to creatinine ratio?

Back 181

Less than 0.2

Front 182

Laboratory evidence of hemolytic anemia:

Back 182

-Elevated reticulocyte count
-Elevated lactate dehydrogenase

Front 183

What diseases associated with a classic triad of: microangiopathic hemolytic anemia, low haptoglobin level, and schistocytes?

Back 183

Hemolytic uremic syndrome. Caused by some strains of E. coli including 0157-h7 that produces Shiga-like toxins.

Front 184

Next test for sustained, isolated proteinuria?

Back 184

Split urine collection: Protein urine collection during the day and collection during the night. to a valve for the benign condition of orthostatic pastoral proteinuria.

Front 185

What is the normal urine protein loss over 24 hours?

Back 185

Less than 150 mg/24 hours

Front 186

Which chemotherapeutic agent is well known for causing type 2 RTA and or Fanconi syndrome?

Back 186

Ifosfamide

Front 187

Lab values associated with postinfectious glomerulonephritis secondary to strep or staph:

Back 187

-Low complement levels
-Elevated antistreptolysin O antibodies when associated with streptococcal infection

Note in this condition there should be a latency period between infection and the onset of kidney disease.

Front 188

What two conditions should be thought of in the presence of resistant hypertension?

Back 188

1. Primary hyperaldosteronism
2. Renovascular hypertensio

Front 189

What is the treatment for primary membranous glomerulopathy?

Back 189

Ace inhibitor and Statin

Front 190

What condition is associated with: type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, myocardial abnormalities seen as J point elevation or Brugada like pattern on EKG

Back 190

Propofol-related infusion syndrome

Front 191

Treatment of mild to moderate salicylate toxicity:

Back 191

Sodium bicarb infusion. Alkalinizing the arterial blood to a pH 7.5 to 6.6 is indicated to decrease intracellular uptake and toxicity of salicylic acid. additionally with hydration and urine alkalinization to a pH of 7.5 to 8.0 will promote salicylate excretion. Blood salicylate levels and other electrolyte should be done q2 hours while treating. Any hypokalemia should be corrected to prevent increased salicylate absorption in the distal tubule. Impaired mentation should be treated with intravenous glucose to attenuate salicylate induced neuroglycopenia.

Front 192

When is hemodialysis indicated in salicylate toxicity?

Back 192

-Serum salicylate levels that exceed 80 mg/dL are
-Altered mentation
-Pulmonary edema
-Advanced kidney disease
-When clinical status worsens despite optimal medical therapy

Front 193

Expected lab values in syndrome of inappropriate ADH secretion:

Back 193

-Low plasma osmolality
-Urine sodium level exceeding 40

Front 194

Definition of hyperkalemia:

Back 194

Potassium over 5

Front 195

Definition of abdominal compartment syndrome:

Back 195

Defined by new organ dysfunction in the setting of sustained, abnormal increase in the intra-abdominal pressure. Things that increase pressure include: massive ascites, volume overload, intra abdominal or retroperitoneal bleed.

Front 196

Medication to increase the likelihood of expulsion of ureteral stone if less than 10 mm in diameter?

Back 196

Tamsulosin (Flomax)

Front 197

What two conditions should be thought of in the presence of resistant hypertension?

Back 197

1. Primary hyperaldosteronism
2. Renovascular hypertension.

Front 198

Describe biopsy characteristics of primary membranous glomerulopathy:

Back 198

-Diffuse glomerular membrane thickening
-No cellular infiltration
-Coarsely granular deposits of IgG and C-3 along capillary loops
-moderate podocyte foot process effacement seen on electron microscopy

Front 199

Describe characteristic biopsy results of minimal change glomerulopathy:

Back 199

This condition is common in children and is not an immune complex disease process.

-Normal light and immunofluorescent microscopy but effacement of podocyte foot processes on electron microscopy.

Front 200

How to treat lithium induced partial nephrogenic diabetes insipidus if patient must continue on lithium?

Back 200

Start Amiloride. This agent directly blocks the epithelial sodium channel and decreases lithium uptake, resulting in less long-term damage.

Tolvaptan is not used in this case because the diabetes insipidus caused by lithium is only partial," not complete.

Front 201

When is Hemodialysis of the ofindicated in salicylate toxicity?

Back 201

-Serum salicylate levels that exceed 80 mg/dL are
-Altered mentation
-Pulmonary edema
-Advanced kidney disease
-When clinical status worsens despite optimal medical therapy

Front 202

The primary temporizing measures for hyperkalemia?

