Free USMLE Step 2 CK Nephrology and Electrolytes practice questions

Red or orange urine is evaluated first with the dipstick heme pad, which reacts with intact red cells, free hemoglobin, and myoglobin. A negative heme pad with red or orange urine means pseudohematuria: a pigment that colors the urine without any blood or heme protein. The common causes are drugs (rifampin, phenazopyridine, nitrofurantoin, and others), foods such as beets, and porphyria. This woman started rifampin 12 days ago, and rifampin and its metabolites predictably turn urine, sweat, and tears orange to red. Her heme pad is negative, microscopy shows no red cells, the urine is otherwise bland, and kidney function and hemoglobin are normal, so no further workup is needed.

Management is reassurance and continuing therapy. Patients starting rifampin should be warned that body fluids will be discolored and that soft contact lenses can be permanently stained. This is also a good moment to review its interactions: rifampin induces hepatic enzymes and reduces the effectiveness of estrogen-progestin contraceptives, warfarin, and many other drugs, so a woman relying on hormonal contraception needs a backup method.

B. Myoglobinuria from rhabdomyolysis makes the heme pad strongly positive with few red cells, and she has no muscle pain or injury. C. Rifampin can rarely cause immune hemolysis, but free hemoglobin would also make the heme pad positive, and her hemoglobin is normal. D. Glomerular hematuria requires red cells on microscopy (at least 3 RBC/hpf), usually dysmorphic, often with RBC casts and proteinuria. E. Rifampin can cause acute interstitial nephritis, but that produces a rising creatinine and pyuria, sometimes with WBC casts, none of which is present.

This patient is in the oliguric maintenance phase of ATN, the period of greatest risk for fatal hyperkalemia. His confirmed potassium of 7.2 mEq/L is accompanied by ECG changes (peaked T waves, PR prolongation and QRS widening) and bradycardia, which signal imminent risk of a ventricular arrhythmia or asystole. The first step is always to stabilize the myocardium with IV calcium (calcium gluconate, or calcium chloride through a central line), which antagonizes the membrane effects of hyperkalemia within minutes. It does not lower the potassium, so it is followed immediately by measures that shift potassium into cells (IV insulin with glucose, nebulized albuterol) and then by removal (potassium binders, loop diuretics if he responds, or dialysis). The ECG should be repeated after the dose, which can be repeated if changes persist.

A. Insulin with dextrose lowers potassium within 15 to 30 minutes and should be given next, but it does not protect the heart as quickly as calcium in a patient with a widened QRS. B. Potassium binders remove potassium slowly, over hours, and are not the first treatment for hyperkalemia with ECG changes. D. Hemodialysis is the definitive removal therapy and is likely indicated here (refractory hyperkalemia in oliguric AKI), but arranging access and starting dialysis takes time, and the myocardium must be stabilized first. E. Sodium bicarbonate is a weak potassium-shifting agent, reserved mainly for patients with significant metabolic acidosis, and does not stabilize the cardiac membrane.

An asymptomatic patient with normal kidney function, no potassium-raising drugs, a normal ECG, and a sample reported as hemolyzed after a traumatic draw (tight tourniquet, fist clenching, small needle) most likely has pseudohyperkalemia. Potassium is released from red cells lysed during collection and from forearm muscle during repeated fist clenching, so the measured value does not reflect the true serum level. Pseudohyperkalemia can also occur with marked leukocytosis or thrombocytosis, which are absent here. The correct response is a prompt repeat sample drawn without prolonged tourniquet time or fist clenching, rather than emergency treatment; however, any ECG change or a confirmed level above 6.5 mEq/L would require immediate therapy starting with IV calcium.

