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USMLE Step 1 High‐Yield Renal Topics
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Renal
High Yield USMLE Step 1 Notes
Welcome to the Renal High-Yield Notes for Step 1.
These are the most commonly tested topics on the exam—ideal for quick review in your last 2 weeks before the exam, when you’re short on time, or when you’re just starting out and want to focus on what is high yield. Created and peer-reviewed by physicians who scored 260+ on Step 1 in a Q&A style to reinforce active learning.
How to use this file
- Read the question ➔ cover the answer ➔ self-quiz before revealing.
- Review the NOTES ➔ they include high-yield details you don’t want to miss.
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- Don’t forget to watch the video lessons that go with this file. Learn more here.
Table of Contents
Congenital
1. Fusion of the kidneys at their lower poles. What prevented the kidneys from ascending to the abdomen?
➔ Inferior mesenteric artery
- Note: In a horseshoe kidney, the fused kidneys’ ascent is halted at the level of the inferior mesenteric artery. Patients are often asymptomatic but can have an increased risk of UTIs, hydronephrosis, and nephrolithiasis.
- Note: Horseshoe kidney = fusion of left and right metanephric blastemas.
- The metanephric blastema gives rise to the glomeruli, proximal tubules, loop of Henle, and distal convoluted tubules, while the ureteric bud forms collecting ducts, calyces, renal pelvis, and ureters.
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2. A 5-year-old girl with repeated episodes of fever and abdominal pain. Renal ultrasound shows dilated calyces and kidney cortical atrophy. What is the most likely cause?
➔ Reflux nephropathy
- Note: Vesicoureteral reflux (VUR) allows retrograde flow of urine from the bladder into the ureters and kidneys, leading to recurrent pyelonephritis, renal scarring, and potentially secondary hypertension if untreated.
3. A 2-day-old boy has not urinated since birth. Abdominal examination shows lower abdominal mass. What’s the likely cause?
➔ Posterior urethral valves
- Note: A congenital bladder outlet obstruction. Only in male infants. Often spotted on prenatal ultrasound, showing bladder distension or hydronephrosis (bilateral). Severe obstruction can lead to oligohydramnios and the POTTER sequence.
- In an infant, suspect if: UTI + bladder distention +/- hydronephrosis.
Acute and chronic kidney diseases
4. An elderly patient with poorly controlled HTN presents with elevated creatinine and BUN. Renal biopsy reveals hyaline deposits in small arterioles. The pathology?
➔ Hyaline arteriolosclerosis
- Note: A hallmark of chronic vascular damage, seen in long-standing hypertension or diabetes. Characterized by eosinophilic, PAS-positive material within vessel walls due to plasma protein leakage. Chronic hypertension also leads to glomerulosclerosis.
- Hyaline arteriosclerosis ➔ Diabetes or Hypertension while Hyperplastic arteriosclerosis (onion skin appearance) ➔ severe Hypertension
- Note: In a diabetic patient, ACEi can protect the kidneys from diabetic nephropathy.
5. An adult patient with fever, rash, and decreased urine output one week after starting amoxicillin for sinusitis. Urine microscopy reveals eosinophils, WBCs, and RBCs. What part of the kidney is most likely involved?
➔ Renal interstitium
- Note: Acute interstitial nephritis: A hypersensitivity reaction.
- Most important causes: β-lactams, sulfonamides, NSAIDS, and autoimmune diseases.
- Symptoms: fever, rash, eosinophilia, urinary eosinophils, WBC casts, and signs of AKI.
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6. A hospitalized patient develops oliguria two days after CPR. Urine sediment shows muddy brown casts. Which renal structure is involved?
➔ Proximal tubules
- Note: Ischemia due to hypotension ➔ tubular epithelial cell death yeilding muddy brown casts in urine, and AKI “high BUN and Cr”. The proximal tubules and thick ascending limbs are most vulnerable to ischemic injury.
- Common scenarios of Acute Tubular Necrosis:
Patient after percutaneous intervention “contrast”
Patient receiving aminoglycosides or chemotherapy (cisplatin)
7. A patient with GI bleeding develops AKI. Several days after initial oliguria, his urine output increases significantly. What electrolyte abnormality is most likely to develop during this phase?
➔ Hypokalemia
- Note: Phases of ATN:
Initiation ➔ Injury: Ischemia or toxins.
Maintenance ➔ Oliguria, ↑ Creatinine, ↑K, ↑P, Acidosis
Recovery ➔ ↑ diuresis, electrolyte wasting as K.
8. An old man with hypertension and bilateral renal artery stenosis. He is started on an ACE inhibitor. What changes?
➔ ↓ renal perfusion, ↓ intraglomerular pressure, and ↓filtration fraction
- Note: Bilateral renal artery stenosis, kidneys rely on angiotensin II to constrict the efferent arteriole and maintain glomerular pressure.
- ACEi (captopril, lisinopril) ↓ conversion of angiotensin I to angiotensin II ➔ ↓ in all downstream effects + accumulation of upstream components.
- ➔ ↓ glomerular pressure and filtration ➔ decreased renal perfusion, intraglomerular pressure, and filtration fraction.
- Note: ACEi increases bradykinin and can cause cough and angioedema.
9. An old woman undergoes gynecologic surgery. During the operation, her left ureter is accidentally injured but promptly repaired. Postoperative imaging reveals mild left-sided hydronephrosis. What urodynamic changes are expected?
➔ ↓GFR and ↓filtration fraction (FF)
- Note: Acute ureteral obstruction raises hydrostatic pressure in Bowman’s space, leading to a reduction in GFR. Although renal plasma flow (RPF) may initially be unaffected or slightly elevated, persistent obstruction causes efferent arteriolar constriction that lowers RPF over time. Since GFR falls more than RPF, the filtration fraction also decreases.
- Most asked examples are Afferent arteriole constriction “NSAIDS”, Efferent arteriole constriction “ATII”. Afferent arteriole dilation “PGs”, and Efferent arteriole dilation “ACEI”.
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| Condition | GFR | RPF | Filtration Fraction (FF) | Example |
|---|---|---|---|---|
| Afferent arteriole constriction | ↓ | ↓ | — | NSAID use (↓ prostaglandins → afferent vasoconstriction) |
| Efferent arteriole constriction | ↑ | ↓ | ↑ | Angiotensin II effect (or ACE inhibitor withdrawal) |
| ↑ Plasma protein concentration | ↓ | — | ↓ | Multiple myeloma (increased serum proteins) |
| ↓ Plasma protein concentration | ↑ | — | ↑ | Nephrotic syndrome (hypoalbuminemia) |
| Constriction of ureter | ↓ | — | ↓ | Kidney stone causing urinary tract obstruction |
| Dehydration | ↓ | ↓↓ | ↑ | Severe vomiting or diarrhea leading to volume depletion |
10. An old man with back pain has normocytic anemia and ↑ creatinine. Serum calcium level is ↑. Renal biopsy shows tubular casts with eosinophilic staining. What is the most likely diagnosis?
➔ Multiple myeloma
- Note: Old patient + Bone pain (or fracture) + normocytic anemia + ↑ creatinine + ↑ calcium ➔ Multiple myeloma
Diagnose: Monoclonal paraproteinemia (M-spike) - In MM, monoclonal light chains precipitate in tubules, causing obstructive casts and kidney injury.
11. A young patient is admitted after trauma with massive hemorrhage. After one day, the patient has high BUN and decreased Urine volume. What lab finding confirms prerenal azotemia?
➔ Urine sodium < 20 mEq/L
- Note: Differentiate prerenal AKI (↓ RPF) from ATN (ischemia or toxins):
Prerenal AKI ➔ BUN/CR > 20, Urine Na+ < 20, Hyaline casts
ATN ➔ BUN/CR ~ 10-15, Urine Na+ > 20, Muddy brown casts - Note: When you see abnormal BUN and Cr in USMLE ➔ calculate the ratio to narrow the differential diagnoses.
12. A man, after a prolonged seizure, becomes oliguric. Labs reveal ↑ creatinine and positive blood on urine dipsticks without RBCs. What is the mechanism?
➔ Tubular injury due to rhabdomyolysis
- Note: Rhabdomyolysis: Crush injury, seizure, statin, heroin
↑ creatinine + ↑K, ↑P, ↓Ca + myoglobinuria (In urine: blood +, RBC −) - A common scenario: an IV drug user or alcohol abuser, found unresponsive by relatives. Learn the lab findings, they are very high yield.
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Electrolyte and acid-base imbalance
13. An ESRD patient presents with muscle cramps and tingling in his fingers. Serum calcium level is 6.5 mg/dL. What other electrolyte imbalance will be seen?
➔ Hyperphosphatemia
- Note: CKD ➔ ↓ phosphate excretion ➔ hyperphosphatemia ➔ binds free calcium ➔ ↓ serum calcium levels ➔ secondary ↑PTH ➔ ↑Pathologic fractures, and bone pain.
