NEPHRO

Question 1

Treat diabetic kidney disease with additional medication in patients with persistent albuminuria despite maximal renin-angiotensin system inhibition.

Answer 1

The NSAID mineralocorticoid antagonist finerenone is recommended in patients with T2DM and CKD who have persistent albuminuria despite maximal renin-angiotensin system inhibition and sodium-glucose cotransporter 2 inhibitor treatment, normal serum potassium levels (<4.8 mEq/L [4.8 mmol/L]), and an estimated glomerular filtration rate ≥25 mL/min/1.73 m2, but care must be taken to avoid hyperkalemia.

Question 2

Avoid overly aggressive treatment of chronic isovolemic hypotonic hyponatremia.

Answer 2

Slowly increase the serum sodium by 4-6 mEq/L and not to exceed in a 24-hour time period.
Overly aggressive treatment of chronic hyponatremia can result in osmotic demyelination syndrome.

Question 3

ASPIRIN TOXICITY?

Answer 3

Salicylate toxicity presents in its early phase as respiratory alkalosis and an increased anion gap metabolic acidosis.

Question 4

DIFF between ASA & ETHANOL/METHANOL Toxicity?

Answer 4

Although alcohol toxicity will increase the osmolal gap, it does not cause either a respiratory alkalosis or a high anion gap metabolic acidosis.

Ethylene glycol toxicity and methanol toxicity cause an increase in both anion gap acidosis and the osmolal gap, but neither would be expected to cause a respiratory alkalosis.

Question 5

Treat masked hypertension.

Answer 5

In masked hypertension, antihypertensive medication should be initiated after a 3-month trial of lifestyle modification if daytime ambulatory or home blood pressure remains ≥130/80 mm Hg.

Question 6

Manage focal segmental glomerulosclerosis with subnephrotic proteinuria with conservative therapy.

Answer 6

Subnephrotic proteinuria (<3.5 g/d).

Question 7

Treat hypertension in pregnancy.

Answer 7

Chronic hypertension as a SBP >140 mm Hg or DBP > 90 mm Hg starting before pregnancy or before 20 weeks of gestation or persists longer than 12 weeks postpartum.

Question 8

Treat newly diagnosed primary membranous nephropathy.

Answer 8

Primary membranous nephropathy is typically treated with 3-6 months of conservative therapy before initiating immunosuppression for patients with persistent nephrotic-range proteinuria to allow for spontaneous remission, which occurs in approximately 30% of patients.

Conservative therapy: which comprises renin-angiotensin system blockers, statin therapy, and edema management.

Question 9

Diagnose uric acid nephrolithiasis.

Answer 9

Uric acid crystals can take on a variety of appearances, such as rhomboids, barrels, rosettes, needles, or hexagonal plates.

Question 10

Diagnose struvite calculi.

Answer 10

Struvite crystals typically have a “coffin lid” appearance. Struvite stones occur in the presence of urea-splitting bacteria, such as Proteus, Klebsiella, or, less frequently, Pseudomonas species.

Question 11

Diagnose calcium oxalate stone formation on the basis of calcium oxalate crystals seen on urinalysis.

Answer 11

The urine sediment shown contains envelope-shaped calcium oxalate dihydrate crystals, which are associated with hyperoxaluria and calcium oxalate stone formation. These crystals can also be seen with ethylene glycol ingestion.

Question 12

Identify common drugs as a nonglomerular cause of an increase in serum creatinine level.

Answer 12

Some medications, such as trimethoprim, cimetidine, dolutegravir, and tyrosine kinase inhibitors, reduce proximal tubule secretion of creatinine, which results in a transient and reversible increase in serum creatinine that is not reflective of changes in glomerular filtration rate.

Question 13

Diagnose ANCA-associated glomerulonephritis.

Answer 13

The most common causes of rapidly progressive glomerulonephritis are ANCA-associated glomerulonephritis, lupus nephritis, and anti–glomerular basement membrane antibody disease.

ANCA-associated glomerulonephritis accounts for >50% of all cases of rapidly progressive glomerulonephritis.

Question 14

Screening for antistreptolysin ab.

Answer 14

Poststreptococcal glomerulonephritis has a classic immunofluorescence pattern of granular IgG staining. Similar to lupus nephritis, it presents with reduced serum complement levels.

Question 15

Manage acute kidney injury due to tacrolimus toxicity.

Answer 15

High calcineurin inhibitor levels can cause acute kidney injury (AKI) via afferent arteriole vasoconstriction, and low calcineurin inhibitor levels can cause AKI via acute rejection.

Question 16

Screen for chronic kidney disease in a patient with risk factors.

Answer 16

The American Diabetes Association recommends that patients with type 2 diabetes mellitus undergo annual screening with a spot urine albumin-creatinine ratio and estimated glomerular filtration rate.