A. Hyporeninemic hypoaldosteronism (type 4 RTA) usually occurs with diabetic kidney disease, causes a mild hyperkalemia with a normal anion gap acidosis, and is not suggested by a normal creatinine and bicarbonate. B. His creatinine of 0.9 mg/dL excludes kidney injury as the explanation. C. His bicarbonate is normal, so there is no acidosis to shift potassium out of cells. E. Statin rhabdomyolysis would cause muscle pain, weakness, and dark urine with a markedly elevated CK; this patient is asymptomatic with a normal examination on a long-standing statin.

This starved patient (minimal intake for 2 weeks, BMI below 16, alcohol use disorder) was fed too aggressively at 30 kcal/kg/day and now has refeeding syndrome. The carbohydrate load triggered insulin release that shifted phosphate, potassium, and magnesium into cells. Hypophosphatemia is the hallmark: depletion of ATP and 2,3-BPG explains his respiratory muscle weakness, proximal myopathy, rhabdomyolysis (elevated creatine kinase), and arrhythmia. A phosphorus below 1 mg/dL with symptoms is severe and needs intravenous phosphate. Because he is also hypokalemic and renal function is normal, potassium phosphate corrects both deficits at once, with careful monitoring of levels every few hours. Magnesium should be repleted as well, and feeding has appropriately been slowed. ASPEN consensus recommendations advise slowing the feeding rate and replacing electrolytes intravenously once refeeding syndrome develops, rather than adding more carbohydrate.

B. Dextrose is the precipitant; more glucose stimulates insulin and drives phosphate further into cells. C. Insulin is wrong for the same reason; his glucose is only mildly elevated, and insulin would worsen hypophosphatemia and hypokalemia. D. Calcium carbonate binds phosphate in the gut and is used to treat hyperphosphatemia, so it would deepen the deficit. E. Calcium gluconate is given for hypocalcemia or hyperkalemic cardiac toxicity; giving calcium with phosphate risks precipitation, and his problem is a low phosphate and low potassium, not a calcium disorder.

This patient has anti-GBM disease (Goodpasture disease): diffuse alveolar hemorrhage (hemoptysis, falling hemoglobin, bloody lavage) plus rapidly progressive GN with linear IgG staining and circulating anti-GBM antibodies directed at the alpha-3 chain of type IV collagen, which is shared by glomerular and alveolar basement membranes. Smoking is a classic trigger for lung involvement.

The disease is driven by a circulating pathogenic antibody, so treatment has two arms: remove the antibody that is already present and stop its production. KDIGO recommends starting treatment without delay in all patients with anti-GBM GN except those who are dialysis-dependent with 100% crescents and no pulmonary hemorrhage, and the regimen is plasma exchange (typically daily or every other day, usually for 14 days or until antibodies are undetectable) combined with high-dose glucocorticoids and cyclophosphamide. Plasma exchange is especially urgent with pulmonary hemorrhage, which is the main cause of early death; fresh frozen plasma is included in the replacement fluid when there is active bleeding.

A. Hemodialysis treats complications of kidney failure such as refractory hyperkalemia, acidosis, volume overload, or uremia. He is nonoliguric and euvolemic with a normal potassium, so dialysis is not indicated now and does not remove anti-GBM antibody. B. Topical bronchoscopic therapy is for focal airway bleeding; diffuse alveolar hemorrhage is a capillaritis that requires removing the antibody and immunosuppression. C. Bilateral nephrectomy was an old remedy for refractory pulmonary hemorrhage and is not part of modern management. E. Transplantation is deferred until anti-GBM antibodies have been undetectable for at least 6 months, because circulating antibody attacks the graft; it is not a treatment for active disease.

In CKD, surviving nephrons hyperfilter under high intraglomerular pressure, which drives albuminuria and progressive injury. Angiotensin II preferentially constricts the efferent arteriole, so ACE inhibitors and ARBs dilate the efferent arteriole and lower intraglomerular pressure. Filtration per nephron falls slightly, and serum creatinine rises within the first 1 to 2 weeks. This hemodynamic, protective effect is the same mechanism that reduces albuminuria and slows CKD progression, as shown by her falling UACR.