- Hypocalcemia: Neuromuscular irritability (Trousseau and Chvostek signs), ↑QT, and seizure.
- Another common scenario for Hypocalcemia is after thyroidectomy ➔ excision of the parathyroids ➔ ↓PTH ➔Hypocalcemia
Hints for electrolytes abnormalities:
- Note: Weakness + arrhythmia ➔ think of potassium
- Note: Spasticity + arrhythmia ➔ think of calcium
- Note: resistant hypocalcemia / hypokalemia ➔ think of hypoMagnesemia ➔ administer Mg
14. An old man with CKD. His serum calcium is high and PTH level is high. What’s the diagnosis?
➔ Tertiary hyperparathyroidism
- Note: Tertiary hyperparathyroidism: long standing secondary hyperparathyroidism ➔ autonomous parathyroid gland hyperplasia ➔ persistent PTH elevation even after correction of phosphate and calcium levels.
- Result: Very high PTH with hypercalcemia and hyperphosphatemia.
| Feature | Secondary HPT | Tertiary HPT |
|---|---|---|
| Cause | Response to CKD-induced hypocalcemia | Autonomous PTH secretion after prolonged stimulation |
| PTH | Increased | Greatly increased |
| Calcium | Low or normal | High |
| Phosphate | High | High |
15. An old patient with a history of heart failure presents with worsening lower extremity swelling and shortness of breath (signs of decompensated heart failure). The diuretic used primarily acts on which nephron segment?
➔ Thick ascending limb of Henle’s loop
- Note: Signs of decompensated heart failure (left-sided) ➔ volume overload, pulmonary edema, and peripheral edema. ➔ Treat with loop diuretics
| Site of Action | Drug Class | Example | Main Uses | Major Side Effects |
|---|---|---|---|---|
| Proximal Tubule | Carbonic Anhydrase Inhibitors | Acetazolamide | Glaucoma, altitude sickness, metabolic alkalosis | Metabolic acidosis |
| Descending Limb of Henle & Proximal Tubule | Osmotic Diuretics | Mannitol | Cerebral edema, increased intraocular pressure | Worsens HF |
| Thick Ascending Limb of Henle | Loop Diuretics (Na+/K+/2Cl− blocker) | Furosemide | Pulmonary edema, heart failure, hypercalcemia | Hypokalemia, hypomagnesemia, hypocalcemia, ototoxicity |
| Distal Convoluted Tubule | Thiazide Diuretics Block NaCl reabsorption | Hydrochlorothiazide | Hypertension, calcium stone prevention, mild heart failure, nephrogenic diabetes insipidus | Hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia |
| Collecting Duct | Potassium-Sparing Diuretics | Amiloride, Spironolactone | Heart failure, hyperaldosteronism, prevention of hypokalemia | Hyperkalemia; Spironolactone: gynecomastia, antiandrogen effects |
16. A young man is brought to the emergency department due to confusion and lethargy. Arterial blood gas shows pH 7.54, PaCO₂ 49 mm Hg. What’s the next step in diagnosis?
➔ Urine chloride
- Note: pH > 7.45 ➔ Alkalosis. Next look at HCO3 and PaCO2.
Metabolic Alkalosis ➔ main problem: ↑HCO3, Compensation: ↑PaCO2
Respiratory Alkalosis ➔ Main problem: ↓PaCO2, Compensation: ↓HCO3 - In case of metabolic alkalosis, we want to check if the kidney response is normal or not.
Normal kidney response ➔ Low Urine chloride (<20 mEq/L) to normalize the serum pH.
○ Seen in: Vomiting, diuretic overuse, nasogastric suctioning. (Think volume loss) - Abnormal kidney response ➔ High Urine chloride (>29 mEq/L). Kidney is losing Cl–, resulting in alkalosis.
○ Think mineralocorticoid excess (hyperaldosteronism, Cushing’s)
17. An old man with a history of heavy smoking presents with weakness, hypercalcemia (Ca²⁺ 14 mg/dL), and 2 months history of cough. What can we see in the lab results?
➔ ↓ PTH, ↑PTHrP, ↓Phosphate, Squamous cell carcinoma of lung
- Note: In most cases of hypercalcemia, you’ll be able to diagnose based on the history:
Chronic cough ➔ lung problems (sarcoidosis or Squamous carcinoma of lung).
Heavy smoking➔ Squamous carcinoma of lung producing PTHrP. - PTHrP has all the effects of PTH (↑calcium, ↓phosphate), while in a negative response, PTH ↓.
18. An old man with back pain, Cr: 3, and Hb: 9. The calcium level is 12. What’s the mechanism of hypercalcemia?
➔ Calcium release from bone
- Note: Hypercalcemia of Malignancy:
- Bone Metastases: Seen in a lot of cancers. Remember multiple myeloma as a high yield cause. Associated with bone pain, fractures, and lytic bone lesions. Lab findings: ↓ PTH, ↓ PTHrP, ↓ Vitamin D
- PTHrP Secretion: Squamous cell lung carcinoma and renal cell carcinoma commonly secretes PTHrP, mimicking PTH and causing hypercalcemia. Lab findings: ↓ PTH, ↑ PTHrP
- Overactivation of Vit D: Seen in lymphoma (also in sarcoidosis). Vitamin D activation ➔ ↑ intestinal calcium absorption. Lab findings: ↓ PTH, ↑ 1,25 (OH)2 Vit D, normal 25OH Vit D
19. A 59-year-old man with diabetes and hypertension experiences a mild rise in serum creatinine and potassium three weeks after starting a new medication. Which drug is most likely responsible?
➔ Lisinopril
- Note: ACE inhibitors (e.g., lisinopril) inhibit angiotensin II formation, preventing efferent arteriole constriction. This reduces GFR slightly, leading to mild creatinine rise and potential hyperkalemia.
- It’s usually expected and tolerated unless creatinine rises by >30%. If the rise is > 30% ➔ think about a narrowing in renal artery (keyword is abdominal bruit)
20. A patient is found severely dehydrated. Where in the nephron does the majority of water reabsorption occur?
➔ Proximal tubule
- Note: Proximal tubule (PT) ➔ Majority of water and electrolyte resorption (PT doesn’t care about serum concentration, just absorbs water)
- Collecting duct (under the effect of ADH) ➔ controls the urine and serum concentration.
21. A patient with a history of major depressive disorder presents with altered mental status. Labs show PaCO₂ = 13, HCO₃⁻ = 10, and pH = 7.34. What is the likely acid-base disturbance?
➔ Metabolic acidosis and respiratory alkalosis
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- Note: Giving This patient psychologic disorder plus thinking of suicide makes us think of poisoning, most likely Salicylate poisoning.
- Salicylate poisoning is a very high-yield mixed acid-base disorder: direct stimulation of respiratory centers leads to respiratory alkalosis, and increased salicylic acid accumulation leads to anion-gap metabolic acidosis. A keyword for salicylate poisoning is ringing in the ear.
- Interpretation of arterial blood gas:
This patient has a mild acidosis, and the HCO₃⁻ is very low. ➔ Metabolic Acidosis.
In metabolic acidosis, we want to calculate the expected PaCO₂ to check whether respiratory compensation is appropriate. Here’s the formula:Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
Expected PaCO2 in this patient is (1.5 × 10) + 8 ± 2 = 23 ± 2
But the current PaCO2 is much lower ➔ There’s also an underlying respiratory alkalosis.
22. A young woman with asthma uses excessive doses of albuterol before arriving at the hospital in respiratory distress. Labs show hypokalemia. What is the most likely mechanism
➔ Intracellular shift of potassium
- Note: Intracellular translocation of potassium (shift into cells):
- Insulin (eg, after DKA treatment, refeeding syndrome)
- Beta-adrenergic stimulation
○ Pharmacologic (e.g., albuterol in asthma treatment, dobutamine)
○ Stress (e.g., alcohol withdrawal, acute MI) - Alkalosis (respiratory or metabolic)
- Increased cell production (e.g., acute leukemia, GM-CSF stimulation)
Causes of hypokalemia (other than shift into cells):
- Gastrointestinal loss:
○ Diarrhea, vomiting, hyperaldosteronism - Urinary loss:
○ Hyperaldosteronism, diuretics, renal tubular acidosis (RTA) types 1 and 2
23. A 21-year-old patient with weakness. She has hypokalemia and metabolic acidosis on lab results. She is worried about her appearance and wants to lose weight. BMI = 20. What’s the cause of hypokalemia?
➔ Self-induced diarrhea (e.g., polyethylene glycol overuse.)
- Note: In case of eating disorder: diarrhea, vomiting, and diuretics can be self-induced.