Question 17

Diagnose malabsorption-related calcium oxalate nephrolithiasis.

Answer 17

Patients with fat malabsorption have an increase in the incidence of calcium oxalate kidney stones.

Question 18

In patients with recent diuretic use or who have Gitelman syndrome

Answer 18

urine chloride levels would be elevated.

Question 19

In patients who abuse laxatives, potassium loss is extrarenal; the kidney retains potassium and thus urine potassium would be low.

Answer 19

Furthermore, these patients will typically have metabolic acidosis resulting from the loss of base in the stool.

Question 20

: Diagnose β2-agonist–related hypokalemia.

Answer 20

β2-Agonists can cause hypokalemia by facilitating intercellular shifts of potassium.

When hypokalemia is secondary to acute transcellular shifts, total body potassium is normal and potassium replacement may cause rebound hyperkalemia.

Question 21

Prevent contrast-associated nephropathy.

Answer 21

Contrast-associated nephropathy prophylaxis with intravenous 0.9% saline pre- and post-procedure is indicated for patients who have an estimated glomerular filtration rate <30 mL/min/1.73 m2 or acute kidney injury.

Contrast-associated nephropathy prophylaxis is not indicated for patients with a stable estimated glomerular filtration rate ≥45 mL/min/1.73 m2.

Question 22

Screen for malignancy in an older patient with membranous nephropathy.

Answer 22

The initial step in the management of newly diagnosed membranous nephropathy (MN) is to evaluate for secondary forms of the disease, and cancer screening is particularly important in evaluating for secondary forms of MN in patients >65 years of age.

Testing for phospholipase A2 receptor (PLA2R) antigen is used to help distinguish primary (PLA2R antigen–positive) from secondary (PLA2R antigen–negative) forms of membranous nephropathy.

Question 23

Manage a patient following initiation of a renin-angiotensin system inhibitor.

Answer 23

Following initiation of an ACE inhibitor or angiotensin receptor blocker, a >30% increase in serum creatinine levels necessitates decreasing the dose of or discontinuing these agents.

Question 24

Screen for renal cell carcinoma in a patient with acquired cystic kidney disease.

Answer 24

Patients with end-stage kidney disease are at increased risk for renal cell carcinoma.
Screening for renal cell carcinoma in patients with end-stage kidney disease and acquired cystic kidney disease may be reasonable in patients with a longer life expectancy.

Question 25

Treat a kidney stone with lithotripsy.

Answer 25

Stone passage decreases with increasing size; only 50% of stones >6 mm will pass, and stones >10 mm are extremely unlikely to pass spontaneously.

Question 26

Treat hypermagnesemia in a patient with chronic kidney disease.

Answer 26

Hypermagnesemia decreases neural transmission, resulting in weakness, and blocks both calcium and potassium channels, resulting in hypotension and bradycardia. Symptomatic hypermagnesemia (serum magnesium level >4.8 mg/dL [2.0 mmol/L]) is immediately treated with intravenous calcium gluconate while awaiting hemodialysis.

Question 27

Identify laxative abuse as a cause of normal anion gap metabolic acidosis.

Answer 27

Normal anion gap metabolic acidosis can be caused by gastrointestinal bicarbonate loss, renal loss of bicarbonate, or the inability of the kidney to excrete acid. A negative urine anion gap suggests appropriate kidney excretion of acid and therefore gastrointestinal bicarbonate loss as the cause of normal anion gap metabolic acidosis.

Question 28

Manage acute interstitial nephritis in a patient taking multiple medications.

Answer 28

Acute interstitial nephritis can be caused by NSAIDs and proton pump inhibitors in the absence of fever, rash, or eosinophilia.

Question 29

Treat a patient with diabetic kidney disease using a sodium-glucose cotransporter 2 inhibitor.

Answer 29

Sodium-glucose cotransporter 2 inhibitors slow the progression of chronic kidney disease and reduce the risk for death from kidney or cardiovascular complications in patients with diabetic kidney disease. Glucagon-like peptide-1 receptor agonists reduce the risks for cardiovascular events and hypoglycemia and appear to possibly slow chronic kidney disease progression.

Question 30

Discontinue mycophenolate mofetil in a patient who is planning pregnancy.

Answer 30

Mycophenolate mofetil is teratogenic and is contraindicated in pregnancy. In diseases in which mycophenolate mofetil is used, patients should show stable disease for 3 to 6 months following discontinuation of the agent before proceeding with pregnancy.

Question 31

Treat hyperkalemia.

Answer 31

Potassium binders such as patiromer and sodium zirconium cyclosilicate can be used to treat hyperkalemia in patients with chronic kidney disease. Use of potassium binders in patients with chronic kidney disease may allow continuation of essential medications, such as inhibitors of the renin-angiotensin system.

Question 32

Diagnose crystal-induced acute kidney injury in patients receiving intravenous acyclovir.