Back 202

-Intravenous calcium
-Insulin-dextrose solution

Front 203

Differential diagnoses of combined increased anion gap metabolic acidosis + respiratory alkalosis:

Back 203

-Salicylate toxicity which can be found in oils of wintergreen, aspirin
-Liver disease
-Sepsis

Front 204

What is the best diagnostic test to diagnose fibromuscular dysplasia?

Back 204

Catheter-based kidney angiography

Front 205

Treatment of choice for ESKD and setting of Alport syndrome?

Back 205

Kidney transplantation. There are no specific therapies were Alport syndrome.

Front 206

Types of kidney stones seen post gastric bypass surgery?

Back 206

Calcium oxalate stones secondary to enteric hyper oxaluria. Oxalate absorption is increased because calcium, which normally buns to oxalate in the gut and limits oxalate absorption, binds to fatty acids. Treatment is calcium carbonate supplements, low-fat diet, good hydration.

Front 207

Over-the-counter medications and other nonprescription drugs that can cause hypertension:

Back 207

-Decongestants with pseudoephedrine or phenylephrin
-NSAIDs
-Recent caffeine intake
-Cigarette smoking

Front 208

Best treatment to reduce risk of preeclampsia in patients with high risk?

Back 208

Low-dose aspirin 75 to 150 mg/day

Front 209

Definition of preeclampsia:

Back 209

-Systolic blood pressure greater than or equal to 140 or diastolic BP greater than or equal to 90
-24 hour urine protein greater than 300 mg
-After 20th we could just station in a woman who did not have hypertension or proteinuria early in pregnancy

Front 210

The most common disease associated with rapidly progressive glomerulonephritis?

Back 210

ANCA vasculitis. If severe, patient may require induction therapy with plasmapheresis and then cyclophosphamide and steroids. Followed with maintenance therapy with Azathioprine and steroids

Front 211

If suspecting kidney disease confirmed by laboratory data what is the next test to get?

Back 211

Kidney ultrasound. Do this prior to biopsy to rule out obstruction, determine kidney size, or evaluate for kidney cysts. And remember kidney biopsy is predominately used for patients with glomerular disease.

Front 212

Test to check in cases of metabolic alkalosis?

Back 212

-Blood pressure
-dehydration status
-urine chloride level

Front 213

What is the goal LDL level in CKD?

Back 213

Less than 100 and preferably less than 70.

Front 214

What is the first line medication for management of hypertension during pregnancy?

Back 214

Labetalol. Methyldopa works but may cause sedation and has to be given TID to be effective.

Front 215

What brain conditions should be screened for an autosomal dominant polycystic kidney disease?

Back 215

Cerebral aneurysms with MR angiography.

Front 216

Method of PTH suppression in CKD:

Back 216

Vitamin D treatment. Use vitamin D3 or cholecalciferol if actually vitamin D deficient. If intact PTH level elevated but 25 hydroxy vitamin D be more than 30, use active or vitamin D such as calcitriol.

Front 217

Normotension definition:

Back 217

BP less than 120/80

Front 218

Define chronic hypertension during pregnancy versus hypertensive disorder of pregnancy:

Back 218

Normally during pregnancy BP levels typically decrease early in the first trimester and may remain lower then nun pregnant levels until term. Therefore when hypertension is present before 20 weeks just station, this represents chronic hypertension.

Front 219

What are the lab values associated with gentamicin toxicity:

Back 219

Hypokalemic, metabolic alkalosis

Front 220

What test order for iron deficiency anemia:

Back 220

1. Serum iron level -Typically low
2. Ferritin level -Typically low
3. TIBC -Typically high

Because ferritin is an acute phase reaction it can be normal or elevated in the presence of our deficiency anemia. But generally if ferritin greater than 100 it excludes iron deficiency and is less than 15 confirms iron deficiency.

Front 221

Describe electrolytes and acid base seen in Bartter's syndrome:

Back 221

- Hypokalemia, hypochloremic metabolic alkalosis, spot urinary Cl: greater than 20

Due to abnormal chloride transporters in the ascending loop of Henle. Onset during childhood or adoles.

Front 222

Describe electrolytes and acid base seen in Gitelman's syndrome:

Back 222

- Hypokalemia, hypochloremic metabolic alkalosis, spot urinary Cl: greater than 20

Due to abnormal chloride transporters in the distal tubules. This condition is also associated with hypocalciuria.

Front 223

GFR in stage 2 CKD:

Back 223

60-89

Front 224

GFR in stage 3 CKD:

Back 224

30-59

Front 225

GFR in stage 4 CKD:

Back 225

15-29

Front 226

GFR in stage 5 CKD:

Back 226

Less than 15