- Common scenarios of hypokalemia:
○ A hospitalized asthma patient, after taking a lot of albuterol ➔ Intracellular shift
○ A patient with severe diarrhea ➔ Gastrointestinal loss
○ A new-onset hypertension with hypokalemia ➔ Think of hyperaldosteronism (RAAS activation)
○ A Diabetic ketoacidosis patient, receiving insulin ➔ Intracellular shift - Common scenarios for hyperkalemia:
○ Patient with chronic kidney disease
○ Patient after chemotherapy (Tumor lysis syndrome: hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia)
○ Rhabdomyolysis
24. A 6-year-old kid with vomiting and abdominal pain, and has a severe high-anion-gap metabolic acidosis. BS = 300. Which electrolyte should we be careful about?
➔ Potassium
- Note: Diabetic ketoacidosis (DKA): BS>250, High anion gap metabolic acidosis, and ketonuria. Due to acidosis and decreased insulin, potassium shifts outside the cells in DKA. Ultimately, all DKA patients have low potassium content, but almost all have hyperkalemia in their lab results.
- When treating the DKA with Insulin, we must be aware that insulin will shift potassium back to the cells and result in hypokalemia ➔ Give IV potassium
25. A patient has tall T waves on ECG after receiving chemotherapy for CLL. What’s the next step?
➔ IV Calcium (This is a case of hyperkalemia after tumor lysis syndrome.)
- Note: ECG findings in hyperkalemia: Peaked T wave, Prolonged QRS, Sine wave
Treatment of Hyperkalemia:
1- Prevent arrhythmia by stabilizing the myocytes ➔ IV Calcium (doesn’t affect the level of K)
2- Shift K into cell:
○ Insulin
○ Beta-adrenergic (albuterol)
○ Treat underlying acidosis
3- Excrete K:
○ Into Urine: Diuretic (most commonly loop-diuretics)
○ Into the intestine: Kayexalate, Patiromer
○ Hemodialysis
26. A malnourished man with a history of alcohol use is treated with dextrose-containing fluids. A few hours later, he develops profound muscle weakness. Phosphate = 0.4. What explains his hypophosphatemia?
➔ Redistribution of phosphate into hepatic and muscle cells
- Note: In refeeding syndrome, increased insulin after carbohydrate intake drives phosphate into cells for ATP production, resulting in a dangerous drop in serum phosphate, Mg, and K levels. Treat with IV phosphate.
- Another common scenario for refeeding syndrome is in hospitalized anorexia nervosa patients.
- In alcoholic patients receiving dextrose ➔ Also be careful about Vit B1 deficiency.
27. A patient with persistent vomiting for one week. Dry mucous membranes and delayed capillary refill. Which electrolyte abnormalities are most likely present?
➔ Hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis
- Note: Severe vomiting leads to volume depletion, activation of RAAS, and loss of H⁺, K⁺, and Cl⁻. This causes hypokalemic, hypochloremic metabolic alkalosis. Management includes chloride repletion with saline and addressing the underlying cause.
- Remember: Urine chloride is low in these patients.
28. A patient with gastroenteritis develops watery diarrhea for 3 days. What type of acid-base disturbance do we expect?
➔ Normal anion gap (hyperchloremic) metabolic acidosis
- Note: Diarrhea leads to direct loss of bicarbonate from the GI tract, causing a metabolic acidosis with a normal anion gap. Chloride concentration increases in response (hyperchloremic metabolic acidosis).
29. A young man is brought to the emergency department with confusion. Labs show pH 7.25, bicarbonate 12 mEq/L, PaCO₂ 28 mm Hg, sodium 136 and Chloride 90. What is the most likely acid-base disorder?
➔ Anion gap metabolic acidosis
- Note: A low pH and low bicarbonate indicate metabolic acidosis.
If you see metabolic acidosis, calculate the anion gap (Na+ – (HCO3– + Cl–)).
- Normal anion gap: there’s a problem with HCO3– or Cl–
○ Diarrhea, renal tubular acidosis - High anion gap: The serum has an unmeasured acid (other than HCO3– and Cl–).
○ Uremia, lactic acidosis, ketoacidosis, and toxins
30. A 2-year-old boy with poor weight gain, frequent urination, and laboratory findings of glucosuria, hypophosphatemia, hypokalemia, and a normal anion gap metabolic acidosis. Which structure/function defect?
➔ Proximal convoluted tubule — reabsorption of bicarbonate
- Note: Proximal renal tubular acidosis (type 2) results from impaired bicarbonate reabsorption in the proximal convoluted tubule, leading to metabolic acidosis, glucosuria, phosphaturia, and growth failure (Fanconi syndrome mimics type 2 RTA).
- Tip: A child with growth retardation + normal anion acidosis ➔ Think of RTA
- All types cause non-anion gap metabolic acidosis. Use K+ and Urine PH to differentiate.
| Type 1 (Distal) | Type 2 (Proximal) | Type 4 | |
|---|---|---|---|
| Defect | ↓ H⁺ secretion | ↓ HCO₃⁻ reabsorption | Aldosterone resistance or ↓ secretion |
| Serum K⁺ | Low | Low | High |
| Urine pH | > 5.5 | < 5.5 | Variable |
31. A 72-year-old woman with a history of epilepsy has confusion, nausea, and headache. Labs show severe hyponatremia and concentrated urine. Which medication for treatment?
➔ Carbamazepine
- Note: Syndrome of inappropriate anti-diuretic hormone (SIADH) causes hyponatremia with low serum osmolality and concentrated urine. Clinical signs include confusion, nausea, and euvolemia (no edema or JVD).
- Note: SIADH → Low serum osmolality, high urine osmolality, and high urine sodium.
- It can result from CNS disease as hemmorage or tumors, drugs (carbamazepine, SSRIs), lung infection, or cancer (small-cell lung carcinoma).
Tip: Any form of CNS or Lung pathology + hyponatremia ➔ think of SIADH
32. A patient with constant thirst and excessive urination. Urine osmolality is low. Water deprivation testing shows minimal increase in urine osmolality, but a sharp rise occurs after desmopressin administration. What is the most likely diagnosis?
➔ Central diabetes insipidus (insufficient ADH production)
- Note: Diagnosing a patient with polyuria and polydipsia:
1- Check Urine osmolality: it should be low because the patient produces a lot of urine with a small amount of electrolyte.
2- Water deprivation: if water deprivation ↑, urine osmolality → Primary polydipsia → Treat with water deprivation. No need for next steps
3- Administer Vasopressin: If vasopressin ↑ urine osmolality → Central DI (↓ ADH production) → Treat with Vasopressin (synthetic ADH).
4- If nothing works: Nephrogenic DI (important risk factor: lithium use) → Treat with Thiazide diuretics
Glomerular diseases
33. A 9-year-old boy with cola-colored urine and puffiness around his eyes. BP is 135/85 mmHg. Urinalysis shows +1 protein, many RBCs, and RBC casts. Most likely diagnosis?
➔ Poststreptococcal glomerulonephritis (PSGN)
- Note: Poststreptococcal glomerulonephritis: 2–4 weeks after a streptococcal throat or skin infection. It presents with nephritic syndrome (hematuria with RBC casts, mild proteinuria, edema, hypertension).
- Labs often show low C3 complement levels. Histology reveals hypercellular glomeruli and subepithelial “humps” on electron microscopy, which represent immune complex deposits.
- Differentiate from IgA nephropathy:
○ Post-streptococcal GN: Type III hypersensitivity, subepithelial humps, starry sky IF. More than 2 weeks after tonsillitis or skin infection. ↓Complement levels. Anti-ASO +.
○ IgA Nephropathy (Berger Disease): Mesangial proliferation, IgA deposits, less than 1 week after Upper resp / GI infection. Often in adults. Normal C3 & C4
34. A 17-year-old boy, episodes of painless gross hematuria a few days after mild upper respiratory infections. Renal biopsy=mesangial proliferation. Most likely microscopic finding?
➔ Mesangial deposition of IgA
- Note: IgA nephropathy (Berger disease) is the most common cause of recurrent painless hematuria in young adults, often triggered by respiratory infections.
- It shows mesangial hypercellularity and IgA deposits on immunofluorescence microscopy. It can also be part of Henoch–Schönlein purpura.
35. A 25-year-old man with hemoptysis and worsening dyspnea a few weeks after a flu-like illness. Urinalysis: hematuria and proteinuria. Chest CT: bilateral alveolar infiltrates. Autoantibodies are found against which structure?
➔ Alpha-3 chain of type IV collagen
- Note: Goodpasture syndrome involves autoantibodies against the alpha-3 chain of type IV collagen found in the glomerular and alveolar basement membranes.
- It causes rapidly progressive glomerulonephritis and pulmonary hemorrhage. Immunofluorescence shows linear IgG and C3 deposition along the glomerular basement membrane (GBM). Crescent formation.
36. A 6-year-old boy with generalized body swelling and frothy urine. Periorbital and lower extremity edema. Urinalysis reveals 4+ proteinuria without hematuria. The cholesterol level is high. What’s the cause?