Her creatinine rose about 19%, below the roughly 30% threshold above which KDIGO advises looking for another cause (volume depletion, NSAIDs, or renal artery stenosis) and reducing or stopping the drug. Potassium is mildly higher but under 5.5 mEq/L. The correct course is to continue lisinopril, titrate it to the maximally tolerated dose, recheck creatinine and potassium in 2 to 4 weeks, and add an SGLT2 inhibitor, which causes a similar small initial dip in eGFR through afferent constriction.

A. Bilateral renal artery stenosis typically causes a larger creatinine rise (above 30%), often with resistant hypertension, flash pulmonary edema, or an abdominal bruit. C. Acute interstitial nephritis is usually caused by antibiotics, PPIs, or NSAIDs rather than ACE inhibitors and produces pyuria, WBC casts, or rash. D. Her blood pressure is 128/78 mm Hg, not low enough to cause ischemic tubular injury, and the sediment has no muddy brown casts. E. Disease progression would not produce a step change in 2 weeks coinciding with a fall in albuminuria.

Tacrolimus is metabolized by CYP3A4 and transported by P-glycoprotein in the gut and liver. Fluconazole, like other azoles (more strongly, ketoconazole, itraconazole, voriconazole and posaconazole), inhibits CYP3A4 and can raise tacrolimus levels substantially within days. Excess calcineurin inhibitor causes dose-dependent afferent arteriolar vasoconstriction, producing an acute, usually reversible rise in creatinine. Calcineurin inhibitors also cause hyperkalemia (reduced distal potassium secretion and a type 4 RTA-like state), hypomagnesemia, hypertension, tremor and, less often, thrombotic microangiopathy. The appropriate precaution is to reduce the tacrolimus dose when starting the azole when indicated and to check a tacrolimus trough level and creatinine within several days, then readjust when the azole is stopped. Other drugs that raise calcineurin inhibitor levels include clarithromycin, erythromycin, diltiazem, verapamil, protease inhibitors and grapefruit juice.

A. Rejection results from low calcineurin inhibitor levels, as with CYP3A4 inducers such as rifampin, phenytoin, carbamazepine or St John's wort, not with an inhibitor. C. Calcineurin inhibitors cause hypomagnesemia from renal magnesium wasting and hyperkalemia, the opposite of this pattern. D. Mycophenolate is metabolized by glucuronidation and is not significantly affected by fluconazole. E. Accelerated glucocorticoid metabolism and adrenal insufficiency occur with CYP3A4 inducers such as rifampin; an inhibitor would, if anything, increase prednisolone exposure.

Apply the fixed sequence. The pH of 7.34 is mildly acidemic with a low bicarbonate, so the primary disorder is a metabolic acidosis. Winter formula predicts a PaCO₂ of 1.5 x 16 + 8 = 32 plus or minus 2 (30 to 34), and the measured 31 is appropriate, so there is no separate respiratory disorder. The anion gap is 136 minus (88 + 16) = 32, a high gap from ketoacids (beta-hydroxybutyrate 7.1), consistent with DKA.

The next step is the delta ratio: (AG minus 12)/(24 minus HCO₃) = (32 minus 12)/(24 minus 16) = 20/8 = 2.5. A ratio above 2 means the bicarbonate is higher than the anion gap alone would predict, so a coexisting metabolic alkalosis is present. Three days of vomiting removed hydrogen and chloride (note the low chloride of 88), and volume contraction maintained the alkalosis. This is why the pH is only mildly low despite a very large gap; the vomiting DKA patient is the textbook example.

A. Compensation is appropriate, but stopping there misses the hidden alkalosis that the delta ratio exposes. B. A coexisting normal-gap acidosis would produce a delta ratio below 1, with a disproportionately low bicarbonate and high chloride, as can happen later during saline resuscitation. D. A respiratory acidosis would require a PaCO₂ above 34. E. A respiratory alkalosis would require a PaCO₂ below 30.