High yield! It’s the sexiest buzz word in studying for Step 2. Because time is so precious, there is little to waste. It goes without saying (but we’re going to say it anyway): the questions you are most likely to see on test day are the ones that test high-yield information. These are the UWorld questions that most students are answering correctly (not the esoteric proposed mechanism for intracellular signalling that 18% of students got right).

At this point you may be wondering… other than looking at percentages on UWorld, how do we know what is actually high-yield?

To answer this question, a select team of MST tutors have catalogued each and every UWorld and NBME Step 2 CK-driven question. The data that we gathered from it proves incredibly useful in helping our students excel on test day. Here’s a taste of what we learned from our research:

Renal pathophysiology is huge, and is often an area where students struggle. Here are the top 3 heavily tested concepts in renal diseases that we can (just about) promise you will see on your test:

USMLE Step 2 High-Yield Topic 1: Diabetic Nephropathy

Diabetes is everywhere, and it’s a growing problem. It is no surprise that the disease and its effects on every organ system are tested. This disease really takes its toll on the kidneys (specifically the glomerulus). Remember, diabetes and hypertension are the top two causes of chronic kidney disease, and they often coexist in a single patient.

Here’s what you need to know specifically: the pathophysiology involves the glomeruli. It is there that patients experience mesangial expansion, glomerular basement membrane thickening, and glomerular sclerosis. These all lead to a decreased glomerular filtration rate, and decreased GFR means failing kidneys!

How to best help your patient? Prescribe an angiotensin converting enzyme inhibitor (ACEi). This will prevent the progression of microalbuminuria, a pointed sign of glomerular damage. As we move towards a more preventative mindset, we attempt to thwart progression of the disease’s effects as soon as possible. Therefore, the best screening recommendations include frequent ophthalmologic exam for early detection of retinopathy (which can progress to blindness) and checking urine for microalbumin/creatinine ratio. A rising ratio means more damage to the delicate glomerulus.

Diabetic nephropathy occurs in relationship to both degree and temporal exposure to hyperglycemia; patients with very poor blood glucose control, and those who have had diabetes for decades are most likely to suffer from kidney damage secondary to the disease.

USMLE Step 2 High-Yield Topic 2: Analgesic Nephropathy

The number of questions on patient’s mega-dosing themselves with NSAIDs and becoming oliguric was astounding. Now, unlike diabetic nephropathy, analgesic nephropathy was usually tested as a cause of acute kidney injury. Think of the 55-year old man with worsening arthritis or low back pain who is taking increasing doses of ibuprofen after tweaking his back. That said, cases did present themselves in the chronic form – the rheumatoid arthritis patient who was taking 4g of acetaminophen and round the clock aspirin everyday for a decade.

As far as pathophysiology, the most likely finding is papillary necrosis or chronic tubulointerstitial nephritis. NSAIDs work through a decrease in prostaglandins, which is good for pain relief, but bad for keeping the afferent arterioles wide open. The chronic clamping down from the decrease of prostaglandins starves the kidney for blood and oxygen, and much of the kidney has very little reserve (e.g., renal medulla). On urinalysis, look for proteinuria, WBC casts, and hematuria, all from inflammation in the kidney itself. (As an aside, remember that pathology must be present in the kidney itself in order to get pathologic casts. Pathology in the bladder or urethra will not allow casts to form; they can only solidify in the kidney’s tubules).

What to do? Simply decrease the amount of NSAIDs and acetaminophen your patient is taking, and hope that no irreversible damage is done.

USMLE Step 2 High-Yield Topic 3: Disorders of Calcium Metabolism

The kidneys have a very special role in calcium metabolism, along with their 4 best friends, the parathyroids. The long and short is that you must have this chart memorized, and understand these relationships fully!

(From https://courses.washington.edu/conj/bess/calcium/PTH-action.png)

PTH tells the kidney to hang onto calcium and to dump phosphate. This becomes especially important in the setting of renal failure, when calcium levels drop and serum phosphate increases (this is why we give phosphate binders to patients with chronic kidney disease). These low calcium levels lead to an increase in PTH, dubbed secondary hyperparathyroidism. Signs of hypocalcemia include tetany, muscle cramps, carpopedal spasm, and weakness. Telltale physical exam maneuvers to look out for include Chvostek’s sign (twitching of facial muscles after tapping on the facial nerve) and Trousseau’s sign of latent tetany (spasm of the hand after sustained blood pressure cuff inflation).

The two biggest causes of hypercalcemia are due to factors that take place outside the kidney: primary hyperparathyroidism, in which the parathyroid glands themselves churn out the PTH, and hypercalcemia of malignancy, in which serum calcium levels can be very much elevated (think 12+ mg/dL). Go back to your classic mnemonic, “stones, bones, groans, and psychic overtones.” Hypercalcemia has an association with renal stones, bone pain, GI upset, and changes in mentation.

Remember, this is only scratching the surface of the huge field of renal pathophysiology. Honorable mention goes out to nephrotic and nephritic syndromes, which encompass a great number of distinct pathophysiologies. Expect more on this very soon…

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