➔ Increased liver lipoprotein synthesis
- Note: Minimal Change Disease: The most common nephrotic syndrome in children, effacement of foot processes, responds to steroids. T-cells are involved. It is normal on light microscopy. “Loss of negative charge” and “podocyte foot process fusion” are two important keywords.
- In nephrotic syndromes, we have Podocyte damage → massive proteinuria (>3.5 g/day) → hypoalbuminemia → edema (↓oncotic pressure). Also they have hyperlipidemia.
37. A 64-year-old man with type 2 diabetes presents for routine follow-up. Labs show normal creatinine but elevated urinary albumin excretion. What medication should be started to prevent the progression of his kidney disease?
➔ ACE inhibitor (A case of early diabetic nephropathy characterized by microalbuminuria)
- Note: Diabetic nephropathy pathology: Hyperfiltration → glomerular hypertrophy with ↑GFR → Mild albuminuria and arteriolar hyalinosis → Deposits of Kimmelstiel-Wilson nodules in glomerular capillaries.
- ACE inhibitors ➔ ↓ intraglomerular pressure ➔ ↓ albuminuria and slowing progression to end-stage renal disease.
- In diabetic patients, for early detection of kidney disease → 24-hour Urine Albumin.
If you see Diabetic nephropathy → Screen for retinopathy.
38. A 25-year-old woman with a history of systemic lupus erythematosus (SLE) presents with weight gain, facial puffiness, and proteinuria. Kidney biopsy shows thickening of glomerular capillary walls with subepithelial spikes. What is the most likely diagnosis?
➔ Membranous nephropathy
- Note: Membranous Nephropathy: Thickened capillary walls, subepithelial “spike and dome,” associated with solid tumors, HBV, HCV, and SLE.
- Biopsy shows diffuse capillary wall thickening and “spike and dome” appearance due to subepithelial immune deposits.
39. A 56-year-old man develops worsening lower extremity edema and facial puffiness. Kidney biopsy shows apple-green birefringence under polarized light with Congo red staining. What test would best confirm the underlying diagnosis?
➔ Serum protein electrophoresis (biopsy: Amyloidosis)
- Note: Other amyloidosis related to the kidney:
○ ESRD patient on dialysis → ↓clearance of β2-Microglobulin → Amyloidosis
○ Patient with rheumatoid arthritis or multiple myeloma(chronic inflammation) → nephrotic syndrome. It can also cause Carpal tunnel syndrome + shoulder pain.
40. An adult man with a history of hepatitis C infection has generalized edema and proteinuria. Renal biopsy reveals diffuse glomerular hypercellularity and capillary wall thickening. Immunofluorescence shows granular staining for IgG and C3. Most likely diagnosis?
➔ Membranoproliferative glomerulonephritis (MPGN)
- Note: Summary of serologic evaluation in Glomerulonephritis:
- Complement is low (immune complex-mediated GN):
○ Lupus nephritis: Positive ANA, anti-dsDNA antibodies.
○ Membranoproliferative GN: tram track sign, anti-HCV antibodies.
○ Infection-related GN: Poststreptococcal GN: Positive ASO titers
- Complement is normal (antibody-mediated GN):
○ Goodpasture disease: Positive anti-GBM antibodies.
○ Pauci-immune GN (GPA, MPA, EGPA): Positive ANCA.
Urinary tract tumors
41. A heavy smoker with painless hematuria. Urinalysis confirms blood, and urine cytology shows malignant cells. Cystoscopy reveals a bladder mass. What histologic finding is most associated with poor prognosis in this patient?
➔ Involvement of the muscularis propria
- Note: Diagnosis of bladder cancer:
Painless hematuria (especially in patients with risk factors) → U/A (confirm hematuria) → Urine cytology → Cystoscopy - Penetration into the muscularis propria (muscle layer) indicates a higher stage (T2 or greater) and is associated with a poor prognosis in bladder cancer.
- Risk factor: Smoking and cyclophosphamide.
42. An old man with weight loss, fever, and chest pain. Imaging shows multiple lung nodules. Biopsy of a nodule shows clear cytoplasm and polygonal cells. Which organ is primary site?
➔ Kidney
- Note: Clear cells with lipid/glycogen accumulation. Golden-yellow gross appearance.
- Paraneoplastic syndromes: PTHrP (hypercalcemia), EPO (polycythemia), ACTH, and Renin. Associated with VHL gene (chromosome 3).
- Renal cell carcinoma often metastasizes to the lungs.
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Kidney stones
43. A young man with sudden, severe left-sided flank pain radiating to the groin. He has gross hematuria but no fever. Imaging reveals a small stone in the mid-ureter. What laboratory finding is most likely?
➔ Normocalcemia, hypercalciuria
- Note: Flank pain radiating to the groin w/o hematuria suggests kidney stones.
- Calcium stones (calcium oxalate/phosphate) are the most common kidney stones. Most patients have idiopathic hypercalciuria but normal serum calcium levels
- Envelope-shaped casts.
44. Patient with renal colic is found to have a calcium-oxalate stone. Which drug can lower the risk of stone formation?
➔ Hydrochlorothiazide (Thiazide diuretics lower the calcium in urine)
- Note: Risk factors for calcium stones:
- Hypercalciuria → Hyperparathyroidism, idiopathic Hypercalciuria
- Hyperoxaluria → fat malabsorption (crohn’s disease): calcium binds fat → ↑ free oxalate absorption in gut→ calcium-oxalate stones in the kidney
- Loop diuretics (↑ calcium in urine)
Preventive:
- ↓ sodium, protein, and oxalate intake
- Thiazide diuretics (↓ calcium in urine)
- ↑Fluid intake reduces the risk of kidney stones regardless of stone type.
45. A 55-year-old woman with a history of recurrent urinary tract infections has fever, dysuria, and right flank pain. Imaging reveals a large staghorn calculus. What infection is most likely involved?
➔ Klebsiella infection
- Note: Causes of Staghorn calculi:
- Struvite (Ammonium magnesium phosphate) → radiopaque, coffin-lid shape.
Caused by urease + bacteria (Proteus and Klebsiella). Treatment: eradicate infection, surgery. - Cystine → faintly radiopaque, hexagonal shape. Defect in COLA transporter (cysteine, ornithine, lysine, and arginine).
- Treatment: low-sodium diet, alkalinization, chelators.
46. A 46-year-old woman with a history of ileostomy presents with dehydration and right flank pain. She spontaneously passes a uric acid stone. What is the most likely mechanism leading to stone formation?
➔ Concentrated acidic urine
- Note: Uric acid stones → radiolucent, rhomboid/rosette-shaped.
○ Risk: low pH, hyperuricemia (gout, leukemia).
○ Treatment: alkalinization and allopurinol.
- Common scenarios:
○ A patient with leukemia undergoing chemotherapy → Tumor lysis syndrome
○ Pretreatment with hydration, allopurinol, and rasburicase
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47. A young woman with a burning sensation during urination and increased urinary frequency. She denies fever, flank pain, or vomiting. Urinalysis shows pyuria and bacteriuria. What is the most appropriate initial pharmacologic treatment?
➔ Empiric antibiotic therapy with trimethoprim-sulfamethoxazole
- Note: Acute cystitis is an infection of the urinary bladder typically presenting with dysuria, suprapubic pain, urinary frequency, and urgency, but without systemic symptoms like fever or chills.
- Risk factors include female sex (short urethra), sexual activity, indwelling catheters, diabetes mellitus, and impaired bladder emptying.
- Common pathogens:
○ Escherichia coli (most common), Staphylococcus saprophyticus (especially in sexually active women), Klebsiella, Proteus mirabilis (urine may smell like ammonia). - Urinalysis: Positive leukocyte esterase (WBCs) and nitrites (Enterobacteriaceae).
- Treatment: Empirical antibiotics such as trimethoprim-sulfamethoxazole (TMP-SMX) or nitrofurantoin.
48. An old diabetic woman has fever, chills, flank pain, and nausea. On examination, she has costovertebral angle tenderness. Urinalysis shows white blood cell casts, pyuria, and bacteriuria. What is the most likely diagnosis?
➔ Acute pyelonephritis
- Note: Acute pyelonephritis is an infection of the renal parenchyma, characterized by neutrophilic infiltration of the interstitium and cortex.
- Risk factors:
○ Urinary tract obstruction, Indwelling catheter, Diabetes mellitus, and Pregnancy (progesterone-mediated ureteral tone reduction). - Urinalysis: Pyuria (WBCs in urine) with or without white blood cell casts (WBC casts indicate renal involvement).
49. A 45-year-old man presents with flank pain and blood in the urine. He has a history of hypertension. Imaging reveals multiple fluid-filled cysts in both kidneys. What is the most likely diagnosis?
➔ Autosomal dominant polycystic kidney disease (ADPKD)
- Note: ADPKD is due to mutations in PKD1 or PKD2 and manifests with renal cysts, hypertension, and hematuria. Patients often remain asymptomatic until adulthood, when cyst growth causes renal impairment.