Answer 32

Intravenous acyclovir can cause acute kidney injury due to intratubular obstruction from acyclovir crystal precipitation. Correction of volume depletion is critical for the prevention and treatment of crystal-induced acute kidney injury.

Question 33

Manage edema associated with the nephrotic syndrome.

Answer 33

In patients with the nephrotic syndrome and refractory edema despite high-dose loop diuretics, adding a thiazide diuretic and/or a potassium-sparing diuretic is the appropriate next step in management.

Question 34

Diagnose primary hyperaldosteronism as a secondary cause of hypertension.

Answer 34

Primary hyperaldosteronism is the most common cause of secondary hypertension and should be suspected in patients with resistant hypertension, hypokalemia, family history of early-onset hypertension, blood pressure >160/100 mm Hg, or stroke at age <40 years. The plasma aldosterone concentration/plasma renin activity ratio is the recommended screening test for primary hyperaldosteronism.

Question 35

Treat autosomal dominant polycystic kidney disease with tolvaptan.

Answer 35

Tolvaptan can slow kidney function decline in adults at risk for progressive autosomal dominant polycystic kidney disease. Blockade of the renin-aldosterone system is a staple of treating patients with autosomal dominant polycystic kidney disease, including those on tolvaptan.

Question 36

Treat hepatorenal syndrome.

Answer 36

Type 1 hepatorenal syndrome is characterized by an increase in the serum creatinine level of at least 0.3 mg/dL (26.5 µmol/L) and/or ≥50% from baseline within 48 hours; bland urinalysis; and normal findings on kidney ultrasound. Treatment of type 1 hepatorenal syndrome includes vasoconstrictors and intravenous albumin.

Question 37

Treat IgA nephropathy with blockade of the renin-angiotensin system.

Answer 37

First-line therapy for IgA nephropathy is either an ACE inhibitor or an angiotensin receptor blocker. Treatment of IgA nephropathy with high-dose glucocorticoids is associated with an increased risk for adverse events and may not improve kidney function.

Question 38

Treat acute hyponatremia.

Answer 38

Acute hyponatremia developing in less than 48 hours can cause headaches, seizures, or death. Acute hyponatremia should be treated with a 100-mL bolus of 3% saline.

Question 39

Treat a hypertensive emergency with aortic dissection.

Answer 39

Intravenous short-acting β1-selective adrenergic receptor blockers are an initial first-line treatment to rapidly lower blood pressure in patients with hypertensive emergency and aortic dissection. In adults with a compelling condition (such as aortic dissection, severe preeclampsia or eclampsia, or pheochromocytoma crisis), systolic blood pressure should be reduced to <140 mm Hg during the first hour and to <120 mm Hg in aortic dissection.

Question 40

Diagnose minimal change glomerulopathy with acute kidney injury.

Answer 40

The classic presentation of minimal change glomerulopathy is sudden-onset nephrotic syndrome with abrupt appearance of edema and, eventually, anasarca. Up to 25% of adults with minimal change glomerulopathy may have acute kidney injury, with a particular risk in older patients with hypertension, low serum albumin levels, and heavy proteinuria.

Question 41

Treat hypertension in a patient with chronic kidney disease and an estimated glomerular filtration rate <30 mL/min/1.73 m2.

Answer 41

Sodium retention and volume overload are major contributory factors in the hypertension of chronic kidney disease. Loop diuretics, dosed two or three times daily, are preferred to thiazide diuretics in patients with hypertension and an estimated glomerular filtration rate <20 to 30 mL/min/1.73 m2.

Question 42

Diagnose Gitelman syndrome.

Answer 42

Patients with Gitelman syndrome typically present in late adolescence or early adulthood with low-normal blood pressure, hypokalemic metabolic alkalosis, and, frequently, hypomagnesemia and high-normal serum calcium levels.

Question 43

Diagnose alcoholic ketoacidosis.

Answer 43

Alcoholic ketoacidosis results in an increased anion gap metabolic acidosis and minimal ketones on urine dipstick analysis. Ethylene glycol, methanol, and isopropyl alcohol toxicities are associated with an increased osmolal gap.

Question 44

Evaluate kidney function with serum cystatin C measurement.

Answer 44

Increased or decreased muscle mass can alter the serum creatinine level in the absence of kidney disease. Serum cystatin C is more sensitive in identifying milder decrements in kidney function than serum creatinine.

Question 45

Diagnose renal AL amyloidosis.

Answer 45

The gold standard for pathologic diagnosis of amyloidosis is the characteristic apple-green birefringence with Congo red stain when examined under polarized light.

Question 46

Diagnose type 2 (proximal) renal tubular acidosis.

Answer 46

Type 2 (proximal) renal tubular acidosis is characterized by a normal anion gap metabolic acidosis, hypokalemia, glycosuria (without hyperglycemia), low-molecular-weight proteinuria, and renal phosphate wasting. Type 1 (hypokalemic distal) renal tubular acidosis is characterized by a normal anion gap metabolic acidosis, hypokalemia, urine pH >6.0, and calcium phosphate kidney stones.

Question 47

Identify ferric carboxymaltose as the cause of hypophosphatemia.

Answer 47

Ferric carboxymaltose, an intravenous iron preparation, has been associated with hypophosphatemia by causing renal phosphate wasting.

Question 47

Diagnose focal segmental glomerulosclerosis.

Answer 47

Focal segmental glomerulosclerosis is the most common form of the nephrotic syndrome in patients of African descent, likely mediated in part by variants in the APOL1 gene.

Question 48

Manage arginine vasopressin resistance (nephrogenic diabetes insipidus).

Answer 48

Treatment of lithium-induced arginine vasopressin resistance is best accomplished with amiloride, as it blocks the epithelial sodium channel in the collecting tubule and prevents the uptake of lithium by these cells. If amiloride is ineffective in treating lithium-induced arginine vasopressin resistance and lithium must be continued, treatment is aimed at limiting solute intake and causing mild volume depletion with the use of a thiazide diuretic.

Question 48

Manage vaccinations in a patient with chronic kidney disease.

Answer 48

Patients with chronic kidney disease and end-stage kidney disease or on hemodialysis should receive either the 20-valent pneumococcal conjugate vaccine or the 15-valent pneumococcal conjugate vaccine followed by the 23-valent pneumococcal polysaccharide vaccine. Patients with chronic kidney disease and end-stage kidney disease are at increased risk for influenza-related morbidity and mortality and should receive the influenza vaccine annually.

Question 49

Manage gross hematuria in IgA nephropathy.

Answer 49

In younger patients with IgA nephropathy, recurrent hematuria in the absence of proteinuria usually portends a benign clinical course and treatment is conservative. Recurrent gross hematuria, often occurring at the time of an upper respiratory infection or following strenuous exercise, is a common manifestation of IgA nephropathy in younger patients.

Question 50

Diagnose fibromuscular dysplasia.

Answer 50

Fibromuscular dysplasia typically occurs in young persons, particularly women <35 years of age, with the abrupt onset of hypertension. Renal artery CT angiography is the most appropriate diagnostic test to evaluate for fibromuscular dysplasia.

Question 51

Diagnose abdominal compartment syndrome.

Answer 51

Abdominal compartment syndrome is defined as a sustained intra-abdominal pressure >20 mm Hg that is associated with at least one organ dysfunction. The diagnosis of abdominal compartment syndrome can be confirmed through measurement of bladder pressure via a bladder catheter as a surrogate for intra-abdominal pressure measurement.

Question 52

Diagnose anti–glomerular basement membrane antibody disease.

Answer 52

Anti–glomerular basement membrane antibody disease is characterized by necrotizing and crescentic glomerulonephritis with linear staining for IgG on immunofluorescence. Measurement of anti–glomerular basement membrane (anti-GBM) antibodies confirm the diagnosis of anti-GBM antibody disease and are used to monitor response to treatment.

Question 53

Diagnose IgG4-related disease.

Answer 53

Patients with IgG4-related disease commonly present with a sentinel organ enlargement and dysfunction, but careful evaluation often reveals more extensive disease. Kidney involvement of IgG4-related disease typically manifests as chronic interstitial nephritis with fibrosis and dense lymphoplasmacytic infiltrate.

Question 54

Diagnose surreptitious vomiting as a cause of metabolic alkalosis.

Answer 54

Saline-responsive metabolic alkalosis presents with a low urine chloride of <15 mEq/L (15 mmol/L); the most common causes are vomiting, nasogastric suction, and diuretic use. Patients with high urine chloride (>15 mEq/L [15 mmol/L]), hypertension, and hypokalemia who do not appear to be overtly volume overloaded should be evaluated for a mineralocorticoid excess disorder (saline-resistant metabolic alkalosis) such as Cushing syndrome and primary hyperaldosteronism.

Question 55

Treat acute kidney injury due to tumor lysis syndrome.

Answer 55

Tumor lysis syndrome may spontaneously occur in patients with acute leukemia or high-grade lymphoma and is characterized by acute kidney injury with severe hyperuricemia, hyperphosphatemia, and hypocalcemia. Treatment of tumor lysis syndrome includes prompt initiation of isotonic volume expansion and rasburicase to rapidly reduce serum urate levels.

Question 56

Treat metabolic acidosis in chronic kidney disease.

Answer 56

Metabolic acidosis in patients with chronic kidney disease should be treated with alkali therapy when serum bicarbonate levels are <22 mEq/L (22 mmol/L). Repletion of bicarbonate into the normal range in patients with chronic kidney disease (CKD) attenuates the rate of CKD progression.