- Extra-renal features include liver cysts and cerebral aneurysms.
- ADPKD (autosomal dominant) → Adult onset. ARPKD (autosomal recessive) → childhood onset (dies early, detectable with ultrasound during pregnancy)
50. A 23-year-old pregnant woman undergoes a 20-week ultrasound that shows a male fetus with massively enlarged, cystic kidneys and severe oligohydramnios. What neonatal complication is most likely at birth?
➔ POTTER sequence
- Note: Autosomal recessive polycystic kidney disease (ARPKD) causes impaired fetal urine output, leading to oligohydramnios.
- Oligohydramnios results in POTTER sequence: pulmonary hypoplasia, limb deformities, and facial anomalies.
- POTTER sequence scenarios (anything that results in ↓ fetal urine): ARPKD, posterior urethral valves, in utero ACEi exposure.
51. A 22-year-old man with sudden gross hematuria after minor physical activity. He has no fever, dysuria, or previous episodes, but has a family history of sickle cell disease. What is the most likely cause?
➔ Renal papillary necrosis
- Note: Necrotic renal papillae due to ↓blood flow or arterial occlusion → gross hematuria. it is common in sickle cell disease and NSAID.
- Note: Sickle cell traits are mainly asymptomatic, but there’s a high chance of necrotic renal papillae.
52. A 46-year-old man with difficulty urinating after undergoing laparoscopic hernia repair under general anesthesia. Ultrasound shows a post-void residual volume of 300 mL. What medication would help improve this patient’s bladder emptying?
➔ Bethanechol
- Note: Atonic bladder after surgery:
○ Postoperative urinary retention is common after surgery due to bladder overdistension and detrusor underactivity.
○ Bethanechol, a muscarinic cholinergic agonist, stimulates bladder detrusor muscle contraction (M3 receptor) and improves bladder emptying.
53. A menopause woman with urgency and incontinence episodes. Has to rush to the bathroom, but has incontinence on the way to the bathroom. What pharmacologic action is the best treatment?
➔ Antagonism of muscarinic cholinergic receptors
- Note: Urge incontinence: Due to detrusor muscle overactivity (Upper motor neuron sign); presents as sudden strong urge to urinate.
○ Treated with antimuscarinic drugs (e.g., oxybutynin) to block M3 receptors or by stimulating beta-3 adrenergic receptors (eg, mirabegron).
54. A 45-year-old man with a history of poorly controlled type 1 diabetes reports frequent episodes of involuntary urine leakage and difficulty starting urination.
What would most likely be found on further evaluation?
➔ Increased postvoid residual volume
- Note: Overflow incontinence: Due to impaired bladder emptying, causes constant dribbling and feeling of incomplete voiding.
- Common risk factor: long standing Diabetes and Benign prostatic hyperplasia
○ Treat with intermittent catheterization.
55. A 50-year-old woman with a urinary leakage while coughing or laughing. What is the most likely underlying cause of her condition?
➔ Urethral sphincter dysfunction (or pelvic floor muscle weakness)
- Note: Stress incontinence: Due to weak sphincter or hypermobile urethra (due to weak Levator ani muscle complex). Triggered by increased intra-abdominal pressure (eg, coughing).
○ Risk factor: vaginal delivery and postt menopausal state.
○ Treat with Kegel exercises or a sling supporting the pelvic floor.
56. A young man presents to the emergency department after falling from a height. He has tenderness over his suprapubic area. FAST ultrasound shows intraperitoneal free fluid. His urine dipstick is positive for blood. What injury is most likely present?
➔ Bladder dome rupture
- Note: Bladder dome rupture occurs with blunt trauma when the bladder is distended. The dome is covered by peritoneum, so rupture leads to intraperitoneal urine leakage, seen as free fluid on imaging.
- Suprapubic tenderness and hematuria support the diagnosis.
57. A 28-year-old woman with new-onset severe hypertension dies from an intracranial hemorrhage. Autopsy reveals tortuous carotid arteries with alternating stenosis and dilation.
What vascular abnormality is most likely responsible for her condition?
➔ Fibromuscular dysplasia causing renal artery stenosis
- Note: The findings are classic for fibromuscular dysplasia (FMD), which affects young women (<55 years) and features fibrous webs and aneurysmal dilation of medium-sized arteries.
- Cerebrovascular involvement can result in stroke or aneurysm rupture. Renal artery involvement leads to resistant hypertension by activating the RAAS.
- Renal artery stenosis (Hypertension + abdominal bruit ± hypokalemia):
1- Atherosclerotic: in men, smoking, hyperlipidemia, >40-years-old
2- Fibromuscular dysplasia: women w/o risk factor for atherosclerosis, <40-years-old
58. A patient with new-onset edema has a urinalysis that shows casts with a “Maltese cross” appearance under polarized light. What is the most likely diagnosis?
➔ Nephrotic syndrome
- Note: Commonly Tested casts in USMLE
○ Presence of casts → renal or glomerular origin.
○ RBC casts: Glomerulonephritis, hypertensive emergency.
○ WBC casts: Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.
○ Granular casts: Acute tubular necrosis (ATN); “muddy brown” appearance.
○ Fatty casts: Nephrotic syndrome; associated with “Maltese cross” sign.
○ Waxy casts: End-stage renal disease/chronic kidney disease.
○ Hyaline casts: Nonspecific; seen with dehydration, exercise, diuretics.
○ No casts in hematuria/pyuria from bladder cancer, kidney stones, or cystitis.
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Disclaimer
Version 1.0 May 2025. No part of this document may be reproduced or distributed without written permission. For personal study only. Medical information herein is for educational purposes and does not constitute clinical advice. Always confirm with current guidelines and your institution’s policies.
Prefer a narrative review instead of Q&A style? Scroll down to the section below for high-yield concepts in paragraph format (they cover the same concepts).
Narrative Format
High-Yield Renal Topics
High-yield Renal review for USMLE Step 1. Master kidney development, function, acid-base, electrolytes, diuretics, stones, AKI, CKD, glomerulonephritis, and key testing points.
Table of Contents
- Urinary tract development
- Congenital Abnormalities
○ Vesicoureteral Reflux (VUR) - Nephron Transport
○ Endocrine Functions of the Kidney
○ Renin Angiotensin Aldosterone System (RAAS)
○ High Yield Electrolyte Disturbance symptoms - Casts in Urine
○ Kidney Stones
○ Hydronephrosis
○ Urinary Incontinence - Acute Cystitis
○ Pyelonephritis
○ Acute Kidney Injury - Acute Interstitial Nephritis
- Acute Tubular Necrosis
- Renal Papillary Necrosis
- Polycystic Kidney Diseases
- Renovascular Disease
- Renal Cell Carcinoma
- Bladder Cancer
- RAAS Inhibitors
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Urinary tract development
- Metanephros: Permanent kidney; appears in week 5, nephrogenesis completes by week 36.
○ Ureteric bud (metanephric diverticulum): derived from mesonephric duct → forms ureter, renal pelvis, calyces, collecting ducts.
○ Metanephric mesenchyme (metanephric blastema): Ureteric bud interacts with this tissue to induce glomerular formation (including distal convoluted tubules).
○ Ureteric bud and metanephric blastema reciprocally induce each other to form the kidney.
○ Aberrant interaction → congenital malformations: renal agenesis, multicystic dysplastic kidney.
Congenital Abnormalities
- Ureteropelvic junction (UPJ) obstruction: Most common pathologic cause of prenatal hydronephrosis; last part of ureter to canalize.
- Potter Sequence (due to severe oligohydramnios):
○ Renal failure (bilateral renal agenesis, ARPKD, obstructive uropathy)
○ Oligohydramnios (triggers the rest)
○ Pulmonary hypoplasia (fatal due to respiratory failure)
○ Twisted face (low-set ears, retrognathia, flat nose)
○ Extremity defects (limb deformities)
Created with BioRender.com
Commonly tested: ACEi/ARBs are teratogens, can cause renal agenesis, and result in Potter Sequence.
- Horseshoe kidney: Inferior poles of both kidneys fuse; trapped under inferior mesenteric artery (IMA) → remains low in abdomen.
○ Associated with Turner syndrome, trisomy (13, 18, 21).
○ ↑ Risk of hydronephrosis, renal stones, infection, Wilms tumor. - Posterior urethral valve: Male-only membrane remnant in prostatic urethra → bilateral hydronephrosis, dilated bladder (most common cause of bladder outlet obstruction in male infants).
How it is tested: A newborn male is diagnosed with bilateral renal agenesis. Which of the following findings is most likely to be present? Answer: Any of the Potter sequence features.
A 3-day-old male presents with abdominal distension and decreased urine output. Ultrasound reveals bilateral hydronephrosis and a dilated bladder. What is the most likely diagnosis? Answer: Posterior urethral valve
Renal Blood Flow
- Renal medulla has less blood flow than cortex → more prone to ischemia (e.g., ATN).7
- Left renal vein receives blood from the left suprarenal + left gonadal veins.
- Commonly tested: Obstruction of the left renal vein (e.g., Renal Cell Carcinoma) → Congestion of the left kidney and the left gonadal vein → left-side varicocele.
Ureters
- Path: Arises from renal pelvis → under gonadal arteries → over common iliac artery → under uterine artery/vas deferens.
- Clinical Correlation:
○ Ligation of uterine/ovarian vessels may damage ureter → obstruction or leak.
○ 3 Common points of ureteral obstruction:
§ Ureteropelvic junction
§ Pelvic inlet
§ Ureterovesical junction
A patient undergoes a total abdominal hysterectomy. After surgery, she develops flank pain and hydronephrosis. What structure was most likely injured? Answer: Ureter. Remember, urine in the abdomen leads to distension but doesn’t cause pain or peritonitis.
Vesicoureteral Reflux (VUR)
- Retrograde flow of urine from bladder → upper urinary tract.
○ Primary: Due to abnormal ureter insertion into bladder.
○ Secondary: Due to high bladder pressure (e.g., posterior urethral valves, neurogenic bladder). - Increases risk of recurrent UTIs, pyelonephritis, renal scarring.
Key regulators of filtration:
Prostaglandins Dilate Afferent arteriole.
NSAIDs inhibit prostaglandins → afferent arteriole constriction → ↓ RPF, ↓ GFR, ↓ FF.
Angiotensin II Constricts Efferent arteriole.
ACE inhibitors inhibit Angiotensin II → efferent arteriole dilation → ↑ RPF, ↓ GFR, ↓ FF.
Plasma volume can be measured by radiolabeled albumin.
Extracellular volume can be measured by inulin or mannitol.
How it is tested: A 55-year-old man with hypertension is started on lisinopril. A week later, his serum creatinine increases significantly. What is the most likely cause? Answer: Efferent arteriole dilation (Starting ACEi/ARB in a patient with renal arterial stenosis can result in a rise in serum creatinine and hyperkalemia)
Nephron Transport
Proximal Convoluted Tubule (PCT)
- Reabsorbs glucose, amino acids, Na⁺, Cl⁻, HCO₃⁻, K⁺, PO₄³⁻, uric acid, water.
- Generates & secretes NH₃ (derived from glutamine, buffer for H⁺ excretion).
- Key regulators:
○ PTH inhibits Na⁺/PO₄³⁻ cotransporter → ↑ PO₄³⁻ excretion.
○ Angiotensin II stimulates Na⁺/H⁺ exchange → ↑ Na⁺, HCO₃⁻, and H₂O reabsorption.
Loop of Henle
- Thin Descending Limb:
○ Passively reabsorbs H₂O. Concentrates urine. - Thick Ascending Limb:
○ Actively reabsorbs Na⁺, K⁺, Cl⁻ (via NKCC2 transporter).
○ Indirectly reabsorbs Mg²⁺, Ca²⁺.
○ Loop diuretics inhibit NKCC2 → loss of Na⁺, K⁺, Cl⁻, Mg²⁺, and Ca²⁺.
Distal Convoluted Tubule (DCT)
- Reabsorbs Na⁺, Cl⁻.
- PTH → ↑ Ca²⁺ reabsorption via Na⁺/Ca²⁺ exchanger.
- Thiazide diuretics block Na⁺/Cl⁻ cotransporter → ↑ Ca²⁺ retention.
Collecting duct
The highest concentration of urine can be achieved here.
- Aldosterone:
○ ↑ Na+ reabsorption, ↑ K+/H+ excretion (via α-intercalated cells).
○ Upregulates ENaC, Na⁺/K⁺ pump.
○ Amiloride/triamterene block ENaC.
○ Spironolactone/eplerenone block aldosterone receptor. - ADH:
○ Acts on V₂ receptors → inserts aquaporin H₂O channels → ↑ H₂O reabsorption.
How it is tested: A 45-year-old man with cirrhosis and ascites is prescribed a medication that blocks aldosterone receptors in the collecting tubule. Which electrolyte abnormality is contraindicated when starting this medication? Answer: Hyperkalemia.
Endocrine Functions of the Kidney
- Erythropoietin: Released in response to hypoxia (stimulates RBC production)
- Calciferol (Vitamin D activation): PCT converts 25-OH Vit D → 1,25-(OH) ₂ Vit D via 1α-hydroxylase (activated by PTH).
Commonly tested: In sarcoidosis, overactivation of 1α-hydroxylase in macrophages results in hypercalcemia.
- Prostaglandins: Vasodilate afferent arteriole → ↑ Renal Blood Flow (NSAIDs block this).
Hormonal Regulation of Potassium (K+)
- K+ shifts into cells (↓ serum K+):
○ Alkalosis, β-agonists, insulin - K+ shifts out of cells (↑ serum K+):
○ Acidosis, hyperosmolarity, cell lysis (burns, rhabdomyolysis), digoxin toxicity.
How it is tested: A 65-year-old man with chronic kidney disease presents with normocytic anemia. What is the most likely cause of his anemia? Answer: Erythropoietin deficiency.
A patient with hypocalcemia has increased PTH levels but normal 25-hydroxy vitamin D. What is the most likely site of dysfunction leading to low 1,25-dihydroxy vitamin D?
Answer: Proximal Convoluted Tubule (PCT) – due to impaired 1α-hydroxylase activity.
A patient is hospitalized for a severe asthma attack. One day later she develops weakness. Serum K+ level is 2.9. What drug caused her problem with which mechanism? Answer: A β-agonist. Shifted potassium into cells.
Renin Angiotensin Aldosterone System (RAAS)
- Renin (JG cells) → secreted in response to ↓ BP, ↑ sympathetic tone (β₁), ↓ NaCl delivery (macula densa). Note: Beta-Blockers can block renin release.
- Angiotensin II
○ Vasoconstricts efferent arteriole → preserves GFR in low-volume states.
○ Stimulates Na+/H+ exchange in PCT → ↑ Na+, HCO3-, H2O reabsorption. - Aldosterone → ↑ Na+ reabsorption, ↑ K+/H+ excretion.
- ANP, BNP → Vasodilates afferent arteriole, constricts efferent → ↑ GFR, natriuresis.
High Yield Electrolyte Disturbance symptoms
- Low serum Na⁺: Confusion, Coma, Seizures.
- Low serum K⁺: cramps, spasms, weakness.
- High serum K⁺: Wide QRS & peaked T waves on ECG, arrhythmias.
- Low serum Ca²⁺: Seizures, ↑QT, twitching (Chvostek sign), spasm (Trousseau sign).
- High serum Ca²⁺: Stones, bones, groans, psychiatric overtones.
- Low serum Mg²⁺: Tetany, torsades de pointes, hypokalemia, hypocalcemia.
Acidosis & Alkalosis
- Check arterial PH. Normal 7.35 – 7.45:
○ ↑ PH → Alkalosis
○ ↓ PH → Acidosis - Determine Primary Disorder:
○ If HCO₃⁻ changes in the same direction as PH: Metabolic
○ If HCO₃⁻ changes in the opposite direction as PH: Respiratory
Created with BioRender.com
Metabolic Acidosis
- Next step: Check anion gap (AG = Na⁺ – (Cl⁻ + HCO₃⁻))
○ ↑ Anion Gap (>12 mEq/L) means a new molecule is causing the acidosis:
Glycols (ethylene glycol, propylene glycol)
§ Glycols (ethylene glycol, propylene glycol)
§ Oxoproline (chronic acetaminophen use)
§ L-lactate (lactic acidosis) commonly tested
§ D-lactate (exogenous lactic acid)
§ Methanol
§ Aspirin (late effect) Also results in respiratory alkalosis.
§ Renal failure
§ Ketones (diabetic, alcoholic, starvation) commonly tested
○ Normal Anion Gap (8–12 mEq/L) means there’s a problem with Cl⁻ or HCO₃⁻:
§ Spironolactone
§ Hyperchloremia/hyperalimentation
§ Addison’s disease, acetazolamide use
§ Renal tubular acidosis
§ Diarrhea
§ Saline infusion
How it is tested: A patient with type 1 diabetes presents with nausea and abdominal pain. Lab results show a metabolic acidosis with high anion gap (they’ll give you numbers. Learn to calculate). Which mechanism increased the anion gap? Answer: Ketogenesis (Creation of ketone bodies)
Metabolic Alkalosis
- Check Urine Cl⁻:
○ Urine Cl⁻ > 20 mEq/L (Saline-Resistant) means kidney is the main problem:
§ Hyperaldosteronism
§ Bartter/Gitelman syndrome
§ Loop/thiazide diuretics (chronic use)
○ Urine Cl⁻ < 20 mEq/L (Saline-Responsive) means kidney is ok:
§ Vomiting
§ Recent diuretic use
§ Antacids
How it is tested: A patient with signs and symptoms of bulimia nervosa has metabolic alkalosis and a urine chloride level <20 mEq/L. What is the diagnosis?
Answer: Saline-responsive metabolic alkalosis due to vomiting.
Respiratory Disorders
- Respiratory Acidosis (Hypoventilation):
○ Causes: Airway obstruction, chronic lung disease, opioids/sedatives, respiratory muscle weakness. - Respiratory Alkalosis (Hyperventilation):
○ Causes: Anxiety, panic attack, hypoxemia, salicylates (early), pulmonary embolism, pregnancy.
Renal Tubular Acidosis:
All types cause non-anion gap metabolic acidosis. Use K+ and Urine PH to differentiate.
| Type 1 (distal) | Type 2 (proximal) | Type 4 | |
|---|---|---|---|
| Defect | ↓ H⁺ secretion | ↓ HCO₃⁻ reabsorption | Aldosterone resistance or ↓ secretion |
| Serum K⁺ | Low | Low | High |
| Urine pH | > 5.5 | < 5.5 | < 5.5 |
How it is tested: A patient presents with non-anion gap metabolic acidosis and hypokalemia. Urine pH is 7. What is the most likely type of RTA? Answer: Type 1 (distal) RTA
Renal Tubular Defects
- Fanconi and Sjogren’s syndromes: mimic type 1 RTA.
- Bartter syndrome (loop defect): mimics chronic loop diuretic use.
- Gitelman syndrome (DCT defect): mimics chronic thiazide use.
- Liddle syndrome: excessive Na⁺ reabsorption, low aldosterone (treat with amiloride).
- SAME: cortisol excess, mimicking aldosterone.
Casts in Urine
Commonly Tested
- Presence of casts → renal or glomerular origin.
- No casts in hematuria/pyuria from bladder cancer, kidney stones, or cystitis.
- Cast matrix: Tamm-Horsfall mucoprotein (urodulin) from renal tubular cells.
- RBC casts: Glomerulonephritis, hypertensive emergency.
- WBC casts: Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.
- Granular casts: Acute tubular necrosis (ATN); “muddy brown” appearance.
- Fatty casts: Nephrotic syndrome; associated with “Maltese cross” sign.
- Waxy casts: End-stage renal disease/chronic kidney disease.
- Hyaline casts: Nonspecific; seen with dehydration, exercise, diuretics.
How it is tested: A hospitalized patient is started on cisplatin. Days later, he develops acute kidney injury. Urinalysis shows “muddy brown” granular casts. What is the most likely diagnosis? Answer: Acute tubular necrosis (ATN)
A patient with new-onset edema has a urinalysis that shows casts with a “Maltese cross” appearance under polarized light. What is the most likely diagnosis?
Answer: Nephrotic syndrome
Kidney Stones
(Treatment of all types: increase fluid intake.)
- Calcium oxalate (80% of stones) → radiopaque, envelope/dumbbell-shaped.
○ most common cause: Idiopathic hypercalciuria
○ Causes: hypocitraturia, ethylene glycol, vitamin C overdose, Crohn’s.
○ Treatment: thiazides, citrate, low-sodium diet. - Calcium phosphate → radiopaque, wedge-shaped prism.
○ Treatment: low-sodium diet, thiazides. - Struvite (Ammonium magnesium phosphate) → radiopaque, coffin-lid shape.
○ Caused by urease + bacteria (Proteus, Klebsiella, Staph saprophyticus).
○ Staghorn calculi
○ Treatment: eradicate infection, surgery. - Uric acid → radiolucent, rhomboid/rosette-shaped.
○ Risk: low pH, hyperuricemia (gout, leukemia).
○ Treatment: alkalinization, allopurinol. - Cystine → faintly radiopaque, hexagonal shape. Defect in COLA transporter.
○ Tx: low-sodium diet, alkalinization, chelators.
How it is tested: A patient with recurrent UTIs has large staghorn calculi. What is the most likely pathogen? Answer: Proteus mirabilis, Klebsiella, or Staph saprophyticus.
Hydronephrosis
- Dilation of renal pelvis/calyces.
- Causes: obstruction (stones, BPH, congenital, cancer, retroperitoneal fibrosis, VUR).
- Dilation proximal to obstruction. If bilateral, can cause ↑ creatinine.
- If unilateral, problem in the ureter or kidney. If bilateral, problem usually in bladder or urethra.
Urinary Incontinence
- Stress incontinence → Urethral hypermobility/sphincter deficiency → leak with ↑ intra-abdominal pressure. Treatment: Kegels, weight loss, pessaries.
- Urge incontinence → Detrusor overactivity → leak with urgency. Treatment: bladder training, antimuscarinics (oxybutynin), mirabegron.
- Overflow incontinence → Incomplete emptying (detrusor underactivity or obstruction) → leak with overfilling. ↑ Postvoid residual. Treatment: catheterization, α-blockers for BPH.
How it is tested: A woman leaks urine when she coughs or sneezes. What is the most likely cause? Answer: sphincter deficiency or pelvic floor weakness.
A patient reports frequent sudden urges to urinate and occasional leakage. What is the treatment? Answer: Antimuscarinics (first, we rule out UTI)
Acute Cystitis
Bladder inflammation. Symptoms: suprapubic pain, dysuria, frequency, urgency (no systemic signs). Causes:
- E. coli (most common)
- Staph saprophyticus (sexually active women)
- Klebsiella, Proteus (ammonia scent)
Labs: Leukocyte esterase (+), Nitrites (+) (for gram-negative Enterobacteriaceae)
Sterile pyuria: Consider urethritis, not cystitis (Chlamydia, Gonorrhea).
Treatment: TMP-SMX, nitrofurantoin, cefixime (kids).
How it is tested: A sexually active young woman presents with dysuria, frequency, and suprapubic pain. Urinalysis shows positive leukocyte esterase and nitrites. What is the most likely pathogen? Answer: Escherichia coli, Remember, Staphylococcus saprophyticus is Nitrite negative.
Pyelonephritis
Neutrophilic infiltrate in renal interstitium. Symptoms: fever, flank pain, nausea/vomiting, WBC casts.
Causes: Ascending UTI (E. coli most common), hematogenous spread.
Risk factors: Catheters, obstruction, VUR, diabetes, pregnancy.
Complications: Chronic pyelonephritis, papillary necrosis, perinephric abscess, urosepsis.
Treatment: Antibiotics (3rd gen cephalosporin, Ciprofloxacin to cover gram negative → E.Coli).
Findings suggestive of chronic or recurrent pyelonephritis:
- Corticomedullary scarring, blunted calyces, thyroidization (eosinophilic casts in tubules).
- Risk factor: vesicoureteral reflux
Acute Kidney Injury
Pre-renal azotemia: Hypovolemia, ↓ cardiac output, ↓ effective circulating volume (HF, liver failure). Labs: Urine osm >500, FeNa <1%, BUN/Cr >20.
Intrinsic renal failure: ATN (ischemia, nephrotoxins), acute interstitial nephritis, glomerulonephritis, vasculitis. Labs: Urine osm <350, FeNa >2%, BUN/Cr <15.
Post-renal azotemia: Outflow obstruction (stones, BPH, neoplasm). Labs vary.
Acute Interstitial Nephritis
Drug-induced hypersensitivity reaction. Classic causes: NSAIDs, diuretics, PPIs, rifampin, penicillins, sulfa drugs. Histopathology: Mononuclear cell infiltrate
Symptoms: Fever, rash, pyuria (eosinophils + wbc casts), CVA tenderness.
How it is tested: A patient started on NSAIDs develops fever, rash, and eosinophilia with WBC casts in the urine. What is the most likely diagnosis? Answer: Acute interstitial nephritis.
Acute Tubular Necrosis
Most common intrinsic AKI in hospitalized patients. Key finding: granular “muddy brown” casts. Causes:
- Ischemic: ↓ RBF (hypotension, shock, sepsis, HF, pre-renal azotemia).
- Nephrotoxic: Ethylene glycol, Aminoglycosides, contrast, lead, cisplatin, myoglobinuria.
Stages:
- Inciting event
- Maintenance (oliguric, risk of hyperkalemia, metabolic acidosis, uremia)
- Recovery (polyuric, risk of hypokalemia, renal wasting)
Renal Papillary Necrosis
Sloughing of necrotic renal papillae → gross hematuria. Associated with:
- Sickle cell disease/trait
- Acute pyelonephritis
- NSAIDs
- Diabetes mellitus
How it is tested: A patient with sickle cell disease presents with gross hematuria and sloughing of renal papillae. What is the most likely diagnosis? Answer: Renal papillary necrosis
Polycystic Kidney Diseases
ADPKD: PKD1/2 mutation/autosomal dominant. Adult form.
- Bilateral renal cysts, HTN, berry aneurysms, hepatic cysts.
- Treatment: ACEi, transplant
ARPKD: PKHD1 mutation/autosomal recessive. Infantile form.
- Collecting duct cysts, hepatic fibrosis, Potter sequence.
How it is tested: A 45-year-old patient presents with hypertension and bilateral renal cysts on ultrasound. His father died of hepatic failure at age 45. What is the most likely diagnosis?Answer: Autosomal dominant polycystic kidney disease (ADPKD)
Renovascular Disease
Renal artery stenosis (RAS): ↓ renal perfusion → ↑ renin → HTN.
- Causes: Atherosclerosis (older men, smokers), fibromuscular dysplasia (young/middle-aged women).
- Presentation: Resistant HTN, epigastric/flank bruit.
How it is tested: An elderly man with a history of smoking has resistant hypertension. On physical exam, an epigastric bruit is heard. What is the most likely diagnosis? Answer: Renal artery stenosis due to atherosclerosis.
A 35-year-old woman presents with uncontrolled hypertension. Imaging reveals “string of beads” appearance of the renal artery. What is the most likely diagnosis?
Answer: Fibromuscular dysplasia
Renal Cell Carcinoma
Clear cells with lipid/glycogen accumulation. Golden-yellow gross appearance.
Paraneoplastic syndromes: PTHrP (hypercalcemia), EPO (polycythemia), ACTH, renin.
Associated with VHL gene (chromosome 3).
Wilms Tumor
Known as nephroblastoma, a rare kidney tumor in children.
2-4 years old child + abdominal mass that does NOT cross the midline + hematuria → Wilms tumor
Bladder Cancer
Urothelial carcinoma: Painless hematuria. Risks: Smoking, aniline dyes, cyclophosphamide.
Squamous cell carcinoma: Chronic irritation (stones, Schistosoma haematobium, chronic cystitis).
How it is tested: A 60-year-old man with a history of smoking presents with hematuria, weight loss, and a left-sided varicocele (They may show a microscopic image of Clear Cell Carcinoma, the most common type of RCC). What is the most likely diagnosis? Answer: RCC
How it is tested: A 65-year-old male smoker presents with painless hematuria. Urinalysis confirms hematuria and is otherwise unremarkable. What is the most likely diagnosis?
Answer: Urothelial carcinoma of the bladder
Nephritic vs Nephrotic Syndrome
Nephritic Syndrome: Glomerular inflammation → GBM damage → RBC casts, hematuria, mild proteinuria. Causes:
Post-streptococcal GN, IgA nephropathy, Alport syndrome, RPGN.
Nephrotic Syndrome: Podocyte damage → massive proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, edema. Causes:
Minimal change disease, membranous nephropathy, FSGS, amyloidosis, diabetic nephropathy.
Nephritic Syndromes
- Post-streptococcal GN: Type III hypersensitivity, subepithelial humps, starry sky IF.
More than 2 weeks after tonsillitis or skin infection. low complement levels. Anti ASO +
- IgA Nephropathy (Berger Disease): Mesangial proliferation, IgA deposits, Less than 1 week after URI/GI infection.
- Rapidly Progressive GN (RPGN): Crescents, fibrin, Goodpasture (linear IgG), Pauci-immune (ANCA-associated).
- Diffuse Proliferative GN: Seen in SLE, wire-loop capillaries, subendothelial IgG/C3 deposits.
- Alport Syndrome: Type IV collagen defect, basket-weave GBM. Hearing loss. Eye problems.
Can’t see, can’t pee, can’t hear a bee.
- Membranoproliferative GN: GBM splitting, tram-track, associated with HBV/HCV.
Nephrotic Syndromes
- Minimal Change Disease: Effacement of foot processes, most common in children, responds to steroids. Normal on light microscopy.
- FSGS: Segmental sclerosis, common in African Americans, HIV, heroin use.
- Membranous Nephropathy: Thickened capillary walls, subepithelial “spike and dome,” associated with solid tumors,HBV, HCV, and SLE.
- Amyloidosis: Apple-green birefringence, Congo red stain, associated with chronic inflammatory diseases.
- Diabetic Nephropathy: GBM thickening, Kimmelstiel-Wilson nodules, mesangial expansion, ACE inhibitors slow progression.
How it is tested: A child presents with periorbital edema and proteinuria >3.5 g/day. Electron microscopy shows effacement of foot processes. What is the most likely diagnosis?Answer: Minimal change disease
A child develops hematuria and facial swelling two weeks after a sore throat. Immunofluorescence shows granular deposits. What is the most likely diagnosis? Answer: Post-streptococcal glomerulonephritis
A patient with hepatitis B presents with nephrotic syndrome. Biopsy shows subepithelial immune deposits with “spike and dome” appearance. What is the most likely diagnosis? Answer: Membranous nephropathy
Diuretics: Commonly tested: site of action
- Mannitol (Osmotic Diuretic) – Proximal convoluted tubule
Use: Drug overdose, elevated intracranial/intraocular pressure.
Adverse Effects: Dehydration, hypo/hypernatremia, pulmonary edema.
- Acetazolamide (Carbonic Anhydrase Inhibitor) – Proximal convoluted tubule
Use: Glaucoma, Idiopathic intracranial hypertension, altitude sickness.
Adverse Effects: Proximal RTA, paresthesia, NH₃ toxicity, sulfa allergy, hypokalemia.
- Loop Diuretics (Furosemide, Bumetanide, Torsemide) – Thick ascending loop
Inhibit Na/K/2Cl cotransporter.
Use: HF, cirrhosis, nephrotic syndrome, pulmonary edema, hypercalcemia.
Adverse Effects: Ototoxicity, hypokalemia, metabolic alkalosis, nephritis, gout.
- Thiazide Diuretics (Hydrochlorothiazide, Chlorthalidone) – Distal convoluted tubule
Use: Hypertension, HF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis.
Adverse Effects: Hypokalemia, hyponatremia, hyperglycemia, hyperlipidemia,
Hyperuricemia, hypercalcemia.
- K⁺-Sparing Diuretics (Spironolactone, Eplerenone, Amiloride, Triamterene) – Collecting duct
Use: Hyperaldosteronism, HF, hepatic ascites, nephrogenic DI (amiloride), antiandrogen (spironolactone). If spironolactone results in gynecomastia, switch to eplerenone.
Adverse Effects: Hyperkalemia, gynecomastia, metabolic acidosis.
Diuretics: Effects on Urine Electrolyte
- Carbonic anhydrase inhibitors: ↑ Na⁺, ↑↑ HCO₃⁻, ↑↑ K⁺, ↓ H⁺ → Acidosis.
- Loop diuretics: ↑↑ Na⁺, ↑ K⁺, ↑ Cl⁻, ↑↑ Ca²⁺, ↑ Mg²⁺, ↑ H⁺ → Alkalosis.
- Thiazides: ↑ Na⁺, ↑ K⁺, ↑ Cl⁻, ↓↓ Ca²⁺, ↓ Mg²⁺, ↑ H⁺ → Alkalosis.
- K⁺-sparing diuretics: ↑ Na⁺, ↓ K⁺, ↑ Cl⁻, +/- Ca²⁺, +/- Mg²⁺, ↓ H⁺ → Acidosis.
How it is tested: A patient with cerebral edema is given a diuretic that increases plasma osmolality and promotes free water excretion. What is the most likely drug? Answer: Mannitol
A heart failure patient with edema is started on a new medication recently. He develops hearing loss after one week. What is the most likely drug? Answer: Furosemide (loop diuretic)
RAAS Inhibitors
ACE Inhibitors (Captopril, Enalapril, Lisinopril, Ramipril)
- Mechanism: ↓ AT II → ↓ GFR (prevents constriction of efferent arterioles); prevents bradykinin inactivation in lungs.
- Use: Hypertension, HF (↓ mortality), proteinuria, diabetic nephropathy.
- Adverse Effects: Cough, angioedema, ↑ creatinine, hyperkalemia, hypotension, teratogenic.
ARBs (Losartan, Candesartan, Valsartan)
- Mechanism: Selectively block AT II receptor, similar to ACEi but no bradykinin effect.
- Use: Hypertension, HF, proteinuria, diabetic nephropathy.
- Adverse Effects: Hyperkalemia, ↓ GFR, hypotension, teratogenic.
Aliskiren (Direct Renin Inhibitor)
- Mechanism: Blocks angiotensinogen to angiotensin I conversion.
- Use: Hypertension.
- Adverse Effects: Hyperkalemia, ↓ GFR, hypotension, contraindicated with ACEi/ARBs or in pregnancy.
How it is tested: A diabetic patient has blood pressure of 150/90 mmHg. What is the best first step treatment for hypertension? Answer: ACE inhibitor. Slows diabetic nephropathy.
A patient on an ACE inhibitor develops a persistent dry cough. What is the best alternative medication? Answer: Angiotensin receptor blocker (ARB